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Avian Tuberculosis

Other Names: Avian Mycobacteriosis, Mycobacterium Infection

Avian mycobacteriosis, also known as avian tuberculosis, is a contagious, slow-developing, chronicgranulomatous disease primarily caused by Mycobacterium avium subsp. avium (MAA) and less commonly, Mycobacterium genavense. The disease occurs in all avian species (domestic and wild) and sporadically in mammals. Chickens are more susceptible than other animal species.

Avian tuberculosis can have several different clinical presentations, depending on which organs are involved. In chickens, the intestinal tract and liver are the primary organs affected, with dissemination to other organs such as the spleen, bone marrow, air sacs, lungs, and skin. The infection results in the development of large tubercles or granulomas on the organ(s).

The most common form of avian tuberculosis, the intestinal form, typically causes progressive loss in body condition in the bird. Loss of body fat will cause the chicken’s breast muscles to atrophy, resulting in a prominent keel bone. Their face may appear smaller than normal, due to loss in body fat. Other signs observed include weight loss, white diarrhea sticking to vent feathers (“pasty butt”), dull and ruffled feathers, increased thirst, lethargy, and depression. The chicken’s comb, wattles, and earlobes often become very dry and pale in color.

If granulomas develop in the bone marrow of the bird’s leg bones or joints, the clinical signs often include an abnormally stiff and jerky hopping gait which sometimes leads to complete paralysis. This form is called tuberculous arthritis.

Clinical Signs

Avian tuberculosis has a long incubation period, and during the early stage of infection, clinical signs are subtle and less obvious. Once the disease has advanced, more obvious clinical signs develop. Clinical signs of avian tuberculosis are generally not specific and differ from bird to bird, and depend on the organs involved.

Most frequently observed clinical signs include:
  • Loss in condition: The chicken may progressively experience a loss in body condition. Resulting in moderate to marked loss of pectoral muscle mass and develop a prominent keel. Loss of body fat causes sinking of the eyes within the orbits, making the chicken’s face appear smaller than normal. They will have a low body condition score. However, due to the weight of the granulomas that form inside their bodies, body weight alone is not a reliable form of distinguishing whether a bird has lost weight.
  • Poor quality feathers: Affected chickens may have a delayed molt and preen less often, resulting in dull and poor-quality feathers.
  • Diarrhea: When the intestines are involved, chickens may have persistent diarrhea and frequently stain their vent feathers with feces (pasty butt).
  • Pale comb/wattles: The chicken's face, comb, wattles, and earlobes often become dry, pale, thinner, and occasionally have bluish discoloration.
  • Abdominal enlargement: Chickens may present with marked caudal coelomic distension, with a very firm mass or fluid (ascites).
  • Abnormal gait: Some chickens may develop bone lesions, causing lameness or stiffness, and walk with a peculiar jerky hopping gait.
  • Difficulty breathing: If chickens develop granulomas and lesions in their lungs, or abdominal enlargement, it can interfere with their breathing.
  • Subcutaneous lesions: Localized infections are generally the result of traumatic injuries that inoculate environmental mycobacteria into lesions. They are rare, and often present as nodular, ulcerated, fistulous draining tracts or nonhealing granulomatous or pyogranulomatous wound infections which do not respond to conventional drainage and antimicrobial therapy.


Susceptible chickens are primarily infected by ingesting or inhaling aerosolized Mycobacterium from a contaminated ground surface. Infected birds shed the organism in their droppings, where it can survive in the soil for months to years. There will be higher concentrations of the bacteria in areas which previously or currently house high populations of birds, living in unhygienic conditions. Wild birds, pigs, and certain mammals can act as significant reservoirs. Rodents can also be carriers of the bacteria, transmitting it through their feces to the environment.


History: If the chicken lives in an enclosure where avian tuberculosis was detected or suspected in other birds or previous flocks who lived there.

Blood tests: A CBC and blood chemistry may be helpful, depending on where the mycobacterial granulomas develop in the bird. Mild anemia with leukocytosis and a heterophilia and monocytosis may be seen in infected birds. Blood chemistry revealing an elevated AST, bile acids, or CK.

Radiographs: Radiographs (whole body VD and lateral views) may be useful for evaluating the musculoskeletal system and relative size and position of the viscera. Mycobacterial granulomas on the long bones may appear as osteolytic lesions in the radiographs.

Intradermal skin test: Also referred to as the tuberculin test. The test involves giving an intradermal injection of 0.03-0.05 mL of purified protein derivative tuberculin into one of the chicken's wattles or their comb. A positive reaction is indicated by the presence of the inflammation and swelling of the comb or wattle after a 48 hour duration. In the United States, it must be obtained through the State Animal Health or USDA APHIS –VS District Office. The reliability of this test to detect Mycobacterium infected birds decreases in flocks with high infection rates.

Serological testing: There are several serological tests available at diagnostic veterinary laboratories which can detect the presence of Mycobacterium antibodies. These include ELISA, rapid agglutination tests (RAT), complement fixation tests (CFT), and haemoagglutination tests (HAT). The samples required are serum extracted from blood. The results from these tests are often complicated by the occurrence of false negative reactions in healthy birds.

Fecal test: Mycobacterium can sometimes be detected from fecal samples from infected birds. However, repeat culture examinations are required over a course of several consecutive days. The amount of Mycobacterium shed in the feces of infected birds also depends on the stage of infection and organs affected.

Necropsy: Gross necropsy findings and histopathology may reveal characteristic lesions, and tissue cultures which confirm the presence of Mycobacterium. Granulomas (multifocal to miliary nodules, ranging in size from microscopic up to about 4 cm in diameter) in affected organs are the most common finding in chickens with avian tuberculosis. The organs most frequently affected include the spleen, liver, intestines, lung, and bone marrow. Samples for culture should be stored and shipped at 4 degrees Celsius (39 degrees Fahrenheit). The laboratory should be informed that mycobacteria are suspected because they require specialized media and prolonged incubation for successful isolation.

Clinical Signs

Progressive weight loss
Low body condition score
Diarrhea and soiling of vent feathers (pasty butt)
Poor feathering
Pale, dry, thin comb/wattles
Abdominal enlargement
Abnormal gait
Difficulty breathing
Cutaneous masses


  • History
  • Blood tests
  • Radiographs
  • Lab tests
  • Necropsy

Reported Cases

  • Case 1: Granulomatous conjunctivitis in a Emu An 18-month-old female emu presented to the referring veterinarian for examination of a firm white mass inside one lower eyelid. Epiphora was present. The bird was treated with systemic and topical antibiotics and two biopsy specimens of the conjunctiva were sent to the veterinary pathology lab. Histologic exam results revealed abundant caseonecrotic material infiltrated by numerous heterophils and macrophages and moderate numbers of multinucleate Langhan's giant cells. A diagnosis of granulomatous conjunctivitis caused by Mycobacterium spp was made. Ref

  • Case 2: Avian tuberculosis in a Parakeet An adult female red-crowned parakeet was presented for necropsy and histopathologic evaluation. The bird had died after exhibiting lameness, weight loss, respiratory signs, and hemoptysis. Postmortem radiographs revealed lesions in the diaphysis of the left femur and soft-tissue opacities in the lungs. At necropsy, the muscles of the left femur were pale and swollen, white-yellow small nodules were visible in lungs and air sacs, and the liver and other coelomic organs appeared pale. On histologic examination, areas of necrosis in the lungs were extensively infiltrated with acid-fast positive bacilli surrounded by macrophages, epithelioid cells, and giant cells. Acid-fast bacilli were also present in the left leg muscle and in granulomas in the liver, kidneys, and intestine. Fungal hyphae associated with a Splendore-Hoeppli phenomenon were visible in the left leg muscle. Mycobacterium tuberculosis was confirmed by polymerase chain reaction testing performed on muscle samples. Results were indicative of infection with M. tuberculosis complicated by mycotic myositis. Ref

  • Case 3: Systemic amyloidosis secondary to a chronic disseminated mycobacterial infection in a Duck A male duck was diagnosed with systemic amyloidosis secondary to a chronic disseminated mycobacterial infection. Marked caudal coelomic distension with a very firm mass was noted. Otherwise, the duck showed no clinical signs. A CBC revealed a heterophilic (13,710/ul) leukocytosis (21,240/ul), and on serum chemistry analysis there was marked hypoalbuminemia (0.2 g/dl) and mildly increased uric acid (10.4 mg/dl). Radiographs confirmed a large soft tissue density extending from the mid- to caudal coelomic cavity and displacing the intestines caudally. The duck was euthanized. Ref

  • Case 4: Avian mycobacteriosis in a Pigeons An outbreak of avian mycobacteriosis occurred in a flock of 100 two-year-old pigeons. Over a 6 month period, the sick pigeons developed cachexia followed by death. The affected pigeons were found with granulomatous nodular lesions of various sizes, containing numerous acid-fast bacilli in the liver, spleen, intestine, bone marrow, ovary, and oviduct. Despite their breeding age, atrophy was also found in the ovary and oviduct. Microorganisms belonging to Mycobacterium avium complex were identified in the affected tissues by polymerase chain reaction. Ref

  • Case 5: Avian mycobacteriosis in a Vulture A free-living female Ruppell's griffon vulture of unknown age was captured and brought to live in a zoo. After two years in captivity, the vulture suddenly presented with clinical signs of ataxia, weakness, and cachexia. She was dehydrated, and had lost alot of weight. She had a prominent keel and sinking of her eyes in the orbits. Loss of subcutaneous and cavitary fat was evident, and discoloration and damaged feathers. There was mild subcutaneous swelling on the ventral part of her body in the cloacal region. Her feathers surrounding the cloacal were stained with feces. Systemic antibiotics were attempted but the bird died the second day of treatment. Histopathological examination of the spleen (which was enlarged) showed multiple foci of granulomatous inflammation. Ref

  • Case 6: Avian mycobacteriosis in a Commercial Pekin ducks An outbreak of avian tuberculosis occurred in a commercial Pekin duck flock. Postmortem and histopathologic findings included nodules presenting in the visceral organs of ducks, and granulomas with central caseous necrosis surrounded by infiltrating lymphocytes. The M. avium pathogen was isolated and further identified by Ziehl-Neelsen staining and PCR based on insert sequence IS901 and the 16S rRNA gene. Ref

  • Case 7: Avian mycobacteriosis in a Swan Avian tuberculosis was diagnosed in a 2-year-old, male black-necked swan that was part of a private collection of several exotic birds. Necropsy revealed severe emaciation and multifocal grey-yellow, caseous nodules distributed in multiple organs (lung, liver, spleen, ribs and bone marrow). Histologically, lesions consisted of typical granulomas and numerous acid-fast bacilli. PCR on liver was positive for Mycobacterium avium complex. M. avium was isolated and identified from a selected tissue pool. Ref

  • Case 8: Avian mycobacteriosis in a Bruce's green pigeon A 3-year-old female Bruce's green pigeon was presented with granulomatous inflammation of the cere and underlying tissues with osteomyelitis and bone proliferation of the dorsal premaxilla. Biopsy and culture revealed the presence of Mycobacterium avium-intracellulare complex, and multi-antimicrobial treatment was initiated with clarithromycin, ethambutol, rifabutin, and enrofloxacin. The cere lesion improved and no evidence of systemic granulomas was observed over 4 months of treatment, although leukocytosis and monocytosis persisted. Five months after discontinuation of antibiotic therapy, the white blood cell count had normalized, but distal beak irregularities and partial recurrence of the mass were present. The bird died 15 months after discontinuation of antibiotic therapy and necropsy revealed no evidence of active mycobacteriosis of the beak or cere. Ref

  • Case 9: Mycobacteriosis in a Raptors. Four red-tailed hawks, 1 red-shouldered hawk, and 1 great horned owl were presented for examination after being found on the ground unable to fly. Common clinical findings in these birds included coelomic distention or palpable coelomic mass, nonregenerative anemia, and leukocytosis characterized by heterophilia, monocytosis, and lymphopenia. Results of radiography, ultrasonography, coelomoscopy, and biopsy, in combination with acid-fast staining of specimens obtained by biopsy or fine-needle aspiration, provided evidence of a presumptive diagnosis of mycobacteriosis. All birds were euthanatized (n = 5) or died (n = 1). At necropsy, diffuse granulomas with intralesional acid-fast bacilli were present in all birds. Mycobacteriosis was confirmed by culture in 4 birds, and polymerase chain reaction testing confirmed Mycobacterium avium in 3 of these 4 birds. On the basis of clinical and postmortem findings, mycobacteriosis should be considered as a differential diagnosis in adult raptors that are found debilitated and in poor body condition. Detection of acid-fast bacilli in biopsy or necropsy specimens allows a presumptive diagnosis of mycobacteriosis; however, definitive diagnosis requires mycobacterial culture or polymerase chain reaction analysis. Ref
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  • Case 10: Disseminated avian mycobacteriosis in a Eagle A mature bald eagle was diagnosed with mycobacterial infection after being presented for an inability to fly, emaciation, and a swelling of the left tibiotarsal-tarso metatarsal joint. Results of a complete blood cell count revealed a persistent, marked leukocytosis, with heterophilia, monocytosis, and anemia. Radiographs revealed lysis of the left distal tibiotarsus and soft-tissue swelling around the left tibiotarsal-tarsometatarsal joint, multiple pulmonary opacities, and an enlarged liver. Endoscopic evaluation and biopsy of caseated material within the left caudal coelom revealed acid-fast organisms. The eagle was euthanatized, and results of necropsy and histologic evaluation revealed caseated granulomas of the intestine, lungs, air sacs, and subcutaneous regions of the hock. Results of culture, a polymerase chain reaction testing, and direct deoxyribonucleic acid (DNA) sequencing for mycobacterial 16S ribosomal ribonucleic acid DNA determined this organism most likely to be Mycobacterium avium. Ref

  • Case 11: Disseminated avian mycobacteriosis in a Macaw A 31-year-old male captive scarlet macaw from a zoological garden had a history of a nodular swelling on the right side of their face, one near the nostril and the other under the infraorbital sinus. The bird was bright, alert and responsive without any behavioral issues. They had a normal appetite and good feathering. They had moderate dyspnea, apparent by open beak breathing and tail bobbing with every breath. A fine needle aspiration cytology of the facial mass revealed severe inflammatory infiltrate . The bird was treated with tilosin (20 mg/ml) added to the drinking water for 10 days and a single dose of vitamin A without any improvement. The bird died under anesthesia during a procedure to remove the mass. Necropsy results revealed yellowish firm masses with 0.5-1 cm in diameter in the facial muscles, tracheal lumen, air sac, limbs, and heart. Histopathology results showed granulomas containing a central caseous necrosis, surrounded by macrophages, heterophils, lymphocytes, and moderate amounts of multinucleated giant cells in the liver, spleen, heart and nodular masses. Ref

  • Case 12: Polyclonal mycobacterial disease in a Penguins A group of zoo-housed little penguins was diagnosed with mycobacteriosis. While undergoing multidetector computed tomography (MDCT) imaging for an unrelated research project, pulmonary lesions were detected in multiple individuals. In general, birds appeared healthy and free of outward signs of disease. After the loss of three individuals, polyclonal mycobacterial disease due to Mycobacterium avium-intracellulare complex was confirmed. Surviving birds were treated with rifampin (45 mg/kg), ethambutol (30 mg/kg), clarithromycin (10 mg/kg), and enrofloxacin (30 mg/kg) compounded into a single capsule administered once a day in food. After 3 months of therapy, MDCT imaging documented a decrease in nodule size and number in all remaining birds, with further improvement documented after 13 mo of treatment. MDCT imaging was invaluable for diagnosing disease, documenting disease progression over time, and assessing response to therapy. Early initiation of therapy before the development of outward signs of disease led to resolution of mycobacterial pulmonary lesions in multiple penguins. Ref

  • Case 13: Disseminated avian mycobacteriosis in a White-tailed trogon An adult female white-tailed trogon was presented with abdominal enlargement and hard subcutaneous masses. Necropsy findings included bony masses extending from skeletal structures, disseminated pale foci in the liver, and a pale mass in the kidney. Histological examination revealed multifocal to coalescing granulomatous inflammation in the bone, liver, kidney, lung and spleen. Mycobacterium celatum was isolated from the liver and identified by DNA sequencing. Ref

  • Case 14: Mycobacterial airsacculitis in a Southern rockhopper penguin A 21-year-old male southern rockhopper penguin was presented with a chronic history of intermittently decreased appetite, lethargy, and regurgitation. On the external physical examination, the bird was determined to be in fair-to-thin body condition with the complete blood count and plasma chemistry panel being largely unremarkable. Full-body radiographic images were considered normal, and gastroscopy showed only mild gastritis and duodenitis. The penguin was euthanized shortly thereafter due to acute onset of respiratory distress. During the gross necropsy examination, the bird had severe airsacculitis with thick, yellow-to-tan, moist granular plaques adhering to the surface of many air sacs, as well as regional contiguous pneumonia. Intralesional acid-fast bacilli were observed in histologic sections of air sac tissue, and polymerase chain reaction of the affected air sacs was positive for Mycobacterium fortuitum. Ref

  • Case 15: Granulomatous encephalomyelitis and intestinal ganglionitis in a Parrot An approximately 30-year-old male spectacled Amazon parrot was presented with a 2-week history of ataxia, head shaking, weight loss and seizures. Gross findings on necropsy examination included atrophy of the musculature, ruffled feathers and minimal epicardial and abdominal fat. Microscopically, there were perivascular cuffs of macrophages with fewer lymphocytes in the grey and white matter of the brain and spinal cord. These lesions were accompanied by gliosis and mild vacuolation of the white matter. In the small intestine, up to 70% of the intestinal ganglia were effaced by infiltrates of macrophages and fewer lymphocytes. The intestinal lamina propria contained multiple inflammatory aggregates of a similar nature. Ziehl-Neelsen staining revealed the presence of numerous bacilli within the cytoplasm of macrophages in the central nervous system (CNS) and enteric ganglia. Amplification of the DNAJ gene confirmed a mycobacterial infection and subsequent polymerase chain reaction (PCR) using a species-specific primer confirmed the aetiology as Mycobacterium genavense. Ref

  • Case 16: Avian mycobacteriosis in a Penguin A 19-yr-old female African penguin presented with labored breathing and anorexia. Radiographs revealed soft-tissue density lesions in the left lung fields and fluid in the right. The penguin died during the night. Postmortem examination demonstrated multiple granulomas in the lungs and air sacs. The right coelom was filled with opaque fluid. Histopathology of the lung, liver, kidney, and spleen identified Mycobacterium as a primary disease etiology. Large numbers of acid fast-positive, rod-shaped bacteria were recognized on tissue staining. Mycobacterium genavense was detected by polymerase chain reaction (PCR) using primers specific for the species. Further confirmation of M. genavense was accomplished using PCR with universal Mycobacterium spp. primers followed by sequencing of the amplicon obtained. Ref

  • Case 17: Avian mycobacteriosis in a Amazon parrot A blue-fronted Amazon parrot was presented with a granuloma involving the proximal rhinotheca and extending into the rostral sinuses. Mycobacterium marinum was diagnosed based on results of biopsy and culture. Treatment was initiated with clarithromycin, rifampin, and ethambutol, but the bird died 4 months after the onset of antimicrobial therapy. Additional granulomas were found in the left lung and liver on postmortem examination. Mycobacterial isolation on postmortem samples was unsuccessful. Ref

  • Case 18: Avian mycobacteriosis and amyloidosis in a Rhea Avian tuberculosis was diagnosed in two mature rheas on different ratite farms over a 2-year period. Both birds had died after progressively losing body condition. Caseonecrotic granulomas were scattered throughout the liver and spleen in both birds. Similar granulomas were in the lung of one bird and bilaterally in the subcutis cranial to the shoulder in the other bird. Smears of several granulomas from both rheas revealed large numbers of acid-fast bacilli. Histologically, the granulomas had caseonecrotic, non-mineralized centers surrounded by giant cells. Large numbers of acid-fast bacilli were seen free in the necrotic material and within inflammatory cells. Amyloidosis of the liver and spleen occurred in one rhea. Mycobacterium avium complex was isolated at a reference laboratory from hepatic granulomas submitted from one rhea. Ref


Supportive careIsolate the bird from the flock and place in a safe, comfortable, warm location (your own chicken "intensive care unit") with easy access to water and food. Limit stress. Call your veterinarian.
Ciprofloxacin (use in combination with other drugs)80 mg/kg PO q24hB Speer
Clofazimine (use in combination with other drugs)1-12 mg/kg PO q12-24hB Speer
Ethambutol (use in combination with other drugs)Administered orally at 10-30 mg/kg q12-24hB Speer
Isoniazid (use in combination with other drugs)5-30 mg/kg PO q12-24hB Speer
Rifampicin45 mg/kg PO q 12h
Azitrhomycin43 mg/kg PO



  • Minimize stress - There is a correlation between stress and enhancement of the disease.
  • Reduce contact with wild birds and pigs.
  • Don't house your flock in an area that was previously used to house large concentrations of birds.
  • Maintain good sanitary conditions by cleaning feces regularly.
  • Periodically expose ground surface to sunlight, since the unprotected organism is killed by direct sunlight.
  • Provide vitamins and probiotics to diet to help immune system.



Scientific References

Age Range

Most commonly affects older, adult birds.

Risk Factors

  • Housing chickens in an area that was previously used to house large concentrations of birds
  • Poor immune system
  • Exposure to other birds, especially those kept in zoos.
  • Exposure to pigs
  • Stress
  • Living in the north central states of the United States
  • Chickens with colored feathers (instead of white).
  • Keeping chickens in an unhygienic environment.