Experimental trachoma in subcutaneous conjunctival autografts in macaques.

To study chlamydial conjunctivitis, conjunctival autografts subcutaneously implanted in pockets on the abdomens of rhesus (Macaca mulatta) and pig-tailed (M. nemestrina) monkeys were inoculated percutaneously (4-10 X 10(4) inclusion-forming units per pocket) with trachoma strains of Chlamydia trachomatis (serovars B & C). These conjunctival pockets were removed on days 2, 3, 4, 5, 6, 7, 8, 10, 14 and 16 post-inoculation (pi). Tissues (at least two samples at each time interval) were prepared either for reisolation of the organisms by cell culture or histologic examination by light and electron microscopy. Control tissue, inoculated with either HeLa cell material or UV-inactivated organisms, were prepared in parallel. Bloods were drawn and tear strips taken at weekly intervals for 8 weeks. A total of 221 bulbar and 99 palpebral conjunctival pockets were established over time with the success rate of 75% and 88%, respectively, in six rhesus and ten pig-tailed monkeys. Histological examination revealed widespread infiltration of mixed polymorphonuclear and mononuclear cells on days 2 and 3 pi. By day 5 pi, lymphocytes had migrated into the thinned epithelial layer. Patches of inflammatory infiltrate similar to trachoma follicles were observed, although distinct germinal centers were absent. Surface morphologies of normal and infected pocket conjunctiva were examined by scanning electron microscopy. Normal tissue was characterized by a regular mosaic pattern of closely packed epithelial cells containing numerous microvilli. Infected tissue was edematous, and the continuity of the mucosal surface had been altered. Chlamydiae were reisolated from the pockets on days 2, 3, 6, 8 and 10 pi.(ABSTRACT TRUNCATED AT 250 WORDS)

Experimentally induced ocular chlamydial infection in infant pig-tailed macaques.

Four Macaca nemestrina monkeys were inoculated in the conjunctiva with Chlamydia trachomatis (strain E) at 6 weeks of age. A fifth monkey was inoculated with HeLa cell materials only. Ten weeks later, all monkeys were reinoculated with either strain E or strain C. All inoculated monkeys were susceptible to infection with C. trachomatis as documented by fluorescent antibody staining of smears and reisolation of the organism from conjunctival and nasopharyngeal swab specimens. Rectal and vaginal swab specimens remained negative throughout the study. Three of four inoculated animals responded with IgM titers reaching a peak of 1:16 (M#3) and 1:32 (M#1, M#4) 2 weeks after the primary inoculation. IgG appeared in all inoculated animals and titers rose to peak levels of 1:64 (M#2), 1:128 (M#1, M#3), and 1:256 (M#4). Histopathology documented a dramatic difference in immunological response following secondary inoculation. Primary inoculation elicited a typical inflammatory response characterized by moderate stromal infiltration of polymorphonuclear and mononuclear leukocytes. Plasma cells appeared by week 3 postinoculation (pi). Following a secondary inoculation, classic follicle formation was evident by 1 week pi. Mononuclear markers identified a germinal center composed of B cells and a T cell cap. Epithelial thinning near the cap of the follicle was accompanied by a complete loss of goblet cells. This model may be useful for studying the immunopathology of infant chlamydial infections.