Pathology of Johne's Disease
All animals
- Pathology caused by M. paratuberculosis infection varies between animal species and, to a lesser
extent, between individual animals. Described below are the pathologic features of the
infection that are common to most M. paratuberculosis infections in most all animal species. Following are discussion of some of the gross and histopathologic manifestations of the infection that are distinctive to some
animal species.
- The primary site of M. paratuberculosis infections is most often the ileum (see section on
pathogenesis). Consequently, although secondary sites of infection may have pathology, the
ileum is generally the tissue most severely affected and has the highest burden of M.
paratuberculosis bacteria. Lymph nodes draining the ileum are sites of secondary infection where
pathologic changes are commonly seen. Tertiary sites of infection are the liver, spleen, and
lymph nodes distant from the gastrointestinal tract.
- The earliest cellular changes seen at sites of M. paratuberculosis infection are increased numbers
of mononuclear phagocytes and lymphocytes. Occasionally Langerhans giant cells (351.6K) (macrophages
that have coalesced to form very large cells with multiple nuclei) can be seen. In early lesions,
the number of acid-fast bacteria will be low and sometimes cannot be seen without examination of
many sections of tissue stained by the Ziel-Neelsen acid fast stain.
- As the infection progresses, the mononuclear inflammatory infiltrate becomes pronounced and
giant cells become more numerous. This granulomatous type inflammation is distinguished from
that seen in tuberculosis in that it is diffuse; not walled off or circumscribed by fibrous
connective tissue (see histopathology, 351.6K). In many respects the lesion resembles that of leprosy more than that of
tuberculosis (two other diseases caused by mycobacteria). As in leprosy, some lesions have very
numerous acid-fast bacteria (see acid-fast stain, 351.6K). Such lesions are referred to as lepromatous or multi-bacillary.
Other lesions have few acid-fast bacteria and are referred to as paucibacillary or tuberculoid
(tuberculosis-like in the sense of having few acid-fast bacteria, but not tuberculosis-like in
architecture of the histopathology).
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- In cattle, the inflammatory response progresses due to the presence of mycobacteria, until the
intestinal wall is many times its normal thickness - the result of immigration of numerous
lymphocytes and macrophages. Thickening of the intestine becomes evident on gross
examination of the ileum. The mucosal surface is corrugated and granular in appearance (see comparative pathology, 219.7K). The
ileum does not feel thin and pliable, and can not be stretched to thinness. At necropsy, the upper
jejunum, which is not usually affected, can be used as an example of what the ileum should
normally look and feel like. The serosal surface of the ileum may contain thin white lines that
are thickened and dilated lymphatics. These lymphatics have thickened walls and are congested
with lymphocytes which serve to make them grossly visible - pathology referred to as "cording" (351.6K).
Thickening of the ileum by granulomatous inflammation leads to dysfunction of the intestine and
a condition known as a protein losing enteropathy. Protein absorption is impaired and excess
protein is lost in the feces. The result can be measured as subnormal levels of total serum
proteins. One serum protein in particular, serum albumin, will be extremely low in advanced
stages of paratuberculosis. This hypoalbuminemia impairs the ability of the animal to retain
fluids within the vasculature (blood vessels) leading to edema (fluid-filled tissues). In cattle this
is most noticeable in the submandibular region: a condition referred to as "bottle jaw" (235.4K).
Lymph nodes that drain the ileum (mesenteric, 351.6K; and ileocecal) will be enlarged and lighter color
than normal due to the influx of white blood cells (macrophages and lymphocytes). All other
organs generally appear normal, but in advanced Johne's disease, when animals have had diarrhea
for over a week and shown marked loss of weight, there may be noticeable loss of body fat.
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- In sheep and goats, thickening of the ileum is less commonly seen. However, by histopathology
there is clear evidence of a granulomatous inflammatory response and acid-fast bacteria are
normally quite abundant. Lymph nodes are enlarged, and occasionally calcified causing them to
feel "gritty" when cut with a knife. Clinical signs of Johne's disease are more subtle in sheep
and goats: diarrhea is uncommon and weight loss is masked by a heavy coat of fleece or hair.
Consequently, when animals are submitted for necropsy, the M. paratuberculosis infection is very
advanced, the animals are extremely thin, and if still living, are very weak. In these animals,
necrosis of fat reserves in such animal is another pathologic manifestation of paratuberculosis,
though not one unique to paratuberculosis.
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- In deer and other cervidae, M. paratuberculosis and M. avium can cause very similar diseases.
Cervidae seem more susceptible to these pathogens than are domestic ruminants. The infections
run a faster course. Cervidae infected with these mycobacterial species die at a younger age, and
the infection is more disseminated that in domestic ruminants. Gross and histopathology of
paratuberculosis in cervidae resembles that seen in goats and sheep, but caseation of lymph nodes
occurs more frequently than in other animals. Caseation is when lymphocytes and macrophages
die forming a material the consistency and color of cooked oatmeal. Caseation necrosis is a
hallmark of tuberculosis and can lead to confusion at necropsy as to whether animals have
tuberculosis or paratuberculosis, although TB lesions are more often found in the respiratory tract
and lymph nodes of the head.
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Last revised February 19, 1997.
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All material Copyright © 1996 by the Board of Regents of the University of Wisconsin System. School of Veterinary Medicine, all rights reserved. If you have questions or comments about this page email us at: mcollin5@facstaff.wisc.edu