Johne’s Disease (Mycobacterium avium paratuberculosis) infection in goats

Siobhan O’Sullivan, Lisa Gordon

Animal Health Laboratory, University of Guelph, Guelph, ON.

AHL Newsletter 2024;28(3):9.

Multiple goats from a small herd developed chronic diarrhea, progressive loss of body condition, and lymphadenopathy. On postmortem examination, lymph nodes appeared caseonecrotic, the mesenteric vasculature was dilated, and the wall of the intestine was segmentally thickened. Histopathology revealed granulomatous enteritis and lymphadenitis, with caseous necrosis and mineralization in the lymph node. With modified acid fast staining, a few positively-staining organisms were visualized in macrophages. Fecal samples were positive for Mycobacterium avium subsp. paratuberculosis (MAP) by PCR (cycle threshold [Ct] values 29-35), confirming the diagnosis of Johne’s disease.

Clinical signs of Johne’s disease are secondary to the granulomatous enteritis produced by MAP infection. Intestinal malabsorption of protein results in diarrhea, cachexia, hypoproteinemia, tricavitary effusion, and eventual mortality (Figs. 1,2). Common gross lesions include ileocecal and mesenteric lymphadenopathy, thickening of the mucosa of the ileum and colon into elevated ridges, and thickened, white intestinal lymphatics (lymphangitis) (Figs. 1,2). These lesions can be more subtle and variable in small ruminants than in cattle. Caseous necrosis of the lymph nodes with mineralization is also reported sporadically in infected small ruminants. Histologically, acid fast organisms can be abundant (multibacillary) or sparse (paucibacillary) in macrophages, necessitating a thorough scanning of the tissues to identify the diagnostic bacteria (Fig. 2).

Ruminants are often infected while young, through milk or the fecal-oral route, and can remain asymptomatic for 2-5 years while shedding the organisms through feces. Mature animals eventually develop weight loss and diarrhea. These long-term subclinical individuals act as reservoirs of infection for other animals, making Johne’s difficult to control. Since it is not effectively treatable, management of Johne’s focuses on long-term preventative strategies: removing animals that test positive; acquiring replacements from disease-free stock; and reducing the risk of fecal-oral spread to young animals through sanitation practices.   AHL

Figure 1. Goat, small intestine. Aggregates of macrophages are present in the villus lamina propria.  H&E stain.

Figure 1. Goat, small intestine. Aggregates of macrophages are present in the villus lamina propria.

H&E stain.

Figure 2. Goat, small intestine. Modified acid fast-positive bacteria are present in the cytoplasm of macrophages.

Figure 2. Goat, small intestine. Modified acid fast-positive bacteria are present in the cytoplasm of macrophages. ZN stain.

References

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3. Grieg A. Johne’s disease in sheep and goats. In Practice. 2000;22(3):146-151.