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Diagnosis and Control of Johne's Disease (2003)
Board on Agriculture and Natural Resources (BANR)

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Species

Location

Reference

Gnus

(Connochaetes albojubatus)

Unspecified

Rankin, 1958b

Zebu cattle

(Bos indicus)

Unspecified

Katic, 1961

Wild rabbits

Scotland

Grieg et al., 1999; Beard et al., 2001b

Monogastric animals

Mules

Global

Eveleth and Gifford, 1943

Hogs

Global

Larsen et al., 1971

Chickens

Global

Larsen et al, 1981

Monkeys

Global

Chiodini et al., 1984

Pygmy asses

Global

Van Ulsen, 1970

Mandrills

(Papio sphinx)

Unspecified

Zwick et al., 2002

Horses

Global

Larsen et al., 1972

 

SOURCE: Adapted from Chiodini et al., 1984.

SPECTRUM OF DISEASE IN DOMESTICATED ANIMALS

Cattle

JD is characterized by vague and often variable clinical signs, and the clinical signs and the severity of gross and histological lesions do not always correspond (Allen et al., 1968; Downham, 1950; Hallman and Witter, 1933; Macindoe, 1950; Smyth, 1935; Smyth and Christie, 1950). Whitlock and Buergelt (1996) have described the following progression of disease in cattle (summarized in Table 2–2).

Stage I: Silent Infection

In Stage I, animals typically exhibit no overt evidence of infection with Mycobacterium avium subsp. paratuberculosis (Map). Stage I JD is typically found in calves and heifers, most immature young stock, and many adult cattle. No routine or special clinicopathologic tests or serology will detect disease in these animals. Only postmortum tissue culture or, less often, histopathology can detect infection at this early stage of disease.

Stage II: Subclinical Disease

Most animals in Stage II JD are adults that are carriers of Map. The animals do not exhibit clinical signs typical of JD, but they sometimes have detectable antibodies or exhibit altered cellular immune responses. Many are fecal-culture negative, although they intermittently shed low numbers of organisms in feces. In a small percentage (15–25 percent), disease can be detected by fecal culture, by altered cellular immune response, by serum antibodies, or by histopathology. An unknown proportion of Stage II animals progress slowly to Stage III (clinical disease), but because so many are culled

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