Infarctive encephalopathy in zoo-housed gibbons in North America.

Abstract

Progressive neurologic signs without a known underlying etiology have been observed in managed gibbon populations housed at institutions in North America. In 2018, the Gibbon Species Survival Plan initiated a veterinary survey to evaluate clinical histories among gibbons displaying neurologic signs. The clinical results of this survey as well as the results of a centralized histologic review of brain samples from 5 species of managed gibbons displaying neurologic signs are outlined here. Reported neurologic deficits in gibbons surveyed included tremors (12/12, 100%), ataxia/incoordination (11/12, 92%), fine motor skill deficits (11/12, 92%), weakness (10/12, 83%), and mentation deficits (7/12, 58%). Gross lesions were not identified in the brain. However, in affected animals, histology revealed infarctive lesions in the cerebrocortical (14/15, 93% of animals) and cerebellar (10/15, 67% of animals) gray/white matter. Lesions were absent in the thalamus, mesencephalon, and brainstem. Lesions were typified by areas of parenchymal loss, perivascular foamy macrophage accumulation, and extensive gliosis dominated by gemistocytic astrocytes. In all affected animals, vessels located in the center of the lesions had increased tortuosity with loss of medial distinction, variable medial hyperplasia, and multifocal medial vacuolation that was accentuated by Masson's trichrome staining. Thrombotic lesions were not identified, and amyloid was not identified by Congo red staining. Ionized calcium-binding adaptor molecule 1 (IBA1) immunohistochemistry revealed extensive macrophage infiltration, even in areas in which lesions were not identified on histologic examination. This study reveals a pattern of small-vessel disease among gibbons displaying neurologic signs, and the resulting clinical syndrome is here termed "gibbon infarctive encephalopathy."