Toxic hepatic failure in newborn foals.

The research article discusses a case involving eight newborn foals (baby horses) suffering from toxic hepatic failure or severe liver disease, which resulted in their premature death. It details the clinical symptoms, lab results, and pathological findings, hinting at both prenatal and postnatal exposure to a liver toxin, inducing a blend of potentially infectious and toxic health conditions.

Clinical Signs and Laboratory Findings

• The foals, aged between 2 to 5 days, displayed significant clinical signs such as depression and jaundice (icterus).
• Various laboratory tests revealed abnormal readings. They exhibited higher than normal plasma ammonia content, aromatic-to-branch-chain amino acid ratio, total bilirubin content in the blood serum, gamma glutamyl transferase activity, alkaline phosphatase activity, and packed cell volume (PCV).
• Coagulation tests indicated prolonged partial thromboplastin and prothrombin times, suggesting a possible defect in blood clotting.
• Some foals also presented with high sorbitol dehydrogenase activity.
• All these laboratory results pointed towards a serious underlying liver disease and eventual hepatic failure.

Pathological Findings

• Upon post-mortem examination, noticeable pathological changes were identified primarily in the liver and brain.
• The foals’ livers were significantly smaller than they should have been for their age, and had excessive proliferation of bile ducts, destruction of liver cells (hepatic cell necrosis), and mild fibrosis around the portal area of the liver.
• These observations indicated a likelihood of both prenatal (before birth) and postnatal (after birth) illnesses triggered by exposure to a harmful substance affecting the liver (hepatoxin).
• The primary neurological lesion observed was the presence of Alzheimer type II astrocytes (a specific type of brain cells), which are indicative of a brain disorder associated with liver disease (hepatoencephalopathy).

Possible Causes and Explanations

• Though the presence of fibrosis pointed towards exposure to a toxin in the womb, epidemiological data suggested that liver failure originated more likely from exposure to a toxic product from a microorganism shortly after birth.
• This conclusion is substantiated by their ability to induce the same disease in two other newborn foals by feeding them this microbial product, effectively reproducing the disease and strengthening the link between the toxic product and the observed health conditions.