We are rather fortunate in this State, in that our experiences with outbreaks of Johnes Disease over the last 25 years justify the assumption that climatic conditions are just not favourable for the spread of the disease in New South Wales. It is probable that our extreme summer temperatures affect the viability of the Johnes bacillus on pastures and so reduce the risk of infection.
Despite the fact that the disease never has been a major problem in New South Wales herds, the long incubation period and the unsatisfactory nature of diagnostic tests ensures that the disease will continue to be introduced periodically from overseas in imported cattle, and in most cases will not be detected until such animals have passed through quarantine on to their respective properties. Consequently it is the field officer rather than the quarantine officer who encounters the disease in the first instance.
Since 1930, only nine (9) confirmed cases of Johnes Disease have been recorded in the State, and of these five were in imported bulls. Despite the fact that these infected animals were scouring profusely for varying periods prior to death, with resultant heavy contamination of the pastures with the causal organism, in only three properties has there been any known spread of the disease. On two of the three properties, infection has spread to a single animal only; while on the third property it has affected two other cattle.
In view of the small number of cases, it will be of interest to summarise them briefly as follows:
Case 1. 1930. Holbrook. 6-year-old Shorthorn bull; imported 1928. Failed to thrive for 9 months and scoured profusely for one week prior to death on 2/11/30.
Case 2. 1936. Richmond. Jersey Bull; imported 1932. Persistent diarrhoea for three months prior to destruction on 11/6/36. Diagnosed ante-mortem by rectal smears. One cow subsequently reacted to Johnin test, but was negative at autopsy.
Case 3. 1937. Mullumbimby. 8-year-old Jersey cow bred on the property. Unthrifty for 2½ years prior to death on 29/7/37. Source of infection not traced, but probably from an imported bull introduced on to the property some years previously.
Case 4. 1946. Bombala. Jersey bull; imported 1938. Scoured intermittently for 2 years prior to destruction on 31/1/46. Johnin test slightly suspicious. Two cows and another bull subsequently reacted to Johnin test, but all three were negative at autopsy.
Case 5. 1948. Lismore. Guernsey bull; imported 1947. Scoured profusely for 12 days prior to death on 14/12/48.
Case 6. 1949. Moss Vale A. Imported Guernsey bull scoured for eight months prior to destruction on 20/9/49. Ante-mortem rectal scrapings on three occasions and Johnin test negative. Herd of 144 subsequently Johnin tested with 12 reactors. Two of these reactors were destroyed, but both were negative at autopsy.
Case 7. 1951. Moss Vale Property B. Cow ex Bombala property born 8/9/45; purchased 1947. Never a good doer and scoured profusely for three weeks prior to destruction on 4/6/51.
Case 8. 1953. Moss Vale Property A. 3-year-old Guernsey cow sired by Case 6. Died 20/1/53 after scouring profusely for a few weeks. Ante-mortem rectal scrapings positive. Lesions not obvious macroscopically.
Case 9. 1953. Macksville. 9-vear-old Jersey bull purchased from the Bombala property on 4/9/45 (when 19 months old); and actually 5 months prior to diagnosis of Johnes Disease at Bombala. Lost condition for last six months following injuries and scoured profusely for three weeks before destruction on 5/5/53. Lesions not obvious macroscopically.
Some interesting information is available from the brief details mentioned above.
1. The incubation period of the seven cases on which the information is available has varied from not less than one year to 7½ years.
2. Some of the animals were unthrifty or failed to thrive normally for periods up to 4 years, but in most instances profuse scouring was only in evidence for a few weeks prior to death.
3. The Johnes bacillus was demonstrated in smears made from the rectal mucosa ante-mortem in two of three beasts, but in the third animal smears were negative on three occasions.
4. The Johnin test has proved most unreliable as a diagnostic agent on a limited number of animals. Of two clinically affected animals, one was negative and the other gave only a slightly suspicious reaction. In addition to the false positives mentioned already on a number of the properties, at least four imported animals which have reacted to the Johnin test at the Quarantine Station, have shown no evidence of infection at autopsy.
5. The severity of lesions at autopsy varied considerably, and in three of the cases macroscopic lesions were not obvious.
6. In view of the restricted nature of the lesions which can occur, post-mortem specimens for laboratory examination should include the entire gastro-intestinal tract, from midway through the small intestine to the rectum, and associated lymph glands; with smears and section material from appropriate sites of the tract. Ante-mortem specimens should include a number of smears of rectal mucosa, a faecal sample and unpreserved serum sample. Preliminary serological work using the complement fixation test is being carried out in Melbourne with promising results.