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CEREBROCORTICAL NECROSIS (CCN) (Polioencephalomalacia) DEFINITION This is a sporadic, sudden onset nervous disease of ruminants in which affected individuals are staggering, blind and quickly become recumbent. The syndrome is due an aberration of thiamine metabolism. AETIOLOGY In ruminants, the requirement for the B vitamins is largely met by synthesis in the guts . CCN is considered to be caused by a thiamine deficiency because of the rapid response to thiamine treatment and tissue thiamine levels are lower synthesised (low dietary roughage), an inability to utilise the amounts produced (reduced absorption, impaired phosphorylation, increased rate of excretion), thiamine inhibitors (thiaminase), thiamine analogues acting as anti-metabolites, or simply an increased demand. It has been shown that rapidly growing cattle do have an increased requirement for thiamine and the diet which is usually fed to achieve maximum growth rates is a high cereal, low roughage one. When there is a high cereal intake, lactic acidosis develops and, as the pH falls, the following changes take place: firstly, the microflora in the gut changes from predominantly gram-negative to predominantly gram-positive species with an increase in the proportion of bacilli, secondly there is a decrease in the quantity of thiamine produced, thirdly thiaminase producing bacteria flourish, and fourthly, there is an accumulation of histamine and structurally similar bases which can act as potent thiaminase activators.It has also been suggested that, even in the absence of effective concentrations of thiaminase 1, a deficiency of cobalt may predispose cattle to CCN. This could arise either by following a decrease in the activity of the rumen microorganisms responsible for thiamine synthesis, or by inducing liver damage, which is one of the effects of a prolonged deficiency of cobalt. EPIDEMIOLOGY CCN occurs worldwide not only in cattle, but in almost every farm ruminant species. The incidence is highest in cattle from 6 to 12 months which are being fed large quantities of concentrates and minimal amounts of roughage ie. feedlot conditions. Occasionally, grazing animals may be affected. Usually only single animals develop clinical signs, but group outbreaks can occur (up to 25% affected). The mortality rate varies according to the delay before treatment has begun, but it is of the order of 30 per cent. CLINICAL SIGNS This is a sudden onset disease in which the initial signs are dullness, aimless wandering, disorientation, apparent blindness, staggering gait and muscle tremors, particularly of the head. After several hours, the affected individual collapses and goes into lateral recumbency. They can develop convulsions although their legs can be stopped from paddling relatively easily. The rumen continues to cycle, there may be a history of diarrhoea or the animal may be diarrhoeic, and the temperature is usually within the normal range. Clinical signs tend to be more severe the younger the animal affected. Untreated cases will die after an illness of from 2 to 6 days duration. DIAGNOSIS CCN should be suspected when a young fast growing bovine on a high cereal diet is seen to be wandering aimlessly, or standing alone and apparently blind, or is found in lateral recumbency.TREATMENT Thiamine (Vitamin Bl injection) at 10 mg/kg bodyweight usually repeated after 12 and 24 hours (Vitamin Bl injection). In cases given thiamine immediately after the onset of clinical signs, a beneficial clinical response can often be noticed within 12 hours and there may be an apparently complete clinical recovery after 24 hours. When treatment is delayed, several days may pass before any clinical improvement becomes apparent; such cases firstly begin to eat, then mental awareness returns and, finally, the ability to see returns. However, a few cases remain blind although otherwise they appear to have recovered completely. CONTROLSince CCN is a problem almost wholly associated with young cattle being fed on a high cereal - low roughage diet, the most obvious measure is to increase the proportion of roughage. While this does reduce the danger from CCN, it is probably uneconomic to do so in a feedlot-type operation. Therefore, where CCN has been a problem, supplementary thiamine should be added so that the total dietary intake is about 25 mg/kg dry feed. |
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