ARCHIVE FILE
This article was published in 1980
See the original document
Johnes Disease of Cattle in Southern Irrigation Districts
D.D. Salmon, B.V.Sc., Veterinary Inspector, Deniliquin
Introduction
Johnes Disease or Paratuberculosis is an infectious disease caused by Mycobacterium johnei or M. paratuberculosis. It is almost exclusively a disease of ruminants, but M. johnei has, rarely, been recovered from the mesenteric lymph nodes of horses and pigs.
The clinical picture in Johnes Disease (JD) is described by Blood, Henderson and Radostits (1979) and Jubb and Kennedy (1970) as profuse, odourless, fluid diarrhoea. Clinically affected animals are usually two years or older, and remain alert through the course of the disease. The appetite remains normal until the terminal stages, but emaciation is marked and progressive. In sheep and goats the disease is more a chronic wasting disease with little or no diarrhoea. The course varies but is usually prolonged leading to remarkable emaciation necessitating destruction.
Post-mortem findings are described as being related to severe emaciation with gross pathology confined to the intestine and associated lymph nodes. The mesenteric Lymph nodes are enlarged - sometimes remarkably so, with little corticomedullary distinction and some oedema. There is lymphangitis which is described as being constant. The intestinal change is a diffuse hypertrophy, which may extend from the duodenum to the rectum. This hypertrophy may be minimal, or the mucosa may be many times thicker than normal, and thrown into thick transverse folds which cannot be stretched out. The surface of these rugae may be reddened giving a 'zebra gut' appearance. These changes are usually seen best in the ileum, caecum and upper colon, and the ileocaecal valve is usually involved, although Jubb and Kennedy 'de-emphasise' the significance of this change.
Transmission is by ingestion of food or water contaminated by the faeces of infected animals. Calves are more easily infected than adult cattle. Intrauterine infection has also been reported, and may be more common than generally realised. Vertical transmission (i.e. dam to calf) is by far the most common pattern of spread, although lateral transmission also occurs. There is a long incubation period, so that clinically affected animals are usually more than two years old.
The bacterium M. johnei is very slow growing in all culture media and quite difficult to grow successfully,
Diagnosis of Johnes Disease is difficult. Culture is slow and unreliable, examination of faeces is not reliable due to the large numbers of other mycobacteria in faeces, rectal scrapings are only positive in longstanding clinical cases. The intradermal johnin test is unreliable, and the serological tests are also unreliable.
Case History
JD was diagnosed on a property in the Berriquin Irrigation District. The property had an area of 800 acres in a 16½" rainfall area, supplemented by 440 acre feet of irrigation water. The owners ran a 100 breeding cow Shorthorn stud with some cereals and fat lambs. The cattle were run in groups in small irrigated paddocks, and the group composition was changed regularly as cows calved, were joined or weaned.
The stud was founded in 1960 from a stud in Victoria, but additions had come from many sources and a certain amount of interchange was maintained with the parent stud - usually bulls. A cow imported into the parent stud in the 1950's had developed JD and had been slaughtered with its progeny - there was no further evidence of JD in either mob.
In 1973 the Chief, Division of Animal Health, Victorian Department of Agriculture reported that two bulls sold from the property to Victorian owners had been confirmed as infected with JD in 1972/73. Investigations at the time indicated that no clinical evidence of JD had been seen on the property.
Early in 1974, two cows died, they showed elevated temperatures, anorexia, profuse diarrhoea and death within four to five days of onset. Post-mortem examination showed haemorrhagic enteritis of the ileocaecal valve region. Histopathology confirmed JD. At about the same time, a bull was returned from a Victorian A.I. centre following positive serology. The bull was slaughtered and JD confirmed.
Investigations and results
Eradication of Johnes Disease was undertaken.
Faecal samples from all the breeding animals were cultured for M. johnei, and at the same time blood samples were subjected to the Compliment Fixation Test (CFT) for JD. A total of 201 animals were tested.
There was one cow with a positive culture - reported as 'profuse positive' but even so the growth took four months to appear, and another two months to positively identify. This cow also showed a CFT reaction of 40. After a period, during which the owner reported that she looked 'off', she began scouring and died a few days later - this was before her faecal culture had shown positive.
No other faecal culture was positive.
As well as the cow above, eleven others showed CFT reactions.
- 2 cows CFT 40
- 3 cows CFT 20
- 6 cows CFT 10
Of these, three (1 cow CFT 40, 2 cows CFT 20) were slaughtered, along with three calves from infected cows. The three calves (2 of them had a CFT reaction of 40 and one had CFT 10) which had been CFT and culture negative seven months earlier showed post-mortem signs and were confirmed JD. histopathologically. The CFT positive cows had suspicious post-mortems, but could not be confirmed. Of the remaining nine cows with CFT reactions, two showed reactions on a subsequent test, but were later negative. None of the others had any further reactions.
The whole herd was then sampled for CFT's. Out of 168, 1 COW was CFT - 40 (A) and 1 cow CFT 40 (B). Faeces taken from cow A at the same time showed M. johnei after 12 months culture. Her CFT titre remained 40, although subsequent cultures were negative. She had been unthrifty for some nine months prior to the positive faecal sample being taken, she eventually died three months later - scouring only in the last few hours before death. post-mortem showed dramatic thickening, ridging and reddening of the entire intestinal tract. Again death had occurred before the culture had shown M. johnei. Cow B showed repeated CFT 40 and [?] 40, and eventually died with a massive enteritis - histopathology and culture were negative for JD, but the calf following her from the same cow had been confirmed, so that it is probable that he was infected.
To increase the chance of successful diagnosis on culture, all cows were sampled soon after calving - both faeces and blood. Over a two year period 144 individual faecal samples were cultured. One (cow A, above) was positive.
During the same period 130 sera were subjected to the CFT with the results:
9 samples CFT 10
3 samples CFT 20
5 samples CFT 40
5 samples CFT ≥ 40
The five samples CFT ≥ 40 were all from cows A and B above.
Of the five cows with CFT 40, one died and was confirmed JD infected, the others had subsequent negative CFT's.
One cow with CFT 40 became unthrifty, was destroyed and confirmed infected - it was CFT negative at the time of slaughter.
One cow with CFT 4O had a calf with CFT 10, but no evidence of infection was seen. One cow with CFT 10 had a daughter and grand-daughter with CFT's 10, but there was no evidence of infection.
All calves from infected cows were slaughtered where possible, and in all cases showed signs of JD, although it was not always confirmed.
A total of seven cows died during this time which were probably affected by JD, and one more was destroyed in extremis. No post-mortem examination was performed on two, the other six had changes consistent with JD, although two could not be confirmed on histopathology. A further nine clinically normal cattle were slaughtered, all showed changes consistent with JD, but only four were confirmed.
Of these animals, two which died and two which were slaughtered as progeny of infected cows were not tested previously in any way. Ten were either offspring or maternal siblings of infected animals.
Of the thirteen animals probably infected with JD on which CFT's had been performed, only two had never shown a reaction, seven had CFT's of 40 at some stage and six had shown reactions on more than one occasion.
Discussion
On this property Johnes Disease departed from what is described as the normal clinical picture of eight clinical cases which were either confirmed, or almost certainly Johnes Disease, not one showed chronic diarrhoea. Two showed chronic illthrift for periods of 4-12 months with terminal diarrhoea. This is consistent with the disease described in sheep, but very uncommon in cattle. The other clinically affected animals were apparently normal prior to an acute enteritis with sudden death - a syndrome which is apparently not common.
The post-mortem signs in this group of animals also differed from the more common signs described. The classical picture of intestinal thickening was seen in some cases, but in others there were acute haemorrhagic and catarrhal enteridites. The early stage of JD seen in some clinically normal animals was a patchy enteritis, with reddening of the ileocaecal valve. Ridging of the ileum and colon, with reddening of the crests of these rugae was also fairly consistent.
Histopathology of some infected cows showed from the classical hyperplasia of the mucosa and infiltration of the submucosa by epithelioid cells with large numbers of eosinophils; all epithelioid cells and macrophages being loaded with acid fast organisms. In some cases there was a lack of eosinophils or a lack of acid fast organisms with all other features being present. There were also a few cases where histopathology was not specific; but only one case where no signs of JD were present. In this cow, which was almost certainly a clinical case of Johnes Disease, there was a massive haemorrhagic enteritis and autolysis which may have obscured the changes.
Diagnosis of Johnes Disease has always been recognised as a problem. In this case faecal culture - even immediately post calving when the stress could be expected to increase the shedding of M. johnei - was completely useless as a diagnostic tool. M. johnei was detected in the faeces of only two cows, both of which died before the culture could be classed as positive. One of these cows also had two faecal samples negative on culture. The fact that sections of intestine from nine out of seventeen animals examined had no acid fast organisms visible underline the low numbers of M. johnei which may be present in infected animals. Faecal culture is also a difficult and time consuming procedure, in this case 345 individual faecal samples were cultured for periods of nine months or more, yet made no contribution to the control of JD. In six confirmed infected cows, nine cultures were negative and two positive and in six probably infected cows, twelve negative cultures were obtained.
The Complement Fixation Test appeared to be much more reliable. In 499 tests there were 25 positive reactions in which the animal involved was not suspected to be infected, and eleven negative reactions where the animal was probably infected. This 5% false positive reactions is not unreasonable in view of the fact that there was exposure of the mob to M. johnei. The level and repeatability of the reaction appears to be relevant only three out of eleven animals which reacted and were probably or definitely infected had a subsequent negative test. Only two uninfected animals had more than one test positive, and they eventually went negative.
Histopathology can give good diagnosis of JD, but it is not completely reliable. In the absence of intracellular acid fast organisms and significant infiltration of epithelioid cells into the submucosa JD cannot be definitely confirmed.
Given the difficulty of diagnosis, eradication of JD from a property is correspondingly difficult. The property under investigation has now had no disease resembling JD for two years. This apparent eradication was achieved by culling all infected cows and their progeny. Infection was diagnosed post-mortem in every case, so the procedure actually was the removal of the progeny of cows which had died from JD. The completeness of such eradication must be questionable.
The CFT probably has more merit than is generally recognised, It would be a good herd test to select animals for closer consideration. The closer consideration involved could be repeated blood testing, rectal scrapings or biopsy of the terminal ileum and ileocaecal lymph node. This latter technique is reported by Julian (1975) as being in use in Canada with some success. Even with biopsy the diagnosis would not be clear cut, and it would be necessary to err on the side of severity for maximum benefit.
Because of the long incubation period, symptomless carriers and unreliable diagnostic tests, it is difficult, or even impossible to eliminate Johnes Disease from a herd, and the same factors make it even more difficult to know if this has been achieved.
References
Blood, D.C., Henderson, J.A., & Radostits, O.M.; (1979) Veterinary Medicine, 5th Edition, 535-5401
Jubb, K.V.F. & Kennedy, P.C. (1970) - Pathology of Domestic Animals, 2nd Edition, Volume 2, 135-140
Julian, R.J. (1975) - Can. Vet. Jour. 16: 33-43