Fatal disseminated cercopithecine herpesvirus 1 (herpes B infection in cynomolgus monkeys (Macaca fascicularis).

Two adult female cynomolgus monkeys (Macaca fascicularis) that had been housed together for 4 months died within 2 weeks of each other after brief illnesses. Monkey No. 1 presented with collapse, watery stool, and hypothermia and died overnight. Monkey No. 2 presented with dyspnea, nasal discharge, leukopenia, and hypoproteinemia and was euthanized after 2 days. Both animals had peritoneal effusions, massive necrosis of pharyngeal, esophageal, and gastric mucosa, and multifocal hepatic and pancreatic necrosis. Monkey No. 2 also had lingual ulcers and locally extensive necrosis of spleen, adrenal glands, and lymph nodes. Large numbers of eosinophilic intranuclear inclusion bodies were present in epithelial and syncytial cells adjoining the necrotic foci in Monkey No. 2 but were absent in Monkey No. 1. Monkey No. 1 seroconverted to cercopithecine herpesvirus 1 (CHV-1, commonly known as herpes B) in the month before death. CHV-1 was isolated from a sample of stomach from Monkey No. 2, and electron microscopy of liver from this animal demonstrated herpesvirus particles within hepatocytes. Both animals were seropositive for simian type D retrovirus, and the virus was cultured from the liver of Monkey No. 2. A diagnosis of disseminated CHV-1 infection was made, possibly occurring secondary to immunosuppression due to infection with simian type D retrovirus. Although a high percentage of cynomolgus monkeys are apparently infected with CHV-1, disseminated disease is rare. Because infection with CHV-1 in humans is associated with a high fatality rate, familiarity with the lesions of disseminated infection with this virus is important.

Cerebral infarction in two cynomolgus macaques (Macaca fascicularis) with hypernatremia.

Hypernatremia resulting in neurologic symptoms ranging from lethargy to coma, and with underlying lesions of cerebral hemorrhage and thrombosis, has been reported in human beings. Herein we report two cases of cerebral infarction with venous thrombosis in cynomolgus monkeys. Both animals were severely hypernatremic because of water deprivation, with serum sodium levels of 185 and 193 meq/liter, respectively. At necropsy, there were bilateral multiple hemorrhagic and malacic areas visible on the surface of the cerebrum and extending into the parenchyma, primarily involving the occipital lobes. These lesions were interpreted microscopically as infarcts because, in addition to hemorrhage and necrosis, multiple thrombi were present in small and medium-sized veins of gray matter and meninges. The pathogenesis of hypernatremia-induced cerebral lesions is believed to involve cellular dehydration that caused shrinkage of the brain. Because the vasculature of the brain is tightly adherent to the skull, this shrinkage results in tearing of blood vessels, with consequent hemorrhage and thrombosis.

Gastric infarction in cynomolgus monkeys (Macaca fascicularis).

Five cases of gastric infarction were observed in adolescent or adult cynomolgus monkeys (Macaca fascicularis) over a 20-month period. Gastric infarcts were encountered as striking and unexpected findings at necropsy. Gross and microscopic findings included gastric necrosis, hemorrhage, and edema that involved large areas of the fundus and pylorus. A consistent finding was the presence of thrombi in the gastric microvasculature, particularly in the venous system. All animals had acute clinical episodes with substantial tissue damage resulting from a variety of causes, including trauma, pancreatitis, necrotizing cystitis, and intestinal intussusception. In addition, three animals had microvascular thrombosis in nongastric tissues. Our findings suggest that cynomolgus monkeys may be predisposed to developing gastric infarction under conditions of severe systemic insult that predispose to disseminated intravascular coagulation.