Intra-ocular and CNS listeriosis following systemic infection in Wistar rats with chronic serum sickness.

The relationship of immune complex deposits and cell-mediated immunity to the occurrence of ocular and brain listeriosis following a low (0.007-0.03 LD50) intraperitoneal challenge was investigated in 68 Wistar rats with chronic experimental serum sickness and 68 normally resistant controls. The induction of chronic serum sickness involved long continued immunization with bovine serum albumin which resulted in a high level of immune complex entrapment in both the ciliary processes (92%) and choroid plexus (74%) of eye and brain. The extensive immune deposits were associated with a high (23%) incidence of CNS listeriosis and a much lower rate (5.9%) of ocular listeriosis. The difference in incidence could not be related to impaired cell-mediated immunity based on cultural data in liver and spleen. The results seem to indicate that the eye is less vulnerable to systemic listerial infection in chronic immune complex disease despite comparable immune complex entrapment in the ciliary processes and choroid plexus. The findings reflect biologically significant differences between eye and brain that influence their respective vulnerability to systemic Listeria, an opportunistic bacterium, of clinical importance in patients with chronic immunological disorders.

Increased risk of experimental central nervous system listeriosis in rats with chronic serum sickness. An immunohistopathological study.

The incidence and severity of central nervous system (CNS) infection were increased following the intraperitoneal innoculation of Listeria monocytogenes in adult Wistar rats with experimental chronic serum sickness. The results were attributed to an alteration in the blood-cerebrospinal fluid barrier induced by immune complex deposits in the choroid plexus of animals hyperimmunized with bovine serum albumin. CNS inflammation occurred in 16 of 40 (40%) of the test animals studied; one of 36 (2.8%) controls had CNS inflammation. There were extensive pathological changes in the choroid plexus, subarachnoid space, and neural parenchyma of the test animals, as compared with only small inflammatory foci limited to the choroid plexus and subarachnoid space in the one affected control. This experimental model for inducing bacterial CNS infection simulates certain predisposing conditions in chronic immune disease, and may therefore be useful in studying the pathogenesis of CNS infection in such cases.