Monitoring and management of acidosis in calf diarrhoea.

Abstract

Neonatal diarrhoea is a major cause of morbidity and mortality in calves during the first three weeks of life, resulting in considerable economic loss. Aetiological agents include enterotoxigenic Escherichia coli, Salmonella spp, rotavirus, coronavirus and Cryptosporidium parvum, mixed infection being common1-3. As in other species, the cardinal biochemical features of calf diarrhoea are hypovolaemia, hyponatraemia, pre-renal failure and metabolic acidosis-8. There is no relationship between severity of dehydration and acidosis7. In previous studies7'8, acidosis was found to be widespread and severe amongst diarrhoeic suckler calves, and collapsed calves requiring intravenous fluid therapy (IF) were more severely acidotic than those manageable by oral fluid therapy. Calves less than 6 days old were less acidotic than older calves (Figure 1). Recording similar observations, Naylor4 postulated that the age-related difference in severity of acidosis might be explained in terms of susceptibilities to enteric pathogens: the younger calf is likely to be affected by enterotoxigenic E. coil, with consequent rapid dehydration, reduced tissue perfusion and production of lactic acid by the tissues together with intestinal loss of bicarbonate, whereas the older calf is more