Experimental ocular onchocerciasis in cynomolgus monkeys. II. Chorioretinitis elicited by intravitreal Onchocerca lienalis microfilariae.

Chorioretinitis due to onchocerciasis is a major cause of blindness, and the pathogenesis is poorly understood. We have developed an experimental model for onchocercal chorioretinitis using cynomolgus monkeys (Macaca fascicularis). Two normal monkeys and two monkeys which had received prior sensitization with subcutaneous injections of live Onchocerca lienalis microfilariae were given intravitreal injections of either 0, 10, 50 or 500 live microfilariae. Posterior segment changes included disc edema, venous engorgement, retinal vasculitis, intraretinal hemorrhage, and progressive retinal pigment epithelial (RPE) disturbances. Histopathological findings included perivascular infiltrates with eosinophils, eosinophilic choroiditis, and RPE hypertrophy, hyperplasia and loss of pigment. Microfilariae in the retina had no surrounding inflammation but were found adjacent to areas of RPE alterations. Overall the inflammatory reaction in the two unsensitized monkeys was more severe than that seen in the sensitized monkeys. The retinal appearance of the monkeys resembled that found in human onchocerciasis, and this model appears to be a promising one for future investigations.

Effect of diethylcarbamazine citrate and anti-inflammatory drugs on experimental onchocercal punctate keratitis.

Subconjunctivally injected Onchocerca lienalis microfilariae (Mf) migrate into the guinea pig cornea, resulting, when the microfilariae die, in punctate stromal opacities resembling those of human onchocerciasis. Administration of diethylcarbamazine citrate (DEC-C) following subconjunctival injection of Mf increased the proportion of dead Mf in the cornea, the number of punctate opacities and the extent of peripheral corneal neovascularization. Betamethasone (a synthetic steroid) and lodoxamide tromethamine (an inhibitor of mediator release from mast cells) inhibited the formation of punctate opacities. Chlorpheniramine maleate and cimetidine (H1 and H2 histamine receptor antagonists), given together, did not alter the formation of punctate opacities but inhibited the peripheral corneal neovascularization. These observations suggest that mast cell mediators other than histamine may be of importance in the formation of the corneal punctate opacities.

Punctate keratitis induced by subconjunctivally injected microfilariae of Onchocerca lienalis.

An experimental model of human onchocercal keratitis was produced by injecting guinea pigs subconjunctivally with microfilariae (Mf) of Onchocerca lienalis. Actively motile O lienalis Mf spontaneously penetrated the central cornea and produced gray-white midstromal opacities, 0.2 to 0.4 mm in diameter, resembling those of human onchocercal punctate keratitis. Histologically, small foci of eosinophil and mononuclear cell infiltration associated with small pockets of interstitial edema were present in the central corneal stroma, with eosinophil infiltrates in the conjunctiva, episclera, limbus, and ciliary body. The severity of the punctate keratitis was increased by repeated subconjunctival inoculations of Mf. Punctate lesions were not seen following subconjunctival injection of Mf in animals previously hyperimmunized by three subcutaneous injections of Mf. Hyperimmunization may produce an immune response capable of destroying the subconjunctivally injected Mf and preventing their migration into the central cornea.

Bilharziasis in a Nanday conure.

Natural infection with a schistosome in a pet Nanday conure caused weight loss, blood-flecked diarrhea, and death. Hemorrhagicoulcerative colitis and cloacitis were found at necropsy. The schistosome was not identified but was believed to be Gigantobilharzia sp.