Poultry Husbandry Chapter V: Diagnosis of Poultry Disease

History. A good history will often provide clues that will help solve a problem. Get information on the type of bird, age, feed and water source and consumption rate, growth, production, morbidity and mortality, the description of the case, previous problems, vaccination program, medicine being used etc.

The problems may relate to management, environmental factors, and stress rather than to infection so examine the yard and housing conditions. Is the ventilation adequate? Are ammonia fumes a problem? Is it too hot or too cold? Is the litter wet or is it too dry and dusty? Is the pen too light or too dark? Are there sufficient hours of light for best production? Is the nest area darkened? Are the roosts too high? Do the birds appear comfortable? Chickens can talk and the sounds they make can indicate comfort, hunger, pain, panic, or disease.

Examination of Live Birds. Check the general appearance of the individual or group and try to determine which organ or system is involved in the illness. Note any signs or lesions that might point to a diagnosis, such as small size with poor feathering that suggests infectious stunting (malabsorption syndrome). If the birds show lameness or paralysis, is the lesion in the nervous system, bones, joints, muscles or skin? Some conditions, particularly those affecting locomotion, are easier to diagnose in live birds. Botulism which produces neck paralysis in chickens (leg and wing paralysis are more obvious in turkeys, ducks and pheasants) is an example.

Examine the skin of the head, body and legs for lice and mites, injury (particularly cannibalism), blood, mottling, swellings, anemia, cyanosis, or dermatitis. Listen for unusual breathing sounds (snicking, gurgling) and look for gasping or head-shaking that might indicate respiratory distress. Mouth-breathing (panting) is normal in chickens in hot weather. Exudate from nostrils and eyes and dirty feathers also suggest respiratory infection, or if just the eye, ammonia burn, ILTor eyeworm. Examine the droppings for evidence of diarrhea or other abnormalities. Take a blood sample for hematology or serology if indicated.

Necropsy. If a postmortem examination is to be carried out, birds that are representative of the problem in the flock must be selected. If birds have died, both sick and dead birds should be opened. Cull birds will not provide the answer. If the problem is a drop in production, try to find birds that look like they have recently stopped laying. It is important to do both an external and internal examination and to follow a specific routine to avoid missing important lesions.

CRD – chronic respiratory disease

IB(V) – infectious bronchitis (virus)

ND – Newcastle disease

AI – avian influenza

CA(V) – chicken anemia (virus)

EDS – egg drop syndrome

IBH – inclusion body hepatitis

ILT – infectious laryngotracheitis

IBD – infectious bursal disease


Live birds may be killed by cervical dislocation except when anemia or respiratory disease is suspected.

1. Examine the head, including the eyes, ears, nostrils, comb, wattles, mouth and beak.

Infected eyes and conjunctivitis are seen in CRD, sinusitis, Bordetella and Orthobacterium infection, infectious coryza and in ILT, IB and ND.

Keratoconjunctivitis with central corneal ulcers suggest ammonia burn.

Swollen sinuses are seen in infectious coryza (Parahaemophilus infection) in chickens, sinusitis (mycoplasma), cryptosporidia and Bordetella infection in turkeys and pheasants. They may also be seen as the result of other infections such as influenza.

Chronic fowl cholera causes swollen wattles and sinuses in adult chickens.

Fowl pox causes scabs on the comb, eyelid, and wattle, but must be differentiated from injury. Pox also occurs in turkey, pigeons, doves, canaries and other birds.

If the bird has had its beak trimmed, check for proper healing, overgrowth of the lower beak or over-trimming (cut too short).

Injury on the head, neck or breast or back may indicate predators. Dermatitis and scabby or crusty lesions around the mouth and eyes suggest vitamin B deficiency.

2. Cut across the upper beak and back into the sinuses; then through the mandible and down the esophagus into the crop.

White plaques in the mouth, esophagus, or crop may be caused by capillaria worms, yeast infection (candidiasis, moniliasis), or possibly trichomoniasis or vitamin A deficiency, but most frequently by fowl pox (wet form). White plaques beside the tongue in the mouth are common in hens and turkey breeders and may be caused by mycotoxin or low humidity. Vomitoxin may produce similar lesions in young chickens and turkeys.

If the crop is enlarged and full, it may be an impacted or a sour crop (pendulous crop). The problem may be caused by excess water intake, defects in the crop itself, partial blockage of the proventriculus or gizzard or Marek’s disease. Necrosis of the crop in wild birds is caused by Salmonella infection.

3. Examine the soft palate and larynx and cut down the trachea.

Wet fowl pox lesions are seen on the roof of the mouth, pharynx and larynx.

Granulation, congestion and mucus in the trachea are seen in CRD, IB, coryza, ILT, Orthobacterium, Bordetella, and E. coli infection, or with dust and ammonia fumes.

Hemorrhage and blood clots may occur in ILT and in ND or coryza and may cause severe gasping.

Gapes (gape worms) in pheasants, quail, and other birds is caused by Syngamus infection which also causes gasping. Cyanthastoma cause similar infection in water fowl and tracheal flukes may be found in waterfowl. Tracheal and air sac mites occur in cage birds.

4. Check the abdomen for lice and mites, and the vent for injury and prolapse of the oviduct.

Cut down between the abdomen and the legs and dislocate the hip joints. Peel the skin off the abdomen and breast. Tightly adhering skin and dark tissues indicate dehydration. Remove the breast carefully by cutting through the abdominal muscles, ribs and coracoids.

At this point, examine the thoracic and abdominal organs, paying particular attention to the air sacs, lungs, and liver. Carefully raise the gizzard and intestines and examine the abdominal air sacs, peritoneum, spleen and the ovary in laying birds.

The air sacs are cloudy in respiratory disease such as E. coli infection, Mycoplasma, Aspergillus, IB or early CRD in chickens. If there is also fibrin on the liver and in the pericardial sac, suspect E. coli or Salmonella infection. These lesions in turkeys and other birds might also be due to Chlamydia, or in ducks Anatipestifer infection.

Pneumonia in turkeys is caused by fowl cholera (Pasteurella multocida infection), and the lungs are quite solid. Aspergillosis, ND, AI, E. coli and Ornithobacterium infection can also cause pneumonia.

Peritonitis in layers is usually “egg peritonitis” caused by E. coli infection from the oviduct, although acute fowl cholera also causes peritonitis.

White crystals on the heart, liver and other tissues and organs are uric acid crystals (visceral gout) and are caused by hyperuricemia from urate nephrosis secondary to water deprivation, urolithiasis or other kidney disease.

Large blood clots in the abdomen or hemorrhage and hematoma on the liver are the result of trauma or fatty liver hemorrhage syndrome in chickens, or ruptured aorta in turkeys.

Tumors in or on the organs may be Marek’s disease, lymphoid leukosis, or other varieties of tumors. Multiple small tumors on the organs and peritoneum in adult hens are metastasis from a carcinoma of the oviduct. This may result in ascites.

Ascites may also result from heart or liver disease or from ingestion of some toxic material. Right ventricular failure occurs most frequently in meat-type chickens after 4 weeks. It occurs secondary to pulmonary hypertension causing right ventricular hypertrophy and valvular insufficiency.

Focal white lesions on the organs may be tumors or they may be tuberculosis or coli-granuloma or, if just on the liver, blackhead. Turkeys, pheasants, and peacocks are all quite susceptible to blackhead; chickens are less susceptible. There are prominent cecal cores in blackhead (Histomoniasis) and occasionally in salmonella infection or coccidiosis.

In chicks, turkeys and waterfowl, examine the lungs and air sac for yellow-white foci or plaques caused by brooder pneumonia (Aspergillosis). Gasping in young birds is a sign of tracheal or bronchial epithelial injury, or obstruction and can be caused by irritating fumes or by infection (often IB plus E. coli or Aspergillosis).

In young chicks, look for an infected navel and for yolk-sac infection or peritonitis (mushy chick, omphalitis) in which the abdomen is swollen, wet, and discoloured, and the yolk-sac is infected (due to E. coli, Salmonella, Staph., Proteus, etc.).

Young birds also die because they don’t start to eat (starve-outs) or drink (dehydration). Deaths occur mainly at 3, 4, and 5 days. This may be a management problem (chilling, feed and water not available, etc.) or the chicks/poults may be weak or defective when hatched.

Broiler chickens that die suddenly from sudden death syndrome (dead in good condition) or from heat stroke, or suffocation (piling-up) have congested, edematous lungs, a full digestive tract and congested mottled breast muscle.

5. Examine the circulatory and immune systems, the heart, pericardial sac, blood, spleen, bursa, thymus, and lymphoid tissue of the thigh and intestine.

Birds that die from anemia are pale and the blood is watery. With CAV the thymus is small and bone marrow may be pale. Birds that bleed to death (pick-outs, ruptured fatty liver, acute cecal coccidiosis, ruptured aorta, hemorrhagic enteritis in turkeys, etc.) are also pale.

Sulfa poisoning produces anemia and widespread hemorrhage in the tissues. Chicken anemia virus (CAV) produces similar lesions and is the agent responsible for infectious anemia associated with IBH. Lead poisoning may also cause anemia.

To identify anemia from parasites in blood cells (Plasmodium or leukocytozoon in ducks, turkeys and chickens), blood from a live, sick bird must be examined.

IBD (Gumboro disease) is caused by a virus that damages the bursa causing illness in 2-4 week old chickens or in younger chickens destroys part of the immune system, making birds more susceptible to other infections.

Swelling, congestion and hemorrhage with or without focal necrosis in the spleen, liver and lymphoid tissue suggest septicemia (fowl cholera, fowl typhoid, streptococcosis, or erysipelas) or viremia (ND and duck virus enteritis also affect the lymphoid tissue in the intestine).

Marek’s disease and lymphoid leukosis produce tumors in lymphoid tissue and organs except for the bursa which is mainly affected by lymphoid leukosis (occasional Marek’s lesions may occur in the stroma of the bursa).

Skin leukosis is Marek’s disease virus causing viral dermatitis in the feather follicles. At processing this can be confused with scabby hip or other causes of dermatitis. Marek’s disease can also cause lymphoid neoplasia in the skin.

6. Cut through the proventriculus and remove the digestive tract and liver. Open the proventriculus, gizzard, and small and large intestines to the cloaca. Check the cloaca carefully for evidence of picking injury.

If hens are not properly beak-trimmed or are too fat, mortality from “pick-out” is common. The whole intestine may be picked out through the cloaca. Prolapse of the vagina (and cloaca) (blow-out) may occur from excess fat or straining, secondary to injury or inflammation. Injury is common in flocks that produce large eggs before they become mature.

Examine the digestive tract for lesions and the various kinds of enteritis (hemorrhagic, necrotic, ulcerative, etc.), parasites (tetrameres, roundworms, capillary worms, tapeworms, cecal worms, and coccidia), and gastrointestinal accidents. A large proventriculus in broilers is from lack of fibre in the diet resulting in poor development of the gizzard. A thickened proventriculus sometimes with ulcers or hemorrhage may be Marek’s disease or infectious proventriculitis.

Green staining of the digestive tract is just bile and indicates that the bird is not eating. The liver and spleen may be small (if the bird is thin) and the gallbladder full.

Salmonella pullorum (pullorum disease, bacillary white diarrhea) causes enteritis, diarrhea and death in chicks. It has been eradicated in many countries.

Check the ceca, intestine and liver for lesions of blackhead, TB, coccidiosis or tumor, the liver for other varieties of bacterial, viral or protozoal hepatitis, cholangiohepatitis etc., and the pancreas for tumors.

A large liver may be lymphoid leukosis or Marek’s disease, or it may be caused by bacterial hepatitis (E. coli, campylobacter) or fowl typhoid (Salmonella gallinarum).

Hepatitis with necrosis and hemorrhage that looks like bacterial (vibrionic) hepatitis may be immune damage to veins (vasculitis) from amyloid.

A large, yellow liver may be normal fat storage in a laying bird (estrogen stimulation) but layers die from fatty liver hemorrhage syndrome. This occurs when the liver ruptures because it has become fragile due to excess fat and free radical damage from fat.

A yellow or hemorrhagic liver particularly with focal necrosis may be viral hepatitis (IBH) which is seen in broilers, pigeons, raptors, owls and psittacine (but IBH does not cause infectious anemia).

7. Examine the testes or ovary and open the oviduct. Shrinking ova indicate illness of 2-7 days’ duration or one from which the bird may be recovering. Small, sac-like ova indicate that the bird has been out of lay for a week or more and may be in a molt.

Semi-solid (cooked) ova indicate bacterial infection (such as salmonella).

An impacted oviduct may be secondary to vent-picking, egg-material left in the oviduct, or the bird may be egg-bound. Infection (Mycoplasma, IB, E. coli) can cause salpingitis as well.

A large or small fluid-filled cyst in the right abdomen beside the cloaca is the cystic remnant of the right oviduct (may be normal, but increased by IBV).

A drop in production may be related to clinical or subclinical disease (EDS, IB, MG, AE, AI, ND, etc.) or management faults (lack of light, temperature change, lack of water) or nutritional problems etc.

Deformed shells suggest management faults, superovulation, EDS, IB and soft shells (higher than 1-2%) calcium or vitamin D3 deficiency.

A normal-appearing dead bird with an egg in the shell gland, or just laid has likely died from acute hypocalcemia. These birds often have fragile bones (particulary the femur), lack of medullary bone and rib infolding (osteoporosis, osteopenia, osteomalacia).

Hard (fibrotic) or swollen testes indicate bacterial infection (salmonella).

8. Examine the kidneys and ureters.

Swollen, pale or white spotted kidneys indicate hyperuricemia from urate nephrosis and may be due to lack of water or other kidney disease. Swollen. pale kidneys are also seen in IBH, IBD and fatty liver and kidney disease. Ureters plugged with hard stony material (urolithiasis) indicates a previous low phosphorus diet.

Swollen kidneys and nephritis may be due to IBV (nephrotrophic strain) or E. coli infection and usually causes death from dehydration. Newcastle’s disease causes lympholytic foci in the kidney in pigeons.

9. Examine the skin, integument, muscles, bones and joints.

Emaciation, along with small organs, suggests malnutrition, stunting syndrome, beak injury (poor trimming), peck order (psychological) problems, chronic disease (coccidiosis), bumblefoot or other lameness, or chronic poisoning (lead, insecticide, etc.).

Muscular degeneration due to vitamin E-selenium deficiency can cause lameness, particularly in ducks. Ionophore toxicity causes muscle damage and paralysis in turkeys. Granulomas in the breast muscle are usually a vaccine reaction.

Sarcosporidial cysts produce small, white lesions in the muscle of water fowl.

Examine bones and joints for abnormality and deformity. Angular bone (valgus-varus) deformity of the intertarsal joint is caused by lateral or medial bending of the tibio-tarsal and metatarsal bones and is a common problem in meat-type poultry. It has a variety of possible causes (nutritional, rapid growth, management, etc.). Tibial dyschondroplasia causes backward bending or fracture of the top of the tibia. Slowing growth in young birds will help prevent leg deformity.

Other types of hock and stifle lameness and ruptured tendons are frequent in heavy roaster and turkeys and may be mainly due to injury as the result of heavy weight and fast growth, but some respond to added selenium or B vitamins.

Check for poor bone-breaking strength (osteoporosis) and, in young birds for rubbery bones, soft beaks, and beaded ribs which indicate calcium or Vit. D3 deficiency (rickets). Cage layer fatigue because of fragile bones may be due to phosphorus deficiency. Calcium and Vit. D3 deficiency also cause fragile bones (osteoporosis) in adults, but the most common cause is continuous high production.

Infectious stunting syndrome (malabsorption syndrome, fragile bones, osteoporosis) in young broilers is caused by intestinal damage from viral infection in young chicks. The chickens are small, poorly feathered and there is poorly digested food in the lower intestine. Osteomyelitis also causes fragile bones.

Curly-toe paralysis in young birds may be riboflavin deficiency, but in older birds and turkeys may be genetic or due to lack of roosts.

Cracked feet and foot dermatitis may be pantothenic acid or biotin deficiency, but scaly leg is caused by mites.

Footpad dermatitis and hock lesion are often caused by poor litter conditions.

Toe injury in young birds may be cannibalism or mechanical injury.

Arthritis in the feet or hocks or other joints suggests infectious synovitis (Mycoplasma synoviae) or E. coli or Staph. infection often with osteomyelitis.

Infection in the wing joints in pigeons is usually due to salmonella.

In broilers, roaster and broiler breeders viral arthritis (reovirus infection) may cause lameness or ruptured tendons. Ruptured tendons are usually caused by rapid growth and large body size (heavy weight) and there is usually thickening of the tendon above the hock.

If growing birds are lame, and there is no evidence of infection or rickets, cut into the proximal tibia and look for necrosis caused by osteomyelitis or dyschondroplasia and split the spine at T4 to look for spondylolisthesis (kinky-back), a plug of cartilage impinging on the cord or consider Marek’s disease.

Necrotic dermatitis is caused either by staph. or clostridium infection and is associated with immunosuppression (usually by CAV or IBD). Scabby-hip is usually from overcrowding, poor litter conditions, poor feathering or scratches. Dermatitis or granulation in the neck may be a vaccine reaction, or contaminated vaccine.

10. Disturbances of the nervous system may cause incoordination, staggering, paralysis, walking backwards (with wings flapping for balance), tremors, stargazing, and other odd behavior.

In case of lameness, paralysis, or incoordination, examine the sciatic nerves, spinal cord, and brain. Histologic examination will be required for diagnosis.

ND may produce CNS disturbances in pigeons as well as nervous, respiratory, intestinal and reproductive lesions in chickens, pheasants, turkeys, and wild and cage birds of all ages.

Range paralysis is a form of Marek’s disease affecting the peripheral and central nervous system causing lameness, incoordination and paralysis. Marek’s can also cause botulism-like paralysis and transient paralysis.

Vitamin E deficiency (avian encephalomalacia) causes soft, dark areas of hemorrhage in the cerebellum which may be visible grossly. B vitamin deficiency (thiamine and other) may also cause nervous signs.

Avian encephalomyelitis (AE) (epidemic tremor) affects birds up to 3-4 weeks old from non-immune parents.

Arsenilic acid and other feed additives and toxins (botulism, lead) may cause CNS disturbances, while others like the ionophores and coffee weed seeds (Cassia) cause nerve or muscle damage. Bacterial infection (pasteurella, pseudomonas, salmonella, staph. etc.) and fungi (aspergillus, etc.) also cause meningoencephalitis, occasionally in outbreak proportions.