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A 15-year-old female white-capped pionus parrot (Pionus senilis) was presented to the Veterinary Medical Teaching Hospital, Kansas State University, (Manhattan, KS, USA) because of a 10-day history of a slightly decreased appetite and a 1-week progression of dyspnea. The bird was housed with a male pionus parrot in a small, 8-bird aviary with good husbandry practices. There was no history of recent illness in any of the birds in the aviary. The bird's housing was adequate, and all birds were maintained on a pelleted diet supplemented with fresh vegetables and fruits.

On physical examination, the bird weighed 223 g and was bright, alert, and in fair body condition. The bird had a moderate inspiratory stridor and open-mouth breathing.

A blood sample was collected by venipuncture of the right jugular vein for a complete blood count and plasma biochemical analysis. Although the white blood cell count of 9500 cells/[micro]l was within reference ranges, abnormal hematologic results included the following: lymphocytes, 14% (reference range, 25%-45%); monocytes, 12% (reference range, 0%-2%); 2+ polychromasia; and a 1-2+ anisocytosis. (1) Results of the plasma biochemical analysis revealed a high concentration of aspartate aminotransferase (AST) (1004 IU; reference range, 135-365 IU/L).

Whole-body radiographs were obtained (Figs 1 and 2).



Radiographic findings included multiple midcoelomic masses of soft tissue opacity that caused caudal displacement of the intestines and ventriculus (Figs 3 and 4). There was also increased opacity seen in the lungs, which represented additional mass lesions. On the basis of the radiographic findings, neoplastic or granulomatous disease was suspected.


Differential diagnoses for this case included neoplasia, aspergillosis, mycobacteriosis, infectious bronchopneumonia, and papillomatosis. On the basis of the clinical observations, along with the severity and multisystemic nature of the lesions, the owner declined any further diagnostic testing and the bird was euthanatized. At necropsy, the thoracic viscera, lung parenchyma, and liver contained multifocal, white-yellow nodular masses of varying sizes, with the largest being 1.2 cm in diameter (Fig 5). Representative samples were collected from the major organs and tissues, preserved in 10% neutral buffered formalin, and submitted for histopathologic examination.


Histopathologic examination of the nodular masses in the lungs revealed variably sized granulomas composed of large macrophages with abundant, grainy, basophilic cytoplasm, which contained numerous acid-fast bacilli (Figs 6 and 7). Larger granulomas effaced the pulmonary parenchyma, whereas smaller granulomas were closely associated with parabronchi (Fig 6). Many pulmonary nodules were rimmed by lymphocytes and plasma cells, and the adjacent parenchyma was mildly to moderately congested. The nodules of the thoracic air sacs and proventricular serosa had similar morphology to those in the lungs; however, some of the larger nodules contained areas of central necrosis. The liver parenchyma contained granulomas of similar morphology to those in the lungs. Lymphoplasmacytic portal inflammation was also noted.


Although psittacine birds with mycobacteriosis do not typically present with granuloma formation, the presence of the acid-fast bacilli within the histiocytic infiltrates and the monocytosis are consistent with this disease. (2-4) The owner did not choose to pursue further diagnostic tests required to determine the causative myobacterial species.


Mycobacterial infections in healthy birds are rare but can be a common cause of morbidity and mortality in immunocompromised birds. (2,5) The most common causes of disseminated mycobacteriosis in pet birds are Mycobacterium avium-intracellularae complex and Mycobacterium genavense. (3,5,6) Mycobacterium genavense is genetically distinct from M avium-intracellularae, but infection is clinically and histopathologically indistinguishable. (6)

Mycobacterium species are ubiquitous in the environment and are highly resistant to environmental conditions, surviving in a cage or aviary for months to years. (3,4,7) The fecal-oral route is the most common mode of transmission, although an aerogenous route is possible. (3,4) The extensive pulmonary involvement in this pionus, along with the lack of intestinal lesions, are suggestive of a possible aerogenous mode of infection. (4,6) Susceptibility to mycobacterial infections can vary among species and is likely dependent upon host and bacterial genetic factors, as well as environmental factors. Infection rates increase with environmental and physical stressors, such as overcrowding, malnutrition, or concurrent disease. (6)

Because the intestines serve as the main portal of entry and the bacteria penetrate the mucosa and colonize under the serosa, intestinal lesions are common. (5) Dissemination occurs by hematogenous spread, which often results in inflammation of the reticuloendothelial organs (ie, liver, spleen, and bone marrow); however, any organ can be infected, including the air sacs and lungs. (3,5,6) Common gross lesions include enlargement of the liver and spleen, as well as regional to diffuse thickening of the intestinal wall. (4,5) Multifocal to large, coalescing white to yellow masses may develop throughout the coelomic cavity in some cases. (5) Histologically, there may be diffuse granulomatous inflammation or formation of distinct granulomas. (5) The granulomas do not calcify in pet birds and often have a necrotic, eosinophilic core surrounded by epithelioid macrophages and multinucleate giant cells that contain acid-fast bacilli. (3-5)

The pathologic manifestation of chronic mycobacteriosis in avian species varies and depends on the mycobacterial organism, species infected, host's immune response, and stage of infection. (3,5) There are 3 different types of lesions recognized in avian species: 1) classic tubercules, 2) paratuberculosis-like form, and 3) nontuberculoid form. (3) Granuloma formation is generally not seen in psittacine birds with mycobacteriosis, making this case atypical. (2-4) The paratuberculosis-like form can occur in Amazona, Pionus, Brotogeris, and Psittacula species and in the horned parakeet (Eunymphicus cornutus). (3) This paratuberculosis-like form primarily involves the intestinal tract and is characterized by diffuse tubelike thickening and inflammation of the intestinal wall. (3,4,6) The nontuberculoid form is characterized by diffuse infiltration of foamy histiocytes, which often results in diffuse enlargement of the affected organs as the disease progresses. (3) This form of mycobacteriosis is most commonly seen in Passeriformes, Coraciiformes, and Psittaciformes. (2-4)

Clinical signs of mycobacteriosis are variable, but adult birds commonly present with signs of chronic wasting. (3,5,8) These birds often have dull plumage, are emaciated and lethargic, and may die suddenly or several months after onset of clinical signs. (5,6) Diarrhea is a very common sign, as there is a high incidence of intestinal lesions in avian mycobacteriosis. (6) Although uncommon, dyspnea can occur if there is extensive involvement of the respiratory system, as seen with this case. (3,6) Leukocytosis (with a monocytosis and heterophilia), elevated AST concentration, and a mild anemia are common abnormalities that are helpful in screening for mycobacteriosis. (4,6,8) Antemortem diagnosis can be difficult; however, radiology, endoscopy, hematology, serology, culture, and acid-fast stains of biopsy samples, cytologic preparations, and feces are all useful diagnostic tools. (7) A tentative diagnosis can be made after demonstration of acid-fast bacilli in a biopsy or histologic section of tissue. (4,9) However, determination of the specific etiological agent requires sensitive culture techniques and serotyping. (6,9) New molecular and biochemical techniques have potential for more rapid diagnosis. (6)

Treatment of mycobacteriosis in pet birds has potential problems and should be pursued with caution. Because M avium isolates from birds differ from human isolates in antibiotic susceptibility, serovars, and genetic sequencing, pet birds are an unlikely source of M avium in people (except in immunocompromised individuals). (10,11) Transmission to other birds, mammals, and immunocompromised people in contact with the infected bird, along with the duration of therapy, and the potential for poor compliance by the owner are reasons why humane euthanasia is often selected. (3,6,7) If medical treatment is chosen, there are numerous antimycobacterial agents that can be used, such as ethambutol, rifampin, rifabutin, isoniazid, ciprofloxacin, enrofloxacin, and clarithromycin, among others. (1,4) Treatment of avian mycobacteriosis is often lifelong for the bird, and treatment does not necessarily prevent shedding. Concurrent to drug therapy, strict husbandry practices must be used in the attempt to contain and eliminate the infection.

After diagnosis of mycobacteriosis in the pionus in this case, acid-fast stains were performed on fecal samples of the other birds in the aviary. Despite a lack of clinical signs, results indicated that the cagemate, also a pionus, was shedding acid-fast bacilli, and the bird was euthanatized. Although there were no gross lesions observed in this bird at necropsy that were suggestive of avian mycobacteriosis, histopathologic findings in the liver and small intestines were consistent with a mycobacterial infection. No other birds tested positive despite numerous acid-fast examinations of their feces. The remaining birds, therefore, were temporarily removed from the aviary and the enclosures were thoroughly disinfected. The birds were later returned to the aviary and routinely monitored, and it was recommended that no new birds be added.

The mycobacteriosis in this pionus parrot was atypical because it appears to have been acquired aerogenously instead of per os. In addition, the white blood cell count was within normal limits; avian mycobacteriosis almost always results in a marked leukocytosis and heterophilia, as well as a monocytosis. Furthermore, this pionus presented with classic tubercles and granuloma formation, a presentation not typical of psittacine birds. Despite the extensive granulomatous nature of the disease in this bird, clinical signs (ie, dyspnea) were not observed until very late in the course of the infection.

Acknowledgments: We thank the Diagnostic Imaging and Radiology Section, Veterinary Medical Teaching Hospital, College of Veterinary Medicine, Kansas State University, for performing the radiography on this bird.

This case was submitted by Mark G. Ruder, third year veterinary student, and James W. Carpenter, MS, DVM, Dipl ACZM, from the Department of Clinical Sciences, and Brad DeBey, DVM, PhD, Dipl ACVP, from the Department of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506, USA.


(1.) Carpenter JW, ed. Exotic Animal Formulary. 3rd ed. St Louis, MO: Elsevier Inc; 2005:303-304.

(2.) Tell LA, Woods L, Foley J, et al. A model of avian mycobacteriosis: clinical and histopathologic findings in Japanese quail (Coturnix coturnix japonica) intravenously inoculated with Mycobacterium avium. Avian Dis. 2003;47:433-443.

(3.) Gerlach H. Bacteria. In: Ritchie BW, Harrison GJ, Harrison LR, eds. Avian Medicine: Principles and Applications. Lake Worth, FL:Wingers Publishing; 1994:971-975.

(4.) Van Der Heyden N. Mycobacteriosis. In: Rosskopf WJ, Woerpel RW, eds. Diseases of Cage and Aviary Birds. 3rd ed. Baltimore, MD:Williams & Wilkins; 1996:568-571.

(5.) Schmidt RE, Reavill DR, Phalen DN. Pathology of Pet and Aviary Birds. Ames, IA:Iowa State Press; 2003:27-28, 56-57, 76-77.

(6.) Tell LA, Woods L, Cromie RL. Mycobacteriosis in birds. Rev Sci Tech. 2001;20:180-203.

(7.) Dorrestein GM. Bacteriology. In: Altman RB, Clubb SL, Dorrestein GM, Quesenberry K, eds. Avian Medicine and Surgery. Philadelphia, PA:WB Saunders; 1997:275-277.

(8.) Hoefer HL. Diseases of the gastrointestinal tract. In: Altman RB, Clubb SL, Dorrestein GM, Quesenberry K, eds. Avian Medicine and Surgery. Philadelphia, PA:WB Saunders; 1997:434-435.

(9.) Butcher GD, Reed WM, Winterfield RW, Nilipour A. Mycobacterium infection in a gray-cheeked parakeet. Avian Dis. 1990;34:1023-1026.

(10.) Carpenter JW, Gentz EJ. Zoonotic diseases of avian origin. In: Altman RB, Clubb SL, Dorrestein GM, Quesenberry K, eds. Avian Medicine and Surgery. Philadelphia, PA:WB Saunders;1997:350-363.

(11.) Anqulo FJ, Glaser CA, Juranek DD, et al. Caring for pets of immunocompromised persons. J Am Vet Med Assoc. 1994;205:1711-1718.
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Title Annotation:Round Table Discussion
Author:Ruder, Mark G.; Carpenter, James W.; DeBey, Brad
Publication:Journal of Avian Medicine and Surgery
Article Type:Clinical report
Geographic Code:1USA
Date:Sep 1, 2006
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Next Article:Avian Dis: Experimental assessment of the pathogenicity of H5N1 influenza A viruses isolated in Japan.

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