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This article was published in 1960
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.

Entero-Toxaemia in Cattle

D. H. MUMFORD, B.V.Sc., Veterinary Inspector, Dubbo

One of the causes of the greatest loss in sheep in the Central Western districts of New South Wales is Entero-toxaemia, or "Pulpy Kidney". Its presence has been recognised for very many years and the accumulated losses from this disease, if they could be computed, would prove to be staggering in their magnitude.

In contrast to our knowledge of these widespread losses in sheep, the disease in cattle had not been recognised here until comparatively recently. Undoubtedly, the fault was ours and it seems certain that Entero-toxaemia in cattle has been present, but we have failed to recognise it; or, because it is rarely seen as an "explosive" outbreak, cases have not been brought to our notice. It is only since cattle have become so valuable that owners have become more inclined to report mortalities.

Possibly, some of the cases passed off as Bloat were, in fact, Entero-toxaemia.

It is only over the past two years that Entero-toxaemia has been diagnosed in cattle in the Dubbo area. During that period the writer has seen nine outbreaks in Dubbo Pastures Protection District; while Veterinary Officer, Orange, has made available records of twelve outbreaks from some of the other Districts under his control; viz, Molong. Bathurst, Mudgee and Coonamble.

PREDISPOSING CONDITIONS AND SEASONAL INCIDENCE.

In most of the outbreaks seen of this disease, the cattle have been running on very good improved pasture containing such species as Sub. clover, White clover. Lucerne, Rye Grass or natural pasture containing a high proportion of Trefoil. Affected cattle running on sparse pastures were being fed usually some form of concentrate. Only in very odd cases were cattle affected when running on dry, bulky pasture which normally would not be suspected as predisposing towards Entero-toxaemia.

Cattle of all ages have been affected and this is surprising in view of overseas reports, in which calves from a few days old up to a maximum of about three months have succumbed. In this area, cattle eight months old and up to and including a good proportion of adults have generally been affected, although outbreaks have been seen in calves

Animals are in good to fat condition and stock showing a rapid improvement in condition seem to be very susceptible. This may indicate merely that the type of feed which will produce rapid growth rates also will predispose the animal to the disease.

From the limited observations so far, there appears to be a well defined seasonal incidence; with losses commencing in late winter building up to a peak in spring (when pastures are at their lushest stage), and then tailing off into summer.

Naturally enough, properties which have experienced losses from Entero-toxaemia in sheep are generally the ones that are troubled with Entero-toxaemia in cattle. In fact, in one outbreak investigated in calves, losses occurred in a paddock where a severe mortality had been experienced the previous year in sheep.

Doubtless, the same pattern is followed as in the case of sheep: with numbers of apparently healthy animals carrying small populations of the casual organism as normal intestinal inhabitants. Whether the "triggering mechanism" is the same for both sheep and cattle is not known, but it appears very likely that it is.

At least some of the outbreaks seen have been associated with over-eating or sudden changes in feed which would fit in with the hypothesis of Bullen et al. (1957) that one of the main activating factors in the production of Entero-toxaemia in sheep was the upset in ruminal microflora; with the sudden change in feed resulting in the passage of undigested food (as starch granules) into the small intestines, producing a medium extremely favourable for the rapid growth of the organism and the production of large quantities of toxin. Similar conditions would be brought about by over-eating; particularly with grains, but also possibly with lucerne and otheri.e.gumes.

CAUSAL ORGANISM.

The causal organism is Clostridium welchii, (Cl. perfringens), and to date Types A and D have been incriminated in New South Wales. In addition, Types B and have been involved in overseas outbreaks, particularly in young calves.

Briefly summarised, the Cl. welchii Types are as follows:—

TYPE A: (Classical Cl. welchii) Causes Gas Gangrene and Entero-toxaemia. Produces Type A toxin. The homologous antitoxin neutralises only Type A toxin.

TYPE B: (Lamb Dysentery Bacillus). Causes Lamb Dysentery and Entero-toxaemia in calves. Produces Type B toxin. The homologous antitoxin neutralises Types A, B, C and D toxins.

TYPE C: (B. paludis). Causes "Struck" in sheep and Entero-toxaemia in calves. Produces Type C toxin. The homologous antitoxin neutralises Types A, B and C toxins.

TYPE D: (B. ovitoxicus). Causes classical Entero-toxaemia in sheep and cattle. Produces Type D toxin. Homologous antitoxin neutralises Types A and D toxins.

Types B and C have not been recognised to date in New South Wales.

SYMPTOMS.

Generally, the number of animals affected at one time is low, and quite often only individual animals are concerned. In adults particularly, odd animals are lost over a period rather than dying in outbreak proportions over a couple of days, as sometimes is seen in sheep.

The disease is mostly per-acute or acute and animals are found dead (death having occurred quickly) or on the point of death. Bloating sometimes is marked, and in such cases may be suspected as the cause of death. There could possibly be some connection between the two complaints.

Calves usually succumb very quickly and apart from nervous symptoms, which have been likened to those produced by acute lead poisoning and which they show for a short time before death, there is little to be seen. There may or may not be scouring; it is by no means a constant feature.

In those cases, particularly in adults, which last for a day or two, there is extreme depression. The beast is dull, listless, does not eat or drink, may walk aimlessly about or stand with head down; with jaws champing and strings of saliva hanging from the lips. Ataxia was noted in one case in a steer.

Post-mortem examination

Carcases usually show some degree of distension by gas - mostly produced post-mortem but may be evident before death. There may be a fluid or frothy nasal discharge.

Subcutaneous vessels are engorged and the musculature at times has a par-boiled appearance. Cases have been noted with extensive ecchymoses throughout the musculature and connective tissue of the forequarters, and also of the diaphragm. Petechiae are a constant feature in the Thymus. Lymph nodes are congested; sometimes very markedly.

In the thoracic cavity, the lungs are somewhat congested, and if the animal has been dead for a few hours they take on a "smoky" hue.

The pericardial sac contains an excess of straw-coloured fluid which may contain so-called "chicken fat" clots. After the animal has been dead for some time, the fluid becomes sanguineous; due to diffusion of blood pigments from adjacent blood vessels.

Both sub-pericardial (particularly) and sub-endocardial haemorrhages are very well marked.

In the abdominal cavity the picture, as in the thorax, closely parallels that seen in sheep. There is an excess of straw-coloured (later sanguineous) abdominal fluid. A characteristic feature seen on opening the abdominal cavity is the mass of creamy coloured, inflated small intestines. On closer examination of the gastro-intestinal tract, the rumen is found to be full of feed of varying consistency, there is patchy congestion of the abomasum and patchy enteritis throughout the small intestine; the blood vessels of which are intensely congested and show evidence of diffusion of blood pigment into surrounding tissues. The contents of the small intestines are generally sparse and consist mainly of semi-fluid material of creamy to brown colour and of "mayonnaise" consistency. In odd cases in calves, there has been an acute, haemorrhagic enteritis. The small intestines often are degenerated to such a degree that it is quite easy to tear sections apart with the fingers.

The liver shows patchy degeneration with a mottled appearance. Rapid decomposition occurs, and in animals dead several hours the liver is very soft and gassy. Gall gladder is distended and a diffusion of bile stains the surrounding tissues. The spleen is often soft and haemorrhagic. The kidneys in all cases show some change, but those at times may be slight. The "pulpy kidney" as seen in the worst case in sheep is seen rarely in cattle; even in those that have been dead quite some time. However, there may be quite a degree of softening of the cortical region of the lobules. Congestion is well marked, particularly in the cortical zone, and may be universally spread throughout the kidneys or restricted to just a few lobules.

DIAGNOSIS

Confirmation of diagnosis in suspected cases of Entero-toxaemia in cattle is often difficult to obtain, and although some of the confirmatory tests may be positive the others may prove negative. In fact, in some cases where the post-mortem picture has been typical of Entero-toxaemia, it has not been possible to obtain any laboratory confirmation of the diagnosis.

At the Glenfield Veterinary Research Station, confirmation of diagnosis is based on:

1. Toxin - antitoxin neutralisation tests.
2. Examination of bowel smears.
3. Test for glycosuria.

1. Toxin - Antitoxin Neutralisation Tests

Tests are performed using bowel filtrates and Types A and D antitoxin for neutralisation as follows: Mice are used in pairs and each pair is injected with either 0.2 or 0.4 mls of bowel filtrate, or 0.4 mls bowel filtrate neutralised with equal parts of antisera Type A and D. The mice are observed overnight for periods of seventeen to twenty hours. Unprotected mice usually die in a matter of minutes.

It apparently is very difficult to demonstrate the presence of enterotoxin from bowel contents of cattle and Glenfield has had very few specimens from cases of Entero-toxaemia in cattle where it was possible to demonstrate a good enterotoxin. So far there does not appear to be any grounds to suspect that toxin other than epsilon is present.

Some of the reasons for failure to confirm the presence of enterotoxin are:

a. Collection made when putrefactive changes are too advanced.

b. Failure to collect sample from portion of bowel where enter toxin is being produced.

c. Apart from natural dilution factor due to the capacity of the bovine intestinal tract; bowel contents are often of such thick consistency that they will not filter unless diluted with saline; leading to a further dilution factor.

d. During hot weather chloroform, used as a preservative, may volatilise and the sample ferments before reaching the laboratory.

2. Examination of Bowel Smears

Smears taken at various levels throughout the small intestine may show a characteristic picture of the casual organism. Cl. welchii exists in the form of rather short rods, varying considerably in length. Filaments are not uncommon. It has parallel sides and the ends are truncated or slightly rounded. The organism is non-motile and capsules may be formed in the animal body.

It should be noted that a few Cl. welchii may be found in the small intestines of normal sheep and cattle and confirmation of diagnosis would depend on the discovery of these bacteria in sufficient numbers to cause the death of an animal.

Failure to obtain confirmation from bowel smears may be due to:

a. Smears collected from portion of intestinal tract where organisms were not present.

b. Overgrowth of post-mortem invaders if smears are collected when putrefactive changes are well advanced.

3. Test for Glycosuria

It often is helpful to test the urine for the presence of sugar. It is a characteristic of Type D that Entero-toxaemia from this organism is accompanied by a marked and sudden rise in the blood glucose level shortly before death. This may be followed by a glycosuria detectable by the usual routine tests.

Glycosuria is not, however, a constant feature and cases of Entero-toxaemia which have been confirmed by toxin - antitoxin neutralisation tests and positive bowel smears, have been negative for urine sugar.

Failure to obtain positive tests for sugar in urine may be due to:

a. Hyperglycaemia, and consequently glycosuria, does not occur in all cases; and only Type A is responsible.

b. Destruction of sugar by bacterial fermentation in animals dead for some time, or in unpreserved samples of urine while in transit to the laboratory.

TREATMENT AND CONTROL

Treatment appears to be of little value. In the per-acute and acute types of course, there is not time. Even in more chronic cases, sulphonamides and antibiotics, while perhaps prolonging the course of the disease in some instances, have given little success in treatment.

Prevention may be possible by giving two 10 ml. doses of Entero-toxaemia vaccine, spaced by a month's interval. Little is known, at present, of the efficiency of vaccination in cattle.

References:

Blood. R. C. & Helwig. D. M. (1927) - Aust, vet. J., 33 : 144
Bullen, J. J. & Scarisbrick, R. (1957) - J. Path. & Bacto., 73 : 495
Griner. L A., Aichelman, W. W., Brown, G. D. (1956)- J.A.V.M.A. 129 : 8 : 375
Griner, L. A., & Bracken, F. K. (1953)- J.A.V.M.A. 122 : 911 : 99
Helwig. D. M-Pers. Communication
Hepple, J. R. (1952)— Vet. Rec. 64 : 43 : 633
McBarron, E. J-Pers. Communication
Macrae. D. R. Murray, E. G. & Grant, J. J. (1943)- Vet. Rec. 55 : 19 : 203
Rose, A. L., & Edgar, G. (1936)- Aust. vet. J., 12 : 6 : 212
Schofield, F. W. (1955) - J.AV.M.A. 126 : 936 : 192