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This article was published in 1975
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Some Observations of Johne's Disease in the Riverina
E. Scott Rogers, B.V.Sc., Veterinary Inspector , Deniliquin
JOHNE'S DISEASE is described as a chronic, usually fatal, contagious enteritis of cattle, sheep and goats.
This is the standard Text Book (sic)description of the disease as stated in the Diseases of Domestic Animals, Part 5, Vol. 1. Commonwealth Department of Health Service Publication (Veterinary Hygiene) No. 9. This publication gives a good general description and history of the disease in Australia, but hardly paints the true picture of the disease as currently seen in the Riverina, on both sides of the Murray.
whilst Johnes Disease is relatively common in the irrigation districts of Victoria and Gippsland, the disease has been thought to be of little importance in New South Wales. It is known to be well established at Kameruka, on the far South Coast and there has been a recently recorded outbreak in bullocks in the Northern Rivers Region of New South Wales (P Honey). As the irrigation Districts in Southern New South Wales become well established, it is only logical to anticipate a similar incidence of this disease in these areas as in the older established irrigation Districts of Victoria, just across the Murray River and under similar climatic conditions.
In order to stress how important this may be in the future to the irrigation areas of New South Wales, some information on the incidence of the disease across the Murray from the Deniliquin district, may be given as an example.
In the Stanhope, Girgarre, Tongala, Bawmawn Extension and Echuca irrigation area, approximately 60 properties have had clinical cases over the last 10 years and probably 85% of the properties harbour the disease (personal communication). As the organism is excreted with the faeces, officers in these areas consider that spread is via the drainage channels with clinical cases occurring on mismanaged properties. Stress factors play an important part in the manifestation of clinical cases and these can be calving, malnutrition, or transportation, the effects of which are all accentuated on mis-managed properties.
The disease in these areas is insidious with few deaths but with a heavy financial loss due to destruction of clinical cases, (for which Compensation is payable) and a big drop in milk production in sub-clinical cases.
A few of the salient points might be cited to refresh the memories of those who have not yet come in contact with the disease.
1). The incubation period in natural infections varies from 12 months to three years and even up to seven years and the disease is most commonly seen in cows between two and three years, usually after calving.
2). Carriers can occur in a herd which show no clinical symptoms but have extensive lesions on post-mortem.
3). It affects both beef and dairy cattle.
4). Diagnosis is not easy; The Johnin test is unreliable in clinical cases, whilst the C.F. test is only reliable in advanced cases (80-85%). Smears from rectal scrapings in well advanced cases will show clumps of the typical acid-fast M. paratuberculosis bacilli but the animals need not necessarily be showing clinical symptoms even though the infection must be down as far as the mucous membrane of the rectum.
However, V.R.I. has indicated that of 100 bowel specimens submitted for confirmation of Johne's Disease and found negative on direct smear examination, 22 were found positive and four suggestive of the disease on histology. Only 10 of the 22 were also positive to C.F. test.
It is now considered that faecal cultures may be the best diagnostic tool but they have to be cultured for from 2 - 9 months before a result can be obtained. The use of this method is limited by capacity of the Laboratory to handle the specimens and the time factor involved.
5). It is surprising how small the macroscopic lesions of Johne's Disease may be in clinical cases or even in cases dying of the disease.
6). Text books state that in clinical cases, temperatures are not raised and animals do not lose their appetite. Where the clinical symptoms have been of short duration before death, say up to a week, a marked rise in temperature (106°F) and anorexia, have both been noted in cattle in this area (histologically confirmed).
On the incidence of the disease, the history of one outbreak in a Shorthorn Stud in New South Wales makes interesting reading. In 1973, C.D.A.H. Victoria reported that V.R.I. had confirmed the presence of Johne's Disease in a bull, 3-4 years old, purchased from above stud some two years ago (previously — ed.). The records showed a similar case had occurred in 1972 from the same stud. Cattle in the stud are tested regularly for tuberculosis and there have been no T.B. positives and the order also reports no history of scouring in his cattle. On trace back, dam of the first bull was negative to C.F. test and negative on rectal scrapings. The dam of the second bull was slaughtered due to an injured back and consequently no history was available. During routine testing last year at an A.I. centre in Victoria, another bull from the same stud gave a positive C.F. test and the owner was requested to remove the bull. This bull had shown no clinical symptoms, but as the owner did not wish to return the bull to his stud, it was consigned for slaughter.
The post-mortem report from the Meat Inspector at the abattoir showed N.V.L. for Johne's Disease and the bull was in excellent condition. The specimen advice report from the D.V.O. who collected the specimens stated that Lymph nodes were normal, ileocaecal valve cherry red and swollen. Small and large intestines patchy reddening with nodules and very, wrinkled.
The D.V.R. reported C.F. test negative.
Bacteriology ileocaecal valve grossly thickened and one portion almost pedunculated red with focal yellow areas - possible ulceration. Intestines markedly involved, excess folds, thickened areas of almost tumour-like formation from mucosa (all red and thickened). Smears masses of acid-fast organisms consistent with M. paratuberculosis.
Gross appearance and spears consistent with a long standing case of Johne's Disease.
During January 1974, another bull on holding, 3-5 years old, tucked up, would not eat, died in one week: mortality not investigated.
Also, a cow showed high temperature, 106°F, profuse diarrhoea, anorexia, with death in 2-5 days. P.M. haemorrhagic enteritis of the caecum around ileocaecal valve, fibrotic liver. These were the only abnormalities found on post-mortem. Provisional diagnosis of liver insufficiency due to heliotrope (P.F.)
Diagnosis.
Johne's Disease on histopathology with massive number of acid-fast organisms present within the macrophages. (D.V.R).
As a result of the above history, the owner wishes to identify any sub-clinically affected animals in the herd and to attempt eradication. Faecal and blood samples are being taken from all animals for culture and C.F. test respectively. The samples from the cows have been taken, where possible, soon after calving when stress factors are liable to lead to increased numbers of organisms present. To date only two out of 160 samples have been C.F. positive. This was a cow which was immediately isolated on short feed: it commenced to scour and died in a few days. Unfortunately, a post-mortem examination was not carried out. This cow was not closely related to any of the known positive cases and on the basis of the C.P. tests to date, none of the dams, grand-dams of any of the positive cases or the other progeny of these dams and grand-dams have been positive. The results of faecal culture may alter this picture but to date there is no evidence of vertical transmission of this disease on the holding. In another stud, a M.G. cow (2 years) and calf were purchased in February, 1974 from a Victoria stud for $3000. It commenced to scour on arrival. It was treated empirically by a Veterinary practitioner and showed some improvement. As precautionary measure, he took a blood sample which was C.F. positive for Johne's Disease. The cow and calf were isolated, the scouring cleaned up and she was re-joined. As the cow approached her next calving, both cow and calf were re-bled, rectal smears and faecal samples were obtained.
The cow was still C.F. positive with smears positive for M. paratuberculosis whilst the calf remained C.F. negative. Both were thriving and had shown no clinical evidence of Johne's for ten months. As calving approached, the cow did show some scouring, but calved normally. The new calf was removed at birth and the cow consigned for slaughter as a control measure. On post-mortem at the abattoirs, she was classified Johne's Disease positive and this was confirmed at Wagga Wagga Veterinary Laboratory, with lesions in the ileum, caecum and colon. In the Victorian stud of origin there was no evidence of infection in the records of the Victorian Department of Agriculture and no C.F. positive reactors were found on trace back.
Control
As it appears to be accepted that the majority of animals become infected during the first few months of life, it is a recommendation in the irrigation dairy areas of Victoria, that owners introduce their replacement stock as adults from clean areas instead of breeding their own replacements within the infected herds.
On dairy farms, calves are usually run in small paddocks in close proximity to the milking shed and these paddocks are also frequently used as hospital paddocks, thereby becoming grossly contaminated.
In N.S.W. Circular 68/18 indicates that all holdings on which clinical cases are running shall be quarantined by the use of Form 8; in this regard accurate diagnosis certainly presents a problem. No surveillance is required after disposal of clinical cases and presumably no action in regard to cattle showing positive on C.F. test rectal smear or faecal culture. With head office approval, a policy of selective slaughter will be instituted where applicable.
Personally, I think this disease will become more important in our irrigation districts and a review of current policy on control measures, will need to be instituted. Further research is required on means of eradication, particularly from the various studs which appear to be the reservoir of infection and the source of spread of the disease. Vaccination may prove of considerable value in endemic areas.