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This article was published in 1984
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Johne's Disease in Goats

S. LOVE, B.V.Sc., Veterinary Inspector, ARMIDALE

INTRODUCTION

Johne's disease, also known as paratuberculosis, is a chronic infectious enteritis of cattle, sheep and goats, caused by the bacterium Mycobacterium paratuberculosis.

The disease also occurs in water buffalo and in captive wild ruminants. Mice and hamsters are susceptible and are used extensively in experimental work.

THE ORGANISM

The causative organism is similar in some aspects to the mycobacteria that cause tuberculosis in birds and swine. The organism was first recognised in Germany by Johne and Frothingham in 1895 in the tissues of diseased cattle. Initially the disease was regarded as an atypical form of tuberculosis but was shown in Denmark in 1905 to be a separate entity.

More than one strain of the organism exists. For example, 3 strains of M. paratuberculosis can cause the disease in cattle; the usual bovine strain and 2 sheep strains. Lloyd (1980) states that there are many unsatisfactory aspects of our knowledge of Johne's disease and among the more important is whether strains of the organism from one species can cause the disease in other species.

M. paratuberculosis will survive for long periods outside the animal body under suitable conditions. Contaminated pastures may remain infective for up to a year. The organism is resistant to freezing, but is relatively susceptible to sunlight and drying (Blood et al. (1978); Malmo (1979]). Naturally infected faeces showed viable bacilli when exposed to atmospheric conditions but kept moist for as long as 245 days. (Bruner & Gillespie [1971]).

OCCURENCE

Johne's disease is worldwide in its distribution and is particularly prevalent in temperate climates and in areas of intensive animal production. The disease is most common in cattle and to a lesser extent in sheep and goats. However, Merkal (1983) states 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.

Regarding Johne's disease in goats in N.S.W., a Department of Agriculture report (1983) stated that there were 23 known infected properties. Lloyd in 1980 stated that there were 6 or 8 infected properties in Victoria, with one herd sustaining substantial losses over several years.

Johne's disease was first confirmed in N.S.W. in goats in 1978 and in sheep in 1980. In cattle and goats in N.S.W., the disease has been widespread but in sheep has been recognised only in the Central West. In goats in N.S.W, the clinical disease is currently recognised only in dairy breeds. (Eamens [1983]).

In a young Angora goat autopsied (1982) by Veterinary Inspector, Braidwood for other reasons, enlarged mesenteric lymph nodes were found. From these, M. paratuberculosis was cultured. However, clinical Johne's disease has not been noted thus far in Angoras in N.S.W. It may only be a matter of time before this situation changes. (Hart (1984]).

TRANSMISSION

Natural infection is by ingestion of food and water contaminated by the faeces of infected animals. Congenital infection is also a possibility. (For example, the organism has been isolated from the genitalia and the semen of infected bulls, and survives antibiotic addition and freezing. As a result, intrauterine infection is said to occur commonly in cattle. (Blood et al. [1978]). Because of the long incubation period, infected animals may excrete organisms in the faeces for 15 to 18 months before clinical signs appear. (The youngest clinical case seen by the writer was a doe 16-18 months of age). Also, animals reared in an infected environment may become permanent or temporary carriers of disease without becoming clinically affected.

DEVELOPMENT OF THE DISEASE

The organism has a predilection for the intestinal tract, the intestine being the main site of bacterial proliferation and action.

Young animals seem to be more susceptible and in most cases the organisms are thought to be ingested prior to weaning. Some infected clinically normal animals may recover over a period of time. The remainder become carriers, with the organism persisting and proliferating slowly in the intestinal tract and associated lymph nodes. (Other parts of the body may be infected, e.g. in clinically normal cattle, prenatal infection can occur). Clinical cases arise from among the carriers.

CLINICAL FINDINGS

Clinical cases may only occur sporadically because of the slow rate of development of the disease. In flocks where the disease is established there are probably a number of asymptomatic animals harbouring or shedding the organism for every goat showing clinical signs. In infected herds of cattle for example, it is said that carrier animals may be up to 20 times as frequent as clinical cases. (Withers [1959]).

The course of the clinical disease may extend over weeks or months. Clinical signs include progressive weight loss and the development of a harsh coat. Diarrhoea is not marked as in cattle; the faeces may even remain pelleted. This depends somewhat on the type of feed, worm burdens etc. Appetite for the most part is maintained. Temporary remissions may occur, especially with supplementary feeding or attempts at treatment, but the course is inexorable, with the terminal weakness and emaciation necessitating destruction.

POST-MORTEM FINDINGS

Changes are found in the intestine and associated lymph nodes but may be slight and could be missed by untrained persons. Autopsies should be performed by veterinarians with appropriate samples being collected for laboratory analysis.

LABORATORY TESTS

Ante-mortem diagnosis of Johne's disease in individual animals may be difficult because of the overall lack of dependability of the available tests. Different allergic and serologic tests behave differently at different stages of the disease and false positive and false negative results have been a problem. Examination and culture of faeces, although useful, is not entirely satisfactory as animals shedding organisms intermittently or in low numbers may escape detection. Also, because the organism grows slowly, culture results may not be available for 2-3 months.

As the disease progresses through pre-clinical, to clinical, to the post-mortem stage, a diagnosis becomes easier to verify, with histopathology (microscopic examination of tissues) and bacteriology (culture of tissues etc.) providing a definitive diagnosis of autopsy.

The gel test in goats is showing considerable promise in N.S.W., with gel test positive animals correlating well with histopathology (at autopsy) and vice versa. However, asymptomatic carrier animals may remain gel test negative until they reach a certain stage in the disease, so that the test is not likely to detect all the infected animals in a herd at a given time.

TREATMENT

M. paratuberculosis is more resistant than M. tuberculosis to chemotherapeutic agents. Treatment is only likely to result in a transient improvement and merely serves to extend the period that affected animals are shedding the organism.

CONTROL

Control or eradication of Johne's disease is difficult. The following husbandry recommendations largely based on those suggested by Merkal (1983), should be considered:

1. Remove newborn animals from their dams at birth and raise them in separate, non-contaminated quarters.

2. Feed the young animals only pasteurised milk or milk replacer.

3. Make sure that no faecal contamination from the adult herd is carried on footwear, feed supplies, etc., to the young animals.

4. Do not mix the replacement animals with the adult herd until they are at least one year old.

5. Animals should be regularly monitored (e.g. using faecal sampling and the gel test in goats). Animals shedding the organism or exhibiting clinical signs should be slaughtered. In one N.S.W. herd attempting eradication, all get test positive animals are slaughtered. (Hart [1984]).

6. Equipment, pens, etc. that need to be disinfected should be cleaned thoroughly to remove all traces of faeces, then be soaked in a disinfectant that contains ortho-phenylphenol and a detergent. Quaternary disinfectants will not kill M. paratuberculosis.

7. Contaminated feedlots and similar areas should be ploughed and covered with 6 inches of fresh, non-contaminated soil.

8. Manure should not be spread on pastures.

9. Merkal (1983) has also suggested the following in U.S.A., with cattle particularly in mind:

'Vaccination should be used only when the above husbandry recommendations are not feasible, and even then as many of the recommendations as possible should be followed because exposure of the young animals to large numbers of organisms overwhelms the protective effect of the vaccine. If a vaccination programme is to be used, the bacterin should be administered during the animal's first month of life. Because the bacterin can produce a serious lesion if accidentally injected into human tissue, it should be administered only by a state-approved veterinarian trained in its use.'

A vaccine is not available in Australia. Vaccination, which first proved useful in sheep, is said also to be of value for young calves. However, vaccination prevents the use of certain testing procedures for detection of infected animals.

REGULATORY ASPECTS - N.S.W.

Where Johne's disease is diagnosed in goats, the herd is placed in quarantine and:

i) all clinically affected animals are slaughtered; and

ii) the remainder of the herd is tested (using the gel diffusion precipitin test) and all positive reactors removed and slaughtered.

Additionally, the immediate offspring, or dams, of clinical cases are slaughtered.

Quarantine is revoked when these requirements have been met satisfactorily. The owner, however, is encouraged to undertake a regular surveillance programme to monitor the prevalence of infection in the herd.

ARCHIVE FILE

This article was published in 1984 See the original document

Johne's Disease in Goats

S. LOVE, B.V.Sc., Veterinary Inspector, ARMIDALE

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This article was published in 1984
See the original document