Pregnancy disease was induced in well-conditioned Merino sheep by subjecting
them to sudden changes of diet, short term starvation or oral dosing of Sulphadimidine.
The blood levels of ketones and glucose were followed daily throughout the
preclinical, clinical and postclinical stages of this metabolic disorder.
Typical clinical symptoms of cerebral dysfunction were obtained in six pregnant
ewes entering their last month of gestation, a non-pregnant ewe, and a wether.
No relation was found between clinical symptoms, minimum blood glucose or
maximum blood ketone levels or the time at which these occurred, thus indicating
that the nervous symptoms were not due to either the low levels of circulating blood
glucose or the high levels of ketone bodies per se.
The appearance of clinical symptoms amongst the pregnant ewes was invariably
preceded by both a persistent hypoglycaemia and a persistent ketosis ; this was less
clearly defined in the case of the non-pregnant ewe and the wether.
The possibility that the nervous symptoms could have been due to impaired
glucose utilization by the cerebral cells, brought about by adrenal cortical hyperactivity