Diarrhoea in calves during the neonatal period (i.e. the first four weeks of life) is very common. Various microbiological agents have been associated with the syndrome and the fate of affected calves is dependent on the severity of the biochemical changes. Diarrhoea caused by Salmonella is described under Salmonellosis.

AETIOLOGY

E.coli has been associated with neonatal calf diarrhoea since before the beginning of this century. Particular strains of E.coli are more effective than others at inducing disease. There are also numerous viruses and other microbiological agents that have been identified in diarrhoeic calf faeces; rotavirus, coronavirus, parvovirus, enterovirus, astrovirus, calicivirus, small cubic virus and a villous epithelial cell syncytia inducing virus. The two most important, and certainly most studied, viruses are rotavirus and coronavirus. Both these viruses will produce diarrhoea in colostrum-deprived calves, although strain differences do exist.

Among the other agents which have been associated with diarrhoea in neonatal calves, the small protozoan parasite of the genus Cryptosporidium is the most important.

INCIDENCE

CLINICAL SIGNS

Only the clinical syndrome associated with E.coli is sufficiently distinct to enable an clinical diagnosis to be made with reasonable accuracy. Even then, confirmation by laboratory techniques would be required.

The syndrome produced by E.coli occurs in very young calves, usually less than 5 days of age and frequently as young as 24 hours old. The onset of the syndrome is very sudden, and the diarrhoea is very profuse, with a brownish-yellow colour. Affected calves can lose up to 15% of their bodyweight within 24 hours of the onset of diarrhoea. They quickly become dull, lethargic and dehydrated. Mortality rates can be very high among affected calves.

Generally, however, neonatal calf diarrhoea occurs mainly during the second and third weeks of life, but death occurs only in a proportion of affected calves. When death occurs it usually does so after three or four days of profuse diarrhoea, during which time there is marked loss of weight and increasing dullness. The faeces, which become progressively more fluid, rarely contain blood, and tend to impart a yellowish stain on the hindquarters and tail. If the diarrhoea continues calves become recumbent, or have great difficulty in rising and are very weak. Some calves become reluctant to feed early in the course of the condition, whereas others continue to take milk readily even after they become recumbent. Eventually, severely affected calves go into lateral recumbency and become comatose.

Calves which have died as a result of severe diarrhoea are severely dehydrated. If the illness has lasted for several days they are also very thin and have little perirenal fat. Many have a grossly distended urinary bladder, presumably due to the fact that calves do not urinate while recumbent. 

PATHOGENESIS

The cause of death in severe neonatal calf diarrhoea is the severe depletion of fluid and electrolytes resulting from the diarrhoea. Briefly, in calves which are fed milk until death, diarrhoea results in a fall in plasma sodium and bicarbonate concentrations and in blood pH, whereas a rise is found in plasma urea and chloride concentrations. Plasma potassium concentrations are variable, but frequently are raised and myocardial potassium concentrations are consistently low. There is a fall in the plasma volume.

It is postulated that the diarrhoea results in metabolic acidosis which results in rapid respiration. As a result of acidosis, potassium is withdrawn from the heart muscle which results in terminal cardiac failure.

EPIDEMIOLOGY

Several major facts have emerged from epidemiological studies of calf mortality both in this country and North America, the most important of which is that although the feeding of colostrum to newborn calves does not guarantee survival, colostrum deprivation invariably results in death. Dairy calves first obtaining colostrum from a bucket have a higher mortality rate than similar calves which first ingest colostrum by suckling their dams. Calves born in byres have a much higher mortality rate than calves born in either yards, boxes or in the field. The mortality rate is highest in the first week of life and thereafter it decreases exponentially. The mortality rate in calves in a particular calf-house is directly proportional to the length of time that the building has been occupied by young calves. The mortality rate in dairy calves is at its highest between January and April each year. Ayrshire and Channel Island calves appear to be less resistant to neonatal disease than are Friesians. As the size of the adult cow herd increases, the mortality rate among the calves also increases. The mortality is higher, and the seasonal mortality pattern is much more marked, in Scotland than elsewhere in Great Britain.

The amount of immunoglobulin absorbed by a calf has been shown to be a function of first, the age when fed and second, the mass of immunoglobulin presented. The cessation of immunoglobulin absorption is now known to occur progressively from birth not suddenly at 24-30 hours after birth. This makes the timing of the first feed critical and the value of subsequent feeds of colostrum apparently of only marginal importance in relation to serum immunoglobulin levels.

DIAGNOSIS

In all outbreaks of neonatal diarrhoea, steps must be taken to eliminate the possibility of salmonellosis. Confirmation of one or other of the possible microbiological agents can be readily carried out by diagnostic laboratories

TREATMENT

Almost every available chemotherapeutic agent/antibiotic has been used in the treatment of neonatal calf diarrhoea at some time or other and most with very limited success. Most of the trials which have been carried out have been uncontrolled and few have considered the immune status of the call. The most frequently used treatment regimes consist of antibiotic therapy, combined with some form of food withdrawal and/or fluid replacement.

Fluid therapy has often been used in conjunction with antibiotics. It is clear that the electrolyte and fluid imbalance associated with neonatal calf diarrhoea is a complex disaster resulting in acidosis which, in turn, is probably responsible for death in that it initiates cardiac failure by depleting myocardial potassium. Any attempt at fluid therapy should be based upon a knowledge of the fluid and electrolyte status of a calf and should be administered under conditions of intensive care. Particular care is required in the correction of acidosis in the scouring calf. 

The withdrawal of milk is frequently advocated as an adjunct to the treatment of diarrhoea. Certain proprietary preparations for oral replacement therapy contain appropriate ions and substances such as glycine, glucose and citrate to assist absorption of the electrolytes and are claimed to be of value.

CONTROL

The use of prophylactic antibiotics to control diarrhoea in home-bred calves can be expensive and frequently is not successful. It is the only course open to people purchasing calves for rearing although much of the trouble in these units can be prevented by delaying the purchase of calves until they are about one month old.

Occasionally, despite precautions it is found that a calf with low serum imnmunoglobulin concentration has been produced. This is not due to an inability to absorb colostrum but is a result of either delayed feeding or ingestion of only a small quantity of colostrum. Some dams produce low volumes or concentrations of globulin and "pre-milking" or dripping markedly reduces the concentration of globulin from these quarters. The odd calf with a low serum immunoglobulin level is unlikely to experience diarrhoea if it is mixed with calves with much higher serum levels.

If, for some reason, box calving is not possible, then very large amounts of colostrum should be fed to calves as soon as possible after birth. It is usually possible to feed calves at one hour of age with up to five pints of colostrum. It is suggested that the stockman should be urged to feed up to six pints of colostrum as soon as possible after birth, but at least within the first 4 hours of life. This will not harm the calves although a transient diarrhoea and dullness will occur a few hours after ingesting such amounts. Even in such calves, the absorption of colostral immunoglobulin is very significantly increased if the calves are mothered.

Infection build-up cannot be ignored. Therefore, periodic disinfection should be practiced and calves should be kept in fairly small self-contained groups wherever possible. Obviously, bought-in calves constitute a major hazard to homebred animals and this practice is never consistent with the continued good health of homebred animals.

Other management factors should also be considered here. Newborn dairy calves probably thrive best at an ambient temperature in excess of 13C (55⁰F). Single penning is desirable, not because it limits disease spread, but because the stockman tending the calves gets to know individual animals much more quickly. Successful calf rearing is a time consuming job demanding considerable expertise.

In order to increase the concentrations of specific antibodies to the microbiological agents associated with calf diarrhoea vaccination of the dams in the last few weeks of gestation has been investigated. Rotavec K99  is a vaccine currently available in the U.K. It raises antibody levels in colostrum against both E.coli and bovine rotavirus. Although still dependent on colostral transfer this vaccine gives good results if used appropriately.

However, it is the failure or partial failure in the transfer of colostral immunoglobulins from the cow to the calf that is a major contributory factor to the severity of neonatal calf diarrhoea. Thus increasing the level of specific antibodies in the colostrum is of limited value to a calf which fails to receive sufficient colostrum, at a time when its ability to absorb that colostrum is at a maximum.