ARCHIVE FILE
This article was published in 1957
See the original document
INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Entero-toxaemia in Calves
D. M. HELWIG, B.V.Sc., Veterinary Research Station, Glenfield
There have been few reported cases of confirmed entero-toxaemia in bovines in Australia. In the sixteen months since January, 1956, the Veterinary Research Station, for example, has received specimens from seven cases in which this disease has been suspected. In three of these the laboratory findings were "strongly suggestive" of the condition, but in only one case was a potent entero-toxin demonstrated.
Many specimens have been received from other cases of calf mortality and not infrequently plant or heavy metal poisoning has been suspected; and just as often examination has produced "inconclusive results". It is felt that, had appropriate specimens been available, an examination for entero-toxaemia in some of these may have yielded more definite findings.
In an attempt to outline this condition as it occurs in calves it has been necessary to lean rather heavily on case reports in overseas literature, mainly British and American; in which countries interest in entero-toxaemia in young ruminants has increased over the postwar years.
Aetiology. It is generally accepted that the absorption of Cl. perfringens (Cl. welchii) type toxin from the bowel is the chief cause of the condition, and so far types A, B, C, D and E have been demonstrated. Griner and Bracken (1953) experimentally reproduced the condition in one out of six experimental calves by feeding cultures of the type C organism.
Type of Animal Affected. As in sheep, it is the well-fed, good conditioned calves which appear most susceptible. McRae and Murray (1943) observed that a mortality in calves occurred on the same property which had experienced losses in sheep over a number of years due to Cl. perfringens, or where sheep had died suddenly and inexplicably. Schofield (1955) noted a higher incidence in bucket-fed calves, and suggested excitement associated with feeding as a possible predisposing factor.
Age. Affected animals fall roughly into two age groups:
(a) Young calves between one and ten days of age; in which the disease is often peracute.
(b) Animals two to three months old; showing the acute and less severe forms.
Symptoms. Although a variety of symptoms has been observed, they fall approximately into three types:
(1) Peracute. Showing sudden death without diarrhoea.
(ii) Acute. Affected calves show dullness and inappetence. There may be signs of abdominal pain, with arching of the back. Respiration may be increased. Scouring (straw, white or black in colour) is an inconstant feature and may or may not be bloodstained. A slight increase in temperature up to 104°F. has been reported in some cases This stage can pass to prostration, subnormal temperature and death, or it may give way to nervous symptoms such as mania, bellowing, grinding of the teeth, jaw champing. A "dummy" syndrome may be exhibited, when the animal shows reluctance to move and when forced to do so wanders aimlessly, bumping into objects as though blind, and stands with the head pressed into corners, against objects,etc. Finally, death ensues, often with convulsions.
The acute type may last from two to twelve hours.
(i) Subacute. In which there is progressive depression with scouring, leading to death in two to three days. Animals which recover from this type, without treatment, take about ten to fourteen days to do so (Hepple (1952).
Post-mortem Findings. In the more acute cases there is usually an acute haemorrhagic enteritis with necrosis and desquamation of the mucous membrane. The intestinal contents may be heavily bloodstained. Less acute cases show congestion and often petechial haemorrhages in the small intestine and abomasum. Similar changes may be seen in the caecum and colon. The bowel may be distended with gas, with the contents varying from mayonnaise-like, brown or bloodstained to normal in nature. Changes in other organs include congestion and haemorrhages on the epicardium, endocardium, kidney, spleen, liver thymus and mesenteric lymph nodes. The lungs may be similarly affected. Excess straw-coloured or bloodstained pericardial, pleural and peritoneal fluid may be present.
In most reported cases of entero-toxaemia, treatment with appropriate antiserum or vaccine has appeared to check the mortality.
Laboratory Examination. The specimens are the same as those required from sheep. i.e. bowel smears, bowel contents (including material from caecum and colon), and urine preserved with thymol.
Laboratary diagnosis at the Veterinary Research Station consists of a routine examination of the bowel smears for large numbers of Cl. perfringens type organism, and the injection of bowel nitrate intravenously into mice (the only ones available at present). The mice are observed for twenty-four hours, when the presence of any entero-toxin is indicated by signincant mouse mortality.
In some cases the amount of bowel nitrate available is either small or of a mucoid consistency, in which case dilution with saline is necessary to facilitate filtration. Thus, dilution of any toxin present is unavoidable and may lead to negative results. Between five and ten mls, of bowel contents would be a reasonable working quantity.
Knowledge of the time elapsing between the death of the animal and the collection of the specimens is of assistance in allowing for the discrepancy between post-mortem proliferation of the organisms in the bowel and the suspected deterioration of the toxin.
Cl. perfringens type B may produce beta or epsilon toxin in the bowel, and since epsilon is the chief toxin of the type D organism, then type D antiserum could neutralise type B or type D entero-toxin. Thus, without a full range of antisera it is not possible to differentiate these two types, and a diagnosis of entero-toxaemia due to type D organism is open to question.
References:
Griner, L. A. and Bracken, F. K. (1953)-Amer. Vet. Med. Ass. J., 122 : 99.
McRae, D. R. and Murray, E. G. (1943)- Vet. Rec. 55 : 203.
Schofield, F. W. (1955)-Amer. Vet. Med. Ass. J., 126 : 192.
Hepple, J. R. (1952).-Vet. Rec., 64 : 633.