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Clinical Exposures: Mycobacterium avium infection in a dog


A routine physical examination of a 1.5-year-old spayed female German shepherd that had been presented for vaccinations revealed generalized lymph node adenopathy and a slight fever (102.8 F).

A routine physical examination of a 1.5-year-old spayed female German shepherd that had been presented for vaccinations revealed generalized lymph node adenopathy and a slight fever (102.8 F). A complete blood count revealed anemia.

Figures:- 1, 2, 3, 4 and 5

Oral tetracycline was prescribed because subacute or chronic ehrlichiosis and Rocky Mountain spotted fever were differential diagnoses. The dog developed diarrhea five days after the tetracycline therapy was initiated, so tetracycline was discontinued and chloramphenicol therapy was begun. Two days later, the diarrhea had worsened. Serology results revealed a low antibody titer (1:64) for Rickettsia rickettsii antigens. Chloramphenicol was discontinued, and oral tetracycline therapy was reinstituted.

A wedge-section of prescapular lymph node was submitted for histopathologic examination, and the test results were consistent with mycobacteriosis. The dog's condition deteriorated quickly. The dog had developed rapidly progressive neurologic signs (stilted gait, hyperexcitability, hypermetria, muscle spasm followed by short episodes of ventroflexion and lateral recumbency). Because the prognosis was poor, the owner elected euthanasia.

Necropsy and laboratory findings

Necropsy revealed that the dog was in good body condition. The tonsils (Figure 1) and peripheral and visceral lymph nodes were markedly enlarged and beige. On cut section, the nodes lacked corticomedullary differentiation. Mesenteric lymph nodes (Figure 2) were the largest, measuring up to 30 x 5 x 3 cm; mandibular lymph nodes measured 15 x 4 x 3 cm. The spleen was markedly enlarged and pink and contained numerous yellow-tan to off-white foci and nodules measuring 1 mm to 1 cm (Figure 3). Peyer's patches were prominent and white (Figure 4). The fat in the marrow of the long bones was replaced by pink tissue. The cranioventral lung lobes were wet, had a meaty consistency, and were mottled pink.

A histologic examination of the cerebrum, cerebellum, and brainstem revealed multifocal granulomatous meningoencephalitis of the cerebellum and brainstem. No lesions were observed in the cerebrum. The spinal cord was not examined because the owner requested a cosmetic necropsy. On histologic examination, the parenchyma of the bone marrow, lymph nodes, Peyer's patches, and spleen was replaced by diffuse granulomatous inflammation composed of sheets of large macrophages distended with acid-fast bacilli (Figure 5). The yellow-tan and off-white foci and nodules in the spleen were granulomas with necrotic centers surrounded by neutrophils, macrophages, and giant cells. Edema and mild multifocal granulomatous pneumonia had caused the gross changes in the lungs. Acid-fast stains were performed on impression smears of the spleen taken at necropsy and paraffin-embedded sections of lymph nodes because macrophages in all other organ lesions resembled those seen in the spleen and lymph nodes. Severe diffuse granulomatous enterocolitis affecting the jejunum, ileum, and colon had caused the recent onset of diarrhea.

Aseptically procured swabs of the spleen and lymph nodes were streaked onto Lowenstein-Jensen culture medium, and the isolate was submitted for identification.* The isolate, identified as Mycobacterium avium, was then forwarded to the National Veterinary Services Laboratories in Ames, Iowa, for serotype identification. The infectious agent was determined to be M. avium subspecies avium serotype 1.


Disseminated M. avium infections in dogs are rare.1 Basset hounds and miniature schnauzers appear to be predisposed to the infection, although other breeds are affected. Most reported cases have involved dogs 2 to 4 years of age.1

*The Commonwealth of Virginia, Department of General Services, Division of Consolidated Laboratory Services, Bureau of Microbiological Science Laboratory in Richmond, Va.

The pathogenesis of disseminated M. avium infection in dogs is poorly understood. A mechanism involving immunosuppression has been proposed, but immunologic studies have not revealed abnormalities in T-cell function or CD4+ to CD8+ ratios.1 An infection may develop after a young pup, whose immune system is not fully competent, eats contaminated food.1 (There is an increased danger when feeding a raw diet containing swine or poultry viscera or lymphoid organs. The organism cannot survive in properly processed commercial food.) Ingested organisms may be phagocytized by macrophages in Peyer's patches, persisting and replicating until reaching sufficient numbers to produce overt disease.1

Birds and swine are the primary reservoirs of M. avium.2 Large numbers of organisms are shed in the feces of infected birds and can remain viable in water and soil for at least two years.2 The source of the infection in this case was not determined. The owner reported that the dog had not been exposed to wild or pet birds, chickens, or swine, but the property where the dog resided had been a farm before the dog's owner had purchased it. The owner did not know what type of livestock had been maintained on the farm.

Parvovirus enteritis infection had been diagnosed when the dog was about 10 weeks old, shortly after it had been adopted from a humane shelter. Immune impairment and intestinal damage caused by the parvovirus infection may have allowed the Mycobacterium species in the environment to enter the dog's body and incubate in the lymph nodes draining the digestive tract. Alternatively, the puppy may have been infected with M. avium before its adoption, and the parvovirus infection may have enhanced the organism's ability to establish itself in the host.

Therapy for generalized M. avium infection is often prolonged and ineffective.2 One dog was treated with a combination of clofazimine, ciprofloxacin, and rifampin with limited success, and a dog that received continuous therapy with enrofloxacin, clarithromycin, and clofazimine remained in remission for two years before experiencing a relapse.2

Two more common differential diagnoses for generalized lymph node adenopathy in dogs are malignant lymphoma and histoplasmosis. Clinical signs of M. avium infection are variable but include anorexia, depression, diarrhea, fever, generalized lymphadenopathy, pale mucous membranes, and weight loss.1-3 Additionally, respiratory signs, lameness, and pathological fractures may be seen.3 Mycobacteriosis should be included as a differential diagnosis for intermittent or persistent diarrhea, especially when accompanied by lymphadenopathy. Acid-fast stains should be performed on smears made from swabs of rectal mucosa and fine-needle aspirates or histologic sections of lymph nodes.1

Large numbers of M. avium and closely related organisms may be present in the intestinal tract and mesenteric lymph nodes and can be shed in feces. So infected dogs should not have contact with young children and immunocompromised people and pets.


The author thanks Katherine L. Nicholson, DVM, PhD, Lakeside Animal Hospital, 5206 Lakeside Ave., Suite #6, Richmond, VA 23228, for providing this patient's history and laboratory data and for interpreting these data. Dr. Nicholson's present address is Department of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298.


1. Horn B, Forshaw D, Cousins D, et al. Disseminated Mycobacterium avium infection a dog with chronic diarrhea. Aust Vet J 2000;78:320-325.

2. Greene CE, Gunn-Moore DA. Mycobacterial infections. In: Greene CE, ed. Infectious diseases of the dog and cat. 2nd ed. Philadelphia, Pa: WB Saunders Co, 1998;313-321.

3. Bauer N, Burkhardt S, Kirsch A, et al. Lymphadenopathy and diarrhea in a miniature schnauzer. Vet Clin Pathol 2002;31:61-64.

This case report was provided by Neil Allison, DVM, DACVP, Virginia Department of Agriculture and Consumer Services, 1100 Bank St., Suite 600, Richmond, VA 23239. Dr. Allison’s present address is Experimental Pathology Laboratories, Incorporated, P.O. Box 12766, Research Triangle Park, NC 27709.

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