A 2-year-old pygmy goat with a clinical history of progressive weight loss was submitted for necropsy to the Animal Disease Diagnostic Laboratory.  Two animals (including this one) out of 25 goats were presenting with similar clinical history. 

On necropsy examination, the animal had adequate muscle mass but decreased body fat.The remaining body fat was often gelatinous (serous atrophy of fat). 

  The mesenteric lymph nodes were firm, nodular and enlarged (2-10 cm in diameter; normally they should be 1 cm in diameter) and, on cut surface, contained granularto caseous exudate .  Mesenteric lymphatics were markedly distended.  The serosa of the jejunum and ileum was hyperemic.  The mucosa of the distal jejunum and ileum had a granular appearance and was moderately thickened.

On light microscopic examination, the normal architecture of the mesenteric lymph nodes was disrupted by multifocal to coalescing granulomas that contained necrotic mineralized centers.  Lymphoid sinuses and paracortical areas were more severely affected.

  Macrophages and multinucleated giant cells often had intracytoplasmic acid fast positive bacilli (Ziehl-Neelsen staining).  The remaining lymphoid tissue was depleted of  lymphoid cells.  Thelamina propria of the distal jejunum and ileum was diffusely infiltrated by many macrophages and multinucleated giant cells containing acid fast bacilli, and fewer lymphocytes and eosinophils. The villi were often blunted.  Intestinal lymphatics were ectatic and contained variable infiltration by macrophages.  In the liver, there was granulomatous inflammation around blood vessels of the portal triads

The clinical history of progressive weight loss observed in this goat, in conjunction with the gross and histologic fiindings of granulomatous lymphadenitis, enteritis and hepatitis, and bacterial culture results were consistent with Johne's disease.  Although the epidemiology and pathogenesis of Johne's disease in large and small ruminants are similar, sheep and goats do not develop diarrhea due to the greater efficiency of electrolyte and fluid absorption by the colon; however, pygmy goats are an exception to the course of disease in other small ruminants in that some animals develop explosive diarrhea and die unexpectedly.  This disease, considered to be one of the most serious diseases affecting dairy cattle is characterized by chronic body wasting and hypoproteinemia.  Young animals (approximately six months of age) are most susceptible to Mycobacterium avium paratuberculosis (M. paratuberculosis)  infection.  Milk, semen, urine, intrauterine secretions, and contaminated feed can transmit this agent to susceptible animals.  Within the enteric mucosa of infected animals, M cells transport this bacterium to Peyer's patches.  M. para-tuberculosis replicates within macrophages; it resides in phagosomes and phagolysosomes inhibiting production of superoxides and preventing fusion of lysosomes and phagosomes.  Iron is also important for this organism to survive.  M. paratuberculosis produces the lipid-soluble siderophore mycobactin (iron transporter) and the water soluble siderophore exochelin (separates the iron from ferritin) which help obtain iron from the infected cell.  The bacterial cell wall protects the organisms within phagolysosomes.  Infected macrophages travel through the lymphatic to the lymph nodes, spleen and liver, causing granulomatous inflammation.  In the small intestine and colon there is granulomatous inflammation within the lamina propria causing crypt atrophy.  Malabsorption of amino acids and plasma protein, resulting in negative nitrogen imbalance, protein-losing enteropathy and emaciation, are the result of crypt atrophy.  PCR, serologic tests (antibodies against M. paratuberculosis including complement fixation, agar gel immunodiffusion test and ELISA) and fecal bacterial cultures are currently available for the diagnosis of this disease.

-by Dr. Ingrid Pardo, ADDL Graduate Student

References

1. Harris NB, Barletta RG: 2001.  Mycobacterium avium subspecies paratuberculosis in Veterinary Medicine.  Clin Microbiol.  Review 14(3): 489-512.

2. Manning EJ, Steinberg H, Krebs V, Collins MT: 2003.  Diagnostic testing patterns of natural Mycobacterium paratuberculosis infection in pygmy goats.  Can J Vet Res 67(3): 213-218.

3. Munjal SK, Tripathi BN, Paliwal OP: 2005.  Progressive immunopathological changes during early stages of experimental infection of goats with Mycobacterium avium subspecies paratuberculosis.  Vet Pathol 42(4): 427-436.

4. Whittington RJ, Marsh IB, Reddacliff LA: 2005.  Survival of Mycobacterium avium subsp. paratuberculosis in dam water and sediment.  Appl Environ Microbiol 71(9): 5304-8.

5. http.vp5.afip.org/systemic/index.php