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This article was published in 1983
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A Vesicular Type Disease in Cattle

K.G. Hart, B.V.Sc., Veterinary Inspector, BRAIDWOOD

INTRODUCTION

I considered the following case history worthy of mention because of its vesicular disease similarities.

The problem was first reported in early April, 1982 on Easter Friday. The first case was seen by the owner on Wednesday, 7/4/82 and by Friday, 9/4/82 there were eighteen cases. The major problem was confined to one mixed mob of sixty Murray Grey and sixty Angus Cows. The owner had been checking his cattle every three days.

Clinical signs described by the owner from paddock observations were:

  1. Rapidity of spread
  2. Bilateral nagal discharge
  3. Skin lifting off nose and some noses very red
  4. Some animals exhibiting difficult breathing
  5. Cows were lethargic, anorexic and not drinking
  6. No excessive salivation or lameness
  7. No scouring
  8. No mortalities

I had never seen the respiratory form of Infectious Bovine Rhinotracheitis (IBR) during eight years in the Braidwood district, but the owner's description was highly suggestive of it. A provisional phone diagnosis of IBR was made, and I recommended:

a. Injection of cows showing serious respiratory symptoms with long-acting penicillin (which the owner had on hand)

b. Contact me the next day if the morbidity rate continued to increase

There was no further contact until the following Tuesday, when the owner was no longer alarmed, reporting no losses, no new cases and the clinical cases slowly recovering. On Thursday, 14th April, I visited the property to examine the worst clinical cases which had been mustered for my inspection.

HISTORY

The property of 1,500 acres is situated at Araluen, a valley at the headwaters of the Moruya River with a semi-coastal climate. The area had just had a drought declaration lifted. Pastures comprised mainly couch, phalaris and clover. A short green cattle pick was available which had been stimulated by useful March rains. The weather throughout the outbreak was mild, warm and dry.

CATTLE

The cattle on the property were in quite reasonable condition, but still suffering from residual drought stress. There were three hundred and forty cows of all ages, joined to calve late winter - early spring. The cattle were divided into four paddock mobs:

a. Sixty Angus and sixty Murray Grey cows

b. Three mobs of Hereford cows

OBSERVED MORBIDITY: (number with observable symptoms in paddock)

By breed:

Angus 0%
Murray Grey 30% (18 ex 60)
Hereford 1% (3 ex 220)

No particular age incidence was obvious.

CLINICAL SIGNS

I examined the cattle at least six days after they had first exhibited symptoms.

a. The Angus/Murray Grey mob were examined in their paddock. Only three animals with any clinical signs could be observed. These cow showed a light, bilateral mucoid nasal discharge with scabs lifting from the nose. Many of the cows in this group mentioned by the owner as showing symptoms appeared to have already recovered.

b. The five worst cases (Four Murray Greys and one old Hereford cow) were yarded for examination.

The following findings were observed in these cattle:

  1. (1) Variable sized, red raw ulcerations on external and internal nares.
  2. Bilateral, mucoid nasal discharge.
  3. Two ex five had elevated temperatures (above 39.3°C).
  4. No excessive salivation.
  5. No lameness or evidence of foot lesions.
  6. Very little eye involvement (mild conjunctivitis only, not necessarily causing discharge).
  7. One cow (the Hereford) showed marked dyspnoea.
  8. Localised dermatitis with hair loss and skin scurfiness on ears, neck and back on two cows.
  9. Swishing of the tail appeared unusually frequent, suggesting some irritation (also observed by the owner in the paddock).
  10. One cow (the Hereford) showed marked dyspnoea.
  11. No gross lesions on vulva/vagina of any cow and no vagina discharge.
  12. One cow (the Hereford) showed marked dyspnoea.
  13. Mouth examination:
    Two ex five cows exhibited large ulcers on the ventral surface of the tongue, about 5cms long by 1cm wide with smaller ulcerations on the tip of the tongue. There were no ulcerations on the buccal surface of the lips or gums in any of the five cows examined. The ulcerations were dull red in colour, with some evidence of healing at the edges. No vesicles were seen, but the ulcers bore a resemblance to ruptured foot and Mouth Disease vesicles.

    This finding forced a reappraisal of the whole disease problem, and I rang the Regional Director of Veterinary Services, Orange (Ralph Bonner) from the property to discuss a course of action.

    It was brought to my attention that Rogers et al. (1978) in the - Australian Veterinary Journal had described a serious IBR problem in Queensland cattle, with ulceration of the buccal mucosa, tongue and gums in many clinically affected animals. On the basis of this revelation, coupled with the history, epidemiology and other clinical findings, it was decided that the possibility of this disease outbreak being caused by a vesicular disease was extremely remote, and the property was merely to be kept under surveillance.

    Treatment of the five worst cases with long-acting penicillin produced a marked response, particularly in alleviating respiratory distress. Antibiotic therapy is advised in serious cases of IBR due to a problem with secondary bacterial respiratory infections often associated with the disease. Complete recovery in the worst cases took three to four weeks from the initial appearance of symptoms. Symptoms took only a few days to disappear in those animals that were initially only mildly affected.

    LABORATORY FINDINGS

    Paired sera were taken twenty-one days apart, with the first sampling six to seven days after the appearance of clinical signs. Unfortunately, I wasn't equipped with specific transport medium for IBR virus at the time, and no attempt was made to collect material for virus isolation.

    The sera were tested for both Mucosal Disease and IBR. Two out of five sera were negative for Mucosal Disease and the others had static or falling titres. Paired IBR serum neutralisation titres were negative in three out of five animals, while one showed a significant rise in titre over twenty-one days and another was static at a high level. A sixth clinical case that was only mustered for the second bleed showed a low Mucosal Disease titre and a high serum neutralisation titre for IBR.

    DISCUSSION

    The most important aspect of this disease investigation was the exclusion of the possibility of a vesicular disease as the cause. This was done on the basis of history, clinical signs and epidemiology.

    The main features of this differentiation were:

    1. Relatively limited spread throughout the hard - especially the lack of clinical signs observed in the Angus cattle which were in close contact with the Murray Greys.
    2. Sudden cessation of spread. Absence of mouth vesicles in all animals examined - tongue ulcers in only two out of five cows.
    3. Absence of lameness or any foot involvement.
    4. Relatively rapid recovery of most affected cows.
    5. The relative isolation of this herd and its lack of contact with other stock capable of carrying vesicular disease also received some consideration.

    If it wasn't a vesicular disease, then what was the cause of the outbreak?

    The possibility of a plant origin for the disease was considered and rejected - the epidemiology of the outbreak, its sudden appearance, disappearance and lack of recurrence in animals grazing the same pastures did not suggest a plant aetiology, nor were the clinical signs very similar to cases of bovine photosensitisation I had previously seen in the Braidwood district.

    The disease had many features of a viral entity. As previously mentioned, I had already made a tentative diagnosis of IBR (Bovine herpes virus type 1) before finding the tongue erosions which widened the diagnostic possibilities. Mucosal Disease was considered and rejected, since the history, epidemiology and clinical signs did not appear to fully support a diagnosis of Mucosal Disease (although there were some similarities). In retrospect, I still suspect IBR as the cause of this outbreak. IBR virus is widespread in N.S.W., but disease is uncommon (Littlejohns, 1979).

    IBR has been shown to be responsible for a wide range of clinical syndromes which include:

    a. The most familiar respiratory and pustular vulvovaginitis forms

    b. Encephalitis

    c. Balanoposthitis

    d. Conjunctivitis

    e. (Overseas) Abortion and occasional cases of gastrointestinal disease.

    The association of tongue lesions with IBR infection is rare.

    Serology performed on the clinical cases showed definite evidence of past infection with IBR in three of six animals examined. Serology is not particularly satisfactory in the diagnosis of IBR, since the development of neutralising antibody can be slow and reach only low titres. In retrospect, I would have been better off attempting virus isolation from the clinicals. Although I wasn't equipped for this on the first visit, virus excretion can occur for long periods of time with IBR infection and it may have been possible to isolate virus even on the second visit in early May. Phosphate buffered gelatine saline is preferred for the transport of swabs for the confirmation of IBR, but boiled water can also be adequate as transport medium if saline is unavailable. (Little johns, 1979).

    The selective morbidity of the Murray Grey cows in the Murray Grey/Angus mob was interesting. This was possibly due to the fact that they were the remnants of a Murray Grey stud in the Braidwood area which had been a closed herd for some years with no boundary contact with other cattle. In contrast, the Angus and Hereford cows were all introductions from the Southern Tablelands area. It is reasonable to assume that the Murray Greys had not been exposed to the ubiquitous Bovine Herpes virus Type 1 and had not had the opportunity to acquire immunity to the virus. If this was the case, the Murray Greys would have constituted a susceptible group within the herd which would explain the rather strange morbidity pattern.

    Immunity following IBR infection is long-lasting, but the carrier situation is also common - recrudescence of clinical infection can sometimes occur due to stress. I suspect this to be the reason for the initiation of the outbreak, with the aged Hereford cow as the most likely candidate for the carrier animal.

    SUMMARY

    An outbreak of suspected viral disease in cattle was investigated during April, 1982. The disease bore some similarity to a vesicular disease, with marked rapidity of onset and tongue ulcerations found in two animals.

    Vesicular disease was excluded on the basis of other clinical findings, history and epidemiology. The cause of the outbreak was not conclusively demonstrated, but evidence suggests that the disease was caused by IBR virus (Bovine Herpes virus Type 1).

    It was noted that tongue and mouth ulcerations had been documented by Rogers et al. (1978) in an IBR outbreak in Southern Queensland.

    REFERENCES

    Beveridge, W.I.B. (1981) - Animal Health in Australia, Vol. 1 Viral Diseases of Farm Livestock (Australian Government Publishing Service) pp 25-29

    Jubb, K.V.F. & Kennedy, P.C. (1970) - Pathology of Domestic Animals, V.1, pp 164-166

    Little johns, I.R. (1979) - University of Sydney Post-Graduate Committee in Veterinary Science. Proceedings No. 42 - Cattle Diseases, pp 456-547

    Rogers, R.J. et al. (1978) Australian Veterinary Journal 54:562

    St. George, T.D. 1982 - University of Sydney Post-Graduate Committee in Veterinary Science. Proceedings No. 60 - Advances in Veterinary Virology. pp 104-109

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