Chronic follicular conjunctivitis associated with Chlamydia psittaci or Chlamydia pneumoniae.

We determined whether patients with chronic conjunctivitis in whom direct fluorescent antibody (DFA) tests revealed genus-specific chlamydial antigens (but not species-specific Chlamydia trachomatis antigens) were infected with Chlamydia psittaci or Chlamydia pneumoniae. Patients were divided into a case group of possible non-trachomatis chlamydial conjunctivitis and a control group of nonchlamydial conjunctivitis on the basis of examination and DFA testing. Species-specific primers were used to amplify C. trachomatis, C. psittaci, and C. pneumoniae DNA with polymerase chain reaction (PCR). Four (27%) of 15 samples from the case group were positive for C. psittaci or C. pneumoniae DNA, whereas none of 24 control samples were positive. Sequencing revealed a C. pneumoniae, an avian C. psittaci, and two mammalian C. psittaci strains. A short course of oral antibiotic treatment appears to be inadequate for patients with non-trachomatis chlamydial conjunctivitis. Ocular infections due to C. pneumoniae and C. psittaci may be more common than previously recognized and can be identified by DFA and PCR.

Persistent infection of mouse fibroblasts (L cells) with Chlamydia psittaci: evidence for a cryptic chlamydial form.

When monolayers of mouse fibroblasts (L cells) were infected with enough Chlamydia psittaci (strain 6BC) to destroy most of the host cells, 1 in every 10(5) to 10(6) originally infected cells gave rise to a colony of L cells persistently infected with strain 6BC. In these populations, the density of L cells and 6BC fluctuated periodically and reciprocally as periods of host cell increase were followed by periods of parasite multiplication. Successive cycles of L-cell and 6BC reproduction were sustained indefinitely by periodic transfer to fresh medium. Isolation of L cells and 6BC from persistent infections provided no evidence that there had been any selection of variants better suited for coexistence. Persistently infected populations consisting mainly of inclusion-free L cells yielded only persistently infected clones, grew more slowly, and cloned less efficiently. They were also almost completely resistant to superinfection with high multiplicities of either 6BC or the lymphogranuloma venereum strain 440L of Chlamydia trachomatis. These properties of persistently infected L cells may be accounted for by assuming that all of the individuals in these populations are cryptically infected with 6BC and that cryptic infection slows the growth of the host cell and makes it immune to infection with exogenous chlamydiae. According to this hypothesis, the fluctuations in host and parasite density occur because some factor periodically sets off the conversion of cryptic chlamydial forms into reticulate bodies that multiply and differentiate into infectious elementary bodies in a conventional chlamydial developmental cycle.