ជំងឺបក្សី (ភាសាអង់គ្លេស)

ពីវិគីភីឌា
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INTRODUCTION

Responding to demand from the international poultry industry, We have created a listing of all major poultry diseases.

For every disease the cause(s), clinical signs, diagnosis and treatment and methods for prevention are explained, often with illustrative pictures. The diseases are categorised alphabetically.

Note: products mentioned may not be registered in the country of the reader

Simply select a letter and choose the disease you want to know more about.

មាតិកា

AFLATOXICOSIS[កែប្រែ]

Note:

  • Occurrence: Worldwide
  • Species affected: All species
  • Age affected: All, young most susceptible

Causes:

Consumption of high moisture grains containing aflatoxins produced by Aspergillus flavus, A. parasiticus, Penicillium puberulum.

Effects:

Sleepiness, depression, paleness, reduced egg production, fertility and hatchability. Depressed growth, feed conversion, increased bruising and downgrading can occur.

Detailed cause:

Muycotoxins are toxin metabolic byproducts of fungal growth on grains. High moisture content of grains can lead to fungal growth and toxin production. Fungi can produce toxins before or after grain harvest. Drought and insect damage to grain increase susceptibility of grain to fungal growth. All species and ages can be affected. The disease course can be acute to chronic dependent upon does, duration of exposure and age of the bird. Acute disease seen if young are given high amounts (1,000 ppb of Aflatoxin B1). Chronic disease seen in birds older than 5 weeks, given low levels (ppb) for several weeks.

Consumption of feed containing grains (usually corn) which contain toxins causes the disease. Aflatoxins are a group of related poisons produced by several fungi: Aspergillus flavus, A. parasiticus and Penicillium puberulum. (Afla comes from Aspergillus flavus "A" for Aspergillus and "fla" for flavus). The most common and toxic aflatoxin is aflatoxin B1 followed by B2, G1 and G2. Aflatoxicol, flatoxitrem and cyclopiazonic acid are other toxic metabolites produced by these fungi on mouldy corn. The longer grain is stored, especially under warm, moist conditions, the more fungi grow and can produce toxins. It is a feed storage problem. Aflatoxins are immunodepressive and carceinogenic. 1.0 ppm or greater of AF B1 can produce morbidity and mortality; 500-1,000 ppb can reduce weight grain and feed efficiency; and 200-500 ppb can produce immune depression.

Clinical signs:

Signs include sleepiness, depression, paleness. Reduced egg production, fertility and hatchability. Depressed growth, feed conversion and increased bruising and downgrading can occur.

Postmortem lesions:

Lesions include scattered haemorrhage in the muscles, skin and intestinal tract, fluid around the heart, enlarged pale kidneys, and pale enlarged fatty livers with haemorrhage and anaemia.

Diagnosis:

The clinical history, and gross and microscopic lesions are important. Microscopically, the liver shows fatty change, swollen hepatocytes and bile duct hyperplasia.

An ultra violet (UV)(black) light can be used to test corn for the presence of cogic acid (blue green fluorescence) producing fungi.

Feed analysis using column chromatography is the only method for a definite diagnosis. Test kits are available for aflatoxin B1 using ELISA methodology or minicolumns.

It simulates infectious bursal disease (IBD), fatty liver syndrome, and malabsorption syndrome.

Detailed treatment:

Feed can be prevented from growing mould by incorporating a mould inhibitor. Aluminosilicates in the feed such as zeolites will bind the inactive aflatoxin. Quality control of feeds is important. Check grains for greater than 16% moisture.

Contaminated feed should be diluted with noncontaminated grain or treated with ammonia, which inactivates aflatoxin. Heat-treatment will kill the fungi. Gentian Violet kills fungi and binds aflatoxin. In general low moisture corn (below 14%) should be fed. Mouldy corn should not be added to the finished feed. Contaminated feed may be given to older pullets, which are less susceptible.

Two feed bins at farm will reduce grain and feed storage time, which reduces fungal growth and toxin formation.

Increasing the protein content of feed by 1%, increasing vitamin and mineral content of feed and adding Gentian violet to feed have a sparing effect on aflatoxin-induced disease.

AORTIC RUPTURE (DISSECTING ANEURISM, TURKEY HEART ATTACK)[កែប្រែ]

Note:

  • Occurrence: Worldwide
  • Species affected: Fast-growing, healthy, heaviest turkeys.
  • Age affected: 7-24 weeks. Higher incidence in males.

Causes:

Unknown mode of transmission, high blood pressure, genetics and/or nutrition may play a role.

Effects:

Heavy, fast-growing birds die suddenly due to internal haemorrhage and flop on their backs.

Detailed causes:

Fast-growing, healthy, heaviest turkeys and broilers may die suddenly between 7 and 24 weeks of age. The disease has a higher incidence in males. The disease is non-contagious, and is caused by the development of intimal plaques in the abdominal aorta. Higher blood pressure in involved, and so genetics and/or nutrition may play a role.

Special note:

Genetic strains differ in blood pressure level and incidence of the disease. Reduction in incidence due to breeding has been seen.

Clinical signs:

Heavy fast growing birds die suddenly due to internal haemorrhage and flop on there backs. Mortality rarely reaches 2% of the flock. It is most common between 12 and 16 weeks of age.

Postmortem lesions

A dissecting aneurysm close to the kidneys or testes is seen with blood in the abdominal cavity. The head, skin and musculature are anaemic. Occasionally, blood will run out of the mouth or the oral cavity will be blood-stained.

Diagnosis:

There is a longitudinal slit in the aorta between the external iliac and the sciatic arteries. A marked intimal thickening or a large fibrous intimal plague often occurs in the region or rupture. These microscopic lesions with clinical signs are characteristic.

Treatment and control:

Slowing growth rate with reduced energy level in the feed, or feed restriction using a lighting programme, or the use of mash feed. These management factors will reduce the disease, but at a cost of reduced growth.

Reserpine in the feed can control the condition.

ARIZONOSIS[កែប្រែ]

Causes:

Bacterium- Salmonella arizona.

Effects:

Same as for other Salmonella infections- Diarrhoea, lameness, somnolence (sleepiness), laboured breathing, blindness and mortality. Mortality up to 100%, peaking at 7-10 days. Tremors, convulsions and twisted necks may also be seen.

Detailed causes:

Arizonsis occurs in young turkeys and is caused by the gram negative, flagellate bacterium Salmonella Arizona. The disease is transmitted in the same way as other salmonella species, ie. from bird to bird and between farms. Common vectors include birds, rodents and sometimes reptiles. Spread via the transovarian route can also occur.

Special note

Not as common as paratyphoid.

Clinical signs:

Signs are the same as for other Salmonella. Opaque eyes (blindness), tremors, convulsions, and twisted necks may be seen.

Postmortem lesions

Lesions are the same as for Salmonella pullorum, which include bacteria septicaemia; peritonitis, and retained yolk sacs.

Congested (filled with blood) duodenum, mottled (white necrotic spots) liver, caseous plugs in caeca, and caseous air sacs can be seen.

Diagnosis:

The organisms must be cultured from post mortem lesions, egg yolk etc. on brilliant green agar for a definitive diagnosis.

Agglutination or ELISA tests using sera from breeders can confirm the presences of S. Arizona.

It simulates pullorum, E. coli and typhoid.

Treatment and control:

Prevention

Prevention is the same as for salmonella. Biosafety measures are a common requirement in many countries. Bacterin for turkey breeders prevents egg transmission. Egg and hatchery sanitation are important.

Breeders should be tested and those that are serologically positive should be slaughtered.

Vector control helps control spread of the organism.

Treatment

Treatments will reduce clinical problems, but birds will remain carriers. SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments. Gentamicin and spectinomycin can be given to day-old-chicks by SQ injection.

ASCARIDIA GALLI INFECTION[កែប្រែ]

Causes:

Parasitic nematode worm- Ascaridia galli.

Effects:

Weight depression. In severe infections, intestinal blockage can occur. At high levels of infection, there is loss of blood, reduced blood sugar content, retarded growth and greatly increased mortality. Parasite can occasionally be seen in commercial eggs.

Detailed causes:

This parasitic nematode worm exists in the lumen of the intestine, occasionally in the oesophagus, crop, gizzard, oviduct, and body cavity.

The life history is simple and direct. Infective eggs hatch in either the proventriculus or the duodenum of the susceptible host. The young larvae, after hatching, live free in the lumen of the posterior protion of the duodenum for the first 9 days, then penetrate the mucosa and cause haemorrhages. The young worms enter the lumen of the duodenum by 17 or 18 days and remain there until maturity, at approximately 28-30 days after ingestion of embryonated eggs. Larvae may enter the tissues as early as the 1st day and remain there as long as 26 days after infection. The majority spend from 8-17 days in the intestinal mucosa. A few of the larvae penetrate deep into the tissue, while the majority undergo only a brief and shallow association with the intestinal mucosa during the "tissue phase". A. galli eggs ingested by grasshoppers or earthworms hatch and are infective to chickens, although no development of the larvae occurs.

Under optimum temperature and moisture conditions, eggs in the droppings become infective in 10-12 days; under less favourable conditions a longer time is necessary. Eggs are quite resistant to lower temperatures.

Clinical signs:

A. galli infection causes weight depression in the host, which correlates with increasing worm burden. In severe infections, intestinal blockage can occur. The nutritional state of the host is also important, since weight depression is greater with high dietary levels of protein (15%) than with low levels (12.5%). Chickens infected with a large number of ascarides suffer from loss of blood, reduced blood sugar content, increased urates, shrunken thymus glands, retarded growth and greatly increased mortality. However, no effects of infection on blood protein level, packed-cell volume, or haemoglobin levels were found. A. galli can also have detrimental effedts through interaction (synergism) with other disease conditions such as coccidiosis and infectious bronchitis. A. galli has also been shown to contain and transmit aian reoviruses.

One of the most striking effects of infection, at least from an aesthetic standpoint, is the occasional finding of this parasite in commercial eggs. Presumably the worms migrate up the oviduct via the cloaca, with subsequent inclusion in the egg. Infected eggs can be detected by candling, thus eliminating a potential consumer complaint.

The age of the host and severity of exposure play a role in A. galli infections. Chickens 3-months or older manifest considerable resistance to infection with A. galli. In older fowl, larvae are recovered that have undergone little or no development since emerging from the egg. Larval development is arrested in the third stage at high dose rates as a result of resistance rather than a dessity-dependent phenomenon. Heavier broiler breeds are more resistant to ascarid infections than are the lighter White Leghorns.

Diagnosis:

Worms have a large, thick, yellowish white head with 3 large lips. The male is 50-76 mm long, 490-1.21 mm wide. It has a preanal sucker oval or circular, with strong chitinous wall with a papilliform interruption on its posterior rim; tail with narrow caudal alae or membranes and 10 pairs of papillae. The first pair of ventral caudal papillae are anterior to the preanal sucker, the fourth pair are widely separated (compare with A. dissimillis); spicules nearly equal and narrow and end blunt with a slight indentation. The female is 60-116 mm long, 900-1.8 mm wide; the vulva is in the anterior part of the body, eggs are elliptical, thick-shelled and not embryonated at time of deposition.

Treatment and control:

Control

Modern poultry practices, especially confinement-rearing of broilers and pullets and caging of laying hens, have significantly influenced the quantity and variety of nematode infections in poultry. Many that caused extensive problems in backyard flocks are seldom seen in commercial operations. Others such as Ascaridia are still commonly found in commercial birds.

For most nematodes, control measures consist of sanitation and breaking the life cycle rather than chemotherapy. Confinement-rearing on litter largely prevents infections with nematodes using outdoor intermediate hosts such as earthworms or grasshoppers. Conversely, nematodes with direct life cycles or those that utilise indoor intermediate hosts such as beetles may prosper. Treatment of the soil or litter to kill intermediate hosts may be beneficial. Insecticides suitable for litter treatment include carbaryl, tetrachlorvinphos (stirofos), or Ronnel®, Safecide®. Treatment is carried out usually only between grow-outs. Extreme care should be taken to ensure that feed and water are not contaminated.

Treatment of range soil to kill ova is only partially successful. Changing litter can reduce infections, but treating floors with oil is not very effective. After the old litter has been removed, spraying with permethrin or a mixture of Rabon and Vapona has proved effective for beetle control.

Raising different species or different ages of birds together or in close proximity is bad practice with regards to parasites. Adult turkeys, which are carriers or gapeworms, can transmit the disease to young chicks or pheasants, although older chickens are almost resistant to infection.

None of the products mentioned are allowed in NL, nor to the best of our knowledge in western Europe.

Treatment

Currently used in chickens are Hygromycin B (at a level of 0.00088-0.00132%) or coumaphos in feed for replacements (0.004%) or layers (0.003%), Piperazine compounds in feed or water have been widely adopted as a method of treatment for ascaridia, since they are practically non-toxic. Piperazine may be administered to chickens in the feed (0.2-0.4%) or water (0.1-0.2%), or as a single treatment (50-100 mg/bird). A high concentration of piperazine in contact with worms at a given time is very important for maximum elimination, therefore, to be most effective it should be consumed by birds in a period of a few hours. Piperazine in drinking water is the most practical method of application for commercial flocks. Since piperazines are available as a wide variety of salts, the level should be calculated on the basis of milligrams of active piperazine. A combination of piperazine (0.11%) and phenothiazine (0.50-0.56%) as a 1-day treatment is only used for removal of both Heterakis and ascarids.

None of these products are registered in the US, where only Flubenol is used as a treatment. 

ASCITES (WATER BELLY, RIGHT VENTRICULAR FAILURE)[កែប្រែ]

Causes:

Non-contagious. Influenced by genetics, breeding, nutrition, growth rate, ambient temperature and oxygen content of the air.

Effects:

Water-belly, abdominal distension, reluctance to move, dyspnoea and cyanotic lesions seen. Affected birds are smaller than normal, and listless with ruffled feathers. Mortality ranges from 0.5-2.0% of the flock.

Detailed causes:

A chronic or acute disease prominent in young, fast growing broilers, ascites is no longer a disease confined to areas of high altitude.

Hypoxia (lack of oxygen) is caused by many agents and leads to constriction of arteries, inducing increased pulmonary arterial pressure which results in right ventricle hypertrophy. The right ventricular valve becomes weak (flabby), which causes back flow of blood and fluid (ascites) in tissues.

It occurs more in males. Hypoxia caused by altitude or gas fumes, carbon monoxide from brooders, worse in winter (tight house), stress of mycotoxins, toxic fat, increased salt in the diet and/or coal tar disinfectants, causes ascites. Respiratory disease can aggravate the problem. It is an important cause of broiler mortality at 5-7 weeks of age, in any area with fast growing broilers, but more so on high altitude. Lighting programmes (reduced photoperiod) to reduce growth rate during the first 2 weeks of age can reduce mortality due to ascites, flip over syndrome and leg problems.

Feeding mash feed instead of pellets also helps to reduce the problem.

Mode of transmission

It is non-contagious and influenced by genetics, breeding, nutrition, growth rate, ambient temperature and amount of oxygen in the air.

Clinical signs

Water belly, abdominal distension, reluctant to move, dyspneic and cyanotic lesions are seen. Affected birds are smaller than normal and listless with ruffled feathers. Mortality ranges from 0.5-20% of the flock.

Postmortem lesions

Water belly (straw-coloured fluid in abdominal cavity), blood clots in lungs, enlargement of right side of the heart, liver scarred, congested or mottled with a greyish capsule and irregular surface and shrunken and the lungs are congested, oedematous and haemorrhagic.

Diagnosis

Clinical signs and postmortem lesions (water belly with enlarged right heart valve) are diagnostic. Microscopically, cartilaginous and osseous nodules occur in the lung, congestion of kidney, oedema, congestion and haemorrhages in the heart, It simulates salt, crotalaria and furazolidone toxicity.

Treatment and control:

Adequate temperature control of the house, good air and litter management, reduced sodium and furazolidone content of diet, and water, feed and/or light restriction with reduce the mortality.

If the altitude cannot be changed, the feed ration should be. A less dense (lower energy) feed practise, mash feeding instead of pellets or use a restrictive lighting programme to reduce growth rate during the first 2 weeks of age. More aeration of the house during the cooler months when gas broilers are in longer use will also help. Keep temperature at recommended level. Too high a temperature can also cause ascites. Control of respiratory disease (MG, IB, TRT, etc) which induce ascites should be carried out.

ASPERGILLOSIS (BROODER PNEUMONIA)[កែប្រែ]

Causes:

Fungal infection caused by Aspergillus fumigatus, A. flavus and A. niger.

Effects:

High mortality, respiratory distress, central nervous dysfunction, sleepiness, inappetance and emaciation. Conjunctivitis and cloudy eyes can be seen.

Detailed causes:

Aspergillosis is mainly seen in young birds as an acute disease. Chronic disease occurs in adults. The fungi Aspergillus fumigatus, A. flavus and A. niger are responsible. It spreads by the aerosol spread of spores, which are common in the hatchery, and less commonly by contaminated dust and litter in the house.

Clinical signs:

Signs include high mortality, respiratory distress (dyspnoea and gasping), central nervous dysfunction (tremors, ataxia, and torticollis) somnolence (sleepy), inappetance, and emaciation (very thin), conjunctivitis and cloudy eyes can be seen.

Postmortem lesions

Yellowish-green or whitish, caseous (cheesy) nodules and/or green, fur-like down in mouth, palate, lungs, trachea, syrinx, viscera, air sacs, brain and eyes may be seen.

Diagnosis:

Fungus can be identified microscopically (20% KOH stain) from culture or special stain of tissues (hyphae, mycelia, conidophores). Isolation of culture in 48 hours on Sabouraud dextrose agar is diagnostic. Stain colony with lactophenol cotton blue to see conidophores. It is similar to colibacillosis, MD, and lymphoid leukosis. Nodules in the lungs and fungal fur-like down in the air sacs are diagnostic.

Treatment and control:

Prevention

Hatchery sanitation includes regular fumigation of eggs, machines and air ducts and regular (monthly) plating of hatchery with media to examine for the presence of fungi. Use clean dry litter and dry cups of nipples to reduce water spills. Quality of the feed is important. An aerosol of thiabenidazole or Clinafarm® pellets can be placed in the hatchery to kill fungus. Formalin fumigation is an effective method to kill Aspergillus in the environment (not in the chicken). This is not allowed in most of the USA.

Treatment

Quaternary ammonium, chlorine, and/or copper sulphate can be added to the water to help reduce the spread of the organism and reduce clinical signs. However, taking preventative measures is more effective.

AVIAN ADENOVIRUS II SPLEENOMEGALY (AAS) (HAEMORRHAGIC ENTERITIS (HE)-RELATED INFECTIONS)[កែប្រែ]

Causes:

Adenovirus is a DNA virus with a diameter of 70-90mm.

Effects:

Paleness, depression, bloody diarrhoea, asphyxia with mortality up to 60%.

Detailed causes:

ASS is caused by a nonenveloped, DNA Adenovirus with icosohedral symmetry of diameter 70-80 mm. there are three serologically distinct avian adenoviruses, which can be differentiated by the AGP test. Serotype I viruses cause IBHV, quail bronchitis, HE and MSDV. Serotype I produces AAS and serotype III virus produces egg drop syndrome. AAS affects chickens of all ages. AAS is spread laterally by the oral route or vertically through the cloaca.

Clinical signs:

Signs include paleness, depression, mortality (to 60%), bloody diarrhoea, and asphyxia (can’t breathe) in AAS.

Postmortem lesions

Lesions include haemorrhages in the gut, liver, proentriculus and gizzard and anaemia. An enlarged mottled spleen and free blood in the intestines can be seen and with MSD oedema and congestion of lungs are also evident.

Diagnosis:

Agar gel precipitin (AGP) test and ELISA can be used to measure antibodies to AAS. Intranuclear inclusion bodies occur in the reticuloendothelial (RE) cells of the spleen. It simulates coccidiosis, VVND, bacteria and fungi.

Treatment and control:

Prevention

Commercial vaccines are available for use at 4 weeks in the water for HE and MSD.

Treatment

None.

AVIAN ENCEPHALOMYELITIS (AE) EPIDEMIC TREMOR[កែប្រែ]

Causes:

Picornavirus.

Effects:

Young birds - drowsiness, lack of coordination, unsteady gait, 5-10% mortality. In adults there is a drop in egg production.

Detailed causes:

AE is a peracute disease affecting all poultry species. Young birds from one and three weeks of age and adult birds in lay are affected. The AE virus is a small RNA picornavirus lacking an envelope. It is spread vertically through the egg for 5-12 days after infection and horizontally by contaminated faeces and fomites.

Clinical signs:

Incubation period is 1-7 days. Signs include trembling of the head, lateral recumbency (birds down on their sides), etaxia, and dull eyes. In chicks, drowsiness, lack of coordination, unsteady gait, and mortality of 5-10% is seen in chicks, a drop in egg production and cataracts (opacity of lens) can be seen in adults.

Diagnosis:

Diagnosis is by virus isolation AE can be confirmed by inoculating susceptible chicks or embryos at 57 days and observing the hatched chicks for clinical signs. Histopathology of the brain (cerebellum), spleen and heart lesions, and virus neutralisation test or ELISA to measure antibodies are helpful. Lateral recumbency in chicks is a presumptive diagnosis for AE. Blindness due to cataracts may develop in chickens that have recovered from an early AE infection during the first three weeks.

Treatment and control:

There is no treatment. Chicks should be purchased only from immune parents. Vaccinate pullets at 10-16 weeks by wingweb or eyedropper. The vaccine spreads rapidly through pullet flocks reared on the floor system (contact with faeces) so all birds do not have to be vaccinated. However, it is advisable to vaccinate all birds when reared in cages or on slats.

AVIAN INFLUENZA (FOWL PLAGUE – BIRD FLU)[កែប្រែ]

Causes:

Type A Orthomyxoviruses.

Effects:

Reportable disease. Respiratory distress, coughing, sneezing, rales, depression, sinusitis, emaciation, feed refusal, nervous signs and diarrhoea. In layers, there is a drop in egg production and shell quality. Mortality is rapid with virulent strains.

Detailed causes:

All birds of all ages are susceptible to avian influenza.

The causative agent, orthomyxovirus, is a single-stranded RNA virus containing 8 segments, and 35 serotypes. Type A viruses are divided into subtypes according to the antigenic nature of haemagglutinin (HA) and neuraminidase (N). The HA is a viral protein which can attacht to the cell surface and the N an enzyme which can brake the virus-cell attachment. Viruses are identified by HA, N, species of animal and year isolated. Antigenic change is common by antigenic shift (reassortment of segments).

Mode of transmission

It is spread by aerosol via the respiratory tract and breathing contaminated faeces. It can also be spread by wild water fowl and contaminated fomites.

Special note

It is a notifiable disease, highly contagious, and spread by waterfowl. The virus is highly unstable and can alter pathotypes quickly by passage in various animal species. Migratory birds spread and transmit human and swine influenza viruses across continents. Ratites (ostriches, emus and rheas) are sometimes infected.

Clinical signs:

The incubation period is hours to days, depending on age, sex, species affected, concurrent infections and pathogenicity of virus.

Respiratory distress, coughing, sneezing, rales, depression, sinusitis, emaciation, off feed, nervous disorder and virulent stains (fowl plague). Multiple pathotypes can occur. A drop in egg production and shell quality, watery eyes, excessive lacrimation, oedema of head and face, and cyanosis may be observed.

Postmortem lesions

Lesions include mucous in trachea, air sacculities, swollen head or wattles, egg peritonitis, sinusitis, watery lungs, and fibrinous enteritis.

Pericarditis, necrosis of skin and GI tract; haemorrhages on wattles, combs and legs’necrotic foci on liver, spleen, kidney and lungs, and haemorrhages at junction of proventriculus and gizzard can be seen with fowl plaque.

Diagnosis:

The AGP and ELISA tests can be used for determining the presence of antibody in the sera.

Isolation and identification of virus from trachea or vent in embryonating eggs or tissue culture is needed. Test haemagglutinating ability of the virus mixed with chicken sera containing antibodies against influenza. The virus can be sub-typed using specific sera against all known HA and N.

It simulates mycoplasmosis, turkey coryza, VVND, ILT, ornithosis, and fowl chlorea.

Treatment and control:

Prevention

•           Killed vaccine is available in limited areas.

•           Quarantine, depopulation and eradication of virulent form is mandated under law in the US.

•           Strict biosecurity is needed.

•           Control of live birds market in large North Eastern US cities is important to prevent the spread of the virus.

•           Recombinant AI vaccine available in Mexico contains H gene cloned into fowl pox vector.

Treatment

Broad-spectrum antibiotics are helpful to control secondary bacteria.

AVIAN PNEUMOVIRUS INFECTIONS. (SWOLLEN HEAD SYNDROME, TURKEY RHINOTRACHEITIS)[កែប្រែ]

Causes:

Pneumovirus is a single-stranded, 80-200nm RNA virus.

Effects:

Sneezing and nasal discharge, foamy conjunctivitis, swelling of infra-orbital sinuses, submandibular oedema, torticollis and cerebral disorientation may occur. Drop in egg production in layers. Mortality 0-10%.

Detailed causes:

Swollen head syndrome is a chronic disease affecting chickens and turkeys of all ages. Avian pneumovirus is a non-hemaggllutinating, nonsegmented, enveloped single stranded RNA virus of the family Paramyxoviridae family with helical capsid symmetry (80-200nm). It is spread by airborne and mechanical routes (feed, water, and equipment). Immunosuppression plays a role, and E. coli is a common secondary invader. In the United States, Pneumovirus is recognised as a pathogen only in turkeys. Swollen heads are typically seen following a severe reaction to NDV-IBV vaccination in stressed immunosuppressed birds.

Special note

Swollen Head Syndrome is a common problem in broiler breeders and occasionally in broilers and layers in Europe and South Africa.

Clinical signs:

Signs include snicking, rales, sneezing, nasal discharge, foamy conjunctivitis, and swelling of the infraorbital sinuses. Submandibular oedema, mortality 0-10%, torticollis, and cerebral disorientation may occur. A drop in egg production, whitish colour of eggs and morbidity approaching 100% of the flock may also be seen.

Postmomrtem lesions

Yellow oedema and/or haemorrhaging in nasal turbinates, laynx, trachea and subcutaneous layer of skin around head can be evident.

Diagnosis:

Viral isolation from the trachea, lungs or nasal exudates in embryonating turkey eggs or chicken organ cultures is diagnostic.

Serological tests include virus neutralisation, and ELISA.

It simulates many respiratory diseases including influenza, bronchitis, mycoplasma, E. coli, and infectious coryza.

Treatment and control:

Live vaccines are usually given by spray or drinking water for broiler breeders and broilers and/or killed vaccines for broiler breeders and breeding turkey are available in Europe, the Middle East, and Latin America.

Antibiotics can be used for secondary invaders. Fresh air in the house and reduced stocking density are helpful.

AVIAN TUBERCULOSIS (TB)[កែប្រែ]

Causes:

Bacterium- Mycobacterium avian.

Effects:

Pale, regressed combs and wattles, depression, emaciation, anaemia, unthriftiness, icterus (yellow skin) and lameness. Public health significance.

Detailed causes:

Avian tuberculosis can be a serious chronic problem in older birds (over 2 years of age) of all species, but in rare in commercial flocks. It is caused by Mycobacterium avian, an acid-fast, bactillary, club-like bacterium. Curved and crooked forms of the bacterium can also occur.

It is spread by older carrier birds, or contaminated faecal material, soil, litter, aerosol, and cannibalism.

Special note

It has public health significance. Some cases of M. avium induced disease can occur in man. Immunosuppressed humans are very susceptible to this organism. It can spread to swine and cattle causing positive skin test. Backyard flocks, zoo and aviary birds over 2 years of age are commonly infected.

Clinical signs:

Pale, regressed combs, wattles, and depression can be seen. Emaciation, anaemia, unthriftiness, icterus (yellow skin) and lameness may occur.

Postmortem lesions

Internal yellow or grey-white pearl-shaped nodules in lungs, liver, spleen, intestines and bone marrow may be seen.

Diagnosis:

Gross lesions (nodules in lungs and bone) and TB skin test of wattles using antigen from state diagnostic laboratory are diagnostic. Acid-fast stain of Tubercle bacilli is also important. Histopathologic observations of tubercule and acid-fast bacilli can be done. Serology tests include ELISA and rapid agglutination test. It simulates lymphoid leucosis and coligranuloma.

Treatment and control:

Prevention

Separate birds by age and remove skin-test-positive birds. Affected flocks should be quarantined.

Treatment

Depopulation of commercial flocks is important. Exotic species can be given isoniazid (30 mg/Kg), ethambutol (30mg/Kg) and rifampicillin (45 mg/Kg) for 18 months.

BIOTIN DEFICIENCY (NUTRITIONAL DERMATITIS[កែប្រែ]

Causes:

Deficiency of biotin in diet. Bioavailability in grains is variable.

Effects:

Skin sores (crusty lesions) on the toes, foot pad and beak and feather loss in young birds. Poor hatchability results from adult deficiency.

Detailed causes:

Biotin is a cofactor is carboxylation and decarboxylation reactions involving fixation of carbon dioxide. The reactions have important roles in anabolic processes and in nitrogen metabolism. Biotin is involved in a coenzyme formation that is needed for proper formation of skin and feathers may be involved in fatty liver and kidney syndrome and acute death syndrome. Hatched embryos have webbing between the third and fourth toes. Young poultry of all species will display clinical signs if biotin is deficient. Bioavailability of biotin in grains is extremely variable and can result in a deficiency.

Clinical signs:

Signs include skin sores (crusty lesions) on the toes, foot pad and beak, feather loss in young birds and poor hatchability in adults.

Portmortem lesions

Fatty livers and kidneys with heart attacks characterised by blood clot in the abdominal cavity can be seen.

Diagnosis:

Postmortem lesions (sterile dermatitis) and histopathology are characteristic. It simulates T-2 toxin, bumblefoot, and bacterial dermatitis.

Treatment and control:

Prevention

Dietary alteration will relieve signs.

Treatment

Restore proper amount of the vitamin in the diet.

BIRD FLU (FOWL PLAGUE – AVIAN INFLUENZA)[កែប្រែ]

Causes:

Type A Orthomyxoviruses.

Effects:

Reportable disease. Respiratory distress, coughing, sneezing, rales, depression, sinusitis, emaciation, feed refusal, nervous signs and diarrhoea. In layers, there is a drop in egg production and shell quality. Mortality is rapid with virulent strains.

Detailed causes:

All birds of all ages are susceptible to avian influenza.

The causative agent, orthomyxovirus, is a single-stranded RNA virus containing 8 segments, and 35 serotypes. Type A viruses are divided into subtypes according to the antigenic nature of haemagglutinin (HA) and neuraminidase (N). The HA is a viral protein which can attacht to the cell surface and the N an enzyme which can brake the virus-cell attachment. Viruses are identified by HA, N, species of animal and year isolated. Antigenic change is common by antigenic shift (reassortment of segments).

Mode of transmission

It is spread by aerosol via the respiratory tract and breathing contaminated faeces. It can also be spread by wild water fowl and contaminated fomites.

Special note

It is a notifiable disease, highly contagious, and spread by waterfowl. The virus is highly unstable and can alter pathotypes quickly by passage in various animal species. Migratory birds spread and transmit human and swine influenza viruses across continents. Ratites (ostriches, emus and rheas) are sometimes infected.

Clinical signs:

The incubation period is hours to days, depending on age, sex, species affected, concurrent infections and pathogenicity of virus.

Respiratory distress, coughing, sneezing, rales, depression, sinusitis, emaciation, off feed, nervous disorder and virulent stains (fowl plague). Multiple pathotypes can occur. A drop in egg production and shell quality, watery eyes, excessive lacrimation, oedema of head and face, and cyanosis may be observed.

Postmortem lesions

Lesions include mucous in trachea, air sacculities, swollen head or wattles, egg peritonitis, sinusitis, watery lungs, and fibrinous enteritis.

Pericarditis, necrosis of skin and GI tract; haemorrhages on wattles, combs and legs’necrotic foci on liver, spleen, kidney and lungs, and haemorrhages at junction of proventriculus and gizzard can be seen with fowl plaque.

Diagnosis:

The AGP and ELISA tests can be used for determining the presence of antibody in the sera.

Isolation and identification of virus from trachea or vent in embryonating eggs or tissue culture is needed. Test haemagglutinating ability of the virus mixed with chicken sera containing antibodies against influenza. The virus can be sub-typed using specific sera against all known HA and N.

It simulates mycoplasmosis, turkey coryza, VVND, ILT, ornithosis, and fowl chlorea.

Treatment and control:

Prevention

•           Killed vaccine is available in limited areas.

•           Quarantine, depopulation and eradication of virulent form is mandated under law in the US.

•           Strict biosecurity is needed.

•           Control of live birds market in large North Eastern US cities is important to prevent the spread of the virus.

•           Recombinant AI vaccine available in Mexico contains H gene cloned into fowl pox vector.

Treatment

Broad-spectrum antibiotics are helpful to control secondary bacteria.

BLACKFLIES[កែប្រែ]

Causes:

Blackflies (family Simuliidae) are also known as turkey or buffalo gnats are blood-sucking insects.

Effects:

Can cause serious damage to humans and livestock, and in dense numbers can cause unthriftiness and anaemia. They also transmit blood protozoan parasites such as leucocytozoon, causing avian malaria.

Detailed causes:

Blackflies (family Simuliidae) are also know as turkey or buffalo gnats. They are similar in size to mosquitoes but are dark, short, chunky, and humpbacked, with short legs; wing venation is distinctive. More than 20 species have been reported to attack domestic poultry in North America. Blackflies usually suck blood during the day and may cause serious damage to people and livestock; in dense numbers they may cause a severe anemia in poultry. They also transmit certain blood protozoans belonging to the genus Leucocytozoon.

Blackfly production sources are restricted to running water such as creeks, streams, or irrigation supply and drainage systems. Eggs are laid on rocks, sticks, or floating vegetation, or are dropped into streams. They may hatch in a few days, but some remain through summer or even until the following spring. Larvae attach to stones or other objects and reach the pupal stage after 3-10 weeks. The pupal stage also occurs under water, lasting from a few days to 1 week or more. Adults or some species emerge in spring, others during summer or early fall. Overwintering occurs in the egg or larval stage. Most temperate-zone species have one generation per year.

Clinical signs:

Blackflies can cause serious damage to humans and livestock, and in dense numbers can cause unthriftiness and anaemia. As blackflies are active during the day, they may be seen on birds or in the house.

Diagnosis:

Signs of anaemia and / or unthriftiness may indicate a heavy infestation with a number of parasites. Blackflies should be distinguished from mosquitoes or houseflies.

Treatment and control:

Control is difficult because these pests develop in streams, often some distance from the poultry farm, where insecticide treatment may be harmful to fish. Successful reduction of larval and subsequent adult blackfly populations, without fish kills, were obtained in infested streams treated monthly by helicopters using 2% temphos granules. Area-wide control programs have been developed using biological control agents such as Bacillus thuringiensis var. israelenis (Bti). These programs involved weekly treatment of all breeding areas in defined geographical areas. Measures recommended for mosquito control, as well as cautions on watershed contamination by pesticides, are also pertinent to blackfly control.

Prevention (red - numbered 1-5)

1.         The synthetic and natural pyrethroid insecticides, organophorus, and carbamate are the main ectoparasite and fly control chemicals used for direct application to poultry, litter, or buildings. In general, chemical insecticides and disinfectants should not be mixed for application together.

2.         Among the botanical insecticides, pyrethrum remains very effective against flies and is a main ingredient of mist and aerosol fly sprays, particularly with synergists.

3.         The chlorinated hydrocarbon insecticides are banned from use on poultry or in poultry houses because of residues in eggs and meat. Under no circumstances should DDT, benzene hexachloride, toxaphene, chlordane, aldrin, dieldrin, endrin, or heptachlor be used on poultry houses or on poultry feed or feed ingredients.

4.         Insecticides are available as wettable powders (WP), emulsifiable concentrates (EC), and water dispersible liquids (WDL), all of which are intended to be applied as a spray or mist. Insecticides are also available as dust and as baits. These low-assay products are prepared, premixed, and ready to use. Care should be taken to ensure that feed and water are not contaminated and that all label directions are strictly adhered to so that tolerances are not exceeded.

5.         Apply the insecticide directly where the pest is located. If birds are being sprayed, the treatment must thoroughly cover the entire bird and the bird should be wet to the skin. If buildings are being treated, the sites where the pests are located must be treated if control is to be adequate. Methods for caged layers include high-pressure sprays of 125 pounds per square inch (psi) from outside the cages. Other treatments are:

•           Dusting. For conventional houses, apply to litter; attempt to cover the area evenly including under roosts, feeders and nest boxes.

•           Spraying. The usual cylindric compressed-air sprayers are satisfactory for treating roosts and walls, as are knapsack sprayers (continuously pumped during spraying) that give a continuous spray. Sprayers powered by an electric or gasoline motor that delivers pressures of 125 psi, and use of a spray gun with a solid-stream nozzle are much more rapid and efficient. When spraying houses, high-pressure and large-volume output are most desirable to drive spray into all cracks and crevices.

•           Misting. Electric mist machines (foggers) are efficient, rapid, and often labour saving. Mist machines are concentrate applicators and do not use the same mixtures as ordinary sprayers. Generally they use 5-10 times the concentration and 1/3пїЅ1/10 the volume. In all fog work, the container should be shaken frequently during spraying to keep insecticide from settling. Mist machines can be used efficiently to dispense fly spray.

BOTULISM (LIMBERNECK, WESTERN DUCK SICKNESS)[កែប្រែ]

Causes:

Soil-borne bacterium- Clostridium botulinum.

Effects:

Loose feathers, sleepiness, neck, wing, eyelid and/or leg paralysis, diarrhoea and high mortality. Dead birds decompose rapidly.

Detailed causes:

Clostridium botulinum is gram-positive and spore-forming rod, anaerobic, and a soil-borne pathogen.

It causes acute paralysis of the neck and frequently occurs in duck populations of the Mid Western US. All species of poultry of any age are susceptible, and it is common in broilers, pullets and wild water fowl.

The organism produces a type A neurotoxin. There are 8 antigenically distinct toxigenic groupings of this type-A toxin.

It is spread by cannibalism and eating insects. There is a 1-2 day incubation period.

Special note

In commercial poultry it is a filth disease caused by poor management and sanitation. Outbreaks in wild ducks in western US can cause mortality in tens of thousands of bird. Large numbers of ducks produce high volumes of organic faecal material. This material produces an anaerobic environment, which favours growth of clostridium that is washed into the area from eroded soil. Flies and maggots feeding on carcasses spread the toxin.

Clinical signs:

Signs include loose feathers, sleepiness, neck, wing, eyelid and/or leg paralysis, diarrhoea, soiled vent, and high mortality. Dead birds decompose rapidly.

Postmortem lesions

Few to no gross lesions are seen. Maggots can be seen in the upper digestive tract.

Diagnosis:

Diagnosis includes rapid central nervous system signs (paralysis) with no gross lesions. The Mouse bioassay includes inoculating mice with serum to determine if toxin is present. If the toxin is present, the mice will show clinical signs.

Fluorescent antibody detection of organism.

It simulates Marek’s disease (MD) and drug and chemical toxicity.

Treatment and control:

Prevention

Pick up and destroy dead birds at regular intervals (twice a day), control flies, remove litter, and disinfect house.

Treatment

None for commercial poultry. Bacitracin, streptomycin, vitamin and mineral therapy are somewhat effective for expensive birds.

CALCIUM, PHOSPHORUS, VITAMIN D DEFICIENCY[កែប្រែ]

Causes:

Deficiency of calcium in the diet caused by dietary variations in calcium and phosphorus content and bioavailability.

Effects:

Soft, brittle bones (rickets) and retarded growth in young birds. In cage layer fatigue, eggs are thin-shelled or shell-less, there may be white areas on brown eggs or a drop in egg production and hatchability.

Detailed causes:

Vitamin D3 is needed for proper metabolism of calcium (Ca) and phosphorus (P), and in the formation of normal skeleton, hard beaks and claws, and strong eggshells. Rickets occurs in young birds and osteomalacia (cage layer fatigue) in mature birds.

Mode of transmission

A deficiency in the diet caused by variations in Ca and P content of animal byproducts and variation in P bioavailability in various mineral sources. A phosphorus deficiency is common in cage layers which don’t have excess to P in the faeces.

Clinical signs:

Soft brittle bones (rickets) occurs in young birds. In adults with cage layer fatigue, there are thin-shelled or shell-less eggs, white areas on brown eggs or a drop in egg production and hatchability.

In young birds with rickets, there is retarded growth.

Postmortem lesions

Beaded ribs, deviated sternum, softening of the beak, claws and keel bone and skeletal distortions can occur.

Diagnosis:

Postmortem lesions and histopathology (widening of epiphyseal plat, hypertrophy and softening of the bone, and irregular patterns of cartilage and bone development in the primary and secondary spongiosa) are diagnostic.

It simulates other deforming leg weaknesses in poultry.

Treatment and control:

Prevention

Quality control of the feed.

Treatment

Restore proper levels to the diet.

Vitamin D3 is needed for absorption of Ca and P from intestine and deposition of calcium in bone. Ca and P are needed for bone growth. Deficiency in Ca or P, or imbalance of either will result in bone and egg shell malformations. Hyper amounts of Vitamin D may cause renal damage and pimpling of egg shells.

CAMPYLOBACTERIOSIS[កែប្រែ]

Occurrence: Worldwide.

Species affected: Chickens, turkeys, ducks, pigeons, game birds, quail, puffins, gulls and geese. Risk for human health.

Age affected: All ages

Causes:

Microaerophile bacteria- Campylobacter jejuni, C. coli and C. lardis.

Effects:

Distension (enlargement) of the intestinal tract, depression, soiled vent, diarrhoea.

Detailed causes:

Campylobacter jejuni, C. coli and C. lardis are microaerophile, gram-negative, spiral and uniflagellate bacteria.

Chickens, turkeys, ducks, pigeons, game birds, quail, puffins, gulls and geese can be affected with acute to chronic disease.

Contaminated feed and water, litter, cannibalism, houseflies, cockroaches, wild free-flying birds and mice can spread the organism.

Special note

People are very susceptible to the organism. Food-borne contamination of uncooked poultry is a significant problem. Up to 2 million causes of enteritis a year may be due to this bacteria.

Clinical signs:

Most chickens are carriers of the bacteria without clinical symptoms. The importance is just for human health.

There is a 24-72 hour incubation period. Depression, soiled vent, and diarrhoea can be seen.

Postmortem lesions

Distension (enlargement) of the intestinal tract, accumulation of mucus, watery fluid and haemorrhages in intestines can be seen.

Focal hepatic necrosis may also be present.

Diagnosis:

Isolation of organism from faeces, intestinal tract, bile, blood or liver is needed. Incubate cultures for 48-72 hours at 43º in a microaerobic atmosphere. Colonies are flat, translucent and grey with a tendency to clump together or be raised, opaque and brown grey with antibiotics including Bacitracin, novobiocin and colistin.

It simulates coccidiosis.

Treatment and control:

Prevention

Biosecurity measures should be put in place, restrict wild birds and vermin to prevent the disease.

Treatment

Kanamycin*, gentamicin, furazolidone* and doxycyline* are effective.

*Not approved for use in the US

CANDIDIASIS (THRUSH, CROP MYCOSIS, YEAST INFECTION)[កែប្រែ]

Occurrence: Worldwide.

Species affected: All.

Age affected: All; young are most susceptible.

Causes:

Yeast-like fungus- Candida albicans, spread through contaminated faeces, litter and dirty drinkers.

Effects:

Emaciation, stunting, listlessness, increased thirst, depression, rough appearance to feathers.

Detailed causes:

Candida albicans is a yeast-like fungus which causes chronic disease in all birds, though young birds are most susceptible. The problem is usually caused by overmedication with antibiotics.

Mode of transmission

It is spread via contaminated faeces, litter, and dirty drinkers.

Clinical signs:

Signs include emaciation, stunting, listlessness, increased thirst, depression, and a rough appearance to the feathers.

Postmortem lesions

Whitish pustules or nodules in mouth, crop and oesophagus, and white towel appearance in upper digestive tract are common.

Ulceration of the mouth and oesophagus, haemorrhagic mucosa in the proventriculus, and focal necrosis of the liver can occur.

Diagnosis:

Slimy white lesions in the upper digestive tract are diagnostic. The organism can be isolated from lesions on Sabouraud’s Dextrose agar. Colonies are whitish, creamy and highly convex. The hyphae and spores can be seen in a fresh smear.

Treatment and control:

Prevention

Clean up water spills, don’t give birds sugar water for more than 1 day, and use water sanitisers to prevent build up of yeast.

Reduce the use of broad spectrum antibiotics.

Treatment

Stop over-use of antibiotics.

Mycostatin, copper sulphate in water, and nystatin (50 g/ton)in the feed can treat the disease.

It is similar to trichomoniasis, Vitamin A deficiency, Wet Pox and T-2 toxicosis.

CANNIBALISM (VENT PICKING, FEATHER PULLING, TOE PICKING, HEAD PICKING)[កែប្រែ]

Occurrence: Worldwide.

Species affected: All.

Age affected: All.

Causes:

Predisposing factors include insufficient feed or feeder space, high density rearing, excessive light, too much heat, nutritional deficiencies or irritation from external parasites.

Effects:

Injuries to the vent, head or feet, missing feathers. Injuries can be severe.

Detailed causes:

Predisposing factors include insufficient feed or feeder space, high density rearing, excessive light, too much heat, nutritional deficiencies or irritation from external parasites.

Clinical signs:

The following are common forms of cannibalism seem in commercial poultry operations:

  • Vent-picking

Picking of the vent or region of the abdomen several inches below the vent is the most severe form of cannibalism. This is generally more common in high-production or overweight pullet flocks. Predisposing factors are prolapse or tearing of the tissues by passage of an abnormally large egg. Vent picking can result in anaemia.

  • Feather-pulling

Frequently seen in flocks kept in close confinement resulting in lack of sufficient exercise. Nutritional deficiencies may contribute to the problem.

  • Toe-picking

Most commonly seen in young birds. Inadequate feeder space or inability of the chick to find the feed will lead to toe-picking.

  • Head picking

Follows injuries to the comb or wattles.

  • Diagnosis:

Injuries seen around the head, vent and feet, or observation of cannibalistic activity are indicative.

Treatment and control:

Prevention

Provide adequate feed and feeding space, reduce bird density, reduce light, beak trimming, toe and comb trimming in breeders and wattle trimming in cage birds. Coloured light can help to reduce the problem. Give "toys" for the birds to play with like straw, branches etc.

(beak trimming, toe and comb trimming and wattle trimming will soon be forbidden in Western Europe).

Chick feeder lids or paper should be filled with feed and be in place prior to the reception of the chicks.

Automatic feeders (pan-shaped or troughs) should be available no later than 7 days of age. Feed lids and automatic feeders should overlap by 3 days to ensure smooth transition between the two feeding systems.

CAPILLARIA (CROP WORM)[កែប្រែ]

Occurrence: Worldwide.

Species affected: All, specificity depending on Capillaria species. Less common in chickens.

Age affected: All

Causes:

Parasitic nematode worms of the genus Capillaria.

Effects:

Depending on Capillaria species involved- In heavy infestations, these worms are extremely pathogenic and can result in death. In chickens, they are less pathogenic. Symptoms include malnutrition and emaciation associated with severe anaemia.

Detailed causes:

Worms of the genus Capillaria are found in the mucosa of the mouth, oesophagus and crop. The body is thread-like, attenuated anteriorly and posteriorly; head with (C. annulata) or without (C. contorta) a cuticular swelling. The male is 8-17 mm long, 60-70 mm wide, has two terminal laterodorsal prominence on tail end a spicule very slender and transparent, about 800 mm long, 120-150 mm wide; the vulva is prominent, circular, and 140-150 mm posterior to beginning of intestine.

The cycle is direct for C. contorta and indirect for C. annulata, which requires the earthworm as an intermediate host. Eggs pass out the rectum and embryonate on the ground or in the earthworm in about 1 month. Embryos or earthworms containing the embryos, are consumed by the bird. Worms mature in the host in about 1 month.

Clinical signs:

When present in large numbers, these worms are extremely pathogenic and can result in death especially in turkeys, partridges, pheasants, guinea and quail. They are less common and less pathogenic in chickens. Signs are principally malnutrition and emaciation, associated with severe anaemia. Usually there is inflammation (thickening and roughening) on the crop and oesophageal walls.

Diagnosis:

When present in large numbers, these worms are extremely pathogenic and can result in death especially in turkeys and game birds. They are less common and less pathogenic in chickens. Signs are principally malnutrition and emaciation, associated with severe anaemia. Usually there is inflammation, thickening and roughening on the crop and oesophageal walls.

Treatment and control:

Coumaphos and Hygromycin B are both approved only for use in chickens. Coumaphos is given to replacement pullets in feed (0.004%) for 10-14 days prior to the onset of egg production. It is given to layers (0.003%) for 14 days as needed, but no sooner than 3 weeks after the end of the preceding treatment. Coumaphos was reported to be effective against A. galli, H. gallinarum, and C. obsignata. In Western Europe, only Flubenol is licensed.

CHICKEN ANAEMIA VIRUS (CAV), (BLUE WING DISEASE)[កែប្រែ]

Occurrence: Worldwide.

Species affected: Chicken.

Age affected: Young birds, 12-28 days.

Causes:

Circo virus of 19-24 nm in diameter.

Effects:

8-10 day incubation period. Anaemia, weight depression and up to 60% mortality can occur. Bluish discolouration of the wing can also occur (Blue wing disease). Immunosuppression, causing often secondary problems (eg Marek’s).

Detailed causes:

CAV is a circovirus of 19-24 nm in diameter. It causes acute to chronic disease in young chickens. The virus is spread horizontally and vertically.

Clinical signs:

There is an 8-10 day incubation period. Signs include anaemia, weight depression and up to 60% mortality.

Postmortem lesions

Lesions include thymic atrophy, the bone marrow is yellow or pink, bursal atrophy, swelling and mottling of the liver, and haemorrhages in the proventriculus and muscles. Bluish discolouration of the wing can also occur. (Blue wing disease).

Diagnosis:

Postmortem lesions and histopathology (widening of epiphyseal plate, hypertrophy and softening of the bone, and irregular patterns of cartilage and bone development in the primary and secondary spongiosa) are diagnostic.

It simulates other deforming leg weaknesses in poultry.

Treatment and control:

Prevention

Control in chickens can be afforded by administration of a live vaccine orally or via drinking water. Exposure of pullets to infected litter before egg production will produce protective maternal immunity in the progeny.

A live vaccine for breeders is available.

Treatment

None.

COCCIDIOSIS[កែប្រែ]

Occurrence: Worldwide.

Species affected: Mostly chicken, some species can also cause disease in turkeys, quail and pheasants.

Age affected: All ages after 7 days of age.

Causes:

Protozoan parasites of the genus Eimeria. Nine species occur in the chicken, of which E. tenella, E. maxima, E. necatrix, and E. acervulina, are the most frequently found in chickens. E. adenoids, E. meleagrimitis and E. dispersa occur in turkeys.

Effects:

Watery and/or bloody droppings, poor weight gain and feed conversion, anaemia, depression, drop in egg production in layers. Morbidity can be as high as 100%, mortality ranges from 0-50%.

Detailed causes:

Nine species of Eimeria occur in the chicken and 6 are important (E. acervulina, E. maxima, E. brunette, E. nexatrix, E. mitis and E. tenella).

All chicken coccidian are species-related (occur only in the chicken) and are tissue tropic (occur in particular areas of the intestine). Infection occurs by the ingestion of sporulated oocysts. For oocysts to sporulate, thus becoming infective, they require moisture and a high temperature, conditions which prevail in poultry houses with poor litter management. The Eimeria oocyst contain 4 sporocysts, each in turn with 2 sporozoites. Once ingested and released there are two cycles of asexual reproduction (schizogony) and one cycle of sexual reproduction (gametogony). The entire process takes 4-7 days depending on the species of Eimeria involved.

Clinical signs:

Coccidia which are deep tissue invaders such as E. maxima, E. necatrix and E. tenella cause severe necrosis, haemorrhage of the intestinal mucosa, and bloody diarrhoea and may result in death.

Signs include watery and/or bloody droppings, mortality (0-50%), and morbidity (0-100%). Culls appear as pale birds with anaemia, depression, poor weight gain and feed conversion, and a drop in egg production.

Postmortem lesions

Enteritis characteristic of Eimeria species is seen. The intestinal tract can be enlarged and have necrotic and/or haemorrhagic foci, undigested feed and gas. Localisation of lesions is species-related.

Diagnosis:

Intestinal scrapings should be examined for oocysts. The site and degree of lesions and size and shape of oocysts and schizonts are all used to differentiate between Eimeria species.

Treatment and control:

The use of virulent vaccines by eye drop at 1 day or in the drinking water or sprayed on the feed during the bird’s first week is a system of controlled exposure.

After 3 complete life cycles (3 weeks), the bird is usually solidly immune to the parasite. If the litter is too moist a second round of infection may cause severe diarrhoea and paleness. If this occurs, birds should be given a curative treatment and/or vitamins and minerals in the water.

Vaccination is only tolerated for pullets and broilers which have at least 8 weeks of rearing. This gives adequate time for the birds to make up for any temporary depression in growth, which may occur after vaccination.

Vaccination by water is less consistent because the oocysts tend to settle down and distribution is not uniform.

Attenuated vaccines are also available, both for breeders, layers (on the floor systems) and broilers. These are safer than the virulent vaccines and usually give adequate protection for life.

Coccidiostats are usually continuously fed to broilers in the feed. A withdrawal period is necessary. Resistance to certain drugs is common. Coccidiostats can be given in the feed, to pullets, for the first 8 weeks.

Treatment

•           Sulphonamides: sulfaquinoxaline (feed) (0.05%)

•           Amprolium Plus (0.024%) (water)

•           Sulfadimethoxine and Ormetoprin (water)

•           Sulfamethazine (0.1%) (water)

•           Sulfachloropyrazine monohydrate (0.03%) (water)

•           Toltrazuril

COLIBACILLOSIS (COLI GRANULOMA, MUSHY CHICK DISEASE, CELLULITIS)[កែប្រែ]

Occurrence: Worldwide.

Species affected: All.

Age affected: All.

Causes:

Gram negative bacteria- Escherichia coli. It is the most common bacterial pathogen of poultry, and the second most common of all poultry pathogens.

Effects:

Low performance in older birds, or high mortality in younger birds. High embryonic mortality, respiratory distress and enteritis can be evident.

Detailed causes:

This disease has a number of names because it causes granulomas in adults and yolk sac infection in chicks.

Coli Granuloma is chronic in mature birds of all species, and may be acute in chicks occurring as omphalitis.

Escherichia coli are gram-negative, non-acid-fast, non-spore-forming bacilli, and many strains have flagella.

Mode of transmission

E. coli may be a primary or secondary invader. It is the most common bacterial pathogen in poultry and second most common of all pathogens of poultry.

Faecal contamination of eggs, transovarian contamination, contaminated water and feed with bacteria can occur commonly.

Aerosol spread may occur.

Special note

E. coli is a normal contaminant in the intestines and may complicate mycoplasma, IBV, LT, and/or NDV in the air sacs, heart, liver and lungs causing air sacculities and/or chronic respiratory disease (CRD). Several serotypes make vaccination difficultur. E. coli is a very important cause of economic losses in poultry due to mortality, drops in weight gain, hatchability and an import cause of Septicemia-toxemia (sept-tox), air sacculities, and IP condemnations in processing plant. Sept-tox is the leading infectious cause of condemnation in the broiler processing plant in the US, air sacculities is the second, and IP the third.

Clinical signs:

Low performance in older birds or high mortality in younger birds, high embryonic mortality, respiratory distress and enteritis (diarrhoea) can be evident.

Postmortem lesions

Cauliflower-like nodules on viscera (granuloma), omphalitis in chicks, discoloured and misshapen yolk (mushy chick) are seen. These lesions are characteristic. Air sacculitis, salpingitis (inflammation of the oviduct), enteritis, synovitis, arthritis, pericarditis, peritonitis, panophthalmitis, or swollen head syndrome are common. Cellulitis, an inflammation of the cellular or connective tissue, can be caused by E. coli. The soft tissue is heavily necrotic and may be gangrenous. It can result in extensive processing plant condemnation. It is sometimes called infectious process or IP.

Diagnosis:

Laboratory isolation of E. coli for lesions, yolk, blood on MacConkey’s or methylene blue agar (EMB). Colonies are pink on MacConkey’s and dark with metallic sheen. It simulates Salmonella, Staphylococcus, Tuberculosis, Fowl cholera, Marek’s disease and Aspergillosis.

Treatment and control:

Prevention

•           Use mycoplasma-free stock to prevent interaction with E. coli.

•           Pellet feed to kill bacteria.

•           Bacterin for breeders or turkeys (serotype 02, 078) egg and hatchery sanitation to reduce organisms.

•           Chlorinate water (3 to 5 ppm) and use nipple drinkers to reduce transmission in water.

•           An inactivated vaccine is available for breeders and layers.

Treatment

Chlortetracycline (CTC) (400 g/ton), Oxytetracycline (OTC), Quinolones (Flumequine), Sulfadimethoxine and Ormetroprim or Trimethoprim, can be used.

Gentamicin can be given by subcutaneous injection at 1 day-of-age. 

Chlorox® in water at 2 to 4 oz/gal for 1-3 weeks or Quinolone in water for 3-5 days to treat clinical signs.

CROTALARIA TOXICITY[កែប្រែ]

Occurrence: Most common in Southeast US, associated with soybean fields.

Species affected: All.

Age affected: All.

Causes:

Ingestion of food containing crotalaris plant material (above 0.23% of diet containing the alkaloid toxin).

Effects:

Increased thirst, dull, inactive, watery diarrhoea, bright yellow-green urates, watery discharge from nose and mouth.

Detailed causes:

Crotalaria is a toxic weed found in the southeastern part of the US. Poultry of all ages are susceptible to acute to chronic toxicity by ingestion of feed containing seed, leaves or stems of Crotalaria spectabilis. Crotalaria contains an alkaloid toxin, which is toxic to poultry at above 0.3% of the diet.

Special note

The week is common in soybean fields in southeast US and is picked up by mechanical pickers. Soybeans are downgraded if crotalaria are present. Crotalaria can be separated from soybeans by a screening process, but this adds to cost of processing.

Clinical signs:

Signs include increased thirst, dull, inactive, watery diarrhoea, bright yellow-green urates, off feed and watery discharge from nose and mouth.

Postmortem lesions

Lesions include atrophied liver, ascites, subcutaneous oedema, hydropericardium, lung oedema, nephritis, hepatitis, and myocardial and skeletal haemorrhage.

Diagnosis:

Diagnosis is by feed analysis. Black mitten-shaped seeds can be seen in the feed. Clinical signs, gross and microscopic lesions are helpful.

Microscopic examination of the liver reveals bile duct hyperplasia.

It simulates salt toxicity, ascites due to metabolic causes, aflatoxicosis, vitamin E or selenium deficiency (exudative diathesis). The seeds are confused with soybean hulls.

Treatment and control:

Prevention

Spot check of feed.

Treatment

Fresh feed.

CRYPTOSPORIDIOSIS[កែប្រែ]

Occurrence: Worldwide.

Species affected: Chickens (broilers), turkey, quail and ducks.

Age affected: Age resistance is apparent (birds more than 3 weeks old are not susceptible).

Causes:

Small coccidian parasites of genus Cryptosporidium. C. baileyi causes disease in chickens, in turkeys, both C. baileyi and C. meleagridis cause disease. In quail, the organism responsible has not yet been identified.

Effects:

Disease has a 3-5 day incubation period. Respiratory signs include open-mouthed breathing, gasping, sneezing and gurgling. Intestinal signs include swelling of the sinuses, diarrhoea, poor weight gain and feed conversion. Morbidity to 40% and mortality to 10% can occur with the respiratory disease.

Detailed causes:

The life cycle of Cryptosporidium species differ from other Eimeria species. The intracellular stages are confined to the microvillus region of the host cell and the oocysts, which sporulate within the host cells, are infective when releases in the faeces. Two types of oocysts are formed, the thin-walled oocyst rupture to release sporozoites which can penetrate adjacent cells and reinitiate the infection. The thick-walled oocysts pass in the faeces and can transmit infection to other hosts. Also, cryptosporidium can invade the mucosal epithelium of a variety of tissues including the intestines, respiratory tract, cloaca, eyelids and bursa of Fabricius. Cryptosporidum in chickens mainly causes a respiratory disease.

It is common in immunodepressed birds and often seen together with IBD and/or reovirus infections.

Chickens. Cryptosporidum baileyi are small coccidian parasites that do not have sporocytes surrounding the 4 sporozoites. The sporocytes lie naked within the oocyst wall. The life cycle is divided into six major developmental stages: excystation (release of infectious sporozoites, gametogony (formation of male and female gametes), fertilisation (union of gametes), oocyst wall formation (to produce an environmentally resistant form), and sporogony (the formation of infective sporozoites within the oocyst wall).

Clinical signs:

3-5 day incubation period.

Respiratory signs include open mouth breathing, gasping, sneezing and gurgling. Intestinal signs include swelling of the sinuses, diarrhoea, poor weight gain and feed conversion.

Morbidity to 40% and mortality to 10% can occur with the respiratory disease.

Postmortem lesions

Respiratory signs – mucous in the trachea, sinuses, turbinates, thickened frothy exudates in the air sacs, and pneumonia.

Intestinal signs – thickened mucosa lining of middle and lower small intestine, which becomes pale and distended with cloudy mucoid fluid and gas bubbles.

Diagnosis:

Clinical signs and gross lesions, and the demonstration of life cycle stages associated with lesions in the tissues are diagnostic.

It simulates coccidiosis, yeast, and viral or bacterial respiratory disease.

Treatment and control:

The organisms are resistant to most chemical disinfectants. No know treatment exists for controlling this organism.

DARKLING BEETLE (LESSER MEAL WORM)[កែប្រែ]

Causes:

Darkling beetle, also known as lesser meal worm. Not true parasites of birds, but may occasionally feed on living skin.

Effects:

Unthriftiness in birds (increased feed intake and decreased production). Darkling beetles are important as vectors for other parasitic, bacterial or viral diseases.

Detailed causes:

Darkling beetles infest poultry houses around the world. The beetles live in the litter where they feed on, feed, manure and dead or moribund birds. The life cycle of darkling beetles requires from 1-3 months for the development of the larvae, and the adults can live for 2 years. Beetles are small (0.5 cm) and can be easily seen under feeders, waterers or along the walls of the house. The larvae are worm-like and will avoid light.

Clinical signs:

Beetles within a poultry house can number up to 1000/m2. They are important to the poultry industry as possible disease vectors, by damage to insulation and as pests. Only adults and late instar larvae-seeking population sites and tunnel in the insulation. Their climbing activity takes place at night. Beetles can be found throughout the poultry house; eggs, larvae, pupae, and adults are in litter and soil.

Diagnosis:

The beetles live in the litter where they feed on, feed, manure, and dead or moribund birds. Beetles are small (0.5 cm) and can be easily seen under feeders, waterers or along the walls or the house. The larvae are worm-like and will avoid light.

Treatment and control:

Due to the beetles’ ability to utilise many niches in the poultry house, control is difficult to achieve with any single approach.

Stored gains and feeds should not be allowed to become infested with insects. Infested material should be fumigated. Control of lesser mealworms and beetles requires an integrated attack that utilises all approaches to manage the population. Any control strategy must take into account that there will be a number of eggs, larvae, pupae and adults in the soil and walls of the building. These life stages will not come into immediate contact with an insecticide, and if the insecticide does not have a long residual life, control of the beetles will be shortened.

The best approach is to clean out after each flock. Another is to utilise carefully timed insecticide treatments. Houses should be treated with an insecticide immediately after the flock is removed. Clean up feed and water spills. The darkling beetle is not tolerant of temperatures below 40ºF. If the air temperature is less than 40º, the house should be opened up at clean-out to allow the temperature of the litter to drop as low as possible. By using cultural controls, low temperature clean-out schedules, and chemicals, beetle populations can be managed and maintained below damaging levels. Other products include permethrins, tetrachlorinphos, and dichlorvos.

None of these products are licensed in Western Europe.

DEEP PECTORAL MYOPATHY (GREEN MUSCLE DISEASE)[កែប្រែ]

Causes:

Localised lack of oxygen due to improper blood supply or necrosis around tissues or blood vessels. There is some evidence of hereditary predisposition, rapid growth rate and increased handling in turkey breeder hens during artificial insemination.

Effects:

Occasionally seen in the field.

Detailed causes:

Ischaemia (inadequate circulation of blood) causes the swelling in a tight fascia (band) of vigorously exercised muscle of growing birds. There is some evidence of hereditary predisposition, rapid growth rate and increased handling in turkey breeder hens during artificial insemination. The condition is occasionally seen in heavy broilers.

The cause is a lack of oxygen due to improper blood supply or necrosis around tissues or blood vessels.

It is non-contagious and no specific nutritional factors may influence the condition.

Clinical signs:

This is a processing plant problem. Problems in the field are still limited, but can be expected in the coming years due to extreme selection for breast meat.

Postmortem lesions

Unilateral or bilateral lesions which do not affect the health of the bird may occur followed by more chronic lesions resulting in dimpling of flattening of the breast muscle which can be palpated.

The whole deep pectoral muscle is swollen, pale and oedematous with necrosis in the middle 1/3-3/5 of the muscle, which is only evident after processing or necropsy.

In other lesions, the oedema disappears and the necrotic muscle becomes more prominent and drier with greenish areas.

Necrotic muscle shrinks and may be enclosed in a fibrous capsule. The sternum adjacent to the necrotic muscle becomes roughened and irregular.

Diagnosis:

Gross (greenish muscles) and microscopic lesions are characteristic. Microscopically the fibres are swollen and eosinophillic with discoid necrosis. Nuclei are absent or faint.

Surrounding the necrotic tissue are inflammatory reactions. Vascular lesions consist of thromboses, intimal proliferation and aneurysm formation.

It simulates bacterial (gangrenous), fungal (favus) or nutritional (exudative diathesis) dermatitis.

Treatment and control:

None.

DEHYDROTION[កែប្រែ]

Causes:

Failure of chicks to find water or newly hatched chicks being kept in machines and hatchery over 24 hours before reaching the farm.

Effects:

Inability of the chick to "peep", insufficient weight for size and age, dehydrated (dark and wrinkled) skin around the shanks. Blood vessels on the skin will be very prominent.

Detailed causes:

Chicks can survive several days without water, but will generally become weak or die after 3-4 days with no water. Dehydration is caused by failure of the chicks to find water or newly hatched chicks being kept in machines and hatchery over 24 hours before reaching the farm.

Clinical signs:

Dehydration can be determined by the inability of the chick to "peep", insufficient weight for the size and age, and dehydrated (dark and wrinkled) skin around the shanks. Blood vessels on the skin will be very prominent. Other changes include blue discolouration of the beak, dry and dark breast musculature, dark kidneys, accumulation of urates in the ureters, and darkening of blood.

Diagnosis:

Dehydration can be determined by the inability of the chick to "peep", insufficient weight for the size and age, and dehydrated (dark and wrinkled) skin around the shanks. Blood vessels on the skin will be very prominent.

Other changes include blue discolouration of the beak, dry and dark breast musculature, dark kidneys, accumulation or urates in the ureters and on visceral organs (Visceral gout), and darkening of blood

Treatment and control:

Prevention

Adequate watering space should be available in the brooding area inside a circular brooding guard. Mini-chick drinkers should be placed in the brooding area prior to the reception of the chicks. Care should be taken to show the birds how to drink from the automatic mini drinkers. Larger automated drinker systems including troughs and bell-shaped drinkers, if used, should be in place no later than 7 days-of-age.

The two watering systems should overlap by at least 3 days to ensure a smooth transitional phase between the two systems. If nipple drinkers are used, rubber bands can be placed over a few or drip catching devices used to aid chicks in learning to drink. Timing of settling, hatching and chick pulling needs to be co-ordinated so that chicks spend no more than 12 hours in the machines after hatching, are processed (vaccinated, debeaked and sexed) in less than 8 hours and reach the house is less than 24 hours after hatching. Chicks should be pulled from the hatcheries when 75% have a small humid ring around the head.

DUCK VIRAL ENTERITIS (DVE, DUCK PLAGUE)[កែប្រែ]

Causes:

Herpes virus.

Effects:

Sudden, high and persistent mortality. Drop in egg production (25-40%). Photophobia- half-closed, pasted eyelids. Inappetance, extreme thirst, droopiness, ataxia, ruffled feathers, nasal discharge, soiled and/or bloodstained vents, watery diarrhoea. Tremors of the head, neck and body, weight loss, blue beaks and mortality (5-100%) may also be seen.

Detailed causes:

Ducks geese and swans of all ages are susceptible to the duck enteritis virus, which is a herpes virus transmitted from bird to bird, by bloodsucking arthropods, or by contact with contaminated environment or water.

Special note

It is immunosuppressive.

Clinical signs:

Signs include sudden, high persistent mortality and a drop in egg production (25-40%). Photophobia can occur as half-closed, pasted eyelids. Inappetence, extreme thirst, droopiness, ataxia, ruffled feathers, nasal discharge, soiled vents and watery diarrhoea may also be evident. Birds may be unable to stand, have droopy outstretched wings, and head down. Tremors of the head, neck and body, loss of weight, blue beaks, blood stained vent, and mortality (5-100%) may be seen.

Postmortem lesions

Lesions include vascular damage (tissue haemorrhages) and free blood in the body cavity. Eruptions in the GI tract and degeneration of lymphoid organs (thymus and bursa) may be seen. Petechial haemorrhage may be seen on the myocardium, on liver, pancreas, intestine, lungs and kidney. Surface haemorrhages and yellow-white crusty plaques on the mucosa of the oral cavity, oesophagus, ceca and cloaca may be evident.

Diagnosis:

Clinical signs and gross lesions in all age ducks are diagnostic. It simulates influenza, duck viral hepatitis and fowl cholera. A live attenuated vaccine can be administered to ducklings and breeders.

Treatment and control:

Prevention

A live attenuated vaccine can be administered to ducklings and breeders.

Treatment

None.

DUCK VIRUS HEPATITIS (DVH)[កែប្រែ]

Causes:

Three types of the Duck hepatitis virus. Types 1 and 3 are unrelated picornaviruses. Type 2 is an astrovirus.

Effects:

Incubation period is 3-4 days. Symptoms depend on type of virus. In DVH-1 infection, birds fall on their side and kick spasmodically. Death is rapid. In DVH-2, convulsions, opisthotonosis (arching of head and neck) and death. In DVH-3, outstretched legs and opisthotonosis occur.

Detailed causes:

Ducklings of 1-4 weeks of age may be affected by this acute disease caused by one of three virus types. DVH type 1 is a 20-40 nm, heat stable picornavirus, DVH type 2 is a 28-30 nm astrovirus. DVH type 3 is also a picornavirus, but is unrelated to DVH type 1 virus.

The virus spreads via airborne and fecal-oral routes.

Clinical signs:

(There is a 3-4 day incubation period)

In DVH-1 birds fall on their sides and kick spasmodically with rapid death. Morbidity can reach 200% and mortality can reach 95%.

In DVH-2 convulsions, opisthotonos (arching of head and neck) and death are evident.

In DVH-3 outstretched legs and opisthotonosis occurs.

Postmortem lesions

DVH-1 produces enlarged liver with punctuated ecchymotic (paint brush) haemorrhages, and enlarged, mottled spleen and the kidney may be swollen and congested.

DVH-2 produces a liver which is pick and has haemorrhages, spleen enlarged, kidneys enlarged and small haemorrhages in the intestinal wall.

DVH-3 lesions are similar to DVH-1.

Diagnosis:

A rapid onset of clinical signs in ducklings with liver lesions is characteristic. Isolation and identification of organism in duck embryonated eggs and staining of virus with specific fluorescent conjugated antisera is diagnostic.

It simulates Chlamydia psittaci, Salmonellosis, aflatoxicosis and avian influenza.

Treatment and control:

Prevention

A live attenuated vaccine is available for use in breeders or ducklings by injection against the DVH-1 type only.

Treatment

None.

EGG DROP SYNDROME (EDS 76)[កែប្រែ]

Causes:

Avian adenovirus.

Effects:

Incubation period is 7-9 days. Loss of colour in pigmented eggs, thin-shelled, soft-shelled or shell-less eggs and a reduction in production up to 40%. Watery albumin and reduction in egg size. Inappetence, dullness and diarrhoea may occur.

Detailed causes:

Egg drop syndrome is an acute to chronic disease affecting laying birds, ie. laying chickens, ducks and guinea fowl. It is caused by the avian adenovirus, which is 70-75 nm in length. All chickens are susceptible, but brown layers are most susceptible.

It can spread vertically through the embryonated egg, by faecal-oral routes, and by contaminated water.

Special note

It occurs worldwide, however, the disease has not been reported in chicks in the US. The virus has been isolated from migratory ducks in the US.

Clinical signs:

(There is a 7-9 day incubation period)

Signs include loss of colour in pigmented eggs, thin-shelled, soft-shelled or shell-less eggs and a reduction in production up to 40%. Watery albumin and reduction in size of the egg, inappetence, dullness and diarrhoea may occur.

Postmortem lesions

Lesions include inactive ovaries and atrophied oviducts, uterine oedema, exudates in the shell gland, flaccid ovules and a mild splenomegaly (enlarged spleen).

Diagnosis:

Clinical signs, gross lesions, and inclusion bodies in the epithelial cells of the shell gland are diagnostic.

Isolation and identification of the virus in embryonated duck eggs from a flock free of EDS is the most sensitive test for EDS.

Immunofluorescent staining of fluids with specific conjugated antisera, and the Haemagglutination-inhibition test and ELISA to check for antibody in blood are also helpful.

It simulates IB.

Treatment and control:

Prevention

Biosecurity is important. An inactivated vaccine can be given during the pullet-rearing phase to help prevent the disease.

Treatment

None.

ENTEROHEPATITIS (BLACKHEAD, HISTOMONASIS)[កែប្រែ]

Causes:

Amoeboid protozoan Histomonas meleagridis.

Effects:

Enterohepatitis has a 7-12 day incubation period. In chickens, morbidity (to 100%) occurs, a cyanotic head and bloody caecal diarrhoea. In turkeys, signs include drowsiness, drooping of wings, stilted gait, closed eyes, head down and anorexia. Mortality occurs up to 100%.

Detailed causes:

It is called blackhead because birds may have a dark discoloured head. Young turkeys, chickens, quail, pheasants, grouse, chukar partridges and guinea fowl are susceptible to this acute to chronic disease. Enterohepatitis is caused by Histomonas meleagridis, a highly pleomorphic amoeboid protozoa with a stout flagellum and pseudopodia.

Mode of transmission

Chicken caecal worm (Heterakis gallinae) engulfs and packages Histomonas oocysts in its egg. Earthworms also consume Histomonas oocysts. Birds become infected by eating caecal or earthworms or caeca worm egg, which contains oocysts. Oocysts can also develop (sporulate) in worms and histomonads enter the tissues of the worm.

Special note

It is quite destructive in turkeys.

Clinical signs:

Enterophepatitis has a 7-12 day incubation period. Signs include drowsiness, drooping of wings, stilted gait, closed eyes, head down and anorexia in turkeys. Mortality and morbidity are high (to 100%) in turkeys, a cyanotic head, and bloody caecal diarrhoea occur in chickens.

Postmortem lesions

The caeca have an ulcerated (cheesy core) or haemorrhagic exudates. Crater-like liver lesions (bulls eye) and an enlarged green coloured liver can also be seen.

Diagnosis:

Coccidiosis should first be eliminated, as enterohepatitis simulates caecal coccidiosis. Clinical signs, gross lesions (intestine and liver lesions) and hestopathologic observations of (diarrhoea) life cycle stages near the lesions are diagnostic.

Treatment and control:

Prevention

Enterohepatitis is controlled by controlling the spread of the helminths, which spread disease. This is done by changing the litter or using antihelmintic drugs in the feed or water. Chickens and turkeys should always be kept separate to prevent introduction of caecal worms.

Treatment

Dimetridazol (0.015%), Carbasone (0.025%), Ipronidazole (0.00625%), Nitarsone (0.01875%) or Furazolidone (0.011%), are effective drugs, though not licensed in Western Europe.

EXUDATIVE DIATHESIS[កែប្រែ]

Causes:

Vitamin E and/or selenium deficiency in the diet.

Effects:

Muscles are pale, chicks stand with their legs far apart. A weeping dermatitis appears as a blue-green lesion.

Detailed causes:

All species of birds at all ages can be affected by exudative diathesis, which is produced by a Vitamin E and/or selenium deficiency in diet.

Special note

Selenium is involved in vitamin E metabolism. Selenium is involved in proper development of skin and muscles and is a mineral involved in coenzyme formation. There is a wide variability in the amount of selenium in soils which can influence the selenium content of grains and hence the diet.

See also Selenium deficiency; Vitamin E deficiency.

Clinical signs:

Muscles are pale, chicks stand with their legs far apart and a weeping dermatitis appearing as a green-blue lesion can be seen.

Postmortem lesions

Greenish-blue exudate under the skin and subcutaneous oedema usually around breast or leg are evident.

Diagnosis:

Gross lesions are adequate for the diagnosis. It simulates gangrenous dermatitis.

Treatment and control:

Prevention

Quality control of dietary selenium content.

Treatment

Restore the normal levels to the diet

FATTY LIVER HAEMORRHAGIC SYNDROME (FLSH)[កែប្រែ]

Causes:

Excessive consumption of high energy diets, where exercise is restricted in cages or overcrowded breeder houses. It may be compounded in hot weather.

Effects:

Straining during oviposition, sudden drop in egg production, thin-shelled eggs, cage layer fatigue, weak, rubbery legs and depressed sternum and rib cages. Hens are overweight with large pale combs and wattles covered with dandruff.

Detailed causes:

Chickens (commercial layers and broiler breeders) can develop this chronic disease. In laying hens, FLHS usually occurs early in production. It is caused by excessive consumption of high-energy diets, where exercise is restricted in cages or overcrowded breeder houses. It may be compounded in hot weather.

There is an over consumption of feed, positive energy balance and excessive fat deposition. It usually occurs because of too low calcium in layer diet when birds are just coming into production. Birds in cages overeat to achieve increased calcium requirement. Elevated serum calcium and cholesterol in affected chickens may be due to a hormone imbalance. Diets high in rapeseed meal may aggravate the condition.

Clinical signs:

Signs include straining during oviposition, sudden drop in egg production, thin-shelled eggs, cage layer fatigue, weak, rubbery legs and depressed sternum and rib cages. Hens are overweight with large pale combs and wattles covered with dandruff.

Postmortem lesions

Lesions include internal haemorrhage, and a fatty, friable, haemorrhagic liver. Haematomas (blood tumours) are dark red to brown within the parenchyma (specific cells within the organ).

Large amounts of fat in the abdominal cavity and around the viscera can be seen.

Diagnosis:

Postmortem lesions (enlarged, yellow, haemorrhagic liver) are characteristic. The fat content of livers exceeds 40% dry weight. Hepatocytes are distended with fat vacuoles, varying sized haemorrhages and organising haematomas.

It simulates aflatoxicosis.

Treatment and control

Lower calorie intake, increase calcium during the onset of lay. And avoid animal fat in the diet increase choline and methionine levels in feed.

FLIES AND MOSQUITOES[កែប្រែ]

Causes:

Order Diptera includes all flies (species of Culicoides, Simulium, Musca and Fannia) and mosquitoes (Culex and Psorophora spp.).

Effects:

Adult flies and mosquitoes are ideal vectors of disease. Can be so numerous as to create a health and public relations concern.

Detailed causes:

The order Diptera includes biting and non-biting flies and mosquitoes. All dipterans have two wings in the adult stage (except degenerate wingless forms) and pass through a complete metamorphosis including a maggot-like larva and a puparium resting stage.

Adult mouthparts are of the piercing-suckling or sponging types. Because of the intermittent nature of their feeding and extensive flight range, adult flies are ideal vectors of disease. Certain species develop in poultry manure and may become so numerous as to create a health and public relations problem. In hot weather the housefly can complete its life cycle in 8 days, in cold weather, this can take over 6 weeks.

Poultry production facilities that utilise lagoons can have problems with mosquitoes breeding in the lagoon.

Although mosquitoes are not as important to poultry as to human beings and other mammals, many species feed on poultry and transmit disease, including fowl pox. Some 140 species of mosquito have been described in North America also and a number of these are known to suck avian blood. Mosquitoes may attack poultry in dense numbers, carrying and transmitting viral agents of Eastern Equine Encephalomyelitis (EEE), St Louis Encephalitis (SLE), and Western Equine Encephalomyelitis (WEE). Fowl pox virus is transmitted by Aedes stimulants, A. aegypti, A. vexans, and many species of culicoides-biting midges. Aedes stimulants may harbour the virus for 2 days, whereas A. vexans may infect birds up to 39 days after contacting the virus of fowl pox and pigeon pox.

Clinical signs:

Flies and mosquitoes are commonly found around poultry house and can be identified by sight.

Adult flies have wings, are active during the daytime and lay eggs in poultry manure, in moist soil, spilled feed or on the carcasses of dead birds. Adult flies, larvae (maggots) and pupae will all be seen in and around the poultry house. Although flies do not commonly cause direct health concerns, they may transmit disease agents.

Most species of mosquito are about 5mm in length and their wings are commonly veined and scaled. Their legs and abdomen are long and the female is provided with elongated mouthparts for piercing the skin. The male does not suck blood. Mosquitoes deposit eggs on pools of water, moist soil or surfaces subject to flooding. Larval and pupal stages develop in water, with adults emerging from pupal cases to mate and then seek a host. In warm weather the life cycle is completed in about 7-14 days. Adults are most active towards evening and at night. Mosquitoes may attack poultry in dense numbers.

Birds may be seen to be agitated and in severe cases anaemia and anorexia may be seen. On close examination bites may be seen on the skin of birds.

Diagnosis:

Adult flies, larvae (maggots) and pupae will all be seen in and around the poultry house. Diagnosis is made by visual identification of adult flies and mosquitoes or their larvae.

Larvae (maggots) may be seen in and around manure and spilled feed. Adults are active during the day.

Treatment and control:

Prevention

Flies can be controlled by management practices such as manure composting, which will generate enough heat to control fly development. The use of dry cups in the house and automatic feeders will keep the litter dry and free of feed. Use of pits and lagoons in cage layer houses will keep faeces from building up in the house. Slats under feeders and waterers will keep the house litter dry and will also allow for easier treatment of the faeces with chemicals.

Treatment

Pyrethrum fly sprays can be fogged in houses or on ranges to obtain quick kill of mosquitoes in an outbreak, but control will not last more than a few hours. Residual sprays of carbaryl, malathion, propoxpur or stirofos can be applied to exterior surfaces of buildings or outdoors to vegetation from which poultry are excluded. If needed, breeding areas can be treated with larvicides or a biological control agent.

Commercial baits are formulated as granules and should be placed in pans or in protected areas. Bait can be placed in fly-traps. To increase the effectiveness of dry bait, such as methomyl, one part field-grade molasses may be diluted with three parts water in a 5-gallon (20 litre) can and covered with a removable window screen lid on which the dry bait is placed. Some commercial baits add a fly attractant.

Control of fly larvae in manure is done with a larvicide, which can be applied as a liquid, dry or in the bird’s feed. Larvicide treatment should only be done on a spot treatment, where large numbers of larvae are see, as larviciding manure disturbs the natural balance of predators and parasites to the larvae. One exception to this rule is the larvicide cyromazine, which is toxic to fly larvae, but not to their predators or parasites.

FOLIC ACID (FOLACIN) DEFICIENCY[កែប្រែ]

Causes:

Deficiency of folic acid in the diet.

Effects:

Shortening and thickening of the long bones leads to lameness. Poor growth and feathering, anaemia and high embryonic mortality may also occur.

Detailed causes:

Folic acid is part of the enzyme system concerned in single-carbon metabolism. It is involved in synthesis of purines and methyl groups of such important metabolites as choline, methionine and thymine. Folic acid, therefore, is required for cell multiplication. A choline, manganese or folic acid deficiency may result in perosis.

Birds of all ages may show symptoms if the diet is deficient in folic acid.

Clinical signs:

Perosis is characterised by a slipped tendon, which causes flattening and enlargement of hocks and long bones. This causes long bones to shorten and thicken and the birds become lame.

Poor growth and feathering, anaemia and high embryonic mortality may also occur.

Postmortem lesions

A slipped gastrocnemius tendon (without haemorrhage) is characteristic for the disease.

Diagnosis:

Gross lesions and analysis of diet are diagnostic. It simulates tibial dyschondroplasia and other leg weaknesses.

Treatment and control:

Prevention

Quality control of the diet.

Treatment

Restore the correct level of the nutrient to the diet.

Perosis is extremely common in broilers and turkeys resulting in trimming in the processing plant. Anywhere from 1-10% of the flock can be affected.

Manganese is an activator of several enzymes and is required for normal growth and reproduction and prevention of perosis.

Choline is present in acetylcholine in body phospholipids and acts as a methyl source in synthesis of methyl – containing compounds such as methionine, creatine and N- methylnicotinamide.

FOWL CHOLERA[កែប្រែ]

Causes:

Gram-negative, spore-forming bacterium- Pasturella multocida. Cats, wild birds and rodents can all act as carriers. Spread from bird to bird by contact. It is a stress disease occurring at point of lay and with seasonal change. 

Effects:

Peractute death without signs can occur.

Acute disease manifests as high fever, thirst, cyanosis, anorexia and ruffled feathers.

Chronic symptoms are torticollis (backwards retraction of head and neck), emaciation, sever mortality, enlargement of wattles, combs, legs, footpads and wing joints. Swollen sinuses, hocks and joints, dehydration, respiratory distress, drop in egg production and hatchability can also occur.

Detailed causes:

Turkeys, chickens, ducks, geese and birds of prey can be affected by peracture to chronic fowl cholera. Young adults are most susceptible. It is caused by a gram-negative, non-spore-forming rod, bipolar bacteria, Pasteurella multocida. Variation in pathogenicity occurs between isolates. At least 16 serotypes have been demonstrated, making vaccination difficult.

Mode of transmission

Sources of infection include carrier birds and clinically diseased poultry that have died from the infection. Wild birds, rodents and cats can all be a source of infection. Spread from infection flocks to healthy flocks with equipment, feed bags and other fomites is possible.

Special note

Infected birds which recover become carriers. Relapse of the disease is common in times of stress such as weather change.

Clinical signs:

Peracute death without signs can occur. Acute disease causes high fever, thirst, cyanotic, anorexia and ruffled feathers.

Chronic disease causes torticollis (retraction of the head and neck backwards), otitis (ear infection) emaciation, severe mortality, enlargement of wattles, combs, legs, footpads and wing joints and peritonitis.

Swollen sinuses and hocks, dehydration, respiratory distress, swollen joints, drop in egg production, fertility and hatchability can also occur.

Postmortem lesions

Peracute disease produces no lesions.

With peracute disease, haemorrhage on heart and fat, conjunctivitis, subepicardial and subserosal haemorrhage, conjested breast and septicaemia can occur.

Diagnosis:

Laboratory isolation of the organism is diagnositic. Pasturella should be cultured on blood agar or meat infusion media. A lever impression smear stained with Wright’s stain will yield bipolar rods, which are diagnostic.

Peracute septicaemic disease in pullets and large swollen necrotic liver give a presumptive diagnosis.

Treatment and control:

Prevention

Vaccinate with a bacterin or a live vaccine. Sixteen serotypes have been demonstrated with limited cross-protection between serotypes. Serotypes 1, 3 and 4 are most common and found in most commercial vaccines.

Treatment

OTC (100-200 g/ton), Erythromycin, Sulfaquinoxaline and Ormetropin/Trimethoprim (0.125% + 0.0075%), and Sulfamethazine (0.49%) and Flumequine are effective.

FOWL POX (AVIAN DIPHTHERIA, POX)[កែប្រែ]

Causes:

Avian pox viruses are single, linear double stranded DNA viruses.

Effects:

Incubation is from 4-10 days. There are two forms of the disease- cutaneous dry and diphtheritic or wet. Both may present in the same flock. The dry form is manifest as pimples or scabs on the skin (mainly on unfeathered parts of the body). The diphtheritic form shows cankers or yellow lesions in the mouth, oesophagus or trachea. Other symptoms include blindness, feed refusal, lowered egg production, facial swelling.

Detailed causes:

Pox viruses are single, linear, double stranded DNA viruses which cause chronic disease in poultry of all species and age.

Mode of transmission

Mosquito bites and mechanical transmission of virus to lacerated skin or eye are common routes of viral spread. Wild birds are a reservoir for the viruses.

Clinical signs:

Incubation period is from 4-10 days. They are two forms of the disease; the cutaneous or dry and the diphtheritic or wet. Both may be present in the same flock or animals.

The dry form shows as a pimple or scab on skin (mainly comb, wattles, eyelids and other unfeathered portions of the body).

The wet-mucous form shows diphtheritic, cankers or yellow lesions in mouth, oesophagus or trachea.

Eye involvement (blindness), off feed, lower egg production, facial swelling and an increase in culls can be seen.

Postmortem lesions

Cankers or false membranes in mouth (wet) are seen as slightly elevated white opaque nodules. Nodules increase in size and coalesce to yellow, cheesy and necrotic membranes.

Grey or black papular eruptions on unfeathered portions of skin (dry) are due to epithelial hyperplasia.

Head, face and feet are most commonly affected, but may spread to feathered portions of the body.

Diagnosis:

Eliminate bacterial dermatitis. Virus isolation on CAM will produce plaques, which will reveal intracytoplasmic inclusion bodies. Gross lesions will reveal inclusion bodies. Presence of scales on skin and cankers in the mouth in the fall of the year is an important characteristic of the disease.

Treatment and control:

Prevention

The normal procedure is to vaccinate once in the wing web between 8-18 weeks of age. In areas with extreme infection pressure, broilers may be vaccinated at day old. Vaccinate replacement pullets 10-12 weeks (wing web) and again at 16-18 weeks to provide long term immunity. Examine site of injection 1 week later for vaccine take (scab).

Control mosquitoes with insecticides and by getting rid of all standing water (pond, etc), where mosquitoes may breed.

Treatment

Broad spectrum antibiotics are helpful to control secondary bacteria.

FOWL TYPHOID (AVIAN DIPTHERIA, POX, CANKER)[កែប្រែ]

Causes:

Rod-shaped gram negative bacteria- Salmonella gallinarum.

Effects:

Elevated temperature to 44-45ºC (109-111ºF), pale combs and wattles, shrunken combs, greenish-yellow diarrhoea, depression and/or anaemia.

Detailed causes:

All birds, especially young adults and mature birds are susceptible to this acute to chronic disease.

The causative agent is Salmonella gallinarum, a rod-shaped bacterium which produces no spore or capsule.

Mode of transmission

It is spread by biological vectors and through the egg. The incubation period is 4-5 days.

Contaminated feed and H2O, fomites (trucks, workers and equipment etc), will transmit the organism. Fomites are inanimate objects which can carry infectious organisms and spread disease.

The organism is species specific (occurs in birds only).

Horizontal spread occurs from bird to bird

Special note

It has been eradicated from most commercial poultry flocks, but is still common in backyard flocks.

Clinical signs:

Birds have elevated temperature 109-111oF (44-45oC), pale combs and wattles, shrunken combs, greenish-yellow diarrhoea, depression, and/or anaemia.

Postmortem lesions

Birds have bronze liver and grey foci in lungs and gizzard.

Congested breast muscle, enteritis often with ulceration, mottled swollen spleens and kidney and thin watery blood are often seen.

Necrotic foci on the liver and heart, misshape rupture ovaries and peritonitis can occur.

Diagnosis:

Laboratory (necropsy, serology, microbial isolation and identification) monitoring is needed for a definitive diagnosis. Culture Salmonella and determine antibiotic sensitivity. It simulates paratyphoid, pullorum and cholera E. coli.

Treatment and control:

Prevention

•           Control vectors

•           Test breeders for positive serum

•           Destroy positive breeders

•           Pellet feeds

•           Use chlorine in the water

•           Vaccines from non pathogenic S. gallinarum are available

Treatment

Neomycin or sulfaquinoxaline.

FUSARIUM TOXICITY[កែប្រែ]

Cause:

Consumption of feed containing grains infected with fungi of the genus Fusarium, containing tricothecene toxins.

Effects:

Symptoms depend on dose of toxin, age of bird and duration of exposure. Signs include feed refusal, impaired growth, uneven and poorly formed feathers and emesis (vomiting). Thin-shelled eggs, reduced egg production, facial swelling, caustic injury to skin, cyanotic (blue coloured) combs and wattles, seizures and tremors may also be seen.

Detailed causes:

Mycotoxins are toxic metabolic byproducts of fungal growth on grains. High moisture content of grains can lead to fungal growth and toxin production. Fungi can produce toxins before or after grain harvest. Drought and insect damage to grain increase susceptibility of grain to fungal growth.

Disease is acute to chronic depending on dosage of toxin (higher-acute), age of bird (young birds have acute, older have chronic), and duration of exposure (longer periods cause chronic toxicosis).

Consumption of feed containing grains infected with fungi producing trichothecenes toxins cause the disease. The following trichothecenes: T-2, diacetoxyscirphenol (DAS) and deoxynivalenal (DON or vomitoxin) can be produced by Fusarium trichinctum, F. calonectria, F. gibberella, F. cephalosporium and F. trichoderma.

Mode of transmission

Feed contaminated with trichothecenes containing toxin which are very caustic. It can occur in corn, sorghum, barley, safflower seed, oats and brewers grain.

Clinical signs:

Signs include feed refusal, impaired growth, uneven and poorly formed feathers, and emesis (vomiting).

Thin shelled eggs, reduced egg production, swelling of the face, caustic injury to skin, cyanotic (blue-coloured) combs and wattles, seizures and tremors may be seen.

Postmortem lesions

Whitish to yellow, focal nodules in based of mouth, near the salivary ducts and tongue can occur. An inflamed GI tract, atrophy of bursa and thymus, necrosis of gizzard and proventriculus, dermatitis on the toes, pale or yellow bone marrow, yellow haemorrhagic liver and gout can also be seen.

Diagnosis:

Feed analysis for toxins and feed refusal in many farm animals are diagnostic. It simulates wet pox, vitamin A deficiency, thrush, trichomoniasis, ochratoxicosis and aflatoxicosis, IBD and visceral gout.

Treatment and control:

Prevention

Feed low moisture corn (below 14%). Do not add mouldy corn to the finished feed. Mouldy feed can be prevented with a mould inhibitor such as proprionic acid. Even so, quality control of feed is necessary. Grains should be checked for B1 (corn with greater than 16% moisture).

Contaminated feed can be diluted with noncontaminated grain or treated with ammonia, which inactivates the toxin. However, local regulations are sometimes prohibitive of these practices.

Contaminated feed can be fed to older pullets, which are less susceptible.

Two feed bins at the farm will reduce grain and feed storage time, which reduces fungal growth and toxin formation.

Aluminosilicates in the feed such as zeolites will bind and inactive aflatoxin. Other binding agents such as those based on glucomannans can be used. Pelleting can kill fungus, but will not always inactivate toxins.  

Gentian violet* kills fungi and binds aflatoxin.

Treatment

Increasing the protein content of feed by 1%, increasing vitamin and mineral content of feed and adding Gentian violet to feed have a sparing effect on aflatoxin induced disease.

*Not approved for use in US feeds.

GANGRENOUS (NECROTIC) DERMATITIS[កែប្រែ]

Causes:

Bacteria- Clostridium septicum, Escherichia coli, Staphylococcus aureus. Disease often occurs in birds which are already immunosuppressed due to a prior infection (Chicken anaemia, Infectious Bursal Disease) or mycotoxin ingestion.

Effects:

Loss of feathers, pale combs and wattles, depression, incoordination, inappetence, leg weakness and ataxia (can’t move) can be seen. Mortality is low, but dead birds decompose quickly.

Detailed causes:

Broilers (over 3 weeks old) and turkeys can be affected by this chronic debilitating disease. It is caused by Clostridium septicum, E. coli and S. aureaus.

Mode of transmission

Transmission is by contact with infected wet, caked litter. The disease often occurs in immunosuppressed birds.

Special note

It causes increased condemnation. Immune depression increases incidence and severity of dermatitis. Immunodepression may be due to a prior infection with IBDV, MDV, ALV or CAV infection(s) or mycotoxin ingestion.

Diagnosis:

Diagnosis is by postmortem lesions, which include congestion, haemorrhage and necrosis of skin with intro lesion bacteria under the microscope.

Bacteria can be isolated anaerobically on 2.5% blood agar.

It simulates erysipelas.

Treatment and control:

Prevention

Clean out house and add new litter to prevent the disease.

Medicate in starter feed Flavomycin, Virginamyciin, Bacitrcin and CTC can reduce bacteria. Virginiamycin and Bacitracin are banned in most countries.

Proper vaccination against IBDV, CAV and MDV prevent mycotoxin formation in the feed, and eliminate ALV in the breeders to prevent immunosuppression.

Treatment

Erythromycin, penicillin in the feed to treat signs. Chlortetracycine, oxytetracycline, copper sulphate can be added to the water to reduce morbidity.

GUMBORO (INFECTIOUS BURSAL DISEASE, IBD)[កែប្រែ]

Causes:

Infectious bursal disease virus is a birnavirus. It is highly stable and resistant to many physical and chemical agents. It is highly contagious and is be spread by contaminated faeces, water and feed. It can also be carried by vectors such as darkling beetles and rats.

Effects:

Elevated body temperature (111ºF), watery urate diarrhoea, anorexia, depression, ruffled feathers, head tremors, sleepiness and lameness can occur. Morbidity approaches 80% in White Leghorns and 50% in broilers. Hypervirulent strains occur and can cause up to 100% morbidity and 80% mortality in laying hens. Normal mortality is not more than 40% in laying hens and 20% in broilers. The virus is immunosuppressive.

Detailed causes:

IBD occurs only in young birds (2-16 weeks) and is seen mainly in chickens. It is a Birnavirus. It is highly stable and resistant to many physical and chemical agents.

Mode of transmission

IBD spreads by contaminated faeces, water and feed.

It is a highly contagious and hardy agent. Other vectors can harbour the virus including the lesser meal worms and rats.

Clinical signs:

Elevated body temperature (111oF/44oC) watery urate diarrhoea, anorexia, depression, ruffled feathers, head trembles, sleepiness and lameness can occur.

Morbidity approaches 80% in white leghorns and 50% in broilers.

Hypervirulent strains occur and can cause up to 100% morbidity and 80% mortality in laying hens. Normal mortality is not more than 40% in laying hens and 20% in broilers. It is immunosuppressive and very common throughout the world.

Postmortem lesions

The bursa is enlarged (2-4 times), haemorrhagic and/or oedematous early (3-5 days) in the course of the infection.

Other lesions include an increase in kidney urates, a swollen necrotic spleen and increased mucous in the intestine.

Later in the infection the bursa is atrophic (7 days), ¼-½ normal size. Thymus may also be atrophic. The bursa remains atrophic through the life of the bird, whereas the thymus can regenerate.

Muscle haemorrhage, rickets, dehydration, haemorrhages at the junction of the proventriculus and gizzard may also be seen especially with the hypervirulent strains.

Diagnosis:

Oedematous involvement of the bursa of Fabricius in young birds is diagnostic.

Treatment and control:

Prevention

Vaccinate parents at 2 and 6 weeks with live vaccine and at 10 and 18 weeks with killed vaccine. Live vaccine can be given between 10-26 days, depending on level of maternal antibodies and type of vaccine used. Virulent strains can be given approximately 5 days broilers. For problem farms, it is recommended to measure maternal antibody levels of ELISA and calculate day(s) of vaccination accordingly.

For breeders, in addition one killed vaccine around 16-18 days in common.

Vaccinate progeny between 1 and/or 14-21 days with attenuated vaccine on problem farms by spray or drinking water. Some vaccine can be given in ovo at 18 days of embryonation mixed with MD vaccine.

There are two serotypes of IBDV. Serotype 1 viruses are pathogenic, whereas serotype 2 viruses are not pathogenic. Serotype 1 viruses are divided into 6 subtypes.

Treatment

Vitamins and minerals and/or sugar in drinking water to prevent dehydration, replace lost electrolytes and provide and energy burst.

HAEMORRAGIC ENTERITIS (HE)[កែប្រែ]

Causes:

HE virus is a double stranded DNA Adenovirus.

Effects:

Incubation period is less than 24 hours. Depression, bloody droppings, dark red to brownish blood on the skin and feathers around the vent can be seen. Mortality is 10-80%.

Detailed causes:

Turkeys of 4 weeks or older may develop this acute viral disease. HE virus is an unenveloped, icosahedral, double-stranded DNA virus. It replicates in the nucleus forming basophilic inclusion bodies (viral factories seen under light microscope).

Mode of transmission

Spreads orally from infectious faeces or litter.

Clinical signs:

(Incubation period is less than 24 hours).

Depression, bloody droppings, mortality (10-80%), dark red to brownish blood on skin, feathers and around vents can be seen.

Postmortem lesions

The skin and flesh are pale, anaemic and dark in colour.

The jejunal mucosa is read and highly congested, spleens are enlarged, friable and mottled, lungs are congested and vascular organs are pale, and the livers are enlarged with haemorrhage.

Diagnosis:

Clinical signs, and gross and microscopic pathology are useful.

Intranuclear inclusion bodies in the reticuloendotheial (RE) system and intestine are diagnostic.

Spleens show RE hyperplasia and inclusion bodies. ELISA or AGP tests can be used to detect antibody.

Treatment and control:

Prevention

Use of a live vaccine in drinking water at 4 and 6 weeks of age can prevent the diseases.

Treatment

None.

HEAT PROSTRATION (HEAT STRESS)[កែប្រែ]

Causes:

High outside temperatures (reaching 100ºF) and high humidity (reaching 90% or more) combined with inadequate ventilation of poultry houses.

Effects:

Birds have no sweat glands, so their only method of cooling is by rapid respiration with mouths open, and hanging wings loosely by their sides. Birds become weak and feed consumption decreases. If continued for several days or weeks, birds will die due to respiratory, circulatory or electrolyte imbalance. There is a dramatic drop in egg production and shell quality will deteriorate.

Detailed causes:

Older birds (over 5 weeks) and adults (especially heavy breeds) in production are more susceptible to high temperatures accompanied by high humidity. Lacking sweat glands, the birds’ only method of cooling is by rapid respiration with mouths open and wings relaxed and hanging loosely at their sides.

When outside temperatures approach 100oF (38oC) and relative humidity reaches 90%, body temperatures rise, the birds become week and feed consumption is decreased. If this continues for several days or weeks, the birds may die due to respiratory, circulatory, or electrolyte imbalances.

Birds in production will show a dramatic decrease in egg production and shell quality will deteriorate.

Diagnosis:

Clinical signs are diagnostic at high environmental temperatures.

Treatment and control:

Every attempt should be made to improve air circulation with additional fans. Insulation of the building and use of white or aluminium paint on the outside of the building will reflect heat. Water sprinkers can be installed on the roof or over side curtains to cool the house.

Installation of high pressure foggers in the ceiling or evaporation coolers on the side walls will also significantly reduce inside temperatures when the relative humidity falls below 75%.

A system of tunnel ventilation (exhaust fans at one end of the house and air inlets at the other end will provide significantly more efficient cooling and heating throughout the year). Reducing bird concentration and providing birds cool water with vitamin C, electrolytes and/or aspirin will also reduce heat stress.

Increasing the nutrient density of the feed (increased energy and protein) and feeding early in the morning are also important during hot weather when the birds’ feed intake is less.

HE-RELATED INFECTIONS- MARBLE SPLEEN DISEASE (MSD) AND AVIAN ADENOVIRUS II SPLEENOMALGY (AAS)[កែប្រែ]

Causes:

Double stranded DNA viruses of the family Adenovirus. There are three serologically-distinct avian adenoviruses. Serotype I viruses cause IBHV, quail bronchitis, HE and MSD. Serotype II virus produces AAS and Serotype III virus causes Egg drop syndrome.

Effects:

Signs include paleness, depression and bloody diarrhoea, with up to 60% mortality. Asphyxia (can’t breathe) also occurs in AAS.

Detailed causes:

Turkeys (HE), pheasants (MSD) and chickens (AAS). All these diseases have acute action. HE occurs at 4-14 weeks; MSD 3-8 months; and AAS is all age chickens. All three diseases are caused by an adenovirus which is a nonenveloped, icosohedral symmetry, DNA virus with diameter of 70-90 nm.

Mode of transmission

It spreads laterally by the oral route or vertically through the cloaca.

Special note

HE can cause a transient low-level immunodepression. There are three serologically distinct avian adenoviruses, which can be differentiated by the AGP test. Serotype I viruses cause IBHV, quail bronchitis, HE and MSDV. Serotype II produces AAS and serotype III virus produces egg drop syndrome.

Clinical signs

Signs include paleness, depression, mortality (to 60%), bloody diarrhoea, and asphyzia (can’t breath) in AAS.

Postmortem lesions

Lesions include haemorrhages in the gut, liver, proventriculus and gizzard and anaemia. An enlarged mottled spleen and free blood in the intestines can be seen and with MSD oedema and congestion of lungs are also evident.

Diagnosis:

Agar gel precipitin (AGP) test and ELISA can be used to measure antibody. Intranuclear inclusion bodies occur in the reticuloendothelial (RE) cells of the spleen. It simulates coccidiosis, VVND, bacterial and fungal diseases.

Treatment and control:

Prevention

Commercial vaccines are available for use at 4 weeks in the water for HE and MSD.

Treatment

None.

HETERAKIS GALLINARIUM (CAECAL WORM)[កែប្រែ]

Causes:

Heterakis gallinarium is a small white caecal parasitic nematode worm, 7-15 mm long.

Effects:

Unthriftiness. The economic importance of H. gallinarium infection is as a vector of the blackhead organism Histomonas meleagridis.

Detailed causes:

The small, white worms are found in the lumen of the caecum. The male is 7-13 mm long, the female is 10-15 mm long.

The chief economic importance of the caecal worm lies in its role as a carrier of the blackhead organism Histomonas meleagridis. The protozoan parasite is found incorporated in the worm egg and its presence identified in the gut wall and in the reproductive systems of the male and female and in the developing eggs of this caecal worm.

Mode of transmission

Eggs pass out in the faeces; within 2 weeks, under favourable conditions of temperature and moisture, they reach the infective stage.

When eggs are swallowed by a susceptible host, the embryos hatch in the upper part of the intestine; at the end of 24 hours most of the young worms have reached the caeca. The larvae are closely associated with or occasionally embedded in the caecal tissue until 12 days post-exposure, with peak association at 3 days.

Tissue association increases with age of birds; nevertheless, a true tissue phase rarely occurs with H. gallinarum. Earthworms may also ingest the eggs of the caecal worms and may be the means of causing infection in poultry.

Clinical signs:

Heterakis infection results in few clinical signs. On postmortem examination, most of the adult worms are found in the tips or blind ends of the caeca. The caeca of experimentally infected birds show marked inflammation and thickening of the walls. The major economic importance of Heterakis infection is as a carrier of the blackhead organism Histomonas.

Diagnosis:

At necropsy most of the adult worms are found in the tips or blind ends of the caeca. The caeca of experimentally infected birds show marked inflammation and thickening of the walls. In heavy infections nodules form in the mucosa and submucosa.

Treatment and control:

Prevention

Modern poultry practices, especially confinement-rearing of broilers and pullets and caging of laying hens, have significantly influenced the quantity and variety of nematode infections in poultry. Many that caused extensive problems in backyard flocks are seldom seen in commercial operations.

For most nematodes, control measures consist of sanitation and breaking the life cycle rather than chemotherapy. Confinement-rearing on litter largely prevents infections with nematodes using outdoor intermediate hosts such as earthworms or grasshoppers. Conversely, nematodes with direct life cycles or those that utilise indoor intermediate hosts such as beetles may proper. Treatment of the soil or litter to kill intermediate hosts may be beneficial. Insecticides suitable for litter treatment include carbaryl, tetrachlorvinphos (stirofos). Treatment is carried out usually only between grow-outs. Extreme care should be taken to ensure that feed and water are not contaminated.

Treatment of range soil to kill ova is not very effective. After the old litter has been removed, spraying with permethrin a mixture of Rabon and Vapona has proven effective for beetle control.

Raising different species or different ages of birds together or in close proximity is bad practice as regards parasites.

Treatment

Phenothiazine is highly effective in the control of caecal worms in chickens (0.5 g/bird) when given for 1 day only. Hygromycin B and Coumaphos are also approved for use in chickens.

HOUSEFLY[កែប្រែ]

Causes:

Common non-biting flies include the housefly (Musca domestica) and species of the genus Fannia.

Effects:

Flies are a health and sanitation problem. Flies need to be controlled to prevent public pressure forcing poultry producers out of business. Flies have also been incriminated as vectors of intestinal diseases, as well as viruses and parasites.

Detailed causes:

The order Diptera includes families whose members suck blood from birds and mammals. All dipterans have two wings in the adult stage (except degenerate wingless forms) and pass through a complete metamorphosis including a maggot-like larva and a puparium resting stage. Adult mouthparts are of the piercing-sucking or sponging types.

Because of the intermittent nature of their feeding and extensive flight range, adult flies are ideal vectors of disease. Non-biting flies produced on poultry farms are a health and sanitation problem to the poultry producer and neighbours. Public pressure against poultry enterprises can force producers to move or go out of business if flies, odours or blowing feathers are not controlled.

Flies lay eggs in manure (some sarcrophagids deposit living larvae), in most spilled feed, or on dead-bird carcasses. In hot weather the housefly can complete its life cycle in 8 days, but in colder weather it may require over 6 weeks. Larvae (maggots) develop in moist manure and then move to drier areas for pupation. The housefly does not diapause, and survives northern winters by slow development in warm indoor locations such as enclosed poultry houses and dairy barns and in towns and cities. Other filth survive northern winters by hibernation.

Location of poultry houses and manure disposal areas needs to be carefully planned to prevent filth fly problems from developing. The poultry industry has an important role in community responsibility to control flies in suburban and urban areas. Poultry producers have met financial disaster as new residential developments have invaded formerly suburban locations where they had built their facilities. In many regions, state and county legislative action has strengthened public health codes, and local ordinances have resulted whereby poultry farms can be closed because of unabated fly sources found on their property.

Clinical signs:

Flies and mosquitoes are commonly found around poultry houses and can be identified by sight.

Adult flies have wings, are active during the daytime and lay eggs in poultry manure, in moist, spilled feed or on the carcasses of dead birds. Adult flies, larvae (maggots) and pupae will all be seen in and around the poultry house. Although flies do not commonly cause direct health concerns, they may transmit disease agents.

Diagnosis:

Flies and mosquitoes

The order Diptera includes families whose members suck blood from birds and mammals. All dipterans have two wings in the adult stage (except degenerate wingless forms) and pass through a complete metamorphosis including a maggot-like larva and a puparium resting stage. Adult mouthparts are of the piercing-sucking or sponging types. Because of the intermittent nature of their feeding and extensive flight range, adult flies are ideal vectors of disease. Non-biting flies produced on poultry farms are a health and sanitation problem to the poultry producer and neighbours. Public pressure against poultry enterprises can force producers to move or go out of business if flies, odours or blowing feathers are not controlled.

Flies lay eggs in manure (some sarcophagids deposit living larvae), in most spilled feed, or on dead-bird carcasses. In hot weather the housefly can complete its life cycle in 8 days, but in colder weather it may require over 6 weeks. Larvae (maggots) develop in moist manure and then move to drier areas for pupation. The housefly does not diapause, and survives northern winters by slow development in warm indoor locations such as enclosed poultry houses and dairy barns and in towns and cities. Other filth flies survive northern winters by hibernation.

Housefly and its relatives

Non-biting flies produced on poultry farms are a health and sanitation problem to the poultry producers and neighbours. Public pressure against poultry enterprises can force producers to move or go out of business if flies, odours, or blowing feathers are not controlled. Modern poultry farms produce a tremendous amount of manure, which must be managed to ensure that it is not attracting flies for breeding or causing an odour problem.

Location of poultry houses and manure disposal areas need to be carefully planned to prevent filth fly problems from developing. The poultry industry has an important role in community responsibility to control flies in suburban and urban areas. Poultry producers have met financial disaster as new residential developments have invaded formerly suburban locations where they had built their facilities. In many regions, state and county legislative action has strengthened public health codes and local ordinances have resulted whereby poultry farms can be closed because of unabated fly sources found on their property.

Treatment and control:

Location of poultry houses and manure disposal areas needs to be carefully planned to prevent filth fly problems from developing. The poultry industry has an important role in community responsibility to control flies in suburban and urban areas. Poultry producers have met financial disaster as new residential developments have invaded formerly suburban locations where they had built their facilities. In many regions, state and county legislative action has strengthened public health codes and local ordinances have resulted whereby poultry farms can be closed because of unabated fly sources found on their property.

  • Flies

Prevention

The synthetic and natural pyrethroid insecticides, organophosphorus and carbamate are the main ectoparasite and fly control chemicals used for direct application to poultry, litter or buildings. In general, chemical insecticides and disinfectants should not be mixed for application together.

Among the botanical insecticides, pyrethrum remains very effective against flies and is a main ingredient of mist and aerosol fly sprays, particularly with synergists.

The chlorinated hydrocarbon insecticides are banned from use on poultry or in poultry houses because of residues in eggs and meat. Under no circumstances should DDT, benzene hexachloride, toxaphene, chlordane, aldrin, dieldrin, endrin or heptachlor be used on poultry houses, poultry feed or feed ingredients.

Insecticides are available as wettable powders (WP), emulsifiable concentrates (EC) and water dispersible liquids (WDL), all of which are intended to be applied as a spray or mist. Insecticides are also available as dusts and as baits. These low-assay products are prepared, premixed and ready to use. Care should be taken to ensure that feed and water are not contaminated and that all label directions are strictly adhered to so that tolerances are not exceeded.

Apply the insecticide directly where the pest is located. If birds are being sprayed, the treatment must thoroughly cover the entire bird and the bird should be wet to the skin. If buildings are being treated, the sites where the pests are located must be treated if control is to be adequate. Methods for caged layers include high-pressure sprays (125 pounds per square inch (psi)) from outside the cages. Other treatments are:

•           Dusting: for conventional houses, apply to litter; attempt to cover the area evenly including under roosts, feeders and nest boxes.

•           Spraying: the usual cylindric compressed-air sprayers are satisfactory for treating roosts and walls, as are knapsack sprayers (continuously pumped during spraying) that give a continuous spray. Sprayers powered by an electric or gasoline motor that delivers pressures of 125 psi, and use of a spray gun with a solid-stream nozzle are much more rapid and efficient. When spraying houses, high-pressure and large-volume output are most desirable to drive spray into all cracks and crevices.

•           Misting: electric mist machines (foggers) are efficient, rapid and often labour saving. Mist machines are concentrate applicators and do not use the same mixtures as ordinary sprayers. Generally they use 5-10 times the concentration and 1/3 – 1/10 the volume. In all fog work, the container should be shaken frequently during spraying to keep insecticide from settling. Mist machines can be used efficiently to dispense fly spray.

Insecticide formulations are water dispersable liquids, wettable powders (WP), and emulsifiable concentrates. The WP formulations will give a longer lasting residue than the other formulations. Dust, type of surface and amount of sunlight on the surface will have an effect on how long the product remains active.

  • Baits

Commercial baits are formulated as granules and should be place in pans or in protected areas. Bait can be placed in fly traps. To increase effectiveness of dry baits such as methomyl, one part field-grade molasses may be diluted with three parts water in a 5-gallon can and covered with a removable window screen lid on which the dry bait is placed. Some commercial baits add a fly attractant such as Muscamone®, which increases their effectiveness.

  • Larvicides

Control of fly larvae in the manure is done with a larvicide, which can be applied as a liquid, dry or in the bird feed. Penetration of the manure with a liquid is difficult, and it is adding water to manure, making it more difficult to dry to reduce breeding. Larviciding manure is also devastating to the predators and parasites living in the manure, causing a further imbalance of the fly larvae and predators and parasites. Larvicide treatment should only be done on a spot basis, where large numbers of larvae are seen. One exception to this rule is the larvicide cyromazine, which is toxic to fly larvae but not to the predators and parasites. Another product, Larvadex®, can be fed to cage layers. The product passes out harmlessly in the faeces and kills developing larvae.

Biological control

One can use larvae from carpenter wasp in the litter. These larvae will consume fly larvae and these wasps are generally not a problem

Management practices

Use of composting bins for poultry litter will generate enough heat to control fly development. Use of dry cups in the house and automatic feeders will keep the litter dry and free of feed. Use of pits and lagoons in cage layer houses will keep faeces from building up in the house. Use of slats under feeders and waters will keep the house litter dry. This will also allow for easy treatment of faeces with chemicals, in confined areas such as under the pits.

INCLUSION BODY HEPATITIS (IBH)[កែប្រែ]

Causes:

Causes by the double stranded DNA Adenovirus. It replicates in the nucleus forming basophilic inclusion bodies. Prior exposure to IBDV or CAV depresses the immune response and makes birds more susceptible to IBH.

Effects:

Depression, ruffled feathers, feed refusal and poor feed conversion. Pale comb and wattles, gangrenous dermatitis, high mortality (up to 50%) and/or anaemia are common secondary findings.

Detailed causes:

IBH is an acute to chronic viral disease affecting chickens, broiler breeder pullets, leghorn pullets aged 2-20 weeks. IBH virus is an undeveloped, icosahedral, double-stranded DNA adenovirus. It replicates in the nucleus forming basophilic inclusion bodies.

Mode of transmission

Infected litter and fomites and transovarian transmission are important means for viral spread.

Special note

Prior exposure to IBDV or CAV depresses the immune response and makes birds more susceptible to IBH.

Clinical signs:

Signs include depression, ruffled feathers, off feed and poor feed conversion. Pale comb and wattles, gangrenous dermatitis, high mortality (up to 50%) and/or anaemia are common secondary findings.

Postmortem lesions

Lesions include fatty and/or haemorrhage liver, pale bone marrow (anaemia), and haemorrhages in the skeletal and heart muscles.

Atrophy of spleen and bursa due to early IBDV or chick anaemia virus (CAV) infections are also a common finding.

Diagnosis:

Microscropic observations of liver cells will reveal diagnostic intranuclear inclusion bodies.

It simulates aflatoxicosis.

Treatment and control:

Prevention

Avoid stress and vaccinate against IBD to help control the disease.

Treatment

Antibiotics are recommended to reduce secondary invaders which may cause dermatitis and anaemia.

INFECTIOUS BRONCHITIS[កែប្រែ]

Causes:

Infectious bronchitis virus is a coronavirus, and is the most contagious viral respiratory disease in poultry.

Effects:

Sneezing and watery eyes are seen early on, followed by depression, coughing and nasal discharge. Producing birds exhibit drop in egg production or weight gain. Eggs have poor shell quality and watery albumin. Layers also have ruffled feathers and wet droppings. Tracheal rales, gasping and urate diarrhoea are also seen.

Detailed causes:

Infectious bronchitis is an acute to chronic respiratory disease of all birds of all ages, although young birds are most susceptible. It is caused by a coronavirus.

Mode of transmission

Very contagious and spreads rapidly by aerosol. Contaminated faeces, litter and fomites spread the virus.

Special note

It is one of the most contagious viral respiratory diseases in poultry.

Clinical signs:

Sneezing and watery eyes are seen early on, followed by depression, coughing and nasal discharge.

Poor egg shell quality, watery albumen, ruffled feathers and wet droppings are seen in laying birds. A drop in egg production and weight gain, tracheal rales, gaping and urate diarrhoea are also seen.

Postmortem lesions

Exudate in trachea, nasal trubinates, air sacs thickened or frothy and pneumonia can be seen. In young birds misshapen (nonpatent and hypoglandular) ova and oviduct, and yolk in abdominal cavity. Occasionally swollen pale kidneys with urates are found.

Diagnosis:

Virus neutralisation, HI or ELISA test for measuring antibody are helpful. Virus isolation in embryos or chicken kidney cell cultures is necessary for a definitive diagnosis. Curling, stunting and death of embryos can be seen in inoculated embryonating eggs. Respiratory signs and lesions with kidney lesions give a presumptive diagnosis.

Treatment and control:

Prevention

Vaccinate birds with multiple serotypes (depending on region) for broad spectrum protection. Internationally, vaccines of the Massachussetts type are generally used (H20 or cloned type Ma5), preferably by spray or eye drop. Inactivated vaccine can be given for breeders or layers at 18-22 weeks of age by injection.

Sanitation, hygiene and biosecurity are also important.

Treatment

Antibiotics for killing secondary bacterial invaders in feed or water are helpful if signs of secondary infections are observed.

INFECTIOUS BURSAL DISEASE (IBD, GUMBORO)[កែប្រែ]

Causes:

Infectious bursal disease virus is a birnavirus. It is highly stable and resistant to many physical and chemical agents. It is highly contagious and is spread by contaminated faeces, water and feed. It can also be carried by vectors such as darkling beetles and rats.

Effects:

Elevated body temperature (111ºF), watery urate diarrhoea, anorexia, depression, ruffled feathers, head tremors, sleepiness and lameness can occur. Morbidity approaches 80% in White Leghorns and 50% in broilers. Hypervirulent strains occur and can cause up to 100% morbidity and 80% mortality in laying hens. Normal mortality is not more than 40% in laying hens and 20% in broilers. The virus is immunosuppressive.

Detailed causes:

IBD occurs only in young birds (2-16 weeks) and is seen mainly in chickens. It is a Birnavirus. It is highly stable and resistant to many physical and chemical agents.

Mode of transmission

IBD spreads by contaminated faeces, water and feed. It is a highly contagious and hardy agent. Other vectors can harbour the virus including the lesser meal worms and rats.

Clinical signs:

Elevated body temperature, (111oF/44oC), watery urate diarrhoea, anorexia, depression, ruffled feathers, head trembles, sleepiness and lameness can occur.

Morbidity approaches 80% in white leghorns and 50% in broilers.

Hypervirulent strains occur and can cause up to 100% morbidity and 80% mortality in laying hens. Normal mortality is not more than 40% in laying hens and 20% in broilers. It is immunosuppressive and very common throughout the world.

Postmortem lesions

The bursa is enlarged (2-4 times), haemorrhagic and/or oedematous early (3-5 days) in the course of the infection.

Other lesions include an increase in kidney urates, a swollen necrotic spleen, and increased mucous in the intestine.

Later in the infection the bursa is atrophic (7 days), ¼ - ½ normal size. Thymus may also be atrophic. The bursa remains atrophic through the life of the bird, whereas the thymus can regenerate.

Muscle haemorrhage, rickets, dehydration, haemorrhages at the junction of the proventriculus and gizzard may also be seen especially with the hypervirulent strains.

Diagnosis:

Oedematous involvement of the bursa of Fabricius in young birds is diagnostic.

Treatment and control:

Prevention

Vaccinate parents at 2 and 6 weeks with live vaccine and at 10 and 18 weeks with killed vaccine. Live vaccine can be given between 10-26 days, depending on level of maternal antibodies and type of vaccine used. Virulent strains can be given approximately 5 days earlier than intermediate vaccines. Layers should be vaccinated 5-7 days later than broilers. For problems farms, it is recommended to measure maternal antibody levels by ELISA and calculate day(s) of vaccination accordingly.

For breeders, in addition one killed vaccine around 16-18 days is common. Vaccinate progeny between 1 and/or 14-21 days with attenuated vaccine on problem farms by spray or drinking water. Some vaccine can be given in ovo at 18 days of embryonation mixed with MD vaccine.

There are two serotypes of IBDV. Serotype 1 viruses are pathogenic, whereas serotype 2 viruses are not pathogenic. Serotype 1 viruses are divided into 6 subtypes.

Treatment

Vitamins and minerals and/or sugar in drinking water to prevent dehydration, replace lost electrolytes and provide and energy burst.

INFECTIOUS LARYNGOTRACHETIS (ILT, LT)[កែប្រែ]

Causes:

Laryngotracheitis virus is a cuboidal, enveloped DNA herpes virus.

Effects:

The virus has an incubation period of 6-12 days. Different pathotypes have differing pathogenicity. Morbidity is 90-100%. Mortality ranges from 5-70% (average 10-20%). In layers there is a drop in egg production. Early sign is watery eyes, followed by nasal discharge, gasping, tracheal rales and stretching necks. Slinging away the blood from the nose causes blood stains to be seen along the sides of the walls.

Detailed causes:

ILT is mainly acute to chronic and affects all birds, though usually those older than 4 weeks. The herpes virus is a cuboidal, enveloped DNA virus.

Mode of transmission

Older carrier birds are a common source of infection. Aerosol, fomites, ingestion of contaminated litter are also common means for viral spread.

Clinical signs:

An incubation period of 6-12 days. There are many pathotypes of the virus. Some are very mild and others can cause severe morbidity and mortality.

Mortality (average 10-20%, range 5-70%), morbidity (90-100%), drop in egg production (10-20%), watery eyes early on, then nasal discharge, gasping, tracheal rales and stretching necks are common sings. Slinging of blood from nose causes blood stains along the sides of walls.

Most birds recover in 10-14 days if infection is not complicated by immunosuppression or a secondary bacterial or mycoplasma infection.

Postmortem lesions

Mucous in trachea is seen first, followed later by necrotic tissue, then blood. Inflammation of bronchi and lungs, foamy air sacs, oedema and congestion of the conjuctive and infraorbital sinuses are commonly seen.

Diagnosis:

Laboratory tests include microscopic observation of intranuclear inclusion bodies in the lesions (usually trachea).

Blood in the trachea is a important lesion.

Treatment and control:

Prevention

Vaccinate chickens with live attenuated product by-water (embryo-drived), spray or eyedrop (cell culture derived) at 2-4 weeks of age only in endemic areas. Broilers are rarely vaccinated for ILT.

Revaccination of pullets at 10-14 weeks by eyedrop. Revaccinate force moulted hens.

Treatment

Antibiotics for secondary invaders are helpful. Vaccinate only in endemic areas and quarantine all affected flocks.

IONOPHORE TOXICITY[កែប្រែ]

Causes:

Ionophores are common anticoccidial and antibacterial feed additives. Toxicity occurs when high levels are ingested through feed.

Effects:

Signs include birds lying on their sides with partial paralysis and legs extended, anorexia, weakness, drop in egg production, dyspnoea and dehydration. Mortality is variable, but may exceed 70%.

Detailed causes:

Ionophores are common anticoccidial and antibacterial feed additives. They facilitate the movement of alkali metallic actions, such as Na+, across cell membranes. Ingestion of food with high levels of ionophores can cause acute toxicity in all birds (adults are most susceptible). Toxic levels cause potassium to leave and calcium to enter the cells, resulting in cell death.

Special note

Monensin and sulphur drugs may accentuate ionophore toxicity.

Clinical signs:

Signs include birds down on their sides with partial paralysis and legs extended, anorezia, weakness, drop in egg production, dyspnoea and dehydration. Mortality is variable, but may exceed 70%.

Postmortem lesions

Lesions include opaque fibrin plaques on the epicardium, haemorrhage in coronary fat and decreased liver weight.

Pallor and atrophy of muscle fibres of the legs and back can also be seen.

Diagnosis:

Diagnosis is by feed analysis.

Clinical signs, gross and microscopic lesions are suggestive. Scattered areas of hyalinisation with heart and muscle necrosis and myofibril degeneration and necrosis are important lesions.

It simulates Marek’s Disease (MD), Nitrofuran Toxicity, Selenium Deficiency (myopathy), Avian Encephalomyelitis (AE), and Cassia Occidentalis (Coffee bean) toxicity.

Treatment and control:

Prevention

Spot checking feed will help prevent the disease.

Treatment

Fresh feed will discontinue clinical signs. About 75% of broiler diets contain ionophores.

LEUKOCYTOZOONOSIS (AVIAN MALARIA)[កែប្រែ]

Causes:

Leucocytozoon is an intracellular protozoan transmitted via the bite of an invertebrate host, usually blackflies. L. simondi is found in ducks and geese, L. smithi is found in turkeys.

Effects:

Depression, somnolence, feed refusal, muscular incoordination, anaemia, increased thirst, reduced mating and respiratory distress. Reduced egg production, egg weight and hatchability, vomiting and green diarrhoea may also be seen. Mortality is high.

Detailed causes:

Leucocytozoonosis is also called avian malaria because it is transmitted by the bite of an insect.

Turkeys, chickens, ducks, geese, pheasants, ruffled grouse. All birds can be affected, but young are most susceptible.

Leucocytozoon is an intracellular protozoan transmitted by the bite of invertebrate host. Its life cycle includes sporogony and schizogony (merogony) in the tissue cells and gametogony in erythrocytes or leukocytes of the insects. Elongated gametocytes with pale cytoplasmic horns exist in erythrocytes. Gamets are found only in leucocytes. Intracellular schizogonous forms are found in the liver. L. simondi is found in ducks and geese, and L. smithi is found in turkeys.

Mode of transmission

It is transmitted by blackfly bites. Sporozoites are in the salivary glands of the black fly. Wild birds and insects are a reservoir for infection.

Special note

It is immunosuppressive and common in turkeys on range in the southeastern United States.

Clinical signs:

Signs include depression, somnolence, off feed, muscular incoordination, high mortality, anaemia, increased thirst, reduced mating and respiratory distress.

Vomiting, decreased egg production, egg weight and hatchability, and green diarrhoea may be seen.

Postmortem lesions

Haemorrhagic liver and enlargement of liver and spleen, congestion of the lungs, spleen and small intestine can occur.

Fluid can occur in the body cavity, and the blood is thin and clotting retarded.

Diagnosis:

Laboratory blood and tissue smears are examined for the presence of parasite. Wright’s Giemsa Stain of red blood cells and lymphocytes show various life-cycle stages.

Treatment and control:

Prevention

Control flies with Carbamate granules distributed by large scale aerial or treatment of grounds.

Eliminate carriers by spraying repellent within the houses to discourage entrance of flies. Clopidol fed continuously at 0.0125–0.0250% also reduce some infection.

Treatment

Clopidol, Phrimethamine (1 ppm) and Sulfadimethoxine (10 ppm) are effective treatment.

LICE[កែប្រែ]

Causes:

Lice are common external parasites of birds, belonging to the order Mallophaga. More than 40 species have been reported for the domestic fowl. Transmitted from one bird species to another if they come in contact.

Effects:

Eat feather products and may consume blood by puncturing soft quills near the bases and gnawing through the covering layers of the skin. Not highly pathogenic to mature birds, but infected chicks may die. Frequently accompanies manifestations of poor health, such as internal parasitism, infectious disease and malnutrition.

Detailed causes:

Lice are common external parasites of birds. They belong in the order Mallophaga, the chewing lice and are characterised by chewing-type mandibles located ventrally on the head, incomplete metamorphosis, no wings, dorsoventrally flattened body, and short antennae with 3-5 segments. More than 40 species have been reported from domesticated fowl. Lice will transfer from one bird species to another if these hosts are in close contact.

Bird lice eat feather products and may consume blood by puncturing soft quills near the bases and gnawing through the covering layers of the skin itself. Hence birds may appear agitated and have ruffled or damaged feathers. Not highly pathogenic to mature birds, but infected chicks may die. Frequently accompanies manifestations of poor health, such as internal parasitism, infectious diseases and malnutrition. In sever infestations, laying birds may refuse to sit on the nest.

Diagnosis:

Pediculosis (lice infestation) of birds is diagnosed by finding the straw-coloured lice on skin or feathers of birds. Lice of domestic birds vary in size from less than 1 mm to over 6 mm in length. Mallophaga up to 10 mm long occur on wild birds. Lice spend their entire life cycle on the host. Eggs are attached to the feathers, often in clusters and require 4.7 days to hatch.

Treatment and control:

Galliform wild or domestic birds should never be allowed contact with poultry flocks. Lice tend to increase during autumn and winter, so flocks should be examined for lice on a regular basis (two times/month minimum) and treated if needed. Birds should be treated twice on a 7-10 day interval. Only the mature and immature forms will be controlled, as none of the available chemicals are ovicidal (egg are not killed). Re-treatment is necessary to control the lice that will hatch after the initial treatment.

In houses, the egg-laden feathers will be a source of re-infestation and when the house is depopulated, a thorough cleanup should be completed. Spraying of birds is the most practical means.

Care should be taken when spraying to ensure that the whole bird is treated, as it is common for lice to move to the neck from the vent when populations are large. In caged-layer flocks it is important that the birds are checked on a regular basis.

LYMPHOID LEUKOSIS (BIG LIVER DISEASE, LYMPHOMATOSIS, VISCERAL LYMPHOMA, J VIRUS)[កែប្រែ]

Causes:

Avian leucosis viruses are RNA retroviruses. There are 10 viral subgroups (A-J). Type A and J are most important. Vertically transmitted some horizontal transmission at young age in case of intensive contact.

Effects:

Paleness, emaciation, weakness, inappetance. Feed/gain ratio increased, decreased egg production and increased culls. External tumours may be seen, and the abdomen is enlarged and feathers are sometimes spotted with urates and bile. The disease is immunosuppressive.

Detailed causes:

The subgroup virus was commonly found in broiler breeders around 1994-1999. Nowadays, it is hardly seen due to severe eradication programs at pedigree level. Osteopetrosis occurs in broiler-age birds.

Lymphoid leukosis virus is an RNA virus in the family of retroviruses. Ten viral subgroups (A-J) are known. Avian leucosis viruses (ALVs) were common around the world, because they are transmitted through the eggs of common commercial breeders.

Mode of transmission

It spreads through the egg (transovarian). It is a ubiquitous organism in commercial poultry flocks.

There is some lateral transmission with congenitally infected chickens.

Special note

It is immunosuppressive and has been a major cause of condemnation in adult broiler breeders and layers.

Clinical signs

Signs include paleness, emaciation, weakness and inappetence. The abdomen is enlarged and feathers are sometimes spotted with urates and bile. The feed/gain ratio is decreased. Increased culls and decreased egg production occurs.

Postmortem lesions

Peripheral nerves are never involved. Bursae are always enlarged and may contain nodular tumours. Visceral tumours are soft, smooth and glistening. Tumours may be nodular, military or diffuse. Tumours are common in gonads, lungs, liver, spleen, heart, kidney, mesentery and bone marrow.

The skin is never affected and skeletal muscles often contain tumours. Eyes are never affected. Bone sometimes contains tumours (especially with J virus). The blood often contains tumours (especially with J virus). Fat tumours are common (Liposarcoma).

Diagnosis:

Tumours in adult birds are characteristic for this disease. Liposarcoma or myeloid tumour (J virus) is also characteristic.

ELISA tests are available to detect both the antigen (P27) and the antibodies against J virus.

Histopathology is confirmatory. It reveals large lymphoblasts in tumours. Lymphoblasts have an ovoid nucleus and a finer, more delicate chromatin network. PCR test is used to select out J virus positive broiler breeder grandparent stock.

ELISA test use specific serum to determine the presence of the organism in serum, vaginal swab or egg albumin. PCR test used for J virus.

Different diagnosis: E. coli, Aspergillus, MD, tuberculosis, erythroblastosis and myelobastosis.

The tumours are grossly distinct from those caused by other ALVs. However, the definitive diagnosis is based on virological isolation or histologic observation of the tumour cells. The myeloid cells can be differentiated from other tumour cell types by a trained histopathologist.

Treatment and control:

Prevention

Select birds on breeding level that are leucosis virus negative using serologic methods to prevent spread of the disease.

Treatment

None.

MALABSORPTION SYNDROME (PALE CHICK OR BIRD SYNDROME, INFECTIOUS PROVENTRICULITIS, RUNTING & STUNTING SYNDROME, HELICOPTER DISEASE)[កែប្រែ]

Causes:

Unknown. Various viruses, eg. REO, Rota, corona, calici, Toga etc. may play a role, combined with nutritional and possibly genetic factors.

Effects:

Incubation period is 7-14 days. Stunting, abnormal feathering, pale comb, wattles and legs are seen. Higher early mortality, weak legs, CNS signs.

Detailed causes:

There are a number of enteric disease conditions affecting young poultry that go undiagnosed with respect to identifying a definite aetiological agent. Thus a group of diseases of the nature have been termed "viral enteritis" but diseases with similar signs have been reported from many different countries under many different names. These include "malabsorption syndrome" "infectious stunting syndrome" broiler runting syndrome" "pale bird syndrome" and "helicopter disease".

Reported observations provide strong evidence that this is an infectious disease, although the involvement of non-infectious agents has not been completely ruled out. Because no recognised enteropathogen(s) has been consistently incriminated as the aetiological agent, research has discovered and/or identified numerous viral agents.

Several viruses have either been observed or isolated from the intestinal tract of chickens experiencing viral enteritis. A number of viral particles resembling either caliciviruses, coronaviruses, togaviruses, parvoviruses and picornalike viruses (pseudopicornaviruses) have been identified. One virus isolated from the intestines of four-day-old chickens showing signs of infectious stunting syndrome has been named the FEW virus. However, it should be remembered that the isolation of a particular viral agent does not in itself constitute a cause and effect relationship for the disease.

Clinical signs:

Incubation period of 7-14 days.

Stunting (stunting or runting syndrome), abnormal feathering (helicopter disease), pale comb, wattles and legs in broilers (pale bird syndrome) are seen.

Higher early mortality, weak legs, CNS signs (tremors, incoordination) and passage of undigested food in faeces can occur.

Postmortem lesions

Enteritis can cause undigested feed in intestines and pale intestines, haemorrhages around heart may also be seen.

Anaemia seen as decreased pigmentation and atrophy of the pancreas and bursa of Fabricius can occur.

An enlarged proventriculus with glandular enlargement and a loss of the normal structural architecture (infectious proventriculitis) may be evident.

Brittle bones and femoral head necrosis with rickets, hydropericardium (water around the heart), a small flaccid (flabby) gizzard and encephalomalacia can often arise.

Diagnosis:

The clinical signs and gross lesions (particularly proventricular hyperplasia and atrophied pancreas) are characteristic.

Treatment and control:

Prevention

A live vaccine at 1-2 days by injection and 6-8 weeks by injection, coarse spray or water and inactivated vaccine at 18-20 weeks for breeders will help control the disease.

Treatment

It responds to antibiotics plus vitamin-mineral supplementation for control of secondary infection.

Vinegar in water (1%) kills viruses by reducing intestinal pH and reduces spread of virus and some clinical signs.

MARBLE SPLEEN DISEASE (MSD)[កែប្រែ]

Causes:

Marble spleen disease is caused by avian adenovirus serotype I.

Effects:

Mortality up to 60% is seen following symptoms of respiratory compromise such as weakness, dyspnoea and asphyxia.

Detailed causes:

Marble spleen disease is an acute viral disease affecting pheasants of 3-8 months. It is caused by an adenovirus, and is spread laterally by the oral route and vertically through the cloaca.

Special note

There are three serologically distinct avian adenoviruses, which can be differentiated by the AGP test. Serotype I viruses cause IBHV, quail bronchitis, HE and MSDV. Serotype II produces AAS and serotype III virus produces egg drop syndrome.

Clinical signs:

Signs include paleness, depression, mortality (to 60%), bloody diarrhoea and asphyxia (can’t breath) in AAS.

Postmortem lesions

Lesions include haemorrhages in the gut, liver, proventriculus and gizzard and anaemia. An enlarged mottled spleen and free blood in the intestines can be seen. MSD oedema and congestion of lungs are also evident.

Diagnosis:

Agar gell precipitin (AGP) test and ELISA can be used to measure antibody. Intranuclear inclusion bodies occur in the reticuloendothelial (RE) cells of the spleen. It simulates coccidiosis, VVND, bacteria and fungi.

Treatment and control:

Prevention

Commercial vaccines are available for use at 4 weeks in the water for HE and MSD.

Treatment

None.

MAREK'S DISEASE (RANGE PARALYSIS)[កែប្រែ]

Causes:

Marek’s disease virus is a cell-associated herpes virus containing double-stranded DNA, of which there are three serotypes. Only serotype 1.

Effects:

It is immunosuppressive and causes increased susceptibility to other diseases. Signs include weakness, paleness, feed refusal, diarrhoea, poor performance culls and blindness. There is paralysis or perisis (partial paralysis), which can be unilateral or bilateral in wings and/or legs, which causes one leg to stretch forward and the other backwards. Tumours and tremors occur. Mortality ensues.

Detailed causes:

It was named after a Hungarian pathologist (Josef Marek) and also because it caused paralysis is chickens, which use to be reared on the range (range paralysis). It affects chickens (all breeds), occasionally pheasants and quail. It occurs worldwide in commercial flocks. Disease is chronic. It takes 4-6 weeks for tumours to form.

Classical type (nervous form) is common in white layers between 6-16 weeks. Visceral type with tumours in various internal organs usually occurs between 16-35 weeks. Infection takes place at very young age, but birds can die of Marek’s disease (MD) near the onset of egg production.

It is caused by a cell-associated Herpes virus containing double-stranded DNA. It has hexagonal naked particles or nucleocapsids of 85 or 100 nm. Marek’s disease viruses and Marek’s disease vaccines are classified into 3 serotypes. Serotype 1 viruses can be oncogenis (cause tumours).

Mode of transmission

It is spread by contaminated litter, dust, down or air-borne (bird to bird). Feather (dust or dander) epithelium contains virus. There is an incubation period of 2 weeks for virus shed and for clinical signs from 3-6 weeks.

Special note

It is immunosuppressive. Tumours are a leading cause of condemnation in broilers and MD is the leading cause of tumours in US broilers. There has been an increase in the incidence of MD in broilers in the US since the change to dry cups and nipple drinkers. These systems make the house drier and dustier, which provides an environment where the virus is more easily spread.

Clinical signs:

It causes increased susceptibility (immunosuppression) to other diseases. Signs include weak, pale, off feed, diarrhoea, poor performance, culls and blindness.

In white leghorn type birds, Classical Marek is common. There is paralysis or perisis (partial paralysis). There can be unilateral or bilateral paralysis of wings and legs, mortality, tumours and central nervous system signs (tremors). One leg stretches forward and the other backwards due to leg paralysis.

Postmortem lesions

The peripheral nerves are often enlarged (vagus, sacaral, sciatic and brachial) with a loss of striations. They can also have grey or yellow discolouration and be edematous (fluid filled).

The bursae are sometimes enlarged with tumours, but most often is strophic. There are enlarged organs (gonads, spleen, heart, lungs, liver, kidneys, proventriculus, intestines etc) with focal to nodular, palpable tumours.

The skeletal muscles have tumours. The eye (iris and pupil) may have diffuse depigmentation, diffuse bluish fading or diffuse grey opacity of the iris. The pupil may be irregular and tiny.

Diagnosis:

The diagnosis is by observation of gross tumours in immature birds. Ocular or skin leucosis and nerve involvement are diagnostic for MD. Histopathologically, small to medium lymphocytes comprise tumours. Lymphoid cells occur in peripheral nerves.

It simulates riboflavin deficiency, lymphoid leucosis, reticuloendotheliosis and colibaccillosis.

Treatment and control:

Prevention

Vaccinate (HVT-serotype 3 alone, or HVT and SB1-serotype 2) chicks at day-old subcutaneously in the hatchery. Some injections are done at 18 days or embryonation (in ovo).

HVT and SB1 are used for broiler breeders and white leghorns at full dosage. HVT is used alone or HVT and SB1 at 1/3-1/4 dosage for broilers if they are to be kept over 50 days, although broiler vaccination is common in the US.

SB1 may cause immunosuppression and increase leucosis is some Leghorn strains. HVT = Herpes virus of turkeys. SB1 = S (susceptible strain) and B1 (pen B1). HVT + SB1 or HVT + Rispens vaccine can be used.

Rispens strain (Serotype 1) may be used alone or in combination with HVT. Outside the USA, Rispens strain is the most commonly used vaccine, usually given by intramuscular injection at day old. In areas with a high infection risk bivalent vaccine (Rispens + HVT) is used.

Treatment

None.

MICE[កែប្រែ]

Causes:

House mouse- Mus musculus is the most common.

Effects:

Contaminate feed and litter with their excrement. Particularly hazardous to Salmonella control programs since they are frequently infected. Burrowing and gnawing activity can undermine foundations and destroy curtains and insulation. They eat and/or contaminate feed, leading to increased feed costs and decreased efficiency. Mice can also carry diseases and ectoparasites.

Detailed causes:

Rodents are common external pests in and around poultry facilities and can parasitise poultry. Rodents can eat or contaminate feed, which increased feed costs and affects feed conversion. Additional problems can be produced by the presence of these pests, since they may carry a variety of disease and ectoparasites.

The house mouse (Mus musculus) is the most common mouse found in and around poultry facilities. Mice will eat almost any kind of food. Mice are active throughout the day, often feeding every hour. However, peak activity occurs at dusk and dawn. Mice breed regularly throughout the year with no seasonal peak.

Clinical signs:

Mice are active throughout the day, often feeding every hour. However, peak activity occurs at dusk and dawn. Mice breed regularly throughout the year with no seasonal peak. If mice are seen during the day, it usually indicates a heavy infestation. Droppings may be seen, especially around spilled feed and gnawing or burrowing activity may be identified around buildings. Scratching noises may be heard.

Size of droppings and visual identification of mice (dead mice may be found) will distinguish mice from rats.

Treatment and control:

Control

Rodent-proofing can be an effective long-term control measure. However, it is impossible to rodent-proof a poultry facility with curtains, wooden sidewalls and/or dirt floors. Access to the building can be restricted by patching or screen holes in the foundation, thus forcing the rodents to burrow into the house, which makes them easier to detect.

Sanitation involves cleaning around the facility. Rodents are secretive creatures, they do not like to move in open areas; therefore, mowing the grass and weeds on a regular basis creates a less favourable habitat. Removing piles of old wood, nests or any other debris helps to make the area less attractive to rodents and aids in making early detection possible. When debris or tall grass is present, rodents can burrow into a facility and go unnoticed. Rolling the house curtains up and down a couple of times a week during summer months will disturb any rodents that are in the curtains and discourage them from living and/or nesting in them.

Treatment

After the control measures have been completed, rodent-killing can be the use of baiting, fumigating, trapping or even shooting. A properly conducted baiting program is easiest and most effective.

There are many products that will kill rodents. The first safe and commonly used baits are the multiple-dose anticoagulants. Products that contain warfarin, fumaric, chlorophacinone or diphacinone as an active ingredient are examples of this type. Multiple-dose anticoagulants must be consumed for several days to be lethal. The effects are cumulative, therefore, it is imperative that enough bait be available for the rodents to eat for several days. These chemicals are safe for people and for non-target animals, because a single dose will not cause death.

MOSQUITOES (AND FLIES)[កែប្រែ]

Cause:

Order Diptera includes all flies (species of Culicoides, Simulium, Musca and Fannia) and mosquitoes (Culex and Psorophora spp.). 

Effects:

Adult flies and mosquitoes are ideal vectors of disease. Can be so numerous as to create a health and public relations concern.

Detailed causes:

The order Diptera includes biting and non-biting flies and mosquitoes. All dipterans have two wings in the adult stage (except degenerate wingless forms) and pass through a complete metamorphosis including a maggot-like larva and puparium resting stage. Adult mouthparts are of the piercing-sucking or sponging types. Because of the intermittent nature of their feeding and extensive flight range, adult flies are ideal vectors of disease. Certain species develop in poultry manure and may become so numerous as to create a health and public relations problems. In hot weather the housefly can complete its life cycle in 8 days, in cold weather this can take over 6 weeks.

Poultry production facilities that utilise lagoons can have problems with mosquitoes breeding in the lagoon.

Although mosquitoes are not as important to poultry as to human beings and other mammals, many species feed on poultry and transmit disease, including fowl pox. Some 140 species of mosquito have been described in North America alone and a number of these are known to suck avian blood. Mosquitoes may attack poultry in dense numbers, carrying and transmitting viral agents of Eastern Equine Encephalomyelitis (EEE), St Louis Encephalitis (SLE) and Western Equine Encephalomyelitis (WEE). Fowl pox virus is transmitted by Aedes stimulants, A. aegypti, A. vexans, and many species of culicoides-biting midges. Aedes stimulants may harbour the virus for 2 days, whereas A. vexans may infect birds up to 39 days after contacting the virus of fowl pox and pigeon pox.

Clinical signs:

Flies and mosquitoes are commonly found around poultry houses and can be identified by sight.

Adult flies have wings, are active during the daytime and lay eggs in poultry manure, in moist soil, spilled feed or on the carcasses of dead birds. Adult flies, larvae (maggots) and pupae will all be seen in and around the poultry house. Although flies do not commonly cause direct health concerns, they may transmit disease agents.

Most species of mosquito are about 5mm in length and their wings are commonly veined and scaled. Their legs and abdomen are long and the female is provided with elongated mouthparts for piercing the skin. The male does not suck blood. Mosquitoes deposit eggs on pools of water, moist soil, or surfaces subject to flooding. Larval and pupal stages develop in water, with adults emerging from pupal cases to mate and then seek a host. In warm weather the life cycle is completed in about 7-14 days. Adults are most active towards evening and at night. Mosquitoes may attack poultry in dense numbers. Birds may be seen to be agitated and in severe cases anaemia and anorexia may be seen. On close examination bites may be seen on the skin of birds.

Diagnosis:

Adult flies, larvae (maggots) and pupae will all be seen in and around the poultry house. Diagnosis is made by visual identification of adult flies and mosquitoes or their larvae. Larvae (maggots) may be seen in and around manure and spilled feed. Adults are active during the day.

Treatment and control:

Prevention

Flies can be controlled by management practices such as manure composting, which will generate enough heat to control fly development. The use of dry cups in the house and automatic feeders will keep the litter dry and free of feed. Use of pits and lagoons in cage layer house will keep faeces from building up in the house. Slats under feeders and waterers will keep the house litter dry and will also allow for easier treatment of the faeces with chemicals.

Treatment

Pyrethrum fly sprays can be fogged in houses or on ranges to obtain quick kill of mosquitoes in an outbreak, but control will not last more than a few hours. Residual sprays of carbaryl, malathion, propoxpur or stirofos can be applied to exterior surfaces of buildings or outdoors to vegetation from which poultry are excluded. If needed, breeding areas can be treated with larvicides or a biological control agent.

Commercial baits are formulated as granules and should be placed in pans or in protected areas. Bait can be placed on fly-traps. To increase the effectiveness of dry bait, such as methomyl, one part field-grade molasses may be diluted with three parts water in a 5-gallon (20 litre) can and covered with a removable window screen lid on which the dry bait is placed. Some commercial baits add a fly attractant.

Control of fly larvae in manure is done with a larvicide, which can be applied as a liquid, dry or in the bird’s feed. Larvicide treatment should only be done on a spot treatment, where large numbers of larvae are seen, as larviciding manure disturbs the natural balance of predators and parasites to the larvae. One exception tot his rule is the larvicide cyromazine, which is toxic to fly larvae, but not to their predators or parasites.

MYCOPLASMA COMPLICATED CHRONIC RESPIRATORY DISEASE (CRD, MYCOPLASMA AIRSACCULITIS MG,MS, MM) [កែប្រែ]

Causes:

Mycoplasma gallisepticum, M. gallinarum, M. synoviae, M. meleagridis, M. iowae and/or TRT. Spread through egg and contact with infected litter, feed or water. Aerosol spread also occurs.

Effects:

Signs include foaming of the eye, conjunctivitis, coughing, tail bobbing when breathing, emaciation, rales, nasal discharge, sneezes, open mouthed breathing, poor growth, decreased feed consumption, lowered egg production and poor shell quality.

Detailed causes:

All species of bird of all ages are susceptible to chronic Mycoplasma infection. A number of different agents are involved in the aetiology of this disease. These include M. synoviae (MS) or M. gallisepticum (MG) in chickens, M. meleagridis (MM) and M. iowae (MI) in turkeys. M. synoviae (MS) is usually less pathogenic. Synergistic effects with E. coli and/or NDV and/or IBV vaccine viruses may occur. ILT can also be involved.

Mode of transmission

It is spread through eggs and contact with infected litter, feed or water. It is also transmitted by people, vehicles etc. E. coli is a secondary invader of mycoplasma-infected birds.

Aerosol spread occurs. Severe ND, IBV or ILT reactions may occur after vaccination, especially if given by spray to chicks previously infected with mycoplasma or E. coli.

Special note

E. coli is a normal contaminant of the intestine, but is a primary pathogen in the respiratory tract. Birds compromised by immunosuppression due to an early infection with IBD commonly develop CRD. It is a major cause of condemnation in the processing plant.

Clinical signs:

Signs include coughing, tail bobbing when breathing, emaciation, rales sneezing, open mouth breathing, poor growth, decreased feed consumption, lowered egg production and shell quality.

Postmortem lesions

Yellow fibrin on the heart, liver and viscera organs, caseous air sacs, muscus in trachea and green livers can be seen.

Diagnosis:

Laboratory isolation and identification of E. coli or mycoplasma from lesions. Detection of mycoplasma colonies using fluorescent antibody test, recombinant probe and hybridisation or antigen capture ELISA.

Serology includes ELISA, plate agglutination and Haemagglutination-inhibition, (HI) testing of sera for antibodies against mycoplasma.

A cheesy exudate in the air sacs is a presumptive diagnosis.

Treatment and control:

Prevention

Hatch stock free of mycoplasma infection. Use pelleted feed to kill E. coli. Vaccinate breeders against E. coli, MG, MS, NDV, IBV, ILT and infectious bursal disease (IBD) to prevent the disease.

Vaccinate progeny against ND, IB, ILT and IBD, hatch and place mycoplasma infected stock separate from mycoplasma negative stock to reduce the spread of the organism. Treat all mycoplasma positive flocks with antibiotics to reduce spread into eggs.

Medicate all mycoplasma-positive broilers for the first 7-10 days in the feed or water.

Treatment

Effective drugs include tylosin, LS 50® and quinolones.

MYCOPLASMA INFECTIOUS SINUSITIS[កែប្រែ]

Causes:

Small procaryotic microorganisms- Mycoplasma gallisepticum; M. meleagridis. Spread vertically through hatching egg contact or contact with infected birds by aerosol.

Effects:

Signs include nasal discharge, emaciation, increased condemnation, sneezing and coughing, swollen infraorbital sinus (above the eye), feed refusal, foaming of the eye and/or air sacculitis.

Detailed cause:

All species of bird or all ages are susceptible to this chronic disease. The agents involved in the aetiology of this disease are Mycoplama gallisepticum (MG) and M. meleagridis (MM) in turkeys. (MM is found only in turkeys).

Mode of transmission

Spread through egg or contact with infected birds by aerosol (also through indirect contact via people and other fomites).

Clinical signs:

Signs include nasal discharge, emaciation, increased condemnation, sneezing and coughing, swollen infraorbital sinus (above the eye), feed refusal, foaming of eye, and/or air sacculitis.

Postmortem lesions

Caseous sinus and air sacculitis can be seen.

Diagnosis:

Serologial tests include plate agglutination, HI or ELISA test.

Isolate organism from the sinus and identify with antigen capture ELISA test and monoclonal antibody; fluorescent antibody or recombinant probe and nucleic acid hybridisation assay.

It simulates many diseases including coryza, NDV, E. coli and IBV.

Treatment and control:

Prevention

Depopulate infected stock, hatch clean stock only, vaccination of pullets for MG with live or killed vaccine to prevent the disease.

Treatment

Drugs, which can be used, include tylosin, LS 50® at (2 g/gal), quinolones and spiramycin*.

*Not approved for use in the US.

MYCOPLASMA INFECTIOUS SYNOVITIS[កែប្រែ]

Causes:

Mycoplasma synoviae. Spread through the egg and laterally by aerosol. Mechanical transmission occurs via people equipment, vehicles etc.

Effects:

Signs include breast blisters, pale or shrunken combs, lameness, ruffled feathers, greenish droppings with large amounts of urates. Birds sit on hocks, are dehydrated, listless, have hot swollen hock and wing joints and foot pads. Layers may have lowered egg production and shell quality. Mycoplasma synoviae can also cause respiratory disease (increased vaccination reaction).

Detailed causes:

Chickens and turkeys of all ages are susceptible to this acute to chronic disease. The aetiology agent involved is M. synoviae.

Mode of transmission

Spread through egg and laterally by aerosol. Also transmitted by people, vehicles etc.

Clinical signs:

Signs include breast blisters, pale or shrunken combs, lameness, ruffled feathers, greenish droppings with large amounts of urates.

Birds sit on hocks, are dehydrated, listless, have hot swollen hock and wing joints and foot pads and/or lowered egg production and shell quality.

Postmortem lesions

Lesions include viscous creamy to grey exudate in yolk, synovial membranes and tendon sheaths, joints, keel bone over breast and hepatospleenomegaly.

Honey coloured fluid on breasts and joints, swollen, mottled and pale kidneys may be present.

Diagnosis:

ELISA test for antibodies is important.

Isolate organism from medium on agar. Identification of the organism using Giemsa stain of culture or antigen capture ELISA with monoclonal antibody, nucleic acid probe test or fluorescent antibody.

It simulates bacterial or viral arthritis.

Honey (yellow) coloured fluid from swollen joints is a presumptive diagnosis.

It simulates synovitis by Staphylococcus aureus.

Treatment and control:

Prevention

Prevention includes regular serological testing of breeder flocks, vaccination of pullets with killed bacterin or temperature sensitive live vaccine by water, one age per farm and all-in-all-out management.

Treatment

Effective drugs include tylosin, LS 50® at 2 g/gal, and quinolones.

MYCOPLASMA TURKEY VENEREAL DISEASE[កែប្រែ]

Causes:

Mycoplasma meleagridis, M. iners. Spread by mating via semen; transovarian route to progeny; and laterally among poults by aerosol.

Effects:

Signs include high embryonic mortality, stunted growth, air sacculitis and lameness. Hock joint swelling, deformation of cervical vertebrae and feather deformities may occur.

Detailed causes:

It spreads through artificial insemination of turkeys with contamination semen. Breeders are susceptible to this chronic disease, often subclinically and pass organism to poults, which slow lameness and feather deformities. The agents involved in the aetiology of this disease include M. meleagridis and M. iowae.

Mode of transmission

Spread by mating via semen or transovarian to progeny and laterally among poults by aerosol.

Clinical signs:

Signs include high embryonic mortality, stunted growth, air sacculitis and lameness (bowing and twisting of legs and shortening of the tarseometatarsal bone). Hock joint swelling, deformation of cervical vertebrae and feather deformities may occur.

Postmortem lesions

Lesions include skeletal deformities especially of the neck and legs and air sacculitis.

Diagnosis:

Diagnosis is by serology (ELISA or HI test) and/or isolation of organism from lesions. It simulates other mycoplasma infections and nutritional deficiencies.

Treatment and control:

Prevention

Prevention is by dipping eggs in tylan or heating eggs to kill mycoplasma. Depopulate infected breeders, hatch only MM or MI clean flocks and/or inject poults or eggs with antibiotics and/or treat in the feed or water.

Treatment

Medications include Tylosin or LS-50® in water, quinolones, gentamycin, nalidixic acid*, tiamulin*, or spiramycin*.

*Not approved in the United States.

NECROTIC ENTERITIS[កែប្រែ]

Causes:

Newcastle disease virus belongs to the family Paramyxoviridae. The organism is transmitted by soil, dust, litter and faeces. Can be induced by choice of raw materials in feed and/or coccidiosis. Clostridium perfringens can become especially prevalent in the small intestine when no growth promoters are used.

Effects:

Ataxia, intoxication, diarrhoea, depression, ruffled feathers, reluctance to move. It may also cause dysbacteriosis, leading to vitamin or mineral deficiency.

Detailed causes:

All types of chickens from two weeks onwards are susceptible to this acute to chronic disease. The agent involved in the aetiology of the disease is Clostridium perfringens which produces types A and C alpha toxin and type C beta toxin. It is also called creepers because chickens are sometimes ataxic (can’t move).

Mode of transmission

Soil, dust, litter and faeces spread the organism.

Special note

It may cause malabsorption syndrome leading to vitamin or mineral deficiency.

Clinical signs:

Ataxia, intoxication, diarrhoea, depression, ruffled feathers and reluctance to move may be seen.

In acute cases death can occur within hours of the disease onset.

Postmortem lesions

Dehydration (darkened skin), emaciation (no breast muscle), congested liver, cooked (ruffled up) intestinal mucosa – primarily of the jejunum and ileum can be seen. Intestines are often distended and filled with gas. There is water in the crop.

In acute cases enteritis occurs with just a grey layer of necrotic material on the mucosa.

Diagnosis:

Diagnosis is based on the gross lesions (ruffled intestinal mucosa), clinical signs and bacterial isolation on blood agar plate. Colonies are surrounded by an inner zone of complete haemolysis and an outer zone of discolouration and incomplete haemolysis.

It simulates coccidiosis and ulcerative enteritis.

Treatment and control:

Prevention

Bacitracin 50 g/ton given continuously in the feed, improved sanitation, lincomycin in feed or water. Rearing birds on wire will prevent the disease.

Treatment

Bacitracin (200 g/T) in the feed and vitamins and minerals in the water to reduce the disease.

Lincomycin, ozytetracycline, amoxicillin and tylosin can also be used to treat the disease.

Note

Bacitracin is now banned in most countries.

NEWCASTLE DISEASE (ND)[កែប្រែ]

Causes:

Virus- Newcastle disease virus is a single-stranded, non-segmented enveloped RNA virus belonging to the family Paramyxoviridae. There are three pathotypes: lentogenic (mild disease), mesogenic (moderate disease) and velogenic (severe morbidity and mortality). Spread is airborne by inhalation or by ingestion of the virus.

Effects:

Incubation period is 2-15 days. Paralysis, incoordination and central nervous signs following the initial respiratory signs are diagnostic of NDV. Watery eyes and a plug in the eye are seen with lentogenic strains. Coughing, gasping and sane mortality are seen with mesogenic strains. Egg production and egg quality are affected. It may [produce torticollis, paralysis and bloody diarrhoea. High morbidity and mortality occur with velogenic pathotype.

Detailed causes:

This disease was named after a town in England where it was first isolated. All species of bird of all ages are susceptible to this acute to chronic disease. It is one of the most common respiratory diseases of poultry and occurs worldwide. The agent involved in the aetiology of this disease is a single-stranded, nonsegmented, enveloped, RNA virus belonging to paramyoviruses. Three pathotypes or strains exist. The lentogenic cause mild disease, the mesogenic produce moderate disease and the velogenic produce severe morbidity and mortality.

Mode of transmission

It is airborne and spread by inhalation or ingestion of virus.

Migratory birds may spread the infection from country to country.

Special note

VVND is a notifiable disease.

It is a very common viral disease of poultry worldwide. Most poultry are vaccinated several times against this virus.

Clinical signs:

(The incubation period is 2-15 days).

Watery eyes and a plug in the eye are seen with lentogenic strains.

Coughing, gasping and sane mortality are seen with mesogenic strains.

It affects egg production and quality (brown broiler eggs turn to white eggs). It may produce torticollis, paralysis and bloody diarrhoea. High morbidity and mortality occur with visceral tropic velogenic (VVND). VVND (exotic) rarely occurs in commercial poultry in the United States. The last outbreak of VVND occurred in 1976 in California and resulted in destruction of 20 million birds. However, outbreaks in pet bird populations are more frequent. It is a common problem in many countries such as the Middle East, Africa and the Far East.

Postmortem lesions

Lesions include cloudy air sacs, congestion and oedema of lungs, abdominal yolk, oedema of bronchi and parbronchi, mucous in trachea and nasal turbinates. Internal haemorrhage may be seen inn VVND (lungs, intestines, gizzard, proventriculus and caecal pouches).

Diagnosis:

The clinical disease (respiratory and central nervous signs) and gross and microscopic lesions in trachea, nasal trubinates and lungs are helpful in the diagnosis.

Paralysis, incoordination, central nervous signs after first respiratory signs, are diagnostic for NDV. It can be complicated by Mycoplasma or E. coli resulting in CRD and severe air sacculitis. Domestic lento or mesogenic NDV cause mild respiratory disease. Isolate and identify virus from trachea of clinically ill birds in cell culture or chicken embryos for definitive diagnosis.

The HI or ELISA test for measuring a rise in antibody titer is helpful.

Treatment and control

Prevention

Vaccinate by coarse spray or eyedrop at one day, or by water or coarse spray at seven days old. In VVND areas, an inactivated vaccine may also be given at 1 and/or 14 days of age.

Revaccination by water or spray is done at 14-21 days.

Breeders or layers can be vaccinated by water or coarse spray at 6-8 week intervals throughout the growing period in areas with high infection pressure.

An inactivated NDV vaccine can be used at around 18 weeks for breeders or layers. Continue live vaccination throughout lay every 6-8 weeks.

In the US the B1 strain is used for the 1st and 2nd vaccination, and lasota or cloned lasota is used thereafter. Outside of US, Hitchner B1 is less used because it gives only limited protection. Instead, primovaccination is given with cloned lasota.

NDV vaccination is usually combined with infectious bronchitis (IB) vaccine. Outside the US, it is preferred to give IB and ND separate to avoid interference of these vaccines. Only in case of cloned IB vaccine, combinations can be used without loosing effect.

Biosecurity is important to control the disease. Imported birds are subject to import quarantine regulations.

Treatment

In many countries, a stamping out policy is used for Newcastle disease. Were allowed, emergency vaccination in case of acute outbreaks help to reduce clinical problems.

A broad-spectrum antibiotic can be given to control secondary invaders, especially E. coli from causing CRD.

NIACIN DEFICIENCY[កែប្រែ]

Causes:

Deficiency of niacin (nicotinic acid) in the diet.

Effects:

Signs include reduced feed consumption, body weight loss and lameness in young birds. Reduced hatchability can occur. Inflammation of the mouth, diarrhoea and reduced feathering may also occur.

Detailed causes:

Nicotinic acid or niacin is the vitamin component of two important coenzymes (NAD and NADP). These enzymes are involved in carbohydrate, fat and protein metabolism. They are especially important in metabolic reactions that yield energy. All species of bird, both young and adults, are susceptible to this disease.

Mode of transmission

Deficiency in the diet.

Clinical causes:

Signs include reduced feed consumption and body weight and lameness in young birds. Reduced hatchability can occur in adults.

Inflammation of the mouth, diarrhoea and reduced feathering may also occur.

Postmortem lesions

Enlargement of the hock joint and bowing of the legs is similar to perosis, however, the tendon rarely slips from its condyles as in perosis.

Diagnosis:

Analysis of feed for niacin is diagnostic.

Treatment and control:

Prevention

Quality control of feed

Treatment

Restore correct levels of niacin to the diet

NITROFURAN TOXICITY[កែប្រែ]

Causes:

Ingestion of food or water with too high a level of nitrofurone antibacterial drug.

Effects:

Incoordination, loud vocalisation, opisthotonos (arching of the head and spine backwards), aimless running, flying, partial paralysis, ascites and convulsions can be seen. Birds are commonly found on their sides.

Detailed causes:

Common antibiotic and anticoccidial compounds. Chickens, turkeys and ducks or all ages, but in particular young, are susceptible to this acute to chronic disease. The agent involved in the aetiology of this disease is nitrofurazone (NFZ), toxicity causes dose-related biventricular cardiomyopathy and prominent dilation of ventricles and thinning of the right or left ventricle.

Mode of transmission

Ingestion of food or water with too high a level of the drug causes the disease.

Special note

It is a drug residue problem. Nitrofurans are commonly added to the water to treat bacterial septicaemia. Nitrofurans are a class of broad-spectrum antibacterial compounds. However, they have been recently withdrawn for use in the United States by the FDA.

Clinical signs:

Incoordination, loud vocalisation, opisthotonos (arching of the head and spine in a backwards direction), aimless running, flying, partial paralysis, ascites and convulsions can be seen.

Birds are commonly down on their sides.

Postmortem lesions

Catarrhal enteritis, lung oedema, congestion of the kidneys of liver, cardiac enlargement, and ascites can be observed.

Diagnosis:

Feed analysis is diagnostic.

Clinical signs, gross and microscopic lesions are helpful. Microscopic heart lesions include oedema, thinning of mycocardial muscle fibres and increased connective tissue.

It simulates coban toxicity, salt toxicity and ascites, which may cause right ventricular hypertrophy.

Treatment and control:

Prevention

A spot check of feed or water is helpful.

Treatment

Fresh feed or water will reverse the disease.

NORTHERN FOWL MITE (LICE AND MITES, CHICKEN MITE, DARKLING BEETLE)[កែប្រែ]

Causes:

A mite of the order Acarina- Dermanyssus gallinae, also know as red mite, roost mite and poultry mite.

Effects:

Increase in feed consumption accompanied by lower production. Serious infestations are associated with anaemia, and can cause death, particularly in chicks and settling or laying hens. Birds may refuse to lay in infested nests. Often resistant to treatments, so difficult to control.

Detailed causes:

The chicken mite (Dermanyssus gallinae), also called red mite, roost mite, or poultry mite, is found worldwide. It is particularly serious in warmer parts of the temperate zone in older poultry house with roosts. The mite is rare in modern large commercial caged-layer operations but is seen frequently in modern broiler breeder farms. It can be identified by the shape of the dorsal plate and by the long whip-like chelicerae that appear to be stylets.

The adult female measures about 0.7mm x 0.4mm, varying in colour from grey to deep red, depending on its blood content. The life cycle may be completed in as few as 7 days. Adult females lay eggs in surroundings of the hosts 12-24 hours after their first blood meal. Eggs hatch in 48-72 hours when warm. The 6-legged larvae moult in 24-48 hours without feeding, becoming first-stage bloodsucking nymphs; they then moult to second-stage nymphs in another 24-48 hours and soon afterwards moult to the adult stage.

Chicken mites can live up to 34 weeks without food.

Clinical signs:

Chickens are the most common hosts, but these mites may occur on turkeys, pigeons, canaries and several species of wild birds. People may also be attacked, and invasions of human dwellings (apartments, hospitals, doctors’ offices) by mites from outdoor pigeon nests are frequently seen. English sparrows may transmit this parasite because of the habit of lining their nests with chicken feathers. These mites may not only produce anaemia, thereby seriously lowering production and increasing feed consumption, but actually kill birds, particularly chicks and settling or laying hens. Birds in production may refuse to lay in infested nests.

An increase in feed consumption accompanied by lower production is a sign that poultry houses should be examined for mites. These mites often can be found by looking under loose clods of manure, under slats in a breeder house, in nests or in cracks and crevices of posts and roof bracing. They are evident as tiny red to blackish dots, often clustered together. Inspection during the night is usually necessary to find mites on birds.

Occasionally these mites may be found on the shanks of both hens and rooster, but care must be taken to differentiate them from northern fowl mites that also appear on the legs.

Diagnosis:

Lice, are members of the Class Insecta, characterised by a body divided into three regions (head, thorax, abdomen), chewing-type mandibles located ventrally on the head incomplete metamorphosis, no wings, dorsoventrally flattened body, and short antennae with 3-5 segments.

It is necessary to examine bedding, roosts, walls, cracks and crevices and beneath manure clods. Nest material, dust and other material collected in the house can be spread out on a white pan and examined. The arthropods can be seen crawling on the pan. Night-time examination of birds may detect parasites that feed on them at night. Poultry infested with parasites exhibit irritation and react by scratching and preening. Any unexplained production drop or increase in feed conversion is cause to look for external parasites.

Mites are more easily seen with a magnifying lens.

Treatment and control:

Prevention

Galliform wild or domestic birds should never be allowed to come into contact with poultry flocks.

To monitor birds in a production facility, 20-50 birds should be checked a minimum of two times a month.

•           Birds should b checked at random and should be chosen from all parts of the house.

•           The vent, head and legs should be closely examined.

•           If parasites are found and cannot be identified at first glance, specimens should be sent to a laboratory to have the specific identity determined.

In caged-layer flocks it is important that the birds are checked on a regular basis.

Treatment

Spraying of birds is the best choice for most practical means. Birds should be treated twice on a 7-10 day interval. Care should be taken when spraying to ensure that the whole bird is treated, as it is common for lice to move to the neck from the vent when populations are large.

In houses, the egg-laden feathers will be a source of re-infestation and when the house is depopulated, a thorough cleanup should be completed.

Many lice are resistant against the commonly used products, so testing of efficacy is recommended.

NUTRITIONAL MUSCULAR DYSTROPHY (VITAMIN E/SELENIUM DEFICIENCY)[កែប្រែ]

Causes:

Deficiency of Vitamin E and/or selenium in the diet.

Effects:

Weakness and signs of unthriftiness.

Detailed causes:

This disease is a vitamin E and/or selenium deficiency. All species of young birds are susceptible to this disease.

Mode of transmission

Deficiency in the diet.

Clinical signs:

Birds are weak and unthrifty signs occur.

Postmortem lesions

Light coloured streaks of easily distinguished affected bundles of muscle fibres in the breast (myopathy), of the gizzard and heart muscles can occur.

Diagnosis:

Gross and microscopic muscle lesions are characteristic. Microscopic lesions include hyaline degeneration, followed by disruption of muscle fibres.

Treatment and control:

Treatment

Restore proper levels in the diet.

OCHRATOXICOSIS[កែប្រែ]

Causes:

Consumption of feed containing grain (corn, wheat and barley) which is contaminated with ochratoxin produced by Aspergillus ochraceous or Penicillium viridicatum.

Effects:

Diarrhoea, depressed growth, reduced pigmentation, soiled eggs, tremors, hypotension and bradycardia (Slow heart rate). In laying hens, reduced egg production, fertility and hatchability, and reduced egg size and shell quality can also occur.

Detailed causes:

Mycotoxins are toxic metabolic by-products of fungal growth on grains. High moisture content of grains can lead to fungal growth and toxin production. Fungi can produce toxins before or after grain harvest. Drought and insect damage to grain increase susceptibility of grain to fungal growth. This happens mainly with grains produced in colder climates.

All ages, but in particular young birds are susceptible. This disease has an acute to chronic action depending on the level of toxin (high levels produce acute disease, low-chronic), duration of exposure (long term-chronic, short term-acute) and the age of the bird (young birds have acute, old-chronic). Consumption of feed containing grain (corn, wheat and barley), which has been contaminated with toxin produced by. Aspergillus ochraceous or Penicillium viridicatum may cause ochratoxin intoxication.

Mode of transmission

Consumption of feed containing toxin causes the disease.

Clinical signs:

Signs include diarrhoea, depressed growth, reduced pigmentation, soiled eggs, tremors, hypotension and bradycardia (slow heart rate).

Reduced egg production, fertility and hatchability and reduced egg size and shell quality can occur.

Postmortem lesions

Fatty liver with haemorrhage, enlarged pale kidneys with urates, heart necrosis, and urate deposits on the liver, spleen and pericardium can be seen.

Diagnosis:

The clinical signs and lesions are helpful, but the only definitive diagnosis is from feed analysis for the presence of toxin.

It simulates aflatoxicosis, visceral gout, infectious bronchitis (IB), IBD, citrinin toxicity and malabsorption syndrome.

Treatment and control:

Prevention

Feed ingredients should be dried thoroughly and feed bins sanitised. Mouldy feed should never be given to birds. Mould inhibitors can be added to the feed and feed storage time reduced to prevent the growth of fungi and toxin production. Toxin binders, have little or no effect on ochratoxin.

Treatment

Increasing the protein, vitamin and mineral and energy content of the diet can alleviate symptoms. Ochratoxin is less common than aflatoxin, but is more toxic (ppb) and immunodepressive.

ORGANIC ARSENICAL TOXICITY[កែប្រែ]

Causes:

Phenylarsonic acids are commonly added to feed as growth promotants, para-ureidobenzenearsonic acid and dimetridazole are used to prevent and control protozoal diseases. Accidental overdose or in dehydrated birds causes toxicity.

Effects:

Peripheral neuropathy causes ataxia and incoordination, stunting, depression and lameness.

Detailed causes:

Organic arsenicals are common growth promotants. All species of bird of all ages are susceptible to this acute disease. The agents involved in the aetiology are Phenylarsonic acids (or 3-nitro, 4-hydroxy Phenylarsonic acid) which are commonly added to improved feed efficiency. Para-ureidobenzenearsonic acid) and dimetridazole are used for prevention and control of various protozoal diseases.

Mode of transmission

Accidental overdose in feed or water.

Clinical signs:

Peripheral neuropathy causes ataxia and incoordination, stunting, depression and lameness.

Postmortem lesions

A small body weight and empty digestive tract are evident.

Diagnosis:

Clinical signs following new feed shipment or initiation of drug treatment in the water, indicate organic arsenical toxicity.

Microscopically, peripheral nerves may show loss of myelin, fragmentation of axons and proliferation of neurilemmal cells.

Diagnosis is by feed analysis. It simulates Newcastle disease, MD, AE and ionophore toxicity.

Treatment and control:

Prevention

The correct level of the drug in feed or water will prevent clinical signs.

Treatment

Fresh feed or water will stop the signs.

ORNITHOBACTER (ORT)[កែប្រែ]

Causes:

Gram-negative, non-sporulating rod shaped bacterium, Ornithobacterium rhinotracheale. Recently isolated, formerly known as a Pasturella-like organism, Kingella or Taxon 28.

Effects:

Broiler breeders (24-52 weeks of age) show slightly increased mortality, decreased feed intake, mild respiratory signs, decreased egg production, poor egg shell quality and decreased egg size. In young chickens, coughing, sinusitis and sometimes respiratory distress and oedema of the head are seen, leading to increased mortality and higher condemnations at processing.

Detailed causes:

The bacterium Ornithobacter rhinotracheale (ORT) was only identified in the 1990’s, but has received much attention since then. Twelve different serotypes of ORT are known. The disease is an acute, contagious respiratory disease of chickens and turkeys. Early research has suggested that the organism is not a primary pathogen and can unfold its pathogenic properties only in association with primary pathogens. However, these results have been disputed, especially through experience in the field with turkeys.

The course and duration of the disease depend on such factors as climate, stocking rate and other simultaneous infections.

Clinical signs:

ORT is often isolated from chickens without obvious clinical signs. Clinical signs are coughing, nasal discharge and sinusitis. Sometimes there is respiratory distress and oedema of the head. In broiler breeders, clinical signs are usually observed early in the production period and consist most importantly of a decrease in egg production of 2-5%, lower egg weight and poor eggshell quality. In broilers, ORT symptoms occur between oedema, depression, increased mortality and low growth. Increased slaughterhouse condemnations may occur.

At postmortem, clinically diseased birds may reveal various gross lesions including rhinitis, sinusitis, tracheitis, airsacculitis, pneumonia, pericarditis and arthritis. Foamy or cheesy exudate in the air sacs is often seen as an indication for ORT.

Diagnosis:

In vitro, ORT bacteria grow slowly and need special growth conditions such as 5-10% CO2. ORT may therefore easily be overgrown by other bacteria that are present, such as E. coli. Suspected chickens should therefore be sampled early in the disease. The addition of gentamicin and polymyxin to the medium contributes to a more selective isolation of ORT.

Treatment and control:

Amoxycillin and doxycyclin are most effective drugs, but resistance often occurs. In the late 1990’s, an inactivated vaccine was developed against ORT. Offspring from broiler breeders vaccinated against ORT have shown increased resistance to the disease for up to three weeks of age.

ORNITHOSIS (PARROT FEVER, PSITTACOSIS)[កែប្រែ]

Causes:

Obligate intracellular bacterium- Chlamydia psittcai. Spread by faeces and airborne route.

Effects:

Has public health significance and is a reportable disease. Signs in poultry include fever and sleepiness, depending on the strain. Toxigenic strains cause high morbidity and mortality, whereas the non-toxigenic strain produces a mild respiratory or gastrointestinal disease. There may also be a drop in egg production and green droppings.

Detailed causes:

It causes fever in man and Pscittacine birds.

The causative agent, Chlamydia psittaci, is an obligate intracellular bacterium. The organism has a complex development cycle, which result in a change from the elementary body to the Reticulate body in the host.

Mode of transmission

It is spread by faeces and airborne. Processing plant exposure may occur for humans.

Special note

Primarily turkeys on range and aviary birds are affected.

It has public health (can cause disease in humans) importance and is a notifiable disease. It can produce high fever, flu-like illness and mortality in humans; causes abortion in cattle. Cats and pigeons spread organisms. Veterinarians, pet bird owners and processing plant employees are a high-risk population.

Clinical signs:

Signs include fever and sleepiness depending on the strain. Toxigenic strain causes high morbidity and mortality, whereas the non-toxic produces a mild respiratory or gastrointestinal disease.

There may be a drop in egg production and green droppings.

Postmortem lesions

There can be a fibrinous pericarditis, air sacculitis and hepatitis. Large congested spleen, pneumonia, congested kidneys, liver, swollen necrotic vent and brain haemorrhage (parrots) can be seen.

Diagnosis:

Eliminate CRD due to mycoplasma, ND or infectious bronchitis (IB) and E. coli. Laboratory isolation of organism in chicken embryos or mice. Serology (complement fixation) test, or latex agglutination test can be done. Recovered birds shed organism up to 42 days.

Giemsa stain from tissue impression smears reveal red EB’s or bluish-green RBs. Antigen capture ELISA will stain Chlamydia smear from swabs or vent or cleft (Abbot or Kodak, Labs.).

It simulates CRD, colibaccillosis, influenza and cholera.

Fibrinous pericarditis, air sacculitis and congested spleen in turkeys is diagnostic.

Treatment and control:

Prevention

Destroy dead birds, prevent wild and free-flying bird exposure and quarantine infected flocks.

Treatment

CTC 400 g/ton (3 weeks) and Doxycyline* are effective drugs.

*Not approved in the United States for use in commercial poultry

OSTEOPETROSIS (MARBLEBONE, THICK LEG DISEASE)[កែប្រែ]

Causes:

RNA retrovirus- belongs to subgroup B of lymphoid leukosis viruses.

Effects:

Incubation period is 1 month. Long bones of legs show a uniform or irregular thickening of the diaphysial or metaphysial regions. A stunted pale bird with "boot-like" shanks, walking with a stilted gait or limp is characteristic of the disease.

Detailed causes:

This is a rare type of leucosis. Chickens of 8-12 weeks are susceptible to this chronic disease. The agent involved in the aetiology is a RNA virus belonging to the family retroviridae, which belongs to subgroup B of lymphoid leucosis viruses.

Mode of transmission

It is spread transovarian or laterally among hatchmates.

Clinical signs:

The incubation period is 1 month.

Long bones of the limbs show a uniform or irregular thickening of the diaphysial or metaphysical regions.

A characteristic sign is a stunted, pale bird, with "boot-like" shanks. The birds walk with a stilted gait or limp.

Postmortem lesions

Bone alternations occur in the diaphysis of the pelvis, shoulder girdle and ribs. Distinct pale yellow foci occur against the grey-white translucent normal bone. The periosteum is thickened and abnormal bone is spongy and is easily cut.

Osteopetrosis and lymphoid leucosis frequently occur together in the same bird.

There can be atrophy of the spleen, bursa and thymus.

Diagnosis:

Gross and microscopic observation of bone tumours are diagnostic. Spongy bone converges centripetally toward the centre of the shaft. There is an increase in size and irregularity of Haversian canals and increase in number and size of lacunae. Osteocytes are more numerous, large and eosinophilic. New bone is basophilic and fibrous.

It simulates rickets and osteoporosis.

Treatment and control:

Prevention

Virus-free breeders should be selected

Treatment

None.

PALE CHICK OR BIRD SYNDROME (MALABSORPTION SYNDROME, INFECTIOUS PROVENTRICULITIS, STUNTING/RUNTING SYNSROME, HELICOPTER DISEASE)[កែប្រែ]

Causes:

Unknown. Various viruses, eg REO, Rota, corona, calici, Toga etc may play a role, combined with nutritional and possibly genetic factors.

Effects:

Incubation period is 7-14 days. Stunting, abnormal feathering, pale comb, wattles and legs are seen. Higher early mortality, weak legs, CNS signs (tremors, incoordination) and passage of undigested food in faeces can also occur. Delayed and poor egg production peaks may occur in layers and breeders.

Detailed causes:

There are a number of enteric disease conditions affecting young poultry that go undiagnosed with respect to identifying a definite aetiological agent. Thus a group of diseases of this nature have been termed "viral enteritis" but diseases with similar signs have been reported from many different countries under many different names. These include "malabsorption syndrome" "infectious stunting syndrome" "broiler runting syndrome" "pale bird syndrome" and "helicopter disease". In turkeys, names such as "turkey viral enteritis" "poults enteritis" "malabsorption syndrome" or "maldigestion syndrome"

Reported observations provide strong evidence that this is an infectious disease, although the involvement of non-infectious agents has not been completely ruled out. Because no recognised enteropathogen has been consistently incriminated as the aetiological agent, research has discovered and/or identified numerous viral agents. Several viruses have either been observed or isolated from the intestinal tract of chickens experiencing viral enteritis. A number of viral particles resembling caliciviruses, coronaviruses, togaviruses, parvoviruses and picornalike viruses (pseudopicornaviruses) have been identified. One virus isolated from the intestines of four-day-old chickens showing signs of infectious stunting syndrome has been named the FEW virus. However, it should be remembered that the isolation of a particular viral agents does not it self constitute a cause and effect relationship for that disease.

Clinical signs:

Incubation period of 7-14 days.

Stunting (stunting or runting syndrome), abnormal feathering (helicopter disease), pale comb, wattles and legs in broilers (pale bird syndrome) are seen.

Higher early mortality, weak legs, CNS signs (tremors, incoordination) and passage of undigested food in faeces can occur.

Delayed and poor egg production peaks may occur in layers and breeders.

Postmortem lesions

Enteritis can cause undigested feed in intestines and pale intestines haemorrhages around heart may also be seen.

Anaemia, seen as decreased pigmentation and atrophy of the pancreas and bursa of Fabricius can occur.

An enlarged proventriculus with glandular enlargement and a loss of the normal structural architecture (infectious proventiculitis) may be evident.

Brittle bones and femoral head necrosis with rickets, hydropericardium (water around the heart), a small flaccid (flabby) gizzard, and encephalomalacia can often arise.

Diagnosis:

The clinical signs and gross lesions (particularly proventricular hyperplasia and atrophied pancreas) are characteristic.

Treatment and control:

Prevention

A live vaccine at 1-2 and 6-8 weeks by injection, coarse spray or water and inactivated malabsorption and VA vaccine at 18-20 weeks for breeders and layers will help control diseases. Some broiler flocks are vaccinated at 1-7 days with VA vaccine.

Treatment

It responds to antibiotics plus vitamin-mineral supplementation for control of secondary infection.

Vinegar in water (1%) kills viruses by reducing intestinal pH, and reduces spread of virus and some clinical signs.

PANTOTHENIC ACID DEFICIENCY[កែប្រែ]

Causes:

Deficiency of pantothenic acid in the diet.

Effects:

Dermatitis, broken feathers, perosis, poor growth and mortality can be seen. Contracting of the eyelids and scabs around the eyes, poor vision, and low hatchability of the eggs can also be evident.

Detailed causes:

Pantothenic acid is a component of coenzyme A, which is involved in the formation of citric acid, synthesis and oxidation of fatty acids, oxidation of ketoacids resulting from deamination of amino acids, acetylation of choline and many other reactions.

Mode of transmission

A deficiency in the feed causes the disease.

Clinical signs:

Dermatitis, broken feathers, perosis, poor growth and mortality can be seen. Sicca (contracting of the eyelids), poor vision and low hatchability of the eggs can be evident.

Postmortem lesions

Pus-like lesions occur at the corner of the mouth and grey-white exudate in proventriculus, hypertrophy of the liver, atrophy of the spleen, and kidneys are enlarged.

Perosis is seen as enlargement of the hock joints, bowing of legs and slipping of tendon. The tibia may also rotate out of the condyle.

Diagnosis:

Feed analysis is needed.

Treatment and control:

Prevention

Quality control of feed.

Treatment

Adjust the nutrient level in the feed.

PARAMYXOVIRUS INFECTIONS[កែប្រែ]

Cause:

Paramyxoviruses are single stranded, non-enveloped RNA viruses. PMV types I (NDV), II and III are serologically distinct.

Effects:

PMV II produces a mild respiratory disease, with sinusitos, elevated mortality, low egg production and reduced fertility and hatchability. PMV III produces a mild respiratory disease with lower egg production and poor shell quality. PMV VI produces a mild respiratory disease and egg production losses.

Detailed causes:

Paramyxovirus (PVM) II affects chickens and turkeys; PMV III affects turkeys, pigeons and pisttacine birds; PMV VI affects turkeys. Birds of all ages can be affected. Paramyxovirus are single-stranded, nonenveloped RNA viruses. PMV I (Newcastle disease virus), PMV II and PMV III are all serologically distinct.

Mode of transmission

Spread is aerosol as with NDV.

Clinical signs:

PMV II produces a mild respiratory disease, sinusitis, elevated mortality, low egg production and reduce fertility and hatchability.

PMV III produces a mild respiratory disease with lower egg production and poor egg shell quality.

PMV VI produces a mild respiratory disease and egg production losses.

Gross lesions

All PMV’s produce mucous in the nasal turbinates, sinuses, trachea and oedematous bronchi, parabronchi and lungs.

Diagnosis:

The clinical disease, and gross and microscopic lesions are helpful aids in the diagnosis. Isolation and identification of virus in chicken embryos or cell culture is necessary for a definitive diagnosis.

Serological analysis of antibodies against PMV’s using ELISA or hemagglutination inhibition is also helpful.

It simulates NDV, IB, Coryza, chronic respiratory disease (CRD), and infectious laryngotracheitis (ILT).

Treatment and control:

Prevention

An inactivated vaccine against PMV IV is available for use in turkeys or pigeons only.

Treatment

Antibiotics in feed and water for secondary invaders are helpful.

PARATYPHOID (SALMONELLOSIS)[កែប្រែ]

Causes:

There are more than 2000 Salmonellas. A lot of them can infect chickens. S. Enteritidis and S. typhimurium are salmonellas. The most important is a facultative anaerobe, with motile flagella, which produces endotoxins. Many routes of transmission. Difficult to eradicate as it can be transmitted by many wild biological vectors.

Effects:

Young birds tremble, whereas birds older than 1 month usually show subclinical disease. Young birds act cold, gasp and are anorectic. Watery diarrhoea, blindness, conjunctivitis, weakness and lameness can occur. Often a carrier without symptoms. Risks for human health.

Detailed causes:

Chickens of all ages, are susceptible to this acute to chronic disease. The agents involved in the aetiology of this disease are Salmonella enteritidis/typhimurium and other species; at least 33 Salmonella shown to infect birds. All are serologically related. They are a facultative anaerobe, with motile flagella and produce endotoxins.

Clinical signs:

  • Young

Young birds tremble, whereas birds older than 1 month are usually subclinical. Young birds act cold, gasp and are anorexic (do not eat). Watery diarrhoea, blindness, conjunctivitis, weakness and lameness can occur.

  • Adults

Subclinical.

Postmortem lesions

Congested organs, caseous caeca, necrotic foci in the heart and air sacs may be seen. Unabsorbed yolks, pericarditis, arthritis, haemorrhagic enteritis in the duodenum and haemorrhagic streaks in the liver can occur.

Diagnosis:

Serologic plate agglutination ELISA haemagglutination test can monitor antibodies in the bird.

Salmonella can be cultured from lesions or faeces on tetrathionate broth base with brilliant green or selenite agar. There are no definitive signs or lesions.

Treatment and control:

Prevention

Fumigation of hatching eggs with formaldehyde on the farms. Collect hatching eggs 5 times per day. Clean eggs, test breeders for positive serum using ELISA.

Inject chicks at day 1 with antibiotics (gentamicin (0.2 mg), naxal or spenctinomycin). Irradiation of meat where available. Chlorinate water in the processing plant. Commercial live and attenuated vaccine available for pullets against S. enteritidis and S. typhimurium. Dipping poultry carcass in trisodium phosphate to prevent attachment of bacteria to the carcass. Probiotics given by feed or water at any early age of life.

Treatment

Nitrofuran (50-200 g/T), neomycin, gentamicin and sulphur drugs can be used. Competitive exclusion of Salmonella from the intestinal tract with Lactobacillus or other probiotic cultures.

Break out an pasteurise all eggs from S. enteriditis-infected flocks.

PHOSPHORUS DEFICIENCY[កែប្រែ]

Causes:

Deficiency of phosphorus in the diet, caused by variations of P content and bioavailability. Phosphorus deficiency is common in caged layers which don’t have access to P in the faeces.

Effects:

Similar to calcium and/or vitamin D deficiency signs. Soft brittle bones (rickets) occurs in young birds, which causes retarded growth. In adults with cage layer fatigue, eggs are thin-shelled or shell-less, there may be white areas on brown eggs, and a drop in egg production and hatchability.

Detailed causes:

Calcium, phosphorus, Vitamin D deficiency

Vitamin D3 is needed for proper metabolism of calcium (Ca) and phosphorus (P) and in the formation of normal skeleton, hard beaks and claws and strong eggshells. It is also required for absorption of Ca and P from intestine and deposition of calcium in bone. Ca and P are needed for bone growth. Deficiency in Ca and P or imbalance of either will result in bone and egg shell malformations. Hyper amounts of Vitamin D may cause renal damage and pimpling of egg shells. Rickets occurs in young birds and osteomalacia (cage layer fatigue) in mature birds.

Mode of transmission

A deficiency in the diet caused by variations in Ca and P content of animal by-products and variation in P bioavailability in various mineral sources. A phosphorus deficiency is common in cage layers, which don’t have access to P in the faeces.

Clinical signs:

Soft brittle bones (rickets) occur in young birds.

In adults with cage layer fatigue, there are thin-shelled or shell-less eggs, white areas on brown eggs or a drop in egg production and hatchability.

In young birds with rickets, there is retarded growth.

Postmortem lesions

Beaded ribs, deviated sternum, softening of the beak, claws and keel bone and skeletal distortions can occur.

Diagnosis:

Postmortem lesions and histopathology (widening of epiphyseal plate, hypertrophy and softening of the bone, and irregular patterns of cartilage and bone development in the primary and secondary spongiosa) are diagnostic.

It simulates other deforming leg weaknesses in poultry.

Treatment and control:

Prevention

Quality control of the feed.

Treatment

Restore proper levels of phosphorus to the diet.

POULT ENTERITIS MORTALITY SYNDROME (PEMS)[កែប្រែ]

Causes:

Unclassified virus (possibly a reovirus). Spread by faecal-oral route.

Effects:

Incubation period is 1-7 days. Depression, sudden death, morbidity to 100% and mortality to 50% can occur. Dehydration, diarrhoea and stunting are common signs.

Detailed causes:

Young turkeys are susceptible to this acute and highly contagious disease. This is an unclassified virus (possibly a reovirus).

Mode of transmission

Spread of faecal-oral route.

Special note

Birds are severely immunosuppressed.

Clinical signs:

(There is a 1-7 day incubation period). Depression, sudden death and morbidity at 100% and mortality to 50% can occur. Dehydration, diarrhoea and stunting.

Postmortem lesions

Lesions include enteritis and peritonitis.

Diagnosis:

Clinical signs and gross lesions in the intestine of young turkeys are characteristic. Isolation of the virus from the liver in the yolk sac of embryonating eggs is helpful and reinoculate day-old poults to reproduce the disease.

Treatment and control:

Prevention

Biosecurity is important and depopulate infected flocks for two consecutive growing cycles.

Treatment

None.

QUAIL BROCHITIS[កែប្រែ]

Causes:

Quail bronchitis virus in an unenveloped double-stranded DNA serotype I avian adenovirus. It is spread by the airborne route.

Effects:

There is a 2-7 day incubation period. Signs include coughing, sneezing, huddling, depression, lachrymation (weeping eyes), conjunctivitis and neurological signs (tremors and paralysis).

Detailed causes:

Mostly young bobwhite quail are susceptible to this acute to chronic disease. The agent involved in the aetiology of this disease is an Adenovirus, which is an unenveloped, icosahedral double-stranded DNA virus, that replicates in the nucleus forming basophilic inclusion bodies.

Mode of transmission

It is spread by airborne route.

Special note

It may cause immunosuppression.

Clinical signs:

(There is a 2-7 day incubation period). Signs include coughing, sneezing, huddling, depression, lacrimation, conjunctivitis and neurological signs (tremors and paralysis).

Postmortem lesions

Lesions include mucous in the trachea or bronchi, cloudy air sacs and corneas, and sinusitis.

Foci in liver, spleen swollen and mottled, lungs are reddened and consolidated, and atrophy of bursa of Fabricius can be seen.

Diagnosis:

Isolation of virus from trachea in embryonated eggs is important. Neutralisation of virus with specific sera is also helpful. It simulates Aspergillosis, and Newcastle Disease.

Treatment and control:

Prevention

Biosecurity and sanitation are helpful to control the disease.

Treatment

Broad-spectrum antibiotics for secondary invaders are also helpful.

QUATERNARY AMMONIUM OR CHLORINE TOXICITY[កែប្រែ]

Causes:

Common water sanitisers are used to remove bacteria, fungi or algae from water lines. Levels of water sanitizer set too high.

Effects:

Birds do not drink, reduced growth, persistent swallowing, continual spitting, facial swelling and ocular or nasal discharge can be seen.

Detailed causes:

Sanitizers are commonly used to remove bacteria, fungi or algae from water lines. Common water sanitizers are the cause of this disease. All species of bird of all ages are susceptible to this acute disease.

Mode of transmission

Water sanitizer levels are too high.

Clinical signs:

Birds to not drink, reduced growth, persistent swallowing, continual spitting, facial swelling and ocular or nasal discharge can be seen.

Postmortem lesions

Ulcers on tongue from epithelial irritation are evident. A pseudomembrane on the mucosa of the mouth, pharynx oesophagus, crop, proventriculus and/or gizzard can be seen.

Diagnosis:

Water analysis of the sanitizers is needed. It simulates T-2 toxin, wet pox, vitamin A deficiency and trichomoniasis.

Treatment and control:

Prevention

Use lower level of the chemicals in the water.

Treatment

Fresh water will reverse the disease.

RAILLIETINA (TAPE WORM, CESTODES)[កែប្រែ]

Causes:

Chicken tapeworm- Raillietina species.

Effects:

Emaciation, degeneration and reduced growth rate.

Detailed causes:

Fifty percent of the intestinal tracts of chickens may contain tapeworms (cestodes) if they are reared on range or in backyard flocks. In contrast, birds confined within poultry houses seldom become infected. Tapeworm infestations are now considered rare in intensive poultry-rearing regions. Over 1400 species of tapeworm have been identified in wild and domestic birds. Of these, three families are 10 genera, including Raillietina species affect poultry.

Tapeworms are flattened, ribbon-shaped, usually segmented worms. Millions of eggs may be required to complete the complicated two-hose or three-hose life cycle. The worms are characterised by complete absence of a digestive tract and obtain their nourishment by absorption from the gut contents of the host.

Mode of transmission

Birds become infected by eating an intermediate host, which transmits a larval stage of the tapeworm to the intestine of the definitive host. The intermediate host may be an insect, crustacean, earthworm, slug, snail or leech depending upon the species of tapeworm. Some larger tapeworms may appear to completely block the intestine of infected birds. Different species vary considerably in pathogenicity so identification as to species is desired.

Clinical signs:

Some large tapeworms may appear to completely block the intestine of infected birds. Different species vary considerably in pathogenicity so identification as to species is desired.

Tapeworms are flattened, ribbon-shaped, usually segmented worms. Millions of eggs may be required to complete the complicate two-hose or three-hose life cycle. The worms are characterised by complete absence of a digestive tract and obtain their nourishment by absorption from the gut contents of the host.

Diagnosis:

Most species of worm appear during postmortem examination of the digestive tract. Acute identification is necessary for effective control. A portion of the worm should be removed and viewed under a microscope for detailed identification.

Tapeworms are flattened, ribbon-shaped, usually segmented worms. The worms are characterised by complete absence of a digestive tract.

Most cestodes are usually host specific for a single or a few closely related birds. Identification of the genus and species may provide a clue to the probable intermediate host.

Treatment and control:

Most cestodes are usually host specific for a single or a few closely related birds. Identification of the genus and species may provide a clue to the probable intermediate host. The diagnositician may then be able to suggest practical control measures.

Completion of a two-host life cycle depends upon a unique set of ecologic conditions. Thus minor changes in flock management may cause a break in the life cycle and affect a useful control measure.

Antihelminthic drugs are not recommended as they are only a short-term remedy. The intermediate host should be identified and controlled.

RATS[កែប្រែ]

Causes:

Norwegian rat (Rattus norvegicus) is the most common rat around poultry houses.

Effects:

Rat harbourage around poultry houses is seen in the form of burrows in the ground and under the foundation, litter under the slats, old nests and debris around the house. Most rat activity occurs at night, and rats seen during the day indicate a large population. Rats eat almost anything, including poultry feed and eggs. They can contaminate feed, and they may carry a variety of diseases (ie Salmonella, Pasteurella) and ectoparasites.

Detailed causes:

Rodents are common external pests in and around poultry facilities and can parasitise poultry. Rodents can eat or contaminate feed, which increases feed costs and affects feed conversion. Additional problems can be produced by the presence of these pests, since they may carry a variety of diseases and ectoparasites.

Rats

The Norwegian rat (Rattus norvegicus) is the most common rat around poultry houses. Rats eat almost any type of food, including eggs and poultry feed; 200 adults rats will consume 25 lbs of feed daily.

Rat harbourage around a poultry house is seen in the form of burrows in the ground and under the foundation, litter under the slats, in wood piles, old nests and other debris near the poultry houses. This type of harbourage must be removed for any control program to be successful.

Most rate activity, including feeding, occurs at night. Rats observed outside their harbourage during the day indicate a large population.

Clinical signs:

Signs of rat activity such as gnawing and burrowing in and around building, droppings around feed, litter under the slats and in woodpiles indicate a rat problem. Old nests may be found. Most rat activity, including feeding occurs at night, so if rats are seen outside their harbourage during the day, a large population is likely.

Diagnosis:

A large population of rats should be suspected if signs of them are seen. The best time to search for rodents and their excrement is at night in the dart with a flash light.

Treatment and control:

Treatment

After the control measures have been completed, rodent-killing can be done by baiting, fumigating, trapping or even shooting. A properly conducted baiting program is easiest and most effective.

There are many products that will kill rodents. The first safe and commonly used baits are the multiple-dose anticoagulants. Products that contain warfarin, fumaric, chlorophacinone or diphacinone as an active ingredient are examples of this type. Multiple-dose anticoagulants must be consumed for several days to be lethal. The effects are cumulative, therefore, it is imperative that enough bait be available for the rodents to eat for several days. These chemicals are safe for people and for non-target animals, because a single dose will not cause death.

Control

Rodent-proofing can be an effective long-term control measure. However, it is impossible to rodent-proof a poultry facility with curtains, wooden side walls and/or dirt floors. Access to the building can be restricted by patching or screening holes in the foundation, thus forcing the rodents to burrow into the house, which makes them easier to detect.

Sanitation involves cleaning around the facility. Rodents are secretive creatures, they do not like to move in open areas; therefore, mowing the grass and weeds on a regular basis creates a less favourable habitat. Removing piles of old wood, nests or any other debris helps to make the area less attractive to rodents and aids in making early detection possible. When debris or tall grass is present, rodents can burrow into a facility and go unnoticed. Rolling the house curtains up and down a couple of times a week during summer months will disturb any rodents that are in the curtains and discourage them from living and/or nesting in them.

RETICULOENDOTHELIOSIS (ACUTE RETICULUM CELL NEOPLASIA, RUNTING DISEASE SYNDROME)[កែប្រែ]

Causes:

Reticuloendotheliosis virus is an RNA retrovirus similar to the avian leukosis/sarcoma group. Some viruses are defective and require a helper virus to complete their replication cycle. It is spread by the transovarian route from hens to offspring, and can also spread laterally via contaminated faeces and litter (although contact infection rarely results in disease).

Effects:

Acute reticulum cell neoplasia results in enlarged abdomen, weakness and death. Runting disease syndrome is seen as stunted, pale birds with abnormal feather development and lameness. Chronic neoplasia, chicken bursal lymphoma, turkey lymphoma and multi-syndromes cause weakness, paleness and anorexia.

Detailed causes:

Turkeys, chickens, pheasants and (rarely) quail of all ages are susceptible to this chronic disease. The agent involved in the aetiology of this disease is an RNA retrovirus similar to avian leukosis/sarcoma group. Some viruses are defective and require a helper virus to complete their replication cycle.

Mode of transmission

It is spread transovarian from infected hens to offspring. The virus can spread laterally by contaminated faeces and litter (although contact infection rarely results in disease).

Clinical signs:

Acute reticulum cell neoplasia results in enlarged abdomen, weakness and death. Runting disease syndrome is seen as stunted, pale birds with abnormal feather development and lameness.

Chronic neoplasia, chicken bursal lymphoma, turkey lymphoma and multi syndromes causes weakness, paleness and anorexia.

Postmortem lesions

Acute reticulum cell neoplasia causes large livers and spleens with infiltrative focal or diffuse lesions. Lesions are also common in the pancreas, gonads, heart and kidney. Runting disease syndrome causes acute hemorrhagic or chronic ulcerative proventriculitis, atrophy of the thymus and bursa enlarged peripheral nerves, enteritis, anemia and necrosis of liver and spleen.

Chicken bursal lymphoma causes tumours in the liver and bursa of Fabricius. Chicken non-bursal lymphoma produces tumours of the heart, liver and spleen, atrophied thymus and enlarged peripheral nerves.

Turkey lymphoma results in tumours in the liver and other visceral organs.

Diagnosis:

Gross and microscopic observations of tumours are necessary. Tumours consist of large vesicular mononuclear cells of the reticuleondothelial system. Areas of necrosis are associated with tumours. Detection of virus using fluorescent antibody test with antibodies can be done. It simulates avian leukosis and MD.

Treatment and control:

Prevention

ELISA testing is used for selection of breeders free of the virus.

Treatment

No effective treatment.

RODENTS (RATS, MICE)[កែប្រែ]

Causes:

The Norwegian rat (Rattus norvegicus) and the house mouse (Mus musculus) are the most common rodents found around poultry houses.

Effects:

Rats and mice cause damage to buildings and their foundations through chewing and burrowing activities. Both will eat poultry feed, and rats may also eat eggs in laying houses. Rats and mice are common vectors for many viral, bacterial and protozoal; diseases and can also carry ectoparasites.

Detailed causes:

Rodents are common external pests in and around poultry facilities and can parasitise poultry. Rodents can eat or contaminate feed, which increases feed costs and affects feed conversion. Additional problems can be produced by the presence of these pests, since they may carry a variety of diseases and ectoparasites.

  • Rats

The Norwegian rate (Rattus norvegicus) is the most common rat around poultry houses. Rats eat almost any type of food, including eggs and poultry feed; 200 adult rats will consume 25 lbs of feed daily.

Rat harbourage around a poultry house is seen in the form of burrows in the ground and under the foundation, litter under the slats, in wood piles, old nests and other debris near the poultry houses. This type of harbourage must be removed for any control program to be successful.

Most rat activity, including feeding, occurs at night. Rats observed outside their harbourage during the day indicate a large population. The best time for search for rodents and their excrement is at night in the dark with a flash light.

  • Mice

The house mouse (Mus musculus) is the most common mouse found in and around poultry facilities. Mice will eat almost any kind of food. Mice are active throughout the day, often feeding every hour. However, peak activity occurs at dusk and dawn. Mice breed regularly throughout the year with no seasonal peak.

Clinical signs:

Rodents can do a tremendous amount of damage if not controlled. They eat the contaminate feed, which increases costs and affects feed conversion. Rats may also eat eggs, so are a problem in layer and breeder houses. If present in very large numbers, rats may also attack birds.

Populations usually decrease during the winter, but in buildings the opposite is often true, as the animals migrate indoors.

Diagnosis:

Mice are more active at dusk and dawn, but are frequently active during the day. Peak rat activity occurs at night, so rats can best be found using a flashlight. Droppings in and around spilled feed and signs of gnawing and burrowing around the poultry house are indicative of rodents.

Treatment and control:

Control

Rodent-proofing can be an effect long-term control measure. However, it is impossible to rodent-proof a poultry facility with curtains, wooden side walls and/or dirt floors. Access to the building can be restricted by patching or screening holes in the foundation, thus forcing the rodents to burrow into the house, which makes them easier to detect.

Sanitation involves cleaning around the facility. Rodents are secretive creatures, they do not like to move in open areas; therefore, mowing the grass and weeds on a regular basis creates a less favourable habitat. Removing piles of old wood, nests, or any other debris helps to make the area less attractive to rodents and aids in making early detection possible. When debris or tall grass is present, rodents can burrow into a facility and go unnoticed. Rolling the house curtains up and down a couple of times a week during summer months will disturb any rodents that are in the curtains and discourage them from living and/or nesting in them.

Treatment

After the control measures have been completed, rodent-killing can be done by baiting, fumigating, trapping or even shooting. A properly conducted baiting program is easiest and most effective.

There are many products that will kill rodents. Safe and commonly used baits are the multiple-dose anticoagulants. Products that contain warfarin, fumaric, chlorophacinone, or diphacinone as an active ingredient are examples of this type. Multiple-dose anticoagulants must be consumed for several days to be lethal. The effects are cumulative therefore, it is imperative that enough bait be available for the rodents to eat for several days. These chemicals are safe for people and for non-target animals, because a single dose will not cause death.

ROTAVIRUS INFECTIONS[កែប្រែ]

Causes:

Rotavirus is a double stranded RNA virus with 11 segments.

Effects:

Incubation period is 2-5 days. Subclinical infection (no signs) to severe diarrhoea may be seen. Other signs include dehydration, poor weight gain, increased mortality (4-7%), restlessness, litter eating and watery droppings.

Detailed causes:

Chickens, turkeys, ducks, pheasants, guinea fowl and pigeons of all ages are susceptible to this acute to chronic disease. The agent involved in the aetiology of the disease is rotavirus, which is a 70 nM-double stranded RNA with 11 segments.

Mode of transmission

Virus is spread by the faecal-oral route.

Clinical signs:

(There is a 2-5 day incubation period). Subclinical (no signs) to severe diarrhoea may occur. Other signs include dehydration, poor weight gain, increased mortality (4-7%), restlessness, litter eating and water droppings.

Postmortem lesions

Lesions include abnormal amounts of fluid and gas in the intestinal tract, dehydration, inflamed vents, vent picking and litter in the gizzard.

Diagnosis:

Diagnosis is by detection of the virus in the faeces using electron microscope and isolation of the virus in cell culture and staining with specific fluorescent conjugated antisera.

It simulates coccidiosis, pale bird syndrome, toxic enteritis, astrovirus, coronavirus and enteric bacteria.

Treatment and control:

Prevention

Biosecurity is important. No vaccine is available.

Treatment

Vitamins, minerals and electrolytes for treating fluid loss are helpful.

SALMONELLOSIS PULLORUM (PULLORUM, BACILLARY WHITE DIARRHEA)[កែប្រែ]

Causes:

Non-motile gram negative bacterium- Salmonella pullorum.

Effects:

Young birds have a pasted vent. White diarrhoea, huddling, lameness, somnolence (sleepiness), laboured breathing and blindness can occur. Mortality peaks at 7-10 days with up to 100% mortality and/or morbidity. Adults usually have subclinical disease, or a drop in egg production, fertility, or hatchability may occur. Occasionally see depression, anorexia, diarrhoea and dehydration. S. pullorum normally affects young birds, while S. typhimurium normally affects older birds.

Detailed causes:

All species of bird of all ages are susceptible to this acute to chronic disease (acute in young birds and chronic in older flocks). The agent involved in the aetiology of the disease is Salmonella pullorum, which is a non-motile, non-spore or capsule forming gram-negative rod-shaped bacteria.

Mode of transmission

Vertically spread through egg (transovarian) or on egg (by faecal contamination) or by feed and water contamination, contamination incubators, exploding eggs, and bird to bird (horizontal) transmission.

It is species specific (occurs in birds only)

Special note

It is a notifiable disease. It has been eradicated from most commercial flocks, but is still common in backyard flocks and commercial flocks in third world countries. A few isolated outbreaks of pullorum have occasionally occurred in broiler breeder and parent stocks.

Clinical signs:

Young birds have a pasted vent. White diarrhoea, huddling, lameness, somnolence (sleepy), laboured breathing and blindness can occur.

Mortality peaks at 7-10 days with up to 100% mortality and/or morbidity and/or morbidity.

Adults are usually infected subclinically and a drop in egg production, fertility or hatchability may occur. Depression, anorexia (won’t eat), diarrhoea and dehydration are occasionally seen.

Postmortem lesions

Young birds have a red-streaked liver, enlarged spleen and grey nodules in the peritoneum.

White caecal plug, misshapen yolk and omphalitis (swollen navel) can occur. White areas on gizzard, liver, heart, lungs, swollen joints urate filled kidneys may be seen.

Adults have misshapen ovaries, testicular abscesses or may be atrophic, swollen joints, nodular myocarditis (inflammation of the cardiac muscle) or pericarditis (inflammation of the sac around the heart).

Diagnosis:

There is no definitive diagnosis based on signs or lesion. Organism should be cultured on Salmonella-Shigella, brilliant green, MacConkey’s or Triple sugar iron agar.

It is a notifiable disease. It simulates paratyphoid and colibaccillosis.

Treatment and control:

Prevention

Testing of breeder flocks by serum aggulatination or enzyme linked immuneosorbent assay (ELISA). Have a good rodent control program in place, as rodents are often carriers of the bacterium.

Spraying and/or fumigation of eggs with formaldehyde. Place paraformaldehyde pellets in nests. Spray eggs in house with 2.5% hydrogen peroxide and 1% quaternary ammonia. Pellet feed to kill bacteria, more difficult to heat inactive bacteria in feed high in energy (5% fat), NF-180® (0.011%) (Neomycin 35g/t). Heating process during Pelleting kills bacteria. National Poultry Improvement Plan (NPIP) monitors hatcheries for Salmonella in the US.

Most countries have a national program for the control of Salmonella pullorum Irradiation of feed to kill bacteria.

Treatment

For young birds only if allowed by local legislation. In many countries, destruction is obligatory. Antibody positive breeders are destroyed.

NF-180® Furazolidone* (feed) (0.055%), Sulfonamide (0.5) in starter mash, 50-100 g/t. (Furox®), *Furacin in water, * Neomycin 70-140 g/t and sulfa drugs in water of young birds will treat the signs.

*Removed from approved drugs by FDA and in most European countries.

SALT TOXICITY[កែប្រែ]

Causes:

Consumption of feed or water with too high level of NaCl.

Effects:

Increased thirst, dehydration, crop filled with water, dyspnoea, depression, watery diarrhoea, stunting, feed refusal, nervous signs and rough dirty wet feathers or down.

Detailed causes:

All species of bird – of all ages, but in particular young, are susceptible tot his acute to chronic disease. The agent involved in the aetiology of the disease is NaC1.

The consumption of feed or water with too high a level of NaC1. Feed normally contains 0.85% water and 0.12% salt, which equals 1200 ppm.

Mode of transmission

Ingestion of food or water with high salt. Over 1% causes clinical diseases and over 10% results in feed refusal.

Some water fowl have salt glands to excrete excess Na+.

Clinical signs:

Signs include increased thirst, dehydration, crop filled with water, dyspnoea, depression, watery diarrhoea, stunting, feed refusal, nervous signs and rough dirty, wet feathers or down.

Postmortem lesions

Lesions include ascites (water belly), excess fluid in lungs, atrophied liver, enteritis, hydropericardium, right side cardiac (biventricular) hypertrophy, nephritis, cystic dilation of seminiferous tubules and gonads and myocardial and skeletal haemorrhage.

Diagnosis:

Diagnosis is by feed analysis. Salt can be tasted in the feed or water (over 2%). Clinical signs and gross lesions are suggestive of salt toxicity.

Ultrastructure changes in the heart muscle include myofibrillar disarrangement and disruption of intercalated discs.

It simulates crotalaria toxicity and ascites.

Treatment and control:

Prevention

Spot check of feed or water will help prevent this disease. May requires filtration of well water.

Treatment

Fresh feed or water will stop the disease and reverse clinical signs within 24 hours. It is a common feed milling problem.

SELENIUM DEFICIENCY (NUTRITIONAL MUSCULAR DYSTROPHY, VITAMIN E DEFICIENCY)[កែប្រែ]

Effects:

Weakness and signs of unthiftiness.

Detailed causes:

This disease is a vitamin E and/or selenium deficiency. All species of young bird are susceptible to this disease.

Mode of transmission

Deficiency in the diet.

Clinical signs:

Birds are weak and unthrifty signs occur.

Postmortem lesions

Light coloured streaks of easily distinguished affected bundles of muscle fibres in the breast (myopathy), of the gizzard and heart muscles can occur.

Diagnosis:

Gross and microscopic muscle lesions are characteristic. Microscopic lesions include hyaline degeneration, followed by disruption of muscle fibres.

Treatment and control:

Treatment

Restore proper levels in the diet.

SKIN LEUKOSIS (MAREK'S DISESE)[កែប្រែ]

Causes:

Marek’s disease virus is a cell-associated herpes virus containing double-stranded DNA of which there are three serotypes. Only serotype 1 is pathogenic.

Effects:

Large scabby lesions on the surface of the skin are usually only seen in the processing plant, resulting in carcass downgrading. Other signs of Marek’s disease include weakness, paleness, feed refusal, diarrhoea, poor performance, culls and blindness. There is paralysis or paresis (partial paralysis), which can be unilateral or bilateral in wings and/or legs, which causes one leg to stretch forward and the other backwards. Tumours and tremors occur. Mortality ensues.

Detailed causes:

Skin leukosis was once recognised as a distinct disease. It is now recognised as a clinical sign associated with Marek’s disease.

Marek’s disease was named after the Hungarian pathologist Josef Marek. It is also know as range paralysis because it caused paralysis in chickens, which use to be reared on the range.

Chickens (all breeds), pheasants and occasionally quail are susceptible to this chronic disease. It occurs worldwide in commercial flocks and takes 4-6 weeks for tumours to form.

The classical type (nervous form) is common in white layers between 6-16 weeks. Visceral type with tumours in various internal organs usually occurs between 16-35 weeks. Infection takes place at a very young age, but birds can die of Marek’s disease (MD) near the onset of egg production.

The agent involved in the aetiology of this disease is a cell-associated Herpes virus containing double-stranded DNA. It has hexagonal naked particles or nucleocapsids of 85 or 100 nm. Enveloped particles of 150-400 nm are occasionally seen in the feather follicle epithelium. There are 3 serotypes. Serotype 1 viruses can be oncogenic (causes tumours).

Mode of transmission

It is spread by contamination litter, dust, down or air-borne (bird to bird). Feather (dust or dander) epithelium contains virus.

There is an incubation period of 2 weeks for virus shed and for clinical signs from 3-6 weeks.

Special note

It is immunosuppressive. Tumours are a leading cause of condemnation in broilers and MD is the leading cause of tumours in US broilers. There has been an increase in the incidence of MD is broilers in the US since the change to dry cups and nipple drinkers. These systems make the house drier and dustier, which provides an environment were the virus is more easily spread.

Clinical signs:

It causes increased susceptibility (immunosuppression) to other diseases. Signs include weak, pale, off feed, diarrhoea, poor performance, culls and blindness.

In white leghorn type birds, Classical Marek is common. There is paralysis or paresis (partial paralysis). There can be unilateral or bilateral paralysis of wings and legs, mortality, tumours and central nervous system signs (tremors). One leg stretches forward and the other backwards due to leg paralysis.

Postmortem lesions

The peripheral nerves are often enlarged (vagus, sacral, sciatic and brachial) with a loss of striations. They can also have grey or yellow discoloration and be oedematous (fluid filled).

The bursae are sometimes enlarged with tumours, but most often is atrophic. There are enlarged organs (gonads, spleen, heart, lungs, liver, kidneys, proventriculus, intestines etc) with focal to nodular white or grey tumours.

The skin has nodular, palpable tumours.

The skeletal muscles have tumours. The eye (iris and pupil) may have diffuse depigmentation, diffuse bluish fading or diffuse grey opacity of the iris. The pupil may be irregular and tiny.

The bone is never involved and the blood and fat sometimes have tumours.

Diagnosis:

The diagnosis is by observation of gross tumours in immature birds. Ocular or skin leukosis and nerve involvement are diagnostic for MD.

Histopathologically, small to medium lymphoid leukosis, reticuloendotheliosis and colibaccillosis.

Treatment and control:

Prevention

Vaccinate (HVT-serotype 3 alone or HVT and SB1-serotype 2) chicks at a day-old SQ in hatchery. Some injections are done at 18 days of embryonation (in ovo). HVT and SB1 are used for broiler breeders and white leghorns at full dosage. HVT is used alone or HVT and SB1 at 1/3-1/4 dosage for broilers. Broilers vaccination is common practice in USA. Outside USA, this is generally only done if broilers are kept over 50 days.

SB1 may cause immunosuppression and increase leukosis in some leghorn strains. HVT=Herpes virus of turkeys. SB1=S (susceptible strain) and B1 (pen B1). HVT + SB1 or HVT + Respins vaccine can be used.

Rispens strain (serotype 1) may be used alone or in combination with HVT.

Outside the USA, Rispens strain is the most commonly used vaccine, usually given by intramuscular injection at day old. In areas with a high infection risk bivalent vaccine (Rispens+HVT) is used.

Treatment

None.

SMOTHERING[កែប្រែ]

Causes:

Smothering occurs due to overcrowding and hence a lack of oxygen. It may occur in chicks that are packed without enough air spaces or ventilation holes, or when birds are moved to new quarters or when they are frightened. It is more common at night.

Effects:

Mortality without signs of any other cause of death. Postmortem, congestion of the trachea and lungs may be seen, or feathers may be worn off where trampling has occurred.

Detailed causes:

Smothering is caused by crowding or pilling in a corner. It may occur when birds are moved to new quarters, when they are frightened by a loud noise or intruder in the house, or when birds are chilled. It is often more common at night. Smothering of chicks occurs in boxes due to overcrowding or when boxes are stacked too high, or there are insufficient air ventilation holes.

Clinical signs:

Sudden death of birds in one area of the house (usually in one corner) without any other signs is indicative that death has occurred by smothering.

Diagnosis:

Postmortem lesions

Necropsy of birds reveals congestion of the trachea and lungs

Treatment and control:

Prevention

The condition can be reduced by encircling chicks around the brooding area with a guard. Guards should be made of a netting material which provides no blockage of air or light and can be easily disinfected.

The house should be pre-warned 24 hours before receiving the chicks.

When the birds are moved to new quarters, lights should be dimmed and birds frequently checked for piling.

Care should be made to prevent frightening the birds by loud intruders. Condition birds to humans and outside noises (trucks, machines) with an inside radio.

SPONDYLOLISTHESIS (KINKY BACK)[កែប្រែ]

Causes:

A deformity of the 6th thoracic vertebra which causes spinal cord compression and posteria paralysis. Influenced by conformation and growth rate. Non-infectious, it is aggravated by fast body development.

Effects:

Incidence of affected birds may reach 2% of the flock. Peak incidence occurs at 3-6 weeks of age. Severely affected birds may become laterally recumbent (lay on their sides) and may die from dehydration if not culled. Lordosis (curving forward) and subclinical spondylolisthesis are common in broilers and develop soon after hatching.

Detailed causes:

Young and fast growing broilers are susceptible to this chronic disease. It is a development disorder influenced by confirmation and growth rate, resulting in a deformity of the 6th thoracic vertebra, which caused spinal cord compression and posterior paralysis.

Mode of transmission

It is a non-infectious metabolic disease of broilers, aggravated by fast body development. It does not occur in breeders, where growth rate is slowed by restricted feeding. It can be increased by genetic selection.

Special note

It is one of many skeletal problems caused by rapid growth rate in broilers.

Clinical signs:

The incidence of affected birds may reach 2% of the flock. Peak incidence occurs at 3-6 weeks of age

Severely affected birds often become laterally recumbent (lay on their sides) and may die from dehydration if not culled.

Lordosis (curving forward) and subclinical spondylolisthesis are common in broilers and develop soon after hatching.

Postmortem lesions

The posterior paralysis results from rotation of the body of the 6th vertebra along the axis of the spine with the posterior part of the body moving dorsal (backward) and anterior (forward), relative to the anterior part.

The rotation causes a kyphotic (humpback) angulation of the floor of the spinal canal between the 6th and 7th thoracic vertebrae and spinal cord compression. The deformation of the spinal column can be readily recognised by palpating the ventral surface of the spinal column during necropsy.

Diagnosis:

Spondylolisthesis is best confirmed by removing, decalcifying and splitting the spinal column along a midline longitudinal plant to allow visualisation of the spinal cord compression.

It simulates other developmental skeletal disorders such as valgus (twisted outward) and various deformation of the intertarsal joint, tibial dyschondroplasia, osteochondrosis, degenerative joint disease and osteoporosis.

A twisted spinal column resulting in a definitive diagnosis can be seen without decalcifying in extreme cases.

Treatment and control:

Prevention

Slowing growth rate as is done in breeders (by restriction of light or feed), and genetic selection of birds that are less susceptible is helpful.

STAPHYLOCOCCOSIS[កែប្រែ]

Causes:

Gram positive, cluster-forming ubiquitous bacterium- Staphylococcus aureus. Common contaminate of skin and secondary infections occur in the joints.

Effects:

Birds are down on their hocks, have swollen feet (bumble foot) and gangrenous dermatitis. Although high mortality may be seen in baby chicks, morbidity and mortality are low with this disease.

Detailed causes:

All species of bird of all ages are susceptible to this acute to chronic disease. The agent involved in the aetiology is Staphylococcus aureus, which is a gram-positive coccoid-shaped, ubiquitous organism found in clusters.

Mode of transmission

Transmission occurs by soiled eggs, secondary infection through wound, contaminated hatchery and wet litter, which cause ammonia burns. Staph readily contaminates burnt skin.

Special note

This organism leads to trimming and downgrading in the processing plant. It is a common contaminate of skin and secondary infections occur in the joints following viral infection or stress. Staph is a leading cause of arthritis and synovitis in poultry. Arthritis and synovitis are a leading cause of condemnation (parts) in the broiler processing plant. Staphylococcosis is the second most common bacterial disease of chickens. Staphylococcal synovitis is a common problem in broiler breeders in the rearing period, often due to feed restrictions and improper feed distribution.

Clinical signs:

Signs include down on hocks, swollen foot pads (bumblefoot) or hocks, high mortality in baby chicks (omphalitis), and gangrenous dermatitis.

Morbidity and mortality are low with this disease.

Postmortem lesions

Lesions may include exudate on heart, liver and yolk in chicks, puss in joints and breast blisters.

Osteomyelitis (focal yellow areas of caseous exudate in the bones) and septicaemia (congestion of liver, spleen, kidney and lungs) may occur.

Diagnosis:

Laboratory isolation of coagulase positive organisms. Staph isolation on blood agar produces white to orange smooth colonies. Type bacteria using phages (bacterial virus).

It simulates Mycoplasma synoviae, viral tenosynovitis, Salmonella, E. coli, Pasteurella and Strephococcus.

Swollen, localised abscesses are characteristic for this disease.

Treatment and control:

Prevention

Fumigate eggs and incubator, remove sharp objects from house, use clean dry litter, and use nipple-drinkers for house to reduce the bacteria.

Treatment

Novobiocin (200-350 g/t), Penicillin, Lincomycin and Strephomycin are effective.

STREPTOCOCCOSIS[កែប្រែ]

Causes:

Gram positive facultatively anaerobic bacteria- Streptococcus. Species include S. zooepidemicus, S. gallinarum, S. avian, S. faecalis and S. durans.

Effects:

Depression, lethargy, lassitude, pale wattles and combs, tremors, decreased egg production, lameness and reduced body weight. In young chickens encephalitis causing torticollis.

Detailed causes:

All species of bird of all ages are susceptible to this acute to chronic disease. The agent involved in the aetiology of this disease is Strephococcosis sp, which includes S. zooepidemicus, S. gallinarum, S. avian, S. faecalis and S. durans. It is a gram-positive, spherical, non-motile, non-spore-forming, facultative anaerobe which occurs in short chains.

Mode of transmission

The organism can be spread by oral and aerosol transmission and with soiled eggs. Secondary infections through wounds, contaminated hatchery and wet litter are also important.

Clinical signs:

Signs include depression, lethargy, lassitude, pale combs and wattles, tremors, drop in egg production, lameness and reduced body weight. Also in young chickens nervous signs, torticollis.

Postmortem lesions

Lesion include spleenomegaly, hepatomegaly (swollen liver), enlarged kidneys, peritonitis, omphalitis (swollen navel), tenosynovitis, arthritis, salpingitis and myocarditis.

In young chickens encephalomyelitis.

Diagnosis:

Laboratory isolation of the organism from yolk, blood and lesions on blood agar. Colonies are small and usually greyish in 24 hours. They may be mucoid to rough.

It simulates Staphylococcus, Mycoplasma synoviae, Salmonella and E. coli. No diagnostic signs or lesions exists.

Treatment and control:

Prevention

Prevention methods include egg and hatchery sanitation, remove sharp objects from the house and use clean, dry litter.

Treatment

Penicillin, erythromycin, novobiocin, nitrofurans and tetracyclines

SUDDEN (ACUTE) DEATH SYNDROME (HEART ATTACK, FLIP-OVER)[កែប្រែ]

Causes:

Unknown, but is probably a metabolic disease due to genetic, environmental and nutritional factors affecting incidence and severity.

Effects:

Greatest losses occur from 3-6 weeks of age. Birds squawk during a sudden attack, characterised by a loss of balance, convulsions and violent flapping. Most birds die on their backs with one or both legs extended or raised.

Detailed causes:

All species of bird of fast growing lines, from 1-8 weeks old are susceptible to this peracute disease. The cause of this disease is unknown, but probably a metabolic disease due to genetic, nutritional and environmental factors affecting the incidence and severity.

Sudden death syndrome of broiler breeders

Occurs mostly during peak production. Acute death, often during feeding time. The cause probably related to K+ deficiency in feed.

Postmortem reveals haemorrhages on heart muscle, heart dilatation.

Clinical signs:

The greatest losses in birds occur from 3-6 weeks of age. Birds squawk during a sudden attack characterised by loss of balance, convulsions and violent flapping.

Most birds die on their backs with one or both legs extended or raised.

Postmortem lesions

Birds are in good health and flesh. Livers are enlarged, pale and friable and gall bladder is empty. Kidneys may be pale and lungs are often congested and oedematous. The ventricles of the heart are generally contracted and the thyroid, thymus and spleen congested. There may be haemorrhages in the kidney.

There may be blood in the abdominal cavity.

Diagnosis:

Clinical signs, gross and microscopic pathology are characteristic. Microscopically there is congestion, oedema and lymphoid oedema in the lungs. Mild degeneration of and infiltration of lymphoid cells in the heart.

It simulates aortic rupture and ascites.

Treatment and control:

Reduced bird density and slow growth and move slowly and quietly through the house to reduce the disease.

Acclimatise flock to sounds using a radio placed in the house

SULPHUR (SULPHONAMIDE) TOXICITY[កែប្រែ]

Causes:

Ingestion of food or water with too high a level of sulphonamide drug. Sulphur drugs are widely used as growth promotants and/or anticoccidials. They are difficult to mix accurately in feed. In summer, birds can accidentally overdose on water-administered sulphonamides due to increased water consumption.

Effects:

Paleness, depression, weight loss and a drop in egg production and shell quality are seen. Secondary bacterial infections may follow due to lymphoid necrosis.

Detailed causes:

All species of bird of all ages are susceptible to this acute to chronic disease. Adults in particular are highly susceptible, resulting in an acute drop in egg production.

Mode of transmission

Ingestion of food or water with too high a level of drug.

Sulpha drugs are difficult to mix in feed accurately. Allowance should be made when adding sulphur to the water when temperatures are high. Birds may over consume water and the drug during hot weather.

Special note

It is a drug residue problem. There is a 4-week withdrawal period for broilers. Sulphonamides are widely used a growth promotants and/or anticoccidial or antibacterial compounds which can be added to the feed or water. Tri or ormetroprim compounds are commonly added to potentiate the sulphonamides by increasing their absorption in the blood. Immunosuppression may follow.

Clinical signs:

Signs include paleness, depression, weight loss and an acute drop in egg production and shell quality.

Secondary bacterial infections may follow due to lymphoid necrosis.

Postmortem lesions

Haemorrhages in the skin (head, comb, face, wattles), muscles and internal organs can be seen.

Haemorrhagic enteritis, haemorrhages in the proventriculus and gizzard, pink to yellow bone marrow and a swollen pale liver may occur. The spleen is enlarge and haemorrhagic and there can be atrophy of the thymus and bursa.

Diagnosis:

Sample feed and water for a definitive diagnosis. Clinical signs and lesions are helpful. Microscopically, areas of caseation necrosis surrounded by giant cells in the liver, spleen, lungs and kidneys can be seen.

It simulates Mycotoxicosis, Fowl plague, Fowl cholera and visceral-trophic velogenic Newcastle disease (VVND)

Treatment and control:

Prevention

Quality control of feed and water

Treatment

Fresh feed and water will reverse clinical signs.

SWOLLEN HEAD SYNDROME (PNEUMOVIRUS)[កែប្រែ]

Effects:

Signs include snicking, rales, sneezing, nasal discharge, foamy conjunctivitis and swelling of the infraorbital sinuses. Submandibular oedema, torticollis and cerebral disorientation may occur. Mortality 0-10%. A drop in egg production and morbidity approaching 100% of the flock may also be seen.

Detailed causes:

All species of bird, in particular turkeys and broiler breeders, of all ages, are susceptible to this acute to chronic disease. The agent involved in the aetiology of this disease is from the Paramyxovirus family (pneumovirus). Various serotypes occur: Type A originated from UK, Type B from European continent and South Africa, Type C was found in Colorado USA.

Mode of transmission

Virus spreads by airborne and mechanical routes (feed, water and equipment).

Clinical signs:

Signs include snicking, ratles, sneezing, nasal discharge, foamy conjunctivitis and swelling of the infraorbital sinuses.

Submandibular oedema, mortality 0-10%, torticollis, and cerebral disorientation may occur. A drop in egg production and morbidity approaching 100% of the flock may also be seen.

Postmortem lesions

Yellow oedema and/or haemorrhaging in nasal turbinates, trachea and subcutaneous layer of skin around head can be evident.

Diagnosis:

Viral isolation from the trachea, lungs or nasal exudate in embryonating turkey eggs or chicken organ cultures are diagnostic. The virus can only be isolated in the very acute stage.

Serological tests include virus neutralisation, ELISA.

Treatment and control:

Prevention

Live vaccines for broilers and breeders and killed vaccines for breeders. Most vaccines are of turkey origin and A type. There also exists a vaccine of the B type and some vaccines of chicken origin. Homologous strains seem more effective as live vaccine.

Treatment

Antibiotics for secondary invaders, fresh air in the house and reduced stocking density are all helpful.

SYNGAMUS TRACHEA (RED WORM, GAPE WORM, FORKED WORM)[កែប្រែ]

Causes:

Parasitic nematode worm Syngamus trachae which may infect the trachea, bronchi and bronchioles.

Effects:

Signs of weakness and emaciation are seen, and infected birds usually spend much time with their eyes closed and head drawn back against the body. Occasionally the bird may throw head forward and upward and gasp for air, sometimes with a convulsive shake in an attempt to remove an obstruction from the trachea. Little or no food is eaten, and death usually ensues.

Detailed causes:

Chickens, turkeys, geese, guinea fowl, pheasants, peafowl and quail can all be infected. The organism is found in the trachea, bronchi and bronchioles.

It is sometimes designated at "redworm" because of its colour or "forked worm", because the male and female are in permanent copulation so that they appear like the letter "Y". The life history of the gapeworm is peculiar in that transmission from bird to bird may be successfully accomplished either directly (by the feeding of embryonated eggs or infective larvae) or indirectly (by ingestion of earthworms containing free or encysted gapeworm larvae they had obtained by feeding on contaminated soil). Gapeworm larvae in the earthworm remain infective to young chickens for as long as 4 years. Slugs and snails may also serve as transfer or auxiliary hosts of larvae. S. trachea is the causative agent of "gapes" (laboured breathing due to parasites) in chickens, turkeys, peacocks and pheasants.

In the artificial rearing of pheasants, gapes are a serious menace. Confinement rearing of young birds has reduced the problem in chickens compared to a few years ago. However, this parasite continues to present an occasional problem with turkeys raised on range.

Young birds are most seriously affected with gapeworms. The rapidly growing worms soon obstruct the lumen of the trachea and cause suffocation. Turkey poults, baby chicks and pheasant chicks are most susceptible to infection. Turkey poults usually develop gapeworm signs earlier and begin to die sooner after infection than young chickens. Full-grown birds rarely show characteristic signs unless heavily infected.

Clinical signs:

Birds infected with gapeworms show signs of weakness and emaciation and usually spend much of their time with eyes closed and head drawn back against the body. From time to time they throw their heads forward and upward and open the mouth wide to draw in air. An infected bird may give its head a convulsive shake in an attempt to remove the obstruction from the trachea so that normal breathing may be resumed. Little or no food is eaten in the advance stages of infection, and death usually ensues.

Diagnosis:

Examination of the trachea of infection birds shows that the mucous membrane is extensively irritated and inflamed. Coughing is apparently the result of this irritation to the mucous lining. Lesions are usually found in the trachea of turkeys and pheasants but seldom if ever in the tracheas of young chickens and guinea fowl. These lesions or the male worm, which remains permanently attached to the tracheal wall throughout the duration of its life. The female worms apparently detach and reattach from time to time in order to obtain a more abundant supply of food.

Treatment and control:

Prevention

Modern poultry practices, especially confinement rearing of broilers and pullets and caging of laying hens, have significantly influenced the quantity and variety of nematode infections in poultry.

For most nematodes, control measures consist of sanitation and breaking the life cycle rather than chemotherapy. Confinement rearing on litter largely prevents infections with nematodes using intermediate hosts such as earthworms or grasshoppers, which are not normally found in poultry houses. Conversely, nematodes with direct life cycles or those that utilise intermediate hosts such as beetles, which are common in poultry houses, may prosper. Treatment of the soil or litter to kill intermediate hosts may be beneficial. Insecticides suitable for litter treatment include carbaryl, tetrachlorvinphos (stirofos). However, treatment is usually done only between grow-outs. Extreme care should be taken to ensure that feed and water are not contaminated. Treatment of range soil to kill ova is only partially successful. Changing litter can reduce infections, but treating floors with oil is not very effective. After the old litter has been removed, spraying with permethrin or a mixture of Rabon and Vapona has proven effective for beetle control.

Raising different species or different ages of birds together or in close proximity is a dangerous procedure as regards parasitism. Adult turkeys, which are carriers of gapeworms, can transmit the disease to young chicks or pheasants, although older chickens are almost resistant to infection.

Treatment

Syngamus approved compounds

Thiabendazole is currently approved for use only in pheasants at a level of 0.05% for 2 weeks and is effective when administered in the feed. Continuous medication of pen-reared birds has been recommended, but is not economical.

Several other compounds have been shown effective against Syngamus under experimental conditions. Methyl 5-benzoyl-2-benzimidazole was 100%efficacious when fed prophylactically at 0.0064% and curatively at 0.0125% to turkey poults. A level of 0.044% for 14 days has also been effective.

5-isopropoxycarbonylamino-2-(4-thizolyl)-benzimidazole was found to be more efficacious than thiabendazole or disophenol (2, 6-diiodo-4-nitrophenol). The level of control with three treatments of cambendazole* on days 3-4, 6-7, and 16-17 post-infection was 94.9% in chickens (2mg/kg x 50mg/kg) and 99.1% in turkeys (2mg/kg x 20mg/kg).

Levamisole*, fed at a level of 0.04% for 2 days or 2 g/gal drinking water for 1 day each month, has proven effective in game birds. Fenbendazole at 20 mg/kg for 3-4 days is also effective.

*Not approved for use in commercial poultry.

TAPEWORMS (RAILIETINA, CESTODES)[កែប្រែ]

Causes:

Common parasitic helminths are species of Ascaridia, Heterakis, Syngamus and Raillietina.

Effects:

Severity and signs dependent of species of parasite. Heavy infestation usually leads to signs of emaciation, feed refusal, anaemia and death.

Detailed causes:

Fifty percent of the intestinal tract of chickens may contain tapeworms (cestodes) if they are reared on range or in backyard flocks. In contrast, birds confined within poultry houses seldom become infected. Tapeworm infestations are now considered rare in intensive poultry-rearing regions. Over 1400 species of tapeworm have been identified in wild and domestic birds. Of these, three families are 10 genera, including Raillietina species affect poultry.

Tapeworms are flattened, ribbon-shaped, usually segmented worms. Millions of eggs may be required to complete the complicated two-hose or three-hose life cycle. The worms are characterised by complete absence of a digestive tract and obtain their nourishment by absorption from the gut contents of the host.

Mode of transmission

Birds become infected by eating an intermediate host, which transmits a larval stage of the tapeworm to the intestine of the definitive host. The intermediate host may be an insect, crustacean, earthworm, slug, snail or leech depending upon the species of tapeworm. Some large tapeworms may appear to completely block the intestine of infected birds. Different species vary considerably in pathogenicity so identification as to species is desired.

Clinical signs:

Some large tapeworms may appear to completely block the intestine to the infected birds. Different species vary considerable in pathogenicity so identification as to species is desired.

Tapeworms are flattened, ribbon-shaped, usually segmented worms. Millions of eggs may be required to complete the complicated two-hose or three-hose life cycle. The worms are characterised by complete absence of the digestive tract and obtain their nourishment by absorption from the gut contents of the host.

Diagnosis:

Most species of worm appear during postmortem examination of the digestive tract. Acute identification is necessary for effective control. A portion of the worm should be removed and viewed under a microscope for detailed identification. Tapeworms are flattened, ribbon-shaped, usually segmented worms. The worms are characterised by complete absence of a digestive tract.

Most cestodes are usually hot specific for a single or a few closely related birds. Identification of the genus and species may provide a clue to the probable intermediate host.

Treatment and control:

Most cestodes are usually host specific for a single or a few closely related birds. Identification of the genus and species may provide a clue to the probable intermediate host. The diagnositician may then be able to suggest practical control measures. Completion of a two-host life cycle depends upon a unique set of ecologic conditions. Thus minor changes in flock management may cause a break in the life cycle and effect a useful control measure. Antihelminthic drugs are not recommended, as they are only a short-term remedy. The intermediate host should be identified and controlled.

THRUSH (CANDIDIASIS, CROP MYCOSIS, YEAST INFECTION)[កែប្រែ]

Causes:

Candida albicans is a yeast-like fungus which is spread via contaminated faeces, litter and dirty waterers. Often occurs after over application of antibiotics.

Effects:

Emaciation, stunting, listlessness, increased thirst, depression, rough appearance to feathers.

Detailed causes:

All species of bird of all ages but in particular the young, are susceptible to this chronic disease. The agent involved in the aetiology of this disease is Candida Albicans, which is a yeast-like fungus.

Mode of transmission

It is spread via contaminated faeces, litter and dirty waterers.

Note

Often seen after too long use of broad spectrum antibiotics.

Clinical signs:

Signs include emaciation, stunting, listlessness, increased thirst, depression and rough appearance to feathers.

Postmortem lesions

Whitish pustules or nodules in mouth, crop and oesophagus, and white towel appearance in upper digestive tract are common.

Ulceration of the mouth and oesophagus, haemorrhagic mucosa in the proventriculus and focal necrosis of the liver can occur.

Diagnosis:

Slimy white lesions in the upper digestive tract are diagnostic. The organism can be isolated from lesions on Sabouraud’s Dextrose agar. Colonies are whitish, creamy and highly convex. The hyphae and spores can be seen in a fresh smear.

Treatment and control:

Prevention

Clean up water spills, don’t give birds sugar water for more than one day and use water sanitisers to prevent build up of yeast.

Treatment

Mycostatin, copper sulphate in water and nystatin (50 g/t) in the feed can treat the disease. It is similar to trichomoniasis, Vitamin A deficiency, Wet Pox and T-2 toxicosis.

TIBIAL DISCHONDROPLASIA[កែប្រែ]

Causes:

Failure of the chondrocytes to hypertrophy (increase in size) results in abnormal cartilage, which cannot be invaded by blood vessels. The disease is not contagious. Genetic and/or dietary (caution-anion ration or high phosphorus relative to calcium) factors may be involved. Grain high in Fusarium roseum or fungicide (tetramethylthiuram) can cause the disease.

Effects:

Bowing of the bones is evident, which is more severe in roaster birds or males kept over 8 weeks for de-boning with body weight over 2.2kg (5lb). Lameness can occur in as many as 30% of the flock, so reluctance to move, stilted gait and bilateral swelling of the femoral;-tibial joints can be seen.

Detailed information

All species of young bird are susceptible to this chronic disease. The aetiology of the disease is the failure of the chondrocytes to hypertrophy (increase in size) resulting in abnormal cartilage, which cannot be invaded by blood vessels. Vascular invasion of the cartilage from the metaphysis is not adequate and/or defective chondrolysis occurs.

Mode of transmission

This disease is not contagious. Genetic and/or dietary (caution – anion ratio or high phosphorus relative to calcium) factors may be involved.

Grain high in Fusarium roseum or fungicide (tetramethyl thiuram sulphate) can cause the disease.

Clinical signs:

Lameness can be seen in as many of 30% of the flock (reluctance to move, a stilted gait and bilateral swelling of the femoral-tibial joints).

Bowing of the bones is evident and is more sever in roaster birds or males kept over 8 weeks for de-boning with body weight over 5 lbs or 2.2 kg.

Postmortem lesions

Proximal tibiotarsal bone is enlarged and contains an abnormal mass of cartilage (failure of cartilage in growth plate to become calcified).

Fractures below the abnormal cartilage may occur.

Diagnosis:

History, clinical signs and postmortem lesions (abnormal mass of cartilage in tibial head) are characteristic. Microscopically, dyschondroplasia is characterised by persistence and accumulation of pre-hypertrophic cartilage and begins as early as the first week of age. Chondrocytes in abnormal cartilage are smaller and shrunken.

It simulates perosis, rickets and osteochondrosis (necrosis of growth plate primarily in the vertebrae and femoral head).

Lyxoscope can detect TD in birds as young as one week of age. This machine is used by basic breeder companies to select out TD in their genetic lines.

Treatment and control

Prevention

Slow the growth rate and select strains with a lower incidence of TD.

Treatment

Diet changes, such as reducing phosphorus relative to the level of calcium, will reduce the disease. Feed a diet free of Fusarium and tetramethyl thiurams sulphate.

TICKS[កែប្រែ]

Causes:

Ticks are large mites belonging to the super-family Ixodoidea of the Acarina. Ticks inhabiting poultry houses belong to the family Argasidae. 

Effects:

Losses caused by tick infestation are threefold- loss of host blood, which may cause death; reduced productivity associated with anaemia, but also possibly due to toxic substances produced by the tick; transmission of avian diseases.

Detailed causes:

The fowl tick is the most important poultry ectoparasite in many tropical countries, being a limiting factor in successful rearing of standard breeds of poultry. Turkeys usually suffer even more than chickens; recently hatched poults and chicks show the highest mortality. These ticks cause skin blemishes on turkeys, reducing price.

Ticks are large mites belonging to the super-family Ixodoidea of the Acarina. Unengorged adults of most common ticks are 2-4 mm long, but fully engorged females may reach more than 10 mm. However, unengorged tick larvae are similar in size to adult mites. Ticks inhabiting poultry houses belong to the family Argasidae.

The fowl tick is capable of transmitting the highly pathogenic spirochete Borrelia anserine in many tropical and temperate parts of the world. Tick-borne avian spirochetosis has been reported in chickens and turkeys in the United States; epizootics of avian spirochetosis in Arizona are associated with infestations by the flow tick.

Fowl ticks have been reported to transmit Aegyptianella pullorum and fowl cholera (Pasteurella multocida) in some regions of the world. All postembryonal stages of the common fowl tick have been found infected with A. pullorum in some areas. However, in other areas transmission of fowl cholera was not shown even though fowl ticks harboured P. multocida for 25 days. Aegyptianellosis has not been reported from the Americas.

Tick paralysis in chickens, a flaccid, afebrile motor paralysis, may result from attacks by A. persicus as well as by A. walkerae in Africa. Aetiology of this sporadic disease is not understood, but most probably a specific paralytic toxin is contained and transmitted in the tick salivary secretions. Clinical signs may be confused with botulism, neural signs of Marek’s Disease, transient paralysis of Newcastle disease, and possible conditions caused by other bacterial or chemical toxins.

Clinical signs

Birds suffer chiefly from attacks of these ticks during the warm dry season. Loss of blood may reach proportions of a fatal anaemia; at least there may be emaciation, weakness, slow growth and lowered production. Ruffled feathers, poor appetite and diarrhoea are signs suggesting tick infestation.

Diagnosis:

Mature blood-engorged females measure about 10 mm x 6 mm. Unfed ticks are relatively easily recognised by their flattened ovoid shape and tan to reddish brown colour.

Females may lay a total of 500-875 eggs in four or five separate batches but require a blood meal before laying each batch of eggs. Eggs are laid in sheltered crevices, including bark of trees. The complete life cycle takes about 7-8 weeks during warm weather and longer during cold seasons. Fowl ticks remain inactive in cracks and crevices during cold weather, and adults may live without a blood meal for more than 4 years.

Diagnosis is made by identification of ticks on the birds, and by clinical signs.

Treatment and control:

Control requires treatment of premises because adult and nymphal ticks are on their hosts only a short time and then hide in the surroundings. The litter, walls, floors and ceilings must be sprayed thoroughly – forcing spray into cracks and behind nest boxes.

Outdoor runs and feed troughs, woodpiles and tree trunks may be treated suing approved insecticides. Other methods for fowl tick control include use of metal construction, elimination of tree roosting, using roosts suspended form ceilings and converting to cage operation. 

Frequent inspection is necessary to combat ticks before their numbers increase to a harmful level. Fowl ticks are rare in modern, large commercial cage-layer operations.

TREPONAEMA (AVIAN INTESTINAL SPIROCHETOSIS)[កែប្រែ]

Cause:

Intestinal spirochete (spiral bacteria) of the genus Treponaema.

Effects:

Layers and breeders have wet faeces or diarrhoea, pasty vents, retarded growth, delayed onset of lay, dirty faecal-stained eggs, reduced egg weight, pale yolks. Turkeys and broilers show growth retardation, diarrhoea, pasted vent.

Detailed causes:

Avian intestinal spirochetosis (AIS) is a subacute to chronic nonsepticaemic disease characterised by spiral bacteria of the genus Spirochaetacae of which Treponaema, Borrlia and Serpulina are pathogenic to animals. The disease is caused by a heterogeneous group of spirochaetes in the rectum and/or colon.

One avian intestinal spirochaete, Serpulina hyodysenteriae, has been classified taxonomically. The remaining are unclassified but have morphological and biochemical features indicating placement in either the genus Serpulina or Treponaema. They have been shown to infect all domesticated poultry and wild birds. Intestinal spirochaetes of poultry are anaerobic gram negative, helix –shaped bacteria.

Initiation and severity of clinical disease is influenced by management, nutrition, environment and genetics. Contributing factors include moulting, onset of egg production, poor feed quality and floor housing. Light laying breeds are more susceptible.

Clinical signs:

Avian intestinal spirochaetes can be divided into three pathotypes, causing: subclinical infection; mild to moderate clinical disease or severe clinical disease. In layers, wet faeces, diarrhoea, pasted vents, retarded growth, delayed onset of lay, production of dirty faecal-stained eggshells, reduced egg weight and reduced egg carotenoid content may all be evident.

In turkeys, broilers and broiler breeders are similar to those in layers except that growth retardation is more severe.

Diagnosis:

Because spirochaetes can be normal flora or produce subclinical infections, characteristic clinical signs and lesions must be present in conjunction with visual demonstration of helical bacteria by dark-field or light microscopy for a presumptive diagnosis of AIS.

Confirmation of bacteria as spirochaetes should be through visualisation of distinctive ultra-structural features, demonstration of spirochaete antigens or by isolation in culture. Culture from fresh faecal droppings or caecal mucosa followed by further characterisation is necessary to confirm a diagnosis. In poultry, spirochaetes identified from faecal specimens should be distinguished from other spiral bacteria such as Campylobacter, Arcobacter, Helicobacter and Spirillum. In case of chronic diarrhoea or pasted vents, nutritional problems such as excess dietary salt, fats or soybean meal should be investigated. Other causes of chronic diarrhoea include enteric salmonellosis, colibaccillosis and coccidiosis.

Treatment and control:

Prevention

AIS is chickens is a mild disease, but prevention is still more economical than treatment. Preventive measures include decreasing contact with faeces by raising birds off floors, frequent changing of litter or manure removal, good rodent and insect control programs, minimising dietary and moulting stress, provision of high quality feed ingredients and use of biosecurity measures.

Treatment

For intestinal spirochaetes of commercial poultry, efficacy of chemotherapeutics varies between isolates. Use of 5-nitromidazole in water at a concentration of 120 ppm for 6 days is generally effective, although re-treatment after 4-8 weeks may be necessary. In some field cases, neomycin has produced clinical improvement.

TRICHOMONIASIS[កែប្រែ]

Causes:

Pear-shaped, flagellated protozoan- Trichomonas gallinae.

Effects:

No specific signs, but lowered feed consumption, spitting up of feed, listlessness, ruffled feathers and emaciation, followed by death may be seen. The crop is distended and filled with fluid, the infected bird has difficulty swallowing, stretches its neck and drools a greenish-yellow fluid. Diarrhoea and a drop in egg production can occur.

Detailed causes:

Growing, chickens, turkeys, pigeons (canker in squabs), doves and falcons (frounce) are susceptible to this chronic disease. Although not common in commercial poultry. The agent involved in the aetiology of this disease is Trichomonas gallinae, which is a pear-shaped protozoan containing four flagella.

Mode of transmission

It is transmitted by consumption of insects, contaminated feed or water and by wild birds. Crop milk can transmit that organism from adult pigeon and doves to young by regurgitation of semi-digested food during feeding.

Clinical signs:

No specific signs occur, but include lowered feed consumption, spitting up of feed, high mortality, listless, ruffled feathers and emaciation.

A large crop filled with fluid, difficulty in swallowing, stretching of neck, drooling greenish to yellowish fluid. Diarrhoea (yellow and watery) and a drop in egg production can occur.

Postmortem lesions

Cone-shaped lesions in the upper digestive tract (mouth, oesophagus and crop, pharynx, liver) proventriculus can occur.

A build up of caseous material may partially or totally occlude (block) the lumen of the oesophagus.

Diagnosis:

The clinical signs and gross lesions (mouth cankers) are characteristic. Histopathologist will demonstrate trichomonads in the lesions.

The organism should be identified from a scraping for a definitive diagnosis. It simulates thrush, T-2 Toxin, Wet Pox, Vitamin A deficiency and Chilomastix gallinarum.

Treatment and control:

Prevention

Eliminate the insect or wild bird carriers.

Treatment

Dimetridazole (0.05%), ipronidizole and nitrasone and effective treatments.

TRICOTHECENE TOXICITY[កែប្រែ]

Causes:

Consumption of feed containing grains infected with fungi producing tricothecene mycotoxins. T-2 toxin; diacetoxyscirphenol (DAS) and deoxynivelanol (DON, vomitoxin) can be produced by the fungi Fusarium trichinctum, F. calonectria, F. gibberella, F. cephalosporium and F. trichoderma.

Effects:

Feed refusal, impaired growth, uneven and poorly formed feathers, vomiting. Thin-shelled eggs, reduced egg production, facial swelling, caustic injury to skin, cyanotic (blue-coloured) combs and wattles, seizures and tremors may be seen.

Detailed causes:

Chickens, turkeys, layers and breeders of all ages are susceptible to this acute to chronic disease. The severity of the disease depends on the dosage of toxin (higher-acute), age of bird (young birds have acute, older have chronic), and duration of exposure (longer periods cause chronic toxicosis). Consumption of feed containing grains infected with fungi producing trichothecenes toxins cause the disease. The following trichothecenes: T-2, diacetoxyscirphenol (DAS) and deoxynivalenal (DON or vomitoxin) can be produced by Fusarium trichinctum, F. calonectria, F. gibberella, F. cephalosporium and F. trichoderma.

Mode of transmission

Feed contaminated with trichothecenes toxins, which are very caustic. It can occur in corn, sorghum, barley, safflower, seed, oats and brewers grain.

Special note

T-2 toxin is the most common and pathogenic of the trichothecenes.

Clinical signs:

Signs include off feed, impaired growth, uneven and poorly formed feathers, and emesis (vomiting). Thin shelled eggs, reduced egg production, swelling of the face, caustic injury to skin, cyanotic (blue-coloured) combs and wattles, seizures and tremors may be seen.

Postmortem lesions

Whitish to yellow focal nodules in base of mouth, near the salivary ducts and tongue can occur. An inflamed GI tract, atrophy of bursa and thymus, necrosis of gizzard and proventriculus, dermatitis on the toes, pale or yellow bone marrow, yellow hemorrhagic liver and gout can also be seen.

Diagnosis:

Feed analysis for toxins and feed refusal in many farm animals is diagnostic. It simulates wet pox, vitamin A deficiency, thrush, trichomoniasis, ochra and aflatoxicosis, IBD and visceral gout.

Treatment and control

Prevention

Prevention is the same as for the other Mycotoxins, including mould inhibitors and use of dry grain only. Mouldy grains should never be added to feed.

Treatment

The treatment is the same as for other mycotoxins, such as aflatoxin. Increasing the protein content of feed by 1%, increasing vitamin and mineral content of feed and adding gentian violet* to feed have a sparing effect on aflatoxin-induced disease.

*Not authorised in the US.

TURKEY CORYZA (TURKEY RHINOTRACHEITIS)[កែប្រែ]

Causes:

Gram negative strictly aerobic bacterium- Bordatella avium. Highly contagious and spread by aerosol.

Effects:

Stunting, huddling, decreased feed and water consumption, respiratory distress, sneezing, dry cough and a tenacious brown nasal discharge can occur. Loss of voice and submaxillary oedema may be seen. Turkeys may have almond-shaped eyes and mortality to 50%. Mortality is low in broilers.

Detailed causes:

Turkeys of more than 3 weeks old are susceptible to this acute to chronic disease. Although broilers can also be affected, it is rarely seen. The agent involved in the aetiology of this disease is Bordetella avium which is a gram-negative, nonfermentative, motile and strictly aerobic bacillus.

Mode of transmission

It is highly contagious and is spread by aerosol. The incubation period is 7-10 days. The organism can contaminate faeces or water for up to 6 months.

Special note

It causes Immunosuppression, which may lead to an outbreak of cholera in turkeys or poor vaccination response to NDV, E. coli or Pasteurella multocida. Coryza means head cold. In Europe, turkey rhinotracheitis is caused by a pneumovirus.

Clinical signs:

Swollen sinuses and tracheal inflammation are characteristic of this disease. Stunting, huddling, decreased consumption of food and water, respiratory distress, sneezing, dry cough and nasal discharge (tenacious brown) can occur.

Loss of voice and submaxillary oedema may be seen. Turkeys may have almond-shaped eyes and mortality to 50%. Mortality is low in broilers.

Postmortem lesions

Mucous in trachea and trubinates, and the trachea is softened and distorted. Pneumonia, edema of the interstitial tissues of head and neck, air sacculitis, pericarditis and bursal atrophy may be evident.

Diagnosis:

Bacteria from the trachea can be cultured on MacConkey’s agar. Colonies are clear and pinpoint and may develop a brownish raised centre.

Microagglutination or ELISA testing will determine antibodies in unvaccinated flocks.

It simulates mycoplasmosis, avian influenza (AI), ornithosis, Newcastle disease (ND) and swollen head syndrome.

Rhinotracheitis in turkeys is characteristic for this disease.

Treatment and control:

Prevention

Sanitation and biosecurity reduces the problem. Bacterin prepared from whole bacterial cells can be given to turkey-breeders at 6 weeks. Live vaccine is a temperature (cold) sensitive mutant (replicates only in upper respiratory tract) given by spray at 1-day and drinking water at 14 days.

Treatment

Aerosol spray of oxytetracycline HCI (10 mm sized particles).

TURKEY VIRAL HEPATITIS[កែប្រែ]

Causes:

A highly contagious, but as yet unclassified virus.

Effects:

Incubation period is 1-7 days. It is often subclinical (no signs). Clinical signs include, depression, morbidity to 100% and mortality to 20%. Death is sudden. Breeder flocks can show reduced production, fertility and hatchability.

Detailed causes:

Turkeys of all ages can be affected with this acute, highly contagious and typically subclinical disease. The virus responsible has not been classified.

Mode of transmission

Spread by faecal-oral route and there may also be vertical transmission.

Clinical signs:

(There is a 1-7 day incubation period). It is often subclinical.

Depression, sudden death and morbidity to 100% and mortality to 25% can occur. Breeder flocks can show reduced production, fertility and hatchability.

Postmortem lesions

Lesions include catarrhal enteritis, bronchopneumonia, peritonitis, or air sacculitis. Focal grey, depressed areas on the liver and circular grey-pink areas on pancreas may be seen.

Diagnosis:

Clinical signs and gross lesions in the liver and pancreas of turkeys are characteristic. Isolation of the virus from the liver in the yolk sac of embryonating eggs is diagnostic. Reinfection of day-old poults to reproduce the disease is also important.

It simulates histomoniasis and bacterial hepatitis.

Treatment and control:

Prevention

Biosecurity is important

Treatment

None.

ULCERATIVE ENTERITIS[កែប្រែ]

Causes:

Gram positive, spore-forming, aerobic, non-motile bacterium- Clostridium colinum.

Effects:

Often accompanies coccidiosis in broilers. Watery diarrhoea, ruffled feathers, dull, listless birds with increased thirst, emaciation and atrophy of pectoral muscles can occur. Mortality in quail is high.

Detailed causes:

Young, quail, broilers, chicken pullets and turkeys of 6-14 weeks are susceptible to this acute to chronic disease. The agent involved in the aetiology of this disease is clostridium colinum, which is spore-forming, gram-positive, aerobic and non-motile.

Mode of transmission

Vectors are faeces, soil and litter containing the bacteria.

Special note

It often accompanies coccidiosis in broilers.

Clinical signs:

High mortality in quail, watery diarrhoea, ruffled feathers, dull, listlessness, increased thirst, emaciation and atrophy of pectoral muscles can occur.

Postmortem lesions

Yellow irregular ulcers on small intestine and caeca, hemorrhagic enteritis are seen. Congested lungs, enlarged haemorrhagic necrotic spleen, light yellow mottling of liver and crop filled with water may occur.

Diagnosis:

Gross lesions (ulcers on intestine and caeca) and bacterial isolation on tryptose – phosphate agar with yeast extract are a definitive diagnosis. Fluorescent antibody test will detect bacteria in organs.

It simulates coccidiosis, necrotic enteritis and histomoniasis.

Treatment and control:

Prevention

Improved sanitation. Adding salt to the soil (500 lbs of salt/house) may kill spores. Raising birds on wire and/or feeding bacitracin at 50-100 g/t will prevent the disease.

Treatment

NF-180 (50-100 g/t), strephomycin (60 g/t) and chlortetracycline, vitamins and minerals in water and/or lincomycin 2 g/t will reduce the signs. Remove dead birds and feed bacitracin (200 g/t)

Note

Bacitracin is not allowed in most countries.

VIRAL ARTHRITIS (VIRAL TENOSYNOVITIS)[កែប្រែ]

Causes:

Double stranded RNA reovirus.

Effects:

Incubation period is 9-13 days. Birds are down on the hocks and have stunted growth, are reluctant to move and have an uneven gait. Swollen tendons above and below the hocks and a ruptured gastrocnemius muscle are also seen.

Detailed causes:

All species of bird from 3-30 weeks old, mostly broilers and broiler breeders, are susceptible to this chronic to debilitating disease. Broilers develop problems from 5-8 weeks and breeder pullets at 10-18 weeks of age. The disease is caused by a reovirus (respiratory, enteric, orphan).

Mode of transmission

Spread laterally from bird to bird or vertically from hen to offspring. Faecal to oral or via respiratory tract transmission can also occur.

Special note

It commonly causes downgrading and trimming in broilers and culling in breeders.

Clinical signs:

Incubation period of 9-13 days. Birds are down on the hocks, have stunted growth, reluctant to move and have an uneven gait. Swollen tendons above and below the hocks and ruptured gastrocnemius tendon is also seen.

Postmortem lesions

Bilateral swelling of tendons (digital flexor and metatarsal extensor) is diagnostic. There is an increase in clear, thick fluid in joints and swelling of the footpad, straw coloured or blood-tinged exudate can be seen in lesions.

Ruptured tendons, haemorrhaging of synovial membrane, erosion of cartilage of distal tibiotarsus can also occur. The condyles (joint capsule) may also be involved.

Diagnosis:

Isolation of virus from lesions on CAM of inoculated embryos and serologic test for VA antibodies (VN or ELISA) are of limited use because birds are routinely infected with non-pathogenic reoviruses.

Histopathology, reveals oedema, coagulation necrosis, heterophil accumulation and perivascular infiltration. Hypertrophy and hyperplasia of synovial cells, infiltration of lymphyocytes, macrophages and reticular cells are also evident.

VA causes excessive or clear straw coloured fluid; Mycoplasma synoviae causes honey coloured fluid and Staphylococcus produces thick white fluid in swollen joints.

Gross and microscopic lesions are diagnostic.

Ruptured gastrocnemius tendon is characteristic.

Treatment and control:

Prevention

Vaccination of parent stocks no later than 20 weeks of age with the S1133 virus strain. This is usually given at 2 weeks (SQ or water) and between 6-10 weeks (water) with live vaccine. Killed virus is given at 18 weeks and possibly again at 40 weeks by SQ injection.

Re-vaccination by drinking water is not allowed in most countries outside the US. SQ is common.

Attenuated live vaccine diluted by 1/3 at 1 day with a full dose of HVT for broilers in problem areas or by coarse spray at one day of age with a full dose. Boosting at 7-10 days by spray or water is sometimes done. This is not allowed is most countries outside the US.

Treatment

None. Antibodies are used to prevent secondary Staph infections.

VITAMIN A DEFICIENCY (NUTRITIONAL ROUP)[កែប្រែ]

Causes:

Deficiency of vitamin A in the diet. May occur when the vitamin is oxidised by rancid fat in the diet, and neomycin, a common antibiotic, decreases the absorption of vitamin A.

Effects:

Caseous eye (no odour), emaciation, weakness, ruffled feathers, incoordination, eyelids stuck together (sicca), watery discharge from throat (roup), nostrils or eyes can be seen in young birds. In adults, egg production and hatchability are decreased.

Detailed causes:

Vitamin A is needed for integrity of epithelial lining of the alimentary, urinary, genital and respiratory systems. Deficiency of this vitamin will interfere with growth, optimal vision and integrity of mucous membranes. All species of bird can be affected by this deficiency.

Mode of transmission

Vitamin A deficiency may occur when the vitamin is oxidised by rancid fat. Neomycin, a common antibiotic, decreases absorption of vitamin A.

Clinical signs:

Caseaous eye (no odour), emaciation, weak, ruffled feathers, incoordination, eyelids stuck together (sicca), water discharge from throat (roup), nostrils or eyes can be seen in young birds.

In adults, egg production and hatchability is decreased.

Postmortem lesions

Lesions include (white pustules) in the throat, nasal passages, oesophagus, pharynx and crop.

Urates (whitish crystals) in kidney (swollen) may lead to gout. Oral lesions are caused by blockage of mucous glands. Blood spots in eggs can also occur.

Diagnosis:

Gross (mouth and eye lesions) and microscopic lesions are characteristic. Microscopic lesions include replacement of original epithelium with stratified squamous keratinised epithelium.

Examine the levels of vitamin A in the diet for a definitive diagnosis.

It simulates T-2 Toxin, Candida, Wet Pox, Trichomoniasis and Infectious bronchitis.

Treatment and control:

Prevention

Check the diet at regular intervals for adequate vitamin level. Add an antioxidant in the feed and remove neomycin.

Treatment

Restore normal level to the diet. Hypervitaminosis A may adversely effect skeletal growth.

VITAMIN B1 (THIAMIN) DEFICIENCY (POLYNEURITIS)[កែប្រែ]

Causes:

Deficiency of vitamin B1 (thiamine) in the diet or Amprol excess can be caused by mouldy feed or oxidation by rancid fat.

Effects:

Nervousness, anorexia, ruffled feathers, leg weakness and an unsteady gait can be seen. Paralysis and star gazing can occur in young birds. Adults may have a blue comb, decreased respiration rate and lowered body temperature.

Detailed causes:

Vitamin B1 is needed for coenzyme formation involved in proper nervous system function. This disease can affect all species of bird. It takes 3 weeks for the deficiency to develop.

Mode of transmission

Vitamin B1 (thiamine) deficiency or amprol excess can be caused by mouldy feed or oxidation by rancid fat. Thiamine is converted in the body to an active form, thiamine pyrophosphate, which is an important cofactor in oxidative decarboxylation reactions and alderhyde exchanges incarbohydrate metabolism.

Clinical signs:

Nervousness, anorexia, ruffled feathers, leg weakness and an unsteady gait can occur. Paralysis (convulsions with head retraction) called polyneuritis and star-gazing (retracted head due to paralysis of the anterior muscles of the neck) can occur in young birds. Adults may have a blue comb, a decrease in respiration rate and lowered body temperature.

Postmortem lesions

Hypertrophy of adrenal glands, cortex and medulla from oedema accumulation, atrophy of the gonads, stomach and intestinal walls are evident.

Diagnosis:

Clinical signs and histopathology are helpful. Microscopically dilated crypts of Lieberkühn occur in the duodenum. Exocrine cells of pancreas show cytoplasmic vacuolation and hyaline body formation.

It simulates Avian encephalomalacia, Newcastle disease and Vitamin E deficiency.

Treatment and control:

Prevention

Quality control of the feed. A correct drug level will help prevent the disease.

Treatment

Alter the drug level or B1 level in the feed. Since most grains are high in B1, it does not need to be added to the diet. Amprol, a common anticoccidial mediation, can bind thiamine.

VITAMIN B2 (RIBOFLAVIN) DEFICIENCY (CURLED TOE PARALYSIS)[កែប្រែ]

Causes:

Deficiency of vitamin B2 (riboflavin) in the diet. Most grains are deficient in vitamin B2, therefore it must be included in the premix.

Effects:

Curled toes, poor growth, weakness and emaciation are seen in young birds. Leg muscles are atrophied and flabby. The skin is dry and harsh. In adults, poor hatchability and egg production can occur. Dead embryos have "clubbed" down feathers. Poults have severe dermatitis of the feet and shanks and incrustations on the corners of the mouth.

Detailed causes:

Vitamin B2 is a cofactor in many enzyme systems. Many are associated with oxidation-reduction reactions that are involved in cell respiration.

Mode of transmission

Most grains are deficient in B2; therefore, it must be added in the premix.

Clinical signs:

Curled toes, poor growth, weak and emaciation are seen in young birds. Leg muscles are atrophied and flabby. The skin is dry and harsh. Poor hatchability and egg production can occur in adults. Dead embryos have "clubbed" down feathers. Poults have severe dermatitis of the feet and shanks and incrustations on the corners of the mouth.

Postmortem lesions

Enlarged sciatic and brachial nerve, leg muscles are atrophied and flabby in young birds. Adults have enlarged fatty (yellow) livers.

Diagnosis:

Postmortem lesions (curled toes) are characteristic.

It simulates Marek’s disease (MD), since both have enlarged peripheral nerves. Histologically, nerves are oedematous for B2 deficiency and contain lymphocytes with MD.

Treatment and control:

Prevention

Quality control of the diet.

Treatment

Increase B2 in diet. Vitamin B2 is needed for correct functioning of the peripheral nervous system.

VITAMIN D DEFICIENCY (RICKETS, OSTEOMALACIA)[កែប្រែ]

Causes:

Deficiency of vitamin D3 in the diet.

Effects:

Vitamin D3 is needed for proper Ca and P metabolism and in the formation of normal skeleton. Signs are therefore similar to Ca and P deficiency. Soft brittle bones (rickets) and retarded growth occur in young birds, whilst cage layer fatigue is seen in mature birds.

Detailed causes:

Vitamin D3 is needed for proper metabolism of calcium (Ca) and phosphorus (P), and in the formation of normal skeleton, hard beaks and claws, and strong eggshells. Rickets occurs in young birds and osteomalacia (cage layer fatigue) in mature birds.

Mode of transmission

A deficiency in the diet caused by variations in Ca and P content of animal by-products and variation in P bioavailability in various mineral sources. A phosphorus deficiency is common in cage layers which don’t have access to P in the faeces.

Clinical signs:

Postmortem lesions and histopathology (widening of epiphyseal plate, hypertrophy and softening of the bone, and irregular patterns of cartilage and bone development in the primary and secondary spongiosa) are diagnostic.

It simulates other deforming leg weaknesses in poultry.

VITAMIN E DEFICIENCY (CRAZY CHICK DISEASE, ENCEPHALOMALACIA)[កែប្រែ]

Causes:

Deficiency of Vitamin E in the diet. Vitamin E is heat labile. It can also be caused by deficiency of selenium. As selenium levels in the soil are very variable, cereal grains are often suboptimal in selenium.

Effects:

Incoordination, tremors, rapid contractions and relaxation of the legs results in the name "crazy chick disease".

Detailed causes:

Vitamin E is required for reproduction and normal integrity of central nervous and muscular system. Vitamin E is also an effective antioxidant. It is an important protector of essential fatty acids, Vitamin A and D3. Young chicks, usually between 15th and 30th day of life are most susceptible.

Mode of transmission

Vitamin E is heat labile. A deficiency of selenium will result in a deficiency of Vitamin E. Selenium levels in some areas are very variable, which may result in suboptimal levels in cereal grains.

Clinical signs:

Incoordination, tremors, rapid contractions and relaxation of the legs results in the name "crazy chick disease".

Postmortem lesions

The cerebellum is softened and oedematous which may progress to haemorrhage and/or necrosis.

Diagnosis:

Histopathology reveals diagnostic lesions in the brain, which includes ischemic necrosis, demyelination and neuronal degeneration.

It simulates Avaian encephalomyelitis (AE), Newcastle disease and vitamin B1 deficiency.

Treatment and control:

Prevention

Proper storage of premixes and finished feed and proper amount of selenium in feed will prevent the disease.

Treatment

Add the dietary ingredient to reduce clinical signs. Selenium is involved in vitamin E metabolism. A deficiency of selenium will cause a deficiency of E. A deficiency in vitamin E will also result in testicular degeneration in adult males and increase embryonic mortality.

VITAMIN K DEFICIENCY[កែប្រែ]

Causes:

Deficiency of Vitamin K in the diet. High levels of sulphaquinoxaline may increase the incidence and severity of the condition.

Effects:

Signs occur 2-3 weeks after the deficiency occurs. Haemorrhaging and anaemia may be seen in young birds. It can cause increased embryonic mortality in breeders and dead embryos can be haemorrhagic.

Detailed causes:

Vitamin K is required for the synthesis of prothrombin. Deficiency in the diet can result in blood clotting difficulties. High levels of sulfaquinoxaline may increase the incidence and severity of the condition.

Clinical signs:

Show 2-3 weeks after the deficiency occurs. Haemorrhaging and anaemia in young birds may be seen. It can cause increased embryonic mortality in breeders and dead embryos can be haemorrhagic.

Postmortem lesions

Lesions include haemorrhages on the breast, legs, wings and/or in the abdominal cavity and a hypoplastic bone marrow.

Diagnosis:

Signs, lesions and determination of the prothrombin time are useful.

Treatment and control:

Correct the deficiency by restoring adequate vitamin K levels to the diet.

WATER SANITIZER TOXICITY[កែប្រែ]

Causes:

Water sanitisers are commonly used to remove bacteria, fungi or algae from water lines. If water sanitizer levels are too high, quaternary ammonium or chloride toxicity may occur.

Effects:

Birds do not drink, reduced growth, persistent swallowing, continual spitting, facial swelling and ocular or nasal discharge can be seen.

Detailed causes:

Water sanitisers are commonly used to remove bacteria, fungi or algae from water lines. However, if the levels are too high, birds can suffer acute toxicity symptoms.

Clinical signs:

Birds to not drink, reduced growth, persistent swallowing, continual spitting, facial swelling and ocular or nasal discharge can be seen.

Postmortem lesions

Ulcers on tongue from epithelial irritation are evident. A pseudomembrane on the mucosa of the mouth, pharynx oesophagus, crop, proventriculus and/or gizzard can be seen.

Diagnosis:

Water analysis of the sanitizers is needed.

It simulates T-2 toxin, Wet pox, Vitamin A deficiency and trichomoniasis.

Treatment and control:

Prevention

Use lower level of the chemicals in the water

Treatment

Fresh water will reverse the disease.

(These articles completed on 201808050852AM 7+UTM)

by PHY PANHA (Nick Name: ARIKOWIN)