INTRODUCTION
Johne's disease (paratuberculosis) is a chronic infectious enteritis of cattle, sheep, goats and other ruminants caused by the bacterium Mycobacterium paratuberculosis.
Merkal (1983), of Iowa, U.S.A., stated that the disease has become increasingly widespread in recent years, especially in cattle and goat herds, as more and more animals are kept in close confinement.
Since the establishment in 1974 of a control facility at Glenfield for the culture of M. paratuberculosis, Johne's Disease has been confirmed in New South Wales in cattle, goats (1978) and sheep (1980) (Eamens [1983]). In cattle and goats in N.S.W., the disease has been relatively widespread but in sheep has only been recognised in the Central West (R.V.O., Orange area). In goats in N.S.W., the clinical disease has thus far only been recognised in dairy breeds (Eamens [1984], however M. paratuberculosis was cultured in 1982 from the mesenteric lymph nodes of a young clinically normal Angora goat (Hart [1984]).
Johne's disease in goats is by no means restricted to high rainfall areas. The writer, for example, has investigated cases of the disease in a herd in a 450 mm. (18") annual rainfall area in northwest N.S.W.
Because the disease is widespread in goats, and because of the increased interest in recent years in goat raising by both established and newer primary producers, a brief review of aspects of Johne's Disease is timely.
CLINICAL ASPECTS
Johne's disease is not a dramatic disease but is insidious and chronic in character. The incubation period is long and irregular with many factors such as age at first infection, size of the infective dose, and stress governing the actual development of clinical disease (Glastonbury (1980)).
Factors which may influence the development of clinical disease include parturition, a low nutritional plane, heavy milk yield, and intercurrent disease (Jubb & Kennedy (1963)). The clinical disease is usually seen in adult goats, occurring sporadically and usually in single animals (the youngest case seen by the writer was a doe about 16 months old).
Wirth (1980) states that Johne's disease in goats differs from the disease in cattle in two important respects:
* the goat suffers an extreme loss of weight and becomes cachectic
* the faeces remain pelleted (with sometimes a mucoid covering). Terminal diarrhoea may occur in a few cases.
However, it has also been observed that diet (e.g. lush green feed) or concurrent gastrointestinal helminthiasis may sometimes result in the passage of soft or fluid faeces in affected goats (Love [1984]).
The coat becomes harsh and lacking in lustre over the course of the clinical disease, which may last from weeks to months. Submandibular oedema may occur in later stages.
Temporary remissions may occur in late pregnancy with clinical signs reappearing, sometimes with increased severity, after parturition. Attempts at treatment or changes in diet may also cause some temporary abatement of clinical signs. The course of the disease, however, is almost invariable inexorable. Although emaciation is progressive and ultimately fatal, it is important to note with respect to differential diagnosis that the appetite is retained and the demeanour remains bright for the most part until the terminal stages.
Clinical signs could be confused with other enteridites, malnutrition, gastrointestinal helminthiasis etc. Goat owners are most likely to confuse the disease with parasitism.
POST-MORTEM ASPECTS
Advanced clinical cases are emaciated, with catabolism of fat depots. Inter-mandibular oedema and serious effusion in the body cavities may also be found. Often there is no correlation between the severity of the clinical syndrome and the severity of lesions found at autopsy.
Specific gross lesions are confined to the intestines, the lymphatics and the regional lymph nodes, with often the least obvious in goats being the changes in the intestines. In cattle, the bowel can be markedly thickened with the development of mucosal folds or corrugations being such that they cannot be smoothed out by stretching. In goats and sheep, however, it is nearly the rule for gross changes to be minimal (Jubb and Kennedy (1963)).
At the level of the ileum, caecum and colon there is moderate intestinal thickening giving a velvety appearance to the mucosa. This is due to thickening of the mucosa and accumulations of epithelioid cells in the submucosa.
Unlike the disease in cattle, small (1 to 4 mm, diameter) white foci or nodules of caseation and calcification, similar to the tubercles that occur in tuberculosis, may occur in lymph nodes, the mucosa, submucosa, lymphatics and on the peritoneum. Lloyd (1980) states that these occur in about 20% of cases but others have found their occurrence to be less frequent (Hart (1984), Love (1984)).
The lymphatics, usually difficult to see, may be corded and knotted, the cording being due to mononuclear cell infiltration of the walls of the lymphatics, and the knots being focal granulomatous accumulations of epithelioid cells and lymphocytes.
Most obvious may be the mesenteric lymph nodes which are enlarged, pale and oedematous, especially in the medulla. The pallor may be such that there is little corticomedullary distinction.
Peritonitis is present in some animals.
Specimens for laboratory examination should include:
* faeces submitted chilled for bacteriology (live animal).
* sections of ileum, caecum, colon, ileocaecal valve and lymph nodes of the ileo-caeco-colonic region in separate containers, submitted chilled for bacteriology.
* sections of ileum, caecum, colon, ileocaecal valve and lymph nodes of the ileo-caeco-colonic region, in buffered formalin for histopathology.
* blood for gel diffusion test (live animal).
Addendum
Attached is also a copy of the paper 'Johne's Disease in Goats' originally written for publication in the Australian Mohair and Angora Journal.
References
Eamens, G.J. (1983) Proc. 66th Ann. Conf., Assoc. of Vet. Inspectors N.S.W. See www.flockandherd.net.au
Eamens, G.J. (1984) Pers. comm.
Glastonbury, J.R.W. (1980) Proc. Gastroenteric Conditions Seminar, Post. Grad. Comm. in Vet. Sc., Uni. Syd.
Hart, K. (1984). Pers. comm.
Jubb, K.V.F. & Kennedy, P.C. (1963) Path. Domest. An.
Love, S. (1984) Pers. comm.
Merkal, R.S. (1983) Unpub. notes. An. Dis. Centre, Ames, Iowa
Wirth, H.J. (1980) Proc. No. 52 (Goats). PGC in Vet. Sc., Uni. Syd.