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Authors: Robyn Gwen Alders, BVSc, Ph.D., Richard Jakowski, DVM, PhD, DACVP
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OCW Zoological Medicine 2008
Poultry Medicine (2008)
R. Alders, DVM / R. Jakowski, DVM
Cummings School of Veterinary Medicine at Tufts University

(This lecture will be updated in the near future.)

1. Learning Objectives

This section pulls together the main diseases and health issues of poultry that students should know. Color coded topics indicate learning objectives that the student should become familiar with.

2. Nutritional Diseases of Poultry

2.1. Vitamin A deficiency

Deficiencies in vitamin A are most likely to occur in chicks under 7 weeks of age. Since a large amount of vitamin A is stored in the egg yolk, this supplies the newly hatched chick with adequate amounts for the first few weeks of life. Laying hens deficient in vitamin A will often produce chicks that show vitamin A deficiency in addition to signs of deficiency in the hen. In certain instances laying hens experience vitamin A deficiency because of increased demands for nutrient associated with egg production.

Vitamin A
Vitamin A

Vitamin A
Vitamin A

2.1.1. Clinical signs

  • Pale comb and wattles

  • Reddened and swollen conjunctiva with watery or scaly ocular exudate.

  • Swollen or exudative infra-orbital sinuses.

  • Nasal exudate may be present suggesting an upper respiratory tract infection.

  • Reduced rate of growth in young birds

  • The normal yellow color of the shanks and feet may be pale or absent.

  • Laying hens show decreased egg production when deficiency has been present for several months.

2.1.2. Diagnosis

Diagnosis is made based on Microscopic lesions associated with vitamin A deficiency consisting of hyperkeratosis of esophageal mucosa in addition to squamous metaplasia of tracheal and esophageal glands. Squamous metaplasia is also present in nasal turbinate epithelium. A concurrent infection of capillariasis may exacerbate vitamin A deficiency since these worms utilized host stores of vitamin A. A careful analysis of the diet is the best way to make the diagnosis of vitamin A deficiency.

Differential diagnoses: infectious coryza of chickens, infectious sinusitis of turkeys and wet pox

2.1.3. Treatment/prevention

Recommendations suggest a minimum of 5000 IU of vitamin A per pound of feed.

2.2. Vitamin D3 deficiency, Ca/P imbalance

(Rickets, Caged layer fatigue, Osteoporosis)

Although an exclusive deficiency of vitamin D can theoretically occur, this nutrient is almost always complicated with deficiencies of calcium and phosphorous. It is important to remember that all birds, including poultry, require the D3 form of vitamin D. The D2 form is nutritionally inert. Laying hens are especially vulnerable to deficiencies of vitamin D3, calcium and phosphorus because of the high demand for these nutrients required for egg production.

Vitamin D, Rickets and growth plate abnormalities seen in poultry
Vitamin D, Rickets and growth plate abnormalities seen in poultry

2.2.1. Clinical signs

  • Growing birds are lame or reluctant to move or walk with a stiff-legged gait.

  • The hocks may show variable swelling.

  • Beading or swelling of the rib costochondral junctions and soft, easily bending bones (rickets). These signs are only seen in young growing animals.

  • Laying hens may show a reluctance to move (caged layer fatigue). In some instances they develop fractures of thoracic vertebrae, wing and leg bones. S-shaped deviations in the cartilaginous portion on the keel may be palpated.

2.2.2. Diagnosis

Diagnosis is based on careful examination of the diet regarding the levels of vitamin D3, calcium and phosphorus. Recommendations suggest 500 IU of vitamin D3 per pound of feed. Gross and microscopic lesions are specific for deficiency states of vitamin D3, calcium and phosphorus but from a practical standpoint it is virtually impossible to state with certainty which of these three nutrients are absent. Soft, rubbery bones and beaks, beaded ribs, broken long bones and vertebrae and enlarged parathyroid glands are all suggestive of deficiency with vitamin D3, calcium and phosphorous.

Note: some references state that only calcium deficiency will result in parathyroid hyperplasia and that deficiency in phosphorous will not cause this lesion.

2.3. Vitamin E deficiency

Vitamin E or selenium deficiency can result in "White muscle disease," muscular dystrophy, encephalomalacia, exudative diathesis or "crazy chick disease". This syndrome can be seen in any animal and is commonly seen in captive waterfowl, chickens and less often in psittacines (most often in cockatiels).

Oil soluble Vitamin E is needed as an antioxidant to protect against peroxidative damage. It neutralizes free radicals which attack cell membranes. Selenium is a cofactor for glutathione peroxidase which performs a similar function.

A deficiency may develop due to a lack of sulfur amino acid (cystine and methionine), due to competition with other fat soluble vitamins (over-supplementation with cod liver oil as a source of vitamin A), or with rancid fats in foods such as dog food. Conditions which produce intestinal malabsorption (giardiasis) may also result in insufficient absorption of Vitamin E.

Three distinct patterns of disease are seen in chickens with vitamin E deficiency: encephalomalacia (crazy chick disease), muscular dystrophy and exudative diathesis. Baby chicks, turkey poults and ducklings all show similar signs of disease with vitamin E deficiency. Almost every case of vitamin E deficiency is associated with diets that are high in polyunsaturated fats (cod liver oil and soy bean oil). Diets contaminated with rancid fat can also lead to vitamin E deficiency.

Dietary Sources of Vitamin E

Vegetable oils

Seed oils (especially wheat germ oil)

Green leafy vegetables

Eggs

Vitamin E, Encephalomalacia in a chick
Vitamin E, Encephalomalacia in a chick

2.3.1. Clinical signs

  • Encephalomalacia

    • Signs are usually seen in 2 - 4 week old chicks

    • Ataxia, loss of balance, and opisthotonos.

  • Muscular dystrophy

    • White streaks in pectoral and leg muscles

    • In turkey poults the gizzard smooth muscle will sometimes show white streaks.

  • Exudative diathesis

    • Red/black or blue/black, gelatinous subcutaneous edema in the ventral abdominal and thoracic region.

    • Similar changes are sometimes present in the intermandibular space and periorbital region.

    • Birds with extensive edema may have difficulty walking and stand with legs apart.

2.3.2. Diagnosis

Diagnosis involves recognition of clinical signs and examination of the feed. Storage time and temperature of the feed is an important consideration in establishing a diagnosis of vitamin E deficiency. Examination of the ration usually reveals rancid feed or inadequate levels of vitamin E and/or selenium.

Differential diagnosis should include the following: Encephalomalacia clinically resembles avian encephalomyelitis. Exudative diathesis can resemble gangrenous dermatitis due to cutaneous Cl. perfringens infection. Subcutaneous crepitation and gas formation is usually present in gangrenous dermatitis but it is not seen in exudative diathesis. Gangrenous dermatitis is a sequela of immunosuppression from a previous infection with infectious bursal disease virus.

2.3.3. Treatment

Recommended levels of vitamin E are 5 -10 IU per pound of feed.

2.4. Angular Limb Deformities

(Perosis, Slipped tendon disease, Chondrodystrophy, Curled toe paralysis)

Perosis is a condition of 4-12 week old chickens, turkeys and pen-reared pheasants and quail. It may also be seen in other rapidly growing birds such as ratites, cranes, waterfowl, etc. This condition occurs as the result of lateral slippage of the gastrocnemius (Achilles) tendon at the tibiotarsal (hock) joint due to a generalized disorder of long bone growth plates resulting in impaired linear growth. Normal bone mineralization is maintained. The tendon is also histologically normal, however there is an enlargement of the hock joints and a secondary varus or valgus deformity of the lower leg. The etiology of perosis is complex and associated with a deficiency or imbalance in dietary manganese, choline, biotin, folic acid, niacin, pyridoxine (vitamin B6) and zinc. Curled toe paralysis is a nutritional problem of chicks associated with a deficiency in riboflavin (vitamin B2). Natural occurrence of this condition is rare.

Perosis
Perosis

2.4.1. Clinical signs

  • Birds are seldom observed with perosis until there is displacement of the tarsus.

  • Unilateral lameness results with hopping on the unaffected leg.

  • The condition can be bilateral..

  • Affected joints are usually swollen.

2.4.2. Diagnosis

Diagnosis is usually based on clinical signs and gross lesions. Analysis of the ration usually reveals that there is a deficiency of manganese, but the other ingredients listed above must also be considered.

Differential diagnosis should include Mycoplasma infections and reovirus which can produce lesions in the hock joints of chicken and turkeys resembling perosis. Tendon displacement does not usually occur with either of these conditions.

3. Viral Diseases of Poultry

3.1. Paramyxovirus, PMV-1, or Newcastle disease

Newcastle, High morbidity and mortality in an outbreak of Velogenic Viscerotropic Newcastle Disease.
Newcastle, High morbidity and mortality in an outbreak of Velogenic Viscerotropic Newcastle Disease.

ND virus (NDV) is a ubiquitous virus that can be isolated from many species of wild and domesticated birds. In addition to chickens - turkeys, peafowl, guinea fowl, pheasants, quail and pigeons are naturally susceptible. A wide range of virulence is encountered in different strains of virus. Identification is based on the antigenic make up of neuraminidase and hemagglutinin receptors on the envelope. NDV cause a wide spectrum of disease in domestic fowl and pet and wild birds.

Lentogenic, mesogenic and velogenic strains of NDV are described in the literature. These terms indicate differences in viral pathogenicity using the chicken as the index species. Lentogenic NDV causes clinically non-apparent disease in chickens but this same virus may kill canaries. Conversely, velogenic NDV causes relatively mild disease in Amazon parrots but this same virus would produce lethal disease in a flock of egg laying hens with 100% mortality. Mesogenic NDV is the most common form of virus isolated from commercial poultry flocks. Many outbreaks present with mild or atypical lesions. This is the result of the common practice of vaccinating commercial poultry with modified live NDV vaccine. The vaccine virus sometimes reverts to mildly virulent virus that may produce clinical disease. Commercial NDV vaccines are usually administered in the drinking water or by aerosol.

Velogenic NDV (VVND) is the most virulent form of the virus. It has been documented to be introduced onto the U.S. through importation of wild psittacine species subsequently sold as pets. This disease is still considered exotic to the US and is REPORTABLE.

Pigeon paramyxovirus (PMV-1 pigeon, PPV) was first seen in Europe and Great Britain in the early 1980s. It has been observed in pigeons in the U.S. since 1984. Paramyxovirus is very common in pigeons, both wild and domestic. Show and racing pigeons are the most common species infected with pigeon paramyxovirus. This form of the virus is also infectious to chickens, Common Blackbirds and House Sparrows. Serologic testing can be performed to confirm the pigeon paramyxovirus. Several vaccines are available to assist in controlling the pigeon disease in captive flocks.

3.1.1. Clinical signs

3.1.1.1. Mesogenic virus in chickens

  • Signs and gross/microscopic lesions non-diagnostic

    • Catarrhal nasal exudate

    • Chicks (1-6 weeks) : anorexia, depression, profound respiratory signs, CNS signs common, paralysis, dehydration ; MORTALITY USUALLY >50%

    • Adults (6 mos.+): mild anorexia, +/- depression, laying hens stop laying

  • Definitive diagnosis requires virus isolation or serology.

3.1.1.2. Velogenic virus in chickens

  • Morbidity/Mortality approaching 100%

  • Mucosal hemorrhages in GI tract, especially proventriculus and cecal tonsils

  • Rapid onset of dyspnea and diarrhea

  • Severe mortality (often approaching 100%)

  • Neurologic signs can be seen birds that survive a few days after the onset of GI disease but such signs are infrequent because of the high mortality.

3.1.1.3. Paramyxovirus in pigeons

  • Anorexia, weight loss, diarrhea and dehydration.

  • CNS signs include leg paralysis and paresis, drooped wings, ataxia, incoordination, and muscle tremors.

3.1.2. Diagnosis

Chick with ND
Chick with ND

Cecal lesions with VVND
Cecal lesions with VVND

Proventricular lesions with VVND
Proventricular lesions with VVND

A suspicion of ND can often be made on the basis of history, clinical signs and gross and microscopic lesions which include: cloudy air sacs with frothy, yellow air sac contents, chronic infection may result in dry caseous exudate in the air sacs. Non-suppurative encephalitis is one of the most consistent microscopic lesions.

VVND usually shows hemorrhagic, ulcerative and necrotizing lesions in gastrointestinal epithelial and lymphoid tissues. It is impossible to confirm a diagnosis of ND without serologic (i.e. rising titre in pair sera), virologic or molecular (e.g. Reverse-transcription polymerase chain reaction (RT-PCR), gene sequencing, and restriction enzyme analysis) confirmation. These include: HA and HAI tests, virus neutralization, FA tests using conjugated anti-NDV serum and demonstration of rising anti-NDV activity in pooled sera.

Newcastle, Lung tissue from a chicken with Newcastle disease.
Newcastle, Lung tissue from a chicken with Newcastle disease.

3.1.2.1. Differential Diagnosis

Laryngotracheitis and Infectious Bronchitis may be difficult to differentiate from mesogenic ND in chickens. Also remember other causes of mild respiratory signs such as low pathogenic avian influenza, mycoplasma and chlamydia. The differential diagnosis for velogenic ND includes Highly Pathogenic Avian Influenza, Laryngotracheitis, Acute Fowl Cholera, Infectious Bursal Disease, Duck Plague (Duck Viral Enteritis) and acute poisonings.

3.1.3. Prevention and Control

Many ND vaccines are available. The commercial vaccines are usually modified live type that are administered by aerosol to large numbers of birds. Other vaccines are administered by eye drop or drops in the nares. Killed, oil-emulsified vaccines are also available for parenteral administration mainly in point of lay pullets. Note that vaccinated birds can still be infected with and replicate NDV, however, the amount of virus shed and the duration of shedding is significantly reduced.

Other components of a ND prevention program are: active and passive surveillance; good biosecurity; and good food safety practices. Components of a control program include: quarantine and movement controls; stamping out; carcase disposal; and decontamination.

3.2. Avian influenza

(AI, Fowl Plague) Avian influenza is caused by an orthomyxovirus of variable pathogenicity. Two principle strains of virus have been identified. Low pathogenic avian influenza (LPAI) is usually seen in domestic turkeys and ducks and causes respiratory disease that rarely exceeds a 15% mortality. Chickens are less often affected and show mild clinical signs. Highly pathogenic forms of AI (fowl plague) is a much more virulent disease that causes high morbidity and mortality in chickens. Avian influenza virus differs from mammalian influenza virus in having the ability to infect and replicate in epithelial cells lining the gastrointestinal tract.

At least 17 different strains of avian influenza virus have been isolated from a variety of birds which include chickens, turkeys, Ring-Necked Pheasants, and Starlings. Migratory waterfowl should always be considered as a potential source of virus when and outbreak of AI occurs in poultry.

Chicken coop
Chicken coop

3.2.1. Highly pathogenic avian influenza (fowl plague)

This disease is caused by more virulent strains of AI virus. In October of 1983 several point mutations of avian influenza virus occurred (antigenic drift) resulting in a severe epidemic in domestic poultry in the eastern U.S. The economic significance of this seemingly trivial biologic event was emphasized by a cost of more than sixty million dollars paid in indemnities for millions of chickens slaughtered in an effort to control the disease. In February of 1993 H5N2 avian influenza virus was identified in a commercial egg laying flocks in New York, New Jersey and Pennsylvania. This disease is REPORTABLE to the USDA APHIS . Some strains are ZOONOTIC (H5N1).

See the Supplemental Readings on TUSK for more reports of outbreaks around the world, including the current global H5N1 outbreak. This strain has still not been reported in North America.

3.2.2. Clinical Signs

3.2.2.1. Low to moderately virulent virus in chickens

  • Coughing, "sneezing", respiratory rales and lacrimation, anorexia, lethargy and emaciation.

  • Egg laying hens may show a drop in egg production.

  • Sinusitis with infraorbital swelling have been reported in some outbreaks however, this finding my be due to secondary infection with Hemophilus paraganinarum (coryza).

  • Sinusitis is a common finding in ducks with avian influenza.

  • Diarrhea, edema of the head and nervous signs are occasionally observed.

    Chicken with Highly Pathogenic Avian Influenza
    Chicken with Highly Pathogenic Avian Influenza

    AI
    AI

3.2.2.2. Highly pathogenic influenza virus in chickens

  • MORBIDITY > 90%, MORTALITY >90%

  • Facial edema with focal cyanosis and hemorrhage of the comb, wattles and non-feathered skin (probably the result of virus induced DIC)

  • Focal mucosal hemorrhage of the proventriculus occurs similar to lesions seen in VVND but in fowl plague this lesion is not associated with submucosal lymphoid tissue necrosis.

3.2.3. Diagnosis

Confirmation of AI must be made on the basis of virus isolation and identification or molecular techniques (e.g. Reverse-transcription polymerase chain reaction; RT-PCR). Serologic information can be useful but seropositive birds may be the result of a previous, sub-clinical infection with a low virulence AI virus.

3.2.3.1. Gross lesions

These vary widely depending on the strain of the virus involved in the outbreak. Reddened tracheal mucosa, sinusitis, cloudy air sacs and conjunctivitis may be the only lesions seen in outbreaks of low virulence AI.

Highly pathogenic strains of AI will produce diffuse petechia and fibrinous exudate on abdominal serosal surfaces. Mucosal hemorrhages in addition to GI tract can also be seen. Microscopic lesions maybe helpful in establishing a diagnosis. These consist of perivascular lymphocytic cuffing in myocardium, lungs, brain, liver and wattles. Additionally, necrosis of splenic lymphoid follicles and pancreatic acinar cells has been seen in highly pathogenic AI.

3.2.3.2. Differential Diagnosis

  • Newcastle disease (mesogenic and velogenic)

  • Mycoplasmosis

  • Chlamydiosis

  • Acute Fowl cholera

  • Laryngotracheitis

  • Infectious Bursal Disease

3.2.4. Prevention

Use of vaccines is controversial and not usually endorsed EXCEPT during a crisis (e.g. H5N1). Note that vaccinated birds can still be infected with and replicate AIV, however, the amount of virus shed and the duration of shedding is significantly reduced if there is a good match between the vaccinal and field strains of virus.

Other components of an AI prevention program are: active and passive surveillance; good biosecurity; and good food safety practices. Components of a control program include: quarantine and movement controls; stamping out; carcase disposal; and decontamination.

3.3. Laryngotracheitis virus (LT)

Laryngotracheitis is an acute, highly contagious, respiratory disease of chickens caused by a herpes virus. The disease is principally seen in chickens and a few rare reports describe an LT-like disease in pheasants and peafowl. Amazon tracheitis virus is a related herpes virus that occasionally causes similar disease in psittacines.

3.3.1. Clinical Signs

  • Nasal discharge, "coughing", gasping, dyspnea and expectoration of blood tinged mucus.

  • Morbidity is high but mortality rarely exceeds 20%.

3.3.2. Diagnosis

The diagnosis of LT usually requires laboratory assistance as other respiratory pathogens of poultry can cause similar clinical signs and lesions. A positive diagnosis can sometimes be made on the basis of gross and microscopic lesions in cases of severe acute LT with high mortality.

Gross appearance of LT
Gross appearance of LT

Gross lesions are confined to the tracheal mucosa and include mucoid and hemorrhagic exudate in addition to fibrinous and heterophil inflammation. Intranuclear, eosinophilic inclusion bodies are usually seen in sloughed tracheal epithelial cells. These inclusions may be difficult to identify forty eight hours after first signs are observed since the damaged tracheal mucosa has been sloughed and is in are generating phase.

Histopathologic lesion of laryngotracheitis virus
Histopathologic lesion of laryngotracheitis virus

3.3.2.1. Differential Diagnosis

LT is rarely confused with other common poultry diseases. However, remember other causes of mild upper respiratory disease: Infectious Bronchitis, mesogenic ND, low pathogenic avian influenza, mycoplasma and chlamydia.

3.3.3. Prevention

Many modified live vaccines are available. They are usually administered by eye drop, aerosol or in the drinking water.

3.4. Fowl pox

3.4.1. Clinical Signs

  • On non-feathered skin

  • Slow spreading with indolent clinical course.

  • Birds with fowl pox behave normally other than showing cutaneous lesions.

  • Raised, proliferative nodular lesions typically appear on non-feathered parts of the body: comb, wattles, shanks and feet.

  • In wet pox, opaque plaques or nodules form on mucus membranes of the mouth, esophagus and trachea. This may result in death secondary to anorexia.

Pox
Pox

Wet Pox
Wet Pox

3.4.2. Diagnosis

Microscopic skin lesions are proliferative with swelling and hydropic changes of the epithelial layer. Intracytoplasmic, eosinophilic inclusions (Bollinger bodies) are apparent on microscopic examination. Fowl pox inclusions will stain positively with histologic stains used for lipids (Sudan IV, Oil red 0: this characteristic is only seen with avian poxviruses).

3.4.2.1. Differential Diagnosis

Vitamin A deficiency can resemble wet pox.

3.4.3. Prevention

Vaccines are available for chickens, turkeys and pigeons. Fowlpox vaccine is commonly applied by the wing-web method to 4-week-old chickens and to pullets about 1—2 months before egg production is expected to start. It is also used to revaccinate chickens held for the second year of egg production. The vaccine is not to be used on hens while they are laying.

3.5. Infectious bursal disease

(IBD, Gumboro disease), a Birnavirus.

Lymphoid cells in the bursa of Fabricius are the target cells of this virus which is currently classified as a birnavirus (double stranded RNA virus). Chickens with a functional bursa of Fabricius (1 day - 16 weeks of age) are susceptible. However, 3-6 week old birds are most apt to show the severest morbidity and mortality. Virus replicates in gut-associated lymphoid tissue with rapid viremia and localization in the bursa of Fabricius. Immunosuppression always occurs in this disease but is variable depending on the age of the bird at time of infection. Recovered birds shed virus in the feces for up to 2 weeks. The virus is extremely stable in the environment. Severely immunosuppressed animals are prone to unusual diseases after recovery from IBD virus infection. Gangrenous dermatitis due to clostridial skin infection and aplastic anemia associated with an avian adenovirus are two examples. Both of these latter diseases are rarely seen in immunocompetent birds and are reminiscent of adenovirus pneumonia and pneumocystosis in foals with CID.

3.5.1. Clinical Signs

  • No clinical disease in chicks under 2 weeks of age

  • Older birds (> 6 weeks) : lethargy, dehydration, bloody feces, death.

  • Initial signs are non-specific and consist of a sudden onset of depression, anorexia, and unsteadiness.

  • Diarrhea and dehydration usually develop with tenesmus, bloody stools and self inflicted vent picking.

  • Morbidity is usually very high but in most instances mortality rarely exceeds 30% except with very virulent IBD strains where mortality can reach over 50%.

3.5.2. Diagnosis

Demonstration of a rising antibody titre in convalescent birds is used to confirm an outbreak of IBD. Gross and microscopic lesions are also definitive: the bursa of Fabricius is enlarged, often twice normal size. Hemorrhagic and gelatinous, yellow fluid is evident below the serosal surface. Necrosis of the bursal lymphoid follicles are seen microscopically. Focal hemorrhagic may be evident in skeletal muscles of the thigh and pectoral region. The kidneys may be swollen with intra-tubular uric acid crystals.

3.5.2.1. Differential Diagnosis

Coccidiosis can mimic many of the clinical signs seen in IBD.

3.5.3. Prevention

A killed vaccine in available. However, it is used mainly in commercial poultry operations.

4. Mycoplasmal Diseases of Poultry

Avian mycoplasmosis represents the most ubiquitous, economically devastating respiratory poultry disease in the United States. A conservative estimate of the annual loss to the commercial poultry industry would be well over 100 million dollars. Similar to mycoplasma infections in mammalian species, once established in a group of animals it is impossible to eradicate the infection unless the entire population is destroyed. Mycoplasma organisms are easily spread by aerosols and it is also possible to transmit the organism in fertilized egg. Although of high importance in poultry, mycoplasma infections in pet bird species are rarely diagnosed.

Respiratory mycoplasma infections in chickens and turkeys result in clinical signs and gross lesions that are remarkably similar to those caused by C. psittaci however avian mycoplasma infections are of no consequence to humans.

Mycoplasma Diseases of Poultry

Mycoplasma gallisepticum

Chronic respiratory disease (chickens)
Infectious choryza (chickens)
Infectious sinusitis (turkeys)

Mycoplasma meleagridis

CRD (turkeys only!)

Mycoplasma synoviae

Synovitis (Enlarged hock disease) Tenovaginitis

Chronic respiratory disease in poultry
Chronic respiratory disease in poultry

  1. Mycoplasma gallisepticum

[MG, Chronic respiratory disease, CRD, Air sacculitis, Infectious sinusitis of turkeys, PPLO infection]

This organism is widespread in the bird population. In addition to the chicken and turkey, natural infections have been documented in pheasants, peafowl, Coturnix and bob white quail, wild turkeys and housefinches. One source claims to have isolated the organism from a yellow-naped Amazon parrot.

4.1. Clinical Signs

4.1.1. Adult chickens

Signs are often non-specific consisting of decreased feed intake and a loss of normal growth rate. Laying chickens will show a variable drop in egg production. Signs of respiratory disease include: ocular and nasal discharge and mild dyspnea.

Mycoplasmal sinusitis in a chicken
Mycoplasmal sinusitis in a chicken

4.1.2. Turkeys

Swelling of the infraorbital sinuses is a common finding in addition to the other signs usually seen in chickens. Nasal exudate is evident on the face, and wings. In general, M. gallisepticum produces a more severe disease in turkeys.

4.2. Diagnosis

Air sacs are almost always affected but may vary in appearance from a mild cloudiness to severe thickening with floccular tan/yellow exudate on the inner lining. In severe cases there is extensive caseous material within the air sacs. Mucoid or mucopurulent exudate is often present in the nasal sinuses, choanae, and trachea. The pericardial sac is often thickened and cloudy. Turkeys may only show swelling of the infraorbital sinuses. However, they may also show air sac and upper airway lesions similar to chickens. A positive diagnosis of MG is usually made with a plate or tube agglutination test. Since this disease is almost always chronic, serum samples from several birds in an involved flock are used for this test. Isolation and identification of the organism is also possible.

4.3. Differential Diagnosis

Chlamydiosis, fowl cholera, colibacillosis, influenza and aspergillosis can resemble MG infections in the turkey and chicken.

4.4. Prevention

The most practical means of controlling M. gallisepticum is through the depopulation of infected flocks with subsequent effort to use stock derived for mycoplasma free breeders. This is often economically unfeasible. A method of immunization by controlled exposure has been practiced in some farms. Vaccine strains of mycoplasma are administered in the drinking water. There are no antibiotics that can be administered to chickens producing meat or eggs for human consumption that will eliminate M. gallisepticum or prevent the transmission of this organism in fertilized eggs.

4.1. Mycoplasma meleagridis (MM)

MM is a mycoplasma disease which only infects domestic turkeys. All age groups are affected. The pathogenesis and transmission are similar to that described above for M. gallisepticum. Although aerosols and egg transmission are the most common means of infection MM has also been shown to be transmissible to humans who handle poults during sex determination by the cloacal examination method. Semen has also been show to harbor the organism and MM can be venereally transmitted.

4.5.1. Clinical Signs

Young poults will often show a mild sinusitis however respiratory signs are rarely observed.

4.5.2. Diagnosis

Young poults show thickened air sacs, often with small amounts of flocculent, yellow material on the inner lining. Sinusitis and synovitis have also been seen in adults with MM infection. A plate agglutination test can be used to serologically confirm an outbreak.

4.5.3. Differential Diagnosis

MG and chlamydial infection must be considered in a provisional diagnosis of MM

4.5.4. Prevention

This disease is controlled in a similar manner as MG. However, the MM organism is somewhat more sensitive to antibiotic therapy and tylosin and tetracycline have been used to control and limit the signs of infection in poults. Lincomycin (spectinomysin) at the rate of 2gm/gal of drinking water has been used for the first 5-10 days of life to reduce the incidence of air sacculitis.

  1. Mycoplasma synoviae

[Synovitis, Enlarged hock disease, MS, Tenovaginitis]

MS is not a respiratory mycoplasma infection but is included here for organizational purposes only. The disease is characterized by swollen hocks with exudates in the hock joints and Achilles tendon sheaths. Chickens and turkeys 4-12 weeks of age are most commonly affected. Guinea fowl are also susceptible. Infection is by aerosols and infected fertile eggs.

4.5.5. Clinical Signs

Lameness is the usual sign. Birds will show swollen hocks and foot pads.

4.5.6. Diagnosis

The hock joints and tendon sheaths contain excessive, creamy to caseous, gray/yellow exudate in the joints and tendon sheaths. The sternal bursa may be filled with caseous material as a result of the birds resting on the keel and being unable to walk. This lesion is sometimes referred to as a "breast blister". Abscesses are sometime seen in the pads on the plantar surfaces of the feet. This lesion is sometime called "bumblefoot".

5. Chlamydiosis in Poultry

Chlamydiosis is covered in more detail in the psittacine section of the syllabus. Follow the link above to read more about the organism and its pathogenesis.

This disease is far more common in turkeys in comparison to chickens. Chickens rarely become clinically ill with ornithosis. Mild outbreaks may be so insignificant as to go unnoticed. In some instances mild respiratory signs and/or diarrhea may be seen. Young birds may develop acute fibrinous pericarditis and hepatitis.

More severe outbreaks in turkeys, ducks, geese or pigeons will show severe depression, anorexia, respiratory distress and nasal discharge. Yellow-green diarrhea may also be evident in addition to vague neurologic signs suggestive of ataxia or paresis. In pigeons, the asymptomatic carrier state may be important as a wild reservoir and continuing source of infection for more susceptible species.

Most often, wild birds are asymptomatic carriers. Some of these strains however may be extremely pathogenic for people, other mammals, and other birds.

  • Airsacculitis is a common gross lesion

  • It is impossible to differentiate this disease from mycoplasmosis on the basis of gross lesions!

  • Impression smears are the best method of making a rapid positive diagnosis.

5.1. Chlamydia Outbreak in Turkeys - an example

In a 1986 Minnesota outbreak, 12 flocks were suspected, and the disease was confirmed in 10. The original source of infection was felt to be from wild birds. The turkeys showed clinical signs of malaise, anorexia, 6% mortality, mild diarrhea, weight loss, and many with no clinical signs. Birds that were treated for less than 3 weeks resulted in a 2% rise in condemnation rate at the slaughter plant. The outbreak cost the producers $120,000. The major problems were with accurate diagnosis. 172 people got sick from the epornitic, including plant and farm workers. There were no human fatalities.

6. Aspergillosis in Poultry

Aspergillosis, Brooder pneumonia lesions in a chick.
Aspergillosis, Brooder pneumonia lesions in a chick.

  • Poultry - Brooder Pneumonia - a disease of poor management and overwhelming exposure

  • In wild birds it is almost always the result of chronic debilitation, stress or immunosupression

7. Parasitic Diseases of Poultry

7.1. Coccidiosis

Coccidiosis is a common, protozoal disease of poultry and other avian species characterized by enteritis and diarrhea. Coccidiosis manifests an enteric disease in most instances but it should be noted that renal coccidiosis in water fowl is caused by Eimeria truncata. Chickens are by far the most common poultry species affected with coccidiosis. Domestic turkeys are also susceptible to infection but the disease is less severe in this species. Intestinal coccidiosis has been reported in geese, ducks, guinea fowl, pigeons, pheasants, quail, and chukar partridge.

Coccidiosis is usually a problem in young chickens but clinical disease can occur in older birds, especially when virulent strains of coccidia are involved. Birds are infected through ingestion of sporulated oocysts in feed, water, litter and soil. Conditions of warmth and high humidity facilitate survival and transmission of the oocysts in litter. The various species of coccidia can be identified by microscopic features of oocysts in addition to the location of shizonts and gametocytes in the GI tract.

Infection with one species of coccidia stimulates immunity to that species only and the host will remain susceptible to other species of coccidia. Birds are often simultaneously infected with more than one species. Clinical disease occurs when susceptible chickens ingest massive numbers of oocysts. This occurs when conditions for sporulation of oocysts are ideal, e.g., the litter is wet and temperatures are warm. If the number of ingested oocysts are low, birds will develop immunity without clinical signs of disease. Chickens maintain immunity to coccidia with repeated exposure. Immune chickens are asymptomatic and shed oocysts for long periods (coccidiasis).

7.1.1. Clinical Signs of coccidiosis

  • Signs in chickens vary depending on the species of coccidia; less pathogenic species produce few or no signs. Pathogenic species cause diarrhea which may be mucoid or bloody. Dehydration often accompanies severe diarrhea. Anemia, listlessness, weakness, retraction of the head and neck and somnolence follow.

  • Laying hens will have a drop in egg production with blanching of the yellow skin pigment.

  • Growing birds, especially broilers, cease to grow satisfactorily.

  • Morbidity and mortality vary - both may be very high.

  • Coccidiosis in turkeys resembles the disease in chickens but diarrhea is seldom bloody and poults over 8 weeks old are seldom affected.

7.1.2. Diagnosis

The diagnosis of coccidiosis is made on the basis of clinical signs and gross lesions. Knowing the location in the digestive where oocysts, sporozoites, merozoites and schizonts are found is useful in determining the species of coccidia involved in the outbreak. Coccidiosis must be differentiated from coccidiasis (subclinical infection in an immune bird). Additionally, oocysts in the mucosal scrapings may be from non-pathogenic or mildly pathogenic species of coccidia which are of no diagnostic significance. It is also important to remember that E. necatrix does not form oocysts at the site where the most severe lesions occur. The pathogenic stage of coccidiosis precedes oocyst formation and schizonts may be overlooked in the mucosal scrapings from birds with severe gross lesions.

The most important species of coccidia produce lesions in specific regions of the GI tract.

Proximal third of the small intestine - Eimeria acervulina

Gray/white striations are often visible on the mucosal surface but may go unrecognized if they coalesce. Oocysts in mucosal scrapings are moderate in size and ovoid shaped. This type of coccidiosis occurs rather frequently in older birds. E. acervulina is a moderately severe pathogen. In severe cases the lesions can extend into more distal portions of the GI tract. Enteritis can be mild to severe and may lead to a thickening of the intestinal mucosa. Frequently, other species of coccidia will be present, complicating the diagnosis.

This location is also favored by 4 non-pathogenic species.

Middle third of the small intestine - Eimeria necatrix

The middle one-third of the intestine is often markedly dilated, and thickened. Yellow/white foci and petechia are visible through the serosa of the unopened gut. Lesions are seen in the middle third of the intestine but extend throughout the intestinal tract in severe cases. Enteritis is characterized by congestion, hemorrhage, necrosis and bloody feces. Oocysts develop in the ceca, and these may be minimal. Mortality may precede the appearance of oocysts in the feces. E. necatrix is a severe pathogen and often causes high mortality

Distal third of the small intestine - Eimeria tenella

Typhlitis with occasional involvement of the adjacent areas of the intestine is the principle lesion. In early cases blood is apparent in the feces and cecal lumena. Later, cheesy cecal cores are found. Large schizonts are found in cecal mucosal scrapings. E. tenella is a severe pathogen producing high mortality in young chickens.

7.1.3. Differential Diagnosis

Other intestinal parasites including Capillaria sp. produce enteric signs that resemble coccidiosis. Ulcerative enteritis and salmonellosis also mimic coccidiosis.

7.1.4. Prevention

A wide range of anti-coccidial drugs are available. Some of the more popular products include Amprolium, Monensin, Clopidol, Buquinolate and Robonidine.

Acervulina
Acervulina

Necatrix
Necatrix

7.2. Histomoniasis

(Blackhead, Enterohepatitis)

Histomoniasis is a protozoal disease of turkeys, pheasants, peafowl, grouse, quail and chickens caused by Histomonas meleagridis. Turkey poults three month of age and younger are the most susceptible. In young poults morbidity and mortality is high and often approaches100%; older birds are more resistant. Birds are infected through ingestion of protozoa contaminated feces. Infected ova of the cecal worm Heterakis gallinarum and earthworms containing larva of infected cecal worms containing the protozoal organisms can also serve as a less common source of infection.

Lesions of histomoniasis are prominent in the liver and cecum. Chickens have low susceptibility to histomoniasis.

7.2.1. Clinical Signs

  • Signs appears 7-12 days after exposure. Initially there is listlessness, moderate anorexia, drooping wings and sulfur colored feces. Comb, wattles and snood may be cyanotic.

  • Mortality in poults can approach 100%.

  • Emaciation is common in chronic cases; this is more likely to occur in older birds.

  • Chickens with histomoniasis may have hematochezia.

7.2.2. Diagnosis

Gross lesions consist of bilateral enlargement of the ceca with thickened cecal walls and ulceration of cecal mucosa. The cecal lumen contains yellow/gray/green, necrotic, laminated cores. Peritonitis may be present if the cecal wall perforates. In quail, the cecal lesions may not be present, even though mortality is high. The natural surfaces of the liver have 1-2 cm diameter, round, depressed, yellow/gray to red, target-like, multifocal and coalescing lesions. Protozoal organisms can sometimes be found in cecal mucosal scrapings or from liver tissue imprints made from the margin of hepatic lesions. Histologic sections of the liver lesion reveal numerous histomonads.

7.2.3. Differential Diagnosis

Clinical signs and some of the gross lesions of histomoniasis are similar to those of cecal coccidiosis.

7.2.4. Prevention

Histomoniasis can be prevented by adding antihistomonal drugs to the ration. Only Ipropan (irpronidazole) and Histostat (nitarsone) are approved for use in poultry. Directions for use provided with for each product should be followed carefully.

7.3. External parasites

Poultry can be infested by a range of external parasites that tend to be location specific. For example, Sticktight fleas (Echidnophaga gallinaceae) tend to attach to the skin around the eyes; the Northern fowl mite (Ornithonyssus sylviarum) will be found in feathered areas and is the commonest and most important permanent parasite of poultry in all major poultry production areas of the United States.

Poultry seriously infested with the common parasites exhibit irritation and react by scratching and preening.

8. Bacterial Diseases of Poultry

8.1. Infectious Coryza

(Coryza, Croup)

Infectious coryza is an upper respiratory diseases of chickens, pheasants and Guinea fowl. The disease is characterized by conjunctivitis, occulonasal discharge and swelling of the infraorbital sinuses. The causative organism is Hemophilus paragallinarum (formerly H. gallinarum) however it is likely that this organism becomes established in the upper respiratory tract and nasal sinuses as a result of a synergistic relation with M. gallisepticum. H. paragallinarum is transmitted by aerosol and has low survivability in the environment. Clinically healthy carriers of this organism are common.

8.1.1. Clinical Signs

Chronic occulonasal discharge with adhered eyelid margins in addition to swollen infraorbital sinuses in the absence of more severe respiratory signs are the typical presenting signs.

8.1.2. Diagnosis

The infraorbital sinuses are usually filled with a caseous, yellow exudate. In chronic cases the infraorbital abscesses may communicate with the choana. Gram stained smears of the exudate reveal small, Gram (-), bipolar, filamentous rods. H. paragallinarum can be grown on blood agar but, similar to all hemophilus organisms, requires the presence of a Staphylococcus aureus nurse colony to produce factor-V necessary for growth.

8.1.3. Differential Diagnosis

The chronic form of fowl cholera can resemble infectious coryza. In young birds fowl pox and Vitamin A deficiency may resemble some of the lesions of coryza.

8.1.4. Prevention

Many antibiotics have been used in the treatment of infectious coryza. The organism is sensitive to streptomycin, erythromycin, spectinomycin, tylosin and many of the sulfa antibacterial drugs.

  1. Avian Pasteurellosis

(Fowl Cholera, Avian hemorrhagic septicemia)

Fowl cholera is an acute, septicemic disease caused by Pasteurella multocida that effects chickens, turkeys, ducks, geese and many species of waterfowl. The disease occurs worldwide and is relatively common. A similar disease has been described in domestic ducks and is known as New Duck Disease, the causative organism is P. anatipestifer.

Fowl cholera almost always seen as an acute, rapidly fatal disease in poultry with a mortality that approaches 100%. The disease is more common in the late summer and fall with mature birds more susceptible than chicks. Recovered birds harbor the organism in the upper respiratory tract and nasopharynx. Wild birds and many mammalian species (cats and cattle ) harbor the organism in the nasopharyngeal region. These species are thought to spread the organism to susceptible birds. Birds that die in acute septicemia have the organism in all tissues and cannibalism is a common means of spreading an infection within the flock.

8.1.5. Clinical signs

  • Acute fowl cholera is dramatic.

  • Sudden deaths: laying hens are often found dead in the nest box, wild birds in large numbers are found in a given area.

  • Toxicity is often suspected in outbreaks of acute fowl cholera.

  • Sick birds are anorexic and depressed.

  • Cyanosis of comb with respiratory rales and nasal and oral mucus discharge.

  • White, watery or green-mucoid diarrhea is sometimes evident.

  • Chronic fowl cholera results in birds with swollen joints, wattles, foot pad and tendon sheaths. Cheesy exudate may also be present in the conjunctival sac, and infraorbital sinuses.

8.1.6. Diagnosis

Gross lesions may be absent in birds that die peracutely. The most common findings are petechia or ecchymoses on the pericardium and serosal surfaces of the gizzard, small intestine, and abdominal fat. Numerous pinpoint grey/white foci may be present on cut surfaces of the liver. The lungs may be dark red with wet cut surfaces. A gram stained blood smear or imprint of the liver usually reveals numerous, gram-negative, bipolar bacilli characteristic of P. multocida. The organism is easily grown on blood agar.

Pasteurellosis may produce epicardial petechiae and/or multifocal hepatic necrosis
Pasteurellosis may produce epicardial petechiae and/or multifocal hepatic necrosis

8.1.7. Differential Diagnosis

Erysipelas and acute colibacillosis in turkeys are clinically similar to fowl cholera.

8.1.8. Prevention

Bactrins are available but are not always effective. A live oral vaccine is available for chickens and turkeys using the CU strain of P. multocida. Many antibiotics and sulfa drugs are available to treat fowl cholera. Culture and sensitivity tests are important since widespread resistance is common with this organism.

9. Neoplastic Diseases

9.1. Avian leukosis virus

Oncornavirus induced tumors:

  • Lymphoid leukosis (lymphosarcoma)

  • Erythroblastosis and myeloblastosis

  • Fibrosarcoma (osteosarcoma and meningioma ?)

  • Nephroblastoma

  • Hemangioma

  • Osteopetrosis

Although spontaneous lymphoid tumors are the most common expression of this oncornavirus virus in chickens, a variety of hematopoietic neoplasms have been experimentally produced. Some of these (erythroblastosis and myeloblastosis) require the experimental inoculation of virus into very young chicks. Spontaneous fibrosarcoma is less common than lymphosarcoma. Other neoplasms such as nephroblastoma, hemangiosarcoma and myelocytoma have been linked to the avian leukosis virus but these tumors are also rarely seen under natural conditions. Osteopetrosis is not a neoplastic disease but rather an over production of periosteal bone in the appendicular skeleton due to over production of well differentiated osteocytes.

Lymphoid tumors produced by the avian leukosis virus for practical purposes are gross and microscopically identical to those produced by the herpes virus which causes Marek's disease. Two major differences exist between these lymphoproliferative diseases. Marek's disease is a T-cell lymphoma seen in young chickens before the onset of sexual maturity (10-12 weeks of age). Lymphoid leukosis is a B-cell lymphoma seen in mature chickens after the onset of sexual maturity.

Lymphoid liver tumor compatible with both leukosis and Mareks disease.
Lymphoid liver tumor compatible with both leukosis and Mareks disease.

9.2. Marek's Disease

  • DNA - herpesvirus

  • "T cell" lymphoma

  • Affects birds before the onset of sexual maturity

  • Virus can cause inflammatory as well as neoplastic lesions (gonadal lymphomas are common)

Classical Marek's ds.
Classical Marek's ds.

Two types of lesions are seen in chickens with MD. Birds less than 6 months of age may develop visceral lymphomas. Birds of any age may also show non-suppurative encephalitis and neuritis with clinical signs of paralysis. Neurologic manifestation of MD in the absence of neoplasia is sometimes referred to as classical Marek's disease. Infectious virus is shed from feather follicle epithelial cells. Antigenically related, non-neoplastic herpes virus isolated from turkeys (HVT) has been used to protect susceptible birds from MD by vaccination at one day of age.

9.2.1. Clinical signs

  • Neuritis and nonsuppurative encephalitis

  • Transient paralysis

  • Ocular lymphomatosis ("gray eye")

  • Lymphomatosis (lymphosarcoma)

  • Neurolymphomatosis (a combination of inflammatory and neoplastic forms)

Swollen lumbosacral plexus/sciatic in Marek's ds.
Swollen lumbosacral plexus/sciatic in Marek's ds.

10. A systems approach to disease in chickens

Clinical signs

Possible reasons

General signs

Depression, listlessness,

Inappetence, drooping wings, low productivity,

Wide range of causes

Emaciation

Chronic, long-lasting disease

Respiratory signs:

- Breathing

With open beak

ND, infectious laryngotracheitis,

Other severe respiratory disease,

Very hot weather

Distressed, noisy, rattling

ND, HPAI, severe respiratory disease

Coughing, sneezing, wheezing, gurgling

Infectious Coryza, IB, CRD, other respiratory disease,

Fowl cholera

- Nostrils

Wet or crusted because of nasal discharge

Infectious coryza, CRD, other respiratory disease

- Eyes

Swelling around the eyes

Infectious coryza, CRD, other respiratory disease,

ND, fowl cholera

Discharge

Infectious Coryza, CRD, other respiratory disease,

Fowl Cholera

Cloudy pupils

Various reasons

Diarrhoea

Dirty cloaca

Coccidia, worms, spirochaete infection

ND, gumboro,

Fowl typhoid, pullorum disease, fowl cholera, colisepticaemia or other infectious diseases

Nervous signs

Twisted neck (torticollis)

ND, HPAI or any other disease affecting the nervous system

Lameness (paralysis)

ND or any other disease affecting the nervous system

Trembling, shaking

ND or any other disease affecting the nervous system

Movement

Lameness

Crusted legs due to scaly leg mites,

Marek’s disease or

Various other reasons

Swollen joints

Fowl Cholera or

Various other reasons

Abnormal position of legs

Marek’s disease,

Nutritional deficiencies,

Any accident or

Various other diseases

Swellings under the feet

Infected injuries

Feathers

Small spots, maybe moving

External parasites- lice or mites

Moulting

Usual moulting process (once a year),

Under stress

Ruffled

Indicates that a chicken is sick

Lesions, damage

Lice,

Feather pecking or cannibalism

Skin

Pale skin

Gumboro (IBD) or

Severe infestation with external parasites, especially the Red Fowl Mite

- Comb

Yellowish to dark brown crusty, spots

Fowl pox

Pale

Chronic diseases or

Severe infestation with parasites

Dark, bluish

Acute feverish diseases affecting the circulatory system (e.g. Fowl Cholera, HPAI)

- Wattle

Yellowish to dark brown lesions

Fowl pox

Dark, bluish

Acute febrile diseases affecting the circulatory system (e.g. Fowl Cholera, HPAI)

Swollen

Fowl Cholera, HPAI

Inside the beak

Yellow-white cheesy looking lesions

Fowl pox

11. References and Resources

11.1. Websites

Poultry Breeds http://www.ansi.okstate.edu/poultry/

Poultry NetVet http://netvet.wustl.edu/birds.htm

Poultry Resource Manual http://www.iowaagopportunity.org/poultry/poultrymanual.html

World Organization for Animal Health (OIE) http://www.oie.int/eng/en_index.htm

11.2. Texts and Articles

Damerow, Gail. The Chicken Health Handbook. Storey Books, 1994).

Diseases of Poultry. 11th ed. / edited by Y. M. Saif, Iowa State University Press, 2003.

Morishita, Teresa Y. Common infectious diseases in backyard chickens and turkeys (from a private practice perspective). Journal of Avian Medicine and Surgery, 10(1), 1996 : 2-11.

Poultry diseases. 5th ed. / edited by F.T.W. Jordan, M. Pattison. London: Bailliere Tindall. 2002.