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This article was published in 1969-70
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The Pathogenesis, Epidemiology and Therapy of Calf Scours

P. J. MYLREA, M.V.Sc., Ph.D. Department of Agriculture, District Veterinary Laboratory, Wollongbar

The term "calf scours" is all embracing and warrants some comments. Scours is a clinical sign and not a disease entity. It can occur as a major or a minor symptom in a number of specific diseases. It can also occur as a prominent sign in many disorders which do not fit into any recognisable disease group. In fact, it is often very difficult to determine the primary cause of scouring in the living animal or at autopsy.

This is probably a reflection of our ignorance of the aetiology and pathogenesis of many of these disorders and to the fact that scours is probably a complex with many different facets.

Scouring can occur in calves at any age but this talk will be restricted to comments on the problem in quite young calves. Before doing so there are some aspects of physiology and bacteriology which warrant a brief mention.

Digestion of Milk in the Young Calf

The young calf is essentially a "monogastric" animal and it is not till two or three months that its digestive system takes on its ruminant characteristics.

During early life milk by-passes the rumen and goes directly into the abomasum via the oesophageal groove. The abomasum acts as a reservoir and regulates the flow into the small intestine. Considerable quantities of digestive secretions are added to the milk while it is in the abomasum. These cause the clotting of the milk and its separation into curd and whey fractions. The whey fraction passes into the small intestine first. Some digestion occurs in the abomasum but there is little absorption.

The main site of digestion and absorption is the small intestine. Lactose, fat and protein are absorbed mainly from the upper part of the small intestine while water and sodium and chloride are absorbed in the lower half. The processes are very efficient and little material passes into the large intestine. The rate of passage along the small intestine is fairly rapid, probably takes about two hours (Mylrea, 1966, a, b; 1968, a).

Some absorption but little digestion occurs in the large intestine. Because of the small bulk of the contents there is little stimulation of the defaecation reflex and defaecation occurs infrequently.

There is little information on the functioning of the gut in scouring calves. However, it seems that in some forms of scouring there is little change in abomasal functioning or in the rate of flow through the small intestine (Mylrea, 1968 b). A major change seems to be in the efficiency of the net absorptive processes for water and electrolytes in the small intestine and an abnormally large volume of content enters the large intestine. This in turn stimulates frequent defaecation of the typical watery diarrhoeal faeces.

ABSORPTION OF COLOSTRUM BY THE NEW BORN CALF

The role of colostrum in the resistance of calves to infectious diseases has been known for a long time and it has also been thought that antibodies are absorbed from the gut during the first 24-36 hours of life. However, recent work (see Smith, O'Neil & Simmons, 1967) has focused attention on the concentrations of immune globulins in the serum of calves during the first few days of life. It has been found that there is a great variation between calves with levels ranging from quite high to extremely low values. Observations indicate that this is not due necessarily to failure to ingest colostrum but to a failure to absorb the immune globulins from the alimentary tract. It may be that some calves lose their ability to absorb antibodies as early as 6-8 hours after birth and it seems that absorption may be affected by stress factors.

This feature could be important from a disease point of view because there appears to be a relationship between the levels of immune globulins and the incidence of calf disease. Thus a number of workers have found a much higher incidence of disease and death in calves with low concentrations than in calves with high levels.

BACTERIAL COLONISATION OF THE DIGESTIVE TRACT

The new born calf has a sterile gut but colonisation occurs very rapidly. The pattern of colonisation seems to follow a fairly constant pattern in terms of species of bacteria, numbers present in different parts of the gut and age effects. Species in the flora of the rumen, abomasum and small intestine include E. coli, Clostridium welchii, enterococci and lactobacilli and counts of the order of one million per ml. contents for each group are quite common. Similar organisms also occur in the large intestine and faeces but here the predominant group is a mixture of anaerobes generally classed as bacteroides. The process of colonisation occurs very rapidly after birth and distribution and counts similar to those of older calves are found throughout the tract at eight hours after birth (Smith, 1965). It seems that most of the gut organisms are derived from the environment in which the calf is born.

The normal gut flora appears to have a considerable protective influence on the resistance of the host to introduced pathogens. Thus recent work in laboratory animals has shown that disturbance of the normal flora (by drugs or dietary changes) can increase greatly the susceptibility of the host to introduced pathogens and to endotoxins. It is considered that the normal flora maintains conditions in the gut lumen that are inimical to introduced pathogens but when the normal flora is disrupted the conditions within the gut alter (in terms of pH, fatty acid concentrations, etc.) and become so favourable to pathogens that they survive and multiply (Dubos et al., 1963).

CAUSES OF SCOURS IN YOUNG CALVES

The two extreme views on the causes of scours are that it is primarily a nutritional problem or that it is essentially bacterial (see Roy, 1964) One reason for the confusion is the difficulty of demarcation between normal and diarrhoeal faeces. Thus at one extreme there are cases of profuse scouring with many accompanying signs of disease. At the other extreme are cases where faeces are altered in quantity, appearance and consistency but the calves are otherwise in apparent good health. Probably it is best to consider "scours" as a complex which can result from many factors acting either alone or in combination.

Many direct and indirect causes for scours have been postulated. Some are well established while others are much more speculative. Some are discussed below:

MANAGEMENT FACTORS

These include such factors as shelter, climatic conditions, transport, etc., many of which can be taken as stress factors. It is difficult to pinpoint specific features which may be critical.

FEEDING

In some cases the feeding of young calves on generous quantities of high fat milk will change the faeces from a scant, thick, brown material to a copious, yellowish-white, gelatinous material containing large amounts of fat. Such calves may show few or no signs of abnormality and these might be better classed as animals with a dietetically induced faecal change rather than a scour.

Overfeeding is another cause which is often postulated. A few comments can be made. First, calves on a regular feeding regime soon adjust their intakes and while they may gorge when first given free access to milk they very quickly adjust to these feeding conditions. Secondly, the reservoir action of the abomasum, mentioned above, operates. Thus, the abomasum can dilate to hold very large quantities of milk and despite its dilatation it continues to regulate the flow into the small intestine, Thirdly, the digestive and absorptive capacity of the small intestine is such that it can handle large intakes without loss of efficiency. The end result of these factors, and possibly others. is that in many calves "overfeeding" does not necessarily produce scours (Mylrea, 1966, c).

Calves are often fed on artificial milk replacers and while it is difficult to quote definite evidence it seems that such calves often experience more trouble with scour than do those fed on whole milk. Some features of milk substitutes which have been incriminated are the nature of dried milk and cereal products used and the type of fat and the method of incorporation, etc. If a reasonable balance is not struck then it is unphysiological and the derangements which occur can include: failure to clot in the abomasum with abnormal entry into the small intestine, presence of carbohydrates for which the appropriate digestive enzymes have not developed, too large fat globule size for efficient digestion, etc. The end result is that there is a considerable amount of undigested material in the gut which is acted upon by bacteria to give the so-called "putrefactive" diarrhoea with possible bacterial complications.

BACTERIAL CAUSES

Salmonellosis can occur in very young calves but the infectious agent most commonly considered in relation to calf scours is E. coli. A considerable amount of work has been devoted to this organism and infections in calves have been divided into three forms (Gay, 1965).

1. The colisepticaemic form of colibacillosis. This is the form which occurs in very young calves. The course is rapid and the calf dies within a day or two of birth. This is a bacterial, septicaemia disease in which scouring may or may not occur as a symptom. The factors of colostrum absorption and gut colonisation could be very important factors in this form.

2. The enteric-toxaemic form is characterised by collapse and death. It is associated with a tremendous proliferation of certain mucoid strains of E. coli in the intestine. There is probably the form studied by earlier workers and which is deeply entrenched in the literature.

3. The enteric form is the type commonly associated with scouring in calves older than those affected by the colisepticaemic form. It can result in dehydration, collapse and death depending on the severity of the scour. Of the three groups mentioned the enteric form is the type in which a connection with E. coli is the most tenuous. E. coli can be recovered from the intestinal contents but seldom from visceral organs.

DIAGNOSIS

As might be surmised from the preceding discussion it is often very difficult to determine the cause of scouring in either living or dead animals. Some specific infectious diseases have clinical signs which are diagnostically useful, e.g. the blood scour of coccidiosis and the mucus scour with intestinal membranes of salmonellosis. However, in many cases there is nothing characteristic and diagnoses have to be based on circumstantial evidence. At a laboratory level some help can be given routinely with infections causes, e.g. E. coli infections and in salmonellosis.

In the living calf the only samples usually available are faeces and rectal swabs. These are useful in the diagnosis of salmonellosis. They are of limited value in coliform infections because E. coli is a normal faecal inhabitant and can be recovered from any faecal sample. The recovery of E. coli would be more useful if the isolate could be serotyped and shown to belong to a known pathogenic group.

Animals which die can be examined by post-mortem and a more intensive series of specimens taken for bacteriology. Some disease, e.g. coccidiosis and chronic salmonellosis can produce definite lesions but in many calves which have died of scours there is often little to be seen. In some cases the intestines may be flaccid and fluid filled but in others they appear quite normal (Smith, 1962; Radostits, 1965). Post-mortem changes could be important and Smith (1962) found that in recently killed calves the tract appeared normal but that by six hours it had taken on the inflamed look that is associated with enteritis.

Specimens for bacteriology should be taken from visceral organs such as the liver and heart. Recovery of E. coli or salmonella is an indication of septicaemia or bacteraemia and this is diagnostically useful. Recoveries of E. coli from the intestinal tract are more difficult to interpret in the absence of serotype. Reasons for this are that E. coli is a normal inhabitant of the gut and that E. coli multiply rapidly in the small intestine after death, with a 10,000-fold increase by 12 hours (Smith, 1962).

CONTROL AND TREATMENT

There do not seem to be any specific control measures that can be employed. There are references in the literature to vaccination with E. coli preparations, either of the dam during pregnancy or of the calf immediately after birth, but these do not appear to have been very successful.

The most common course is to treat clinical cases with chemotherapeutic agents either orally or parenterally. There are some points about their use which are important. Many organisms, including those of the normal gut flora can develop resistance to antibiotics and in certain cases this resistance can develop rapidly, e.g. E. coli to streptomycin within 12 hours (Mylrea, 1968, c). It is also possible for drug resistance to be transferred between strains and even between species. e.g. from E. coli to salmonella and this is called infective drug resistance (Smith, 1967). It is important because use of drugs can induce resistance in the normal gut inhabitants and this resistance can be transferred rapidly to introduced pathogens even though the latter have never been exposed to the antibiotic. Another point relates to antibiotic sensitive tests. These are often requested when material is submitted to a laboratory. They can be very useful when an organism, isolated in the laboratory, can be confidently diagnosed as the cause of the disorder. However, as can be judged from the previous comments it is often not possible to say this about an isolate and to carry out a sensitivity test on such an organism would often be misleading.

Finally, there is the point of supportive therapy mainly with fluid to combat dehydration. This has been studied by many workers with beneficial results (see Dickson, 1968). The main reason why it is not used more widely seems to be due to the difficulties in applying the therapy.

Dickson, J. (1968), Vet. Rec., 83, 428

Dubos, R., Schoedler, R. W and Costello, R. (1963). Fed. Proc., 22, 1322

Mylrea, P. J. (1965 a.). Res. vet. Sci., 7, 333

Mylrea, P. J. (1966 b.). Res. vet. Sci., 7, 394

Mytrea, P. J. (1966 c.). Res. vet, Sci., 7, 407

Mylrea, P. J. (1968 a.). Res. vet. Sci., 9, 1

Mylrea, P. J. (1968 b.). Res. vet. Sci., 9, 5

Mylrea, P. J. (1968 c.). Res. vet. Sci., 9, 14

Radostits, O. M. (1965). J.A.V.M.A., 147, 1367

Roy, J. N. B. (1964). Vet. Rec., 76, 511

Smith, H. W. (1962). J. Path. Bact., 84, 147

Smith, H. W. (1965). J. Path. Bact., 90, 495

Smith, H. W. (1967). New Zealand Veterinary Journal, 15, 153

Smith, H, W., O'Neil, J. A., and Simmons, E. J. (1967). Vet. Rec., 80, 664


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