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This article was published in 1979
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Interesting Case Reports
P.J. Ahrens, B.V.Sc., Veterinary Inspector, Molong
Observations on Ovine Balanitis and Vulvitis
INTRODUCTION
As a result of my involvement with the Canowindra outbreak of balanoposthitis described by G.V. Nash (1978) in which vulvitis appeared to be incriminated, I approached the owner of a Merino flock at Mandagery where vulvitis had been a perennial problem. I asked if examinations of his rams could be undertaken, especially at joining time which in his case was late spring.
Firstly however, closer study of the vulvitis condition would be worthwhile.
VULVITIS
Scab formation on the external labia and especially at the ventral commissure of the vulva was constantly present in a percentage of ewes, even in unmated maidens. At the time of examination in April 1978 at least 75 per cent of the ewes showed evidence of scabs or the scars and deformation of the vulva that result from it. In a small number of sheep the labia appeared to have contracted to leave only a small orifice which must have provided physical difficulties for coitus. Mostly however the ventral commissure was rounded, or contracted, or distorted to one side. The result in a significant percentage of ewes was misdirection of urine to the extent that scalding occurred on the back of the udder or legs. Flystrike was often a problem with these ewes and they had to be culled. Occasional treatment of other affected ewes with Hibitane udder wash had been carried out since my initial visit to this property in 1975.
The vulva scabs were usually soft and light to dark brown in colour, and could often easily be detached revealing normal white skin overlying swollen or rounded labia.
Bacteriology on some recovered scabs carried out at Glenfield revealed Corynebacterium renale type I together with some streps and staphs. This is the organism normally associated with vulvitis in ewes.
POSTHITIS IN WETHERS
To compare this finding with the bacteriology results for wethers on the property, a collection of scabs and swabs from posthitis cases were submitted to Glenfield a few weeks later. About 50 per cent of the wethers were affected with external scab formation around the preputial opening.
No internal ulceration was present at the time but severe posthitis was a problem on this property in good seasons and regular testosterone implantation was employed.
The laboratory reports lists Corynebacterium renale type II against most of the swabs and scab samples obtained but one of the swabs had both type I and type II present. Type II is consistent with ovine posthitis as described by Southcott.
BALANITIS
Initial examination of the rams' penises in April did not reveal any balanitis. There were only 2 Border Leicester rams kept and in one of these I could perhaps imagine a very slight scar on the galea glandis. Joining took place on 6.11.1978. Luckily (or unluckily) the owner had purchased 5 new young Border Leicester rams from Trundle and put these with the 2 older rams for mating a draft of Merinos for crossbred lambs.
At 14 days after the commencement of joining I examined all the rams. None of the Merino rams on the property showed any lesions. The two older Border Leicester rams were healthy. But one of the new rams showed a typical balanitis lesion on the shaft of the penis. I recommended Hibitane wash and sexual rest for this ram, and re-examined the group a week later. The affected ram appeared to be completely healed, but 3 out of the 4 remaining new rams were now affected, one severely. A further examination of the five new rams was carried out three weeks later. By this time the severely affected ram had been 'cured' (with Hibitane washes locally and sulphonamide parenterally) and put back with the ewes for one week. Actually the cure was not complete as two small 1 and 2 mm deep erosions were still present behind the galea glandis at the time of re-joining him. A dramatic remission occurred in this ram, the penis was again severely swollen and haemorrhagic and the ram was obviously in pain. Surface necrosis was again evident on the glans.
The four other rams were all healthy, including the one which had shown no balanitis at any stage.
Laboratory examination of swabs submitted to Glenfield from this last examination showed a moderate pure growth of Corynebacterium pyogenes in the affected ram but only normal flora in the sheath of the healthy and recovered rams.
CONCLUSIONS
Much more work is required on this disease. I do not think there is any great bacterial relationship between the vulvitis described above and the posthitis cases, but perhaps the scabs on the ewes provide a physical agent to abrade the mucosa of the penis. As pointed out by Damens (1968) C. pyogenes could be an opportunist invader of mucosal surfaces which have been traumatised or otherwise devitalised. Vigour of the rams certainly seems to be a factor.
A more thorough examination of the ewes at mating time would have been worthwhile. In the Canowindra outbreak C. pyogenes was isolated in heavy growth from certain severe cases of vulvitis.
REFERENCES
Eamens, G.J. (1978) N.S.W. A.V.A. Veterinary Proceedings, p25
Nash, G.V. (1978) N.S.W. A.V.A. Veterinary Proceedings, p.23.
An Outbreak of Mucosal Disease
INTRODUCTION
I would like to describe briefly the features of an outbreak of Mucosal Disease on a property at Molong. The outbreak, apart from one or two little variations could probably be described as a fairly normal outbreak of Mucosal disease. Four animals died over a period of 18 months but as you will see, the severity of the disease increased with each one. Finally as an experiment, a blood test was carried out on the whole herd to determine the source of infection if possible and a fifth animal was found negative to serology but positive for virus. This last animal was a symptomless carrier. The family relationships of these animals were unknown.
CASES I & II
Case I was not examined, so probably I should not include it as negative to serology and positive for virus. However the owner described it as identical to Case II which I examined in February 1977. My specimen advice notes say it was a 10 month old steer, emaciated, dehydrated, diarrheic and ataxic. The 'ataxia' was probably due to weakness plus interdigital erosion in all four feet. The eyelids were encrusted, the eyes themselves sunken and the temperature was 40°. On my advice the owner destroyed the animal. The laboratory report on my blood sample stated virus isolation positive and gel diffusion test on body negative.
CASE III
In October 1977, some 8 months later, a case was presented, this time at a much earlier stage of the disease. It died 3 weeks later. It was still in good condition when first seen, and exhibited two unusual features: one was blindness which is not a symptom mentioned in any references on mucosal disease. There was a slight keratitis, more on one side than the other but not enough to cause blindness. Both pupils were fully dilated. The second unusual feature but not unlikely as a mucosal disease manifestation, was an extensive scattering of skin plaques. These were about ½ - 1 cm in size and were distributed on the sides of the body and particularly the neck. They were dry, crumbly, raised scabs which could be removed only with difficulty, leaving a raw surface. I thought they may have been mycotic dermatitis lesions but at histopathology later on there was no sign of fungal elements or evidence of mycotic dermatitis.
Blood (1967) states that dermatitis in mucosal disease is associated with enlargement of the local lymph nodes and this was certainly the case in this animal. At post-mortem examination the prescapular lymph glands for instance were quite large and contained a band of haemorrhage 2 - 3 cm in from the capsule.
At virology examination, the prescapular nodes and popliteal nodes were pooled and found to be positive for virus. Virus was also found in the spleen and blood, despite considerable decomposition that had occurred due to delay between death and post-mortem.
CASE IV
Less than a week later another case occurred. The animal was a 12-15 month old Shorthorn steer in good condition. In fact it had been almost ready for market. Death occurred within 48 hours. If I had doubts about the previous case, this one was even more perplexing. At clinical examination I did not think it was mucosal disease. There was a somewhat glazed look about the eyes, which appeared to be slightly sunken, but the animal was not blind. It was grinding its teeth and obviously in some pain. There was a bilateral ocular serous discharge (tears?). The animal was not lame and there was no diarrhoea. Patches of mycotic dermatitis were observed on the escutcheon. Temperature 39.5 degrees.
Some intranasal ulceration could be seen but the nasal plane was dry and otherwise normal. No ulceration could be found in the mouth.
As in the previous cace I advised the owner to give 4 million units of penicillin intramuscularly. The great cure all! Next day the steer remained chose by the water trough apparently drinking from time to time, but in a very depressed state of mind. It was found dead the next morning is sternal recumbency.
AUTOPSY
The post-mortem picture was one of spectacular haemorrhage and I am only sorry I did not have my camera with me. The heart, for instance, had the most dramatic subepicardial haemorrhage I have ever seen. 50% of the heart was almost black with confluent sheet haemorrhage and the remainder was severely ecchymotic. By contrast there were few subendocardial haemorrhages.
Extensive and severe ecchymotic haemorrhage was notable in the ventral half of the thorax on the lungs and pericardial sac. There were sub-pleural haemorrhages in the dorsal thorax.
Blood extravasation was also common in the inter-muscular connective tissue under the scapulae and along the tracheal groove into the pharyngeal area. Extensive severe petechiation was evident subcutaneously on each side of the neck. Interestingly, no endotracheal haemorrhage was present.
Oral ulceration was limited to 1mm erosions on the soft palate and shallow irregular erosion of the floor of the pharynx and the cervical part of the oesophagus. I did not examine the rumen for erosions. The abomasum presented a most striking pattern of red rings ½ - 3 mm in diameter scattered fairly regularly across the mucosa. The less intense lesions looked like petechiated ringworm. The pyloric part of the abomasal mucosa was devoid of these lesions.
A diphtheritic membrane thickly scattered with old haemorrhages formed a tube within the small intestine. In addition to the extensive mucosal erosion, a heavy line of haemorrhage on the serosal surface accompanied the mesentine attachment of the small intestine for much of its length.
The colon was mostly dry by comparison and the colon contents inspissated.
According to histopathology the erosions and diphtheritic membrane in the small intestine section forwarded to Glenfield were not associated with bacterial or fungal invasion. Scrapings taken from the loop on unpreserved intestine I submitted proved positive for mucosal disease virus and a similar result was obtained for the spleen. Unfortunately my lymph node pool was not so clean and it contaminated the cell cultures used for it at Glenfield.
HERD TEST
In consultation with Ian Littlejohns at Glenfield, blood samples were obtained from the rest of this small herd. All the clinical cases had come from the separate section of the herd which is given the best feed, i.e. the calved cows and fattening steers. Only 18 animals were involved. Two animals were negative on serology, and one - a 12 months old red steer - was positive for mucosal disease virus. This animal remained healthy and was sold for slaughter a few weeks later. There have been no further observations of mucosal disease on the property.
The other antibody negative animal was interesting. It was a one month old bull calf whose dam was strongly antibody positive. The D.V.R. questioned how this could be. Had the calf missed out on colostrum? Upon enquiry the owner remembered that the cow was still suckling its previous calf at the time of birth of the second calf. Unusual as this may be, it is a possible explanation of the lack of passively transferred antibody in the calf. The owner removed the older calf as soon as he discovered the anomaly, but the new calf could well have missed out on its quota of colostrum.
The only other action taken was blood sampling of the remaining cattle on the property. All were antibody positive so no attempt was made to look for virus.
Whether blood sampling of herds suffering losses from mucosal disease is worthwhile remains to be seen. This one was done purely as a matter of interest and so far there has been no recurrence of the disease. This may have been the result anyway without my intervention. And I do not imagine I have prevented further outbreaks of the disease on the property.
The diagnosis of mucosal disease on clinical grounds is often difficult, but because of its similarity to certain exotic diseases, bears close attention. Prof. Blood in a paper delivered at an A.V.A. Conference (1967) stressed that clinical examination is never enough for a definite diagnosis and that laboratory confirmation is always necessary. The resemblance of case No. IV to Ibaraki Disease symptomatology is striking, and perhaps Bluetongue could have been considered too (why not?). Rinderpest could be ruled out because there was no diarrhoea (and this was mucosal disease) while the differential diagnosis from the non-ocular form of Bovine Malignant Catarrh is not clear-cut. (c.f. case III with enlarged lymph nodes and cutaneous lesions). A good collection of tissues for histopathology but kept in reserve could be a useful precaution.
REFERENCES.
Blood, D.C. (1967) 'Field Procedures for the Differential Diagnosis of Mucosal Disease in Cattle', Aust. Vet. J., 43: 501-507
French, E.L. & Snowdon, W.A. (1964). 'Mucosal Disease in Australian Cattle' Aust. Vet. J., 40: 178 - 185
Jubb, K.V.F., and Kennedy, P.C., 2nd Edition (1970) 'Pathology of Domestic Animals', Academic Press, pp. 14-23