[Isolation and serial culture of strains of the agents of inclusion conjunctivitis and inclusion blennorrhea].
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BACKGROUND: Diagnosing adult inclusion and neonatal conjunctivitis can be challenging. They are sexually transmitted diseases that can easily be managed without any serious ocular or systemic sequelae if recognized and treated early on. METHODS: A proper differential diagnosis and careful examination is essential in the management of chlamydial conjunctivitis. RESULTS: Two case reports of patients with laboratory-confirmed inclusion conjunctivitis will be presented. CONCLUSIONS: A careful history and ophthalmic evaluation, along with laboratory studies, which revealed inclusion bodies, confirmed the diagnosis of adult inclusion conjunctivitis. Therefore, proper treatment and management of each case occurred.
A 14-month-old girl had inclusion conjunctivitis although there had been no signs or symptoms that required medical attention in her first year. By 2 1/2 years of age, the child had extensive pannus and corneal scarring that severely reduced vision. The infection was caused by a genital strain of Chlamydia trachomatis, TRIC type E, that was probably acquired at birth. Although genitally transmitted chlamydial strains normally cause a self-limiting inclusion conjunctivitis in areas where trachoma is not endemic, this case illustrates that they may occasionally cause severe trachoma. Possibly local idoxuridine (IDU) treatment (administered to this patient before the correct diagnosis was made) contributed to the severity of this infection.
The infectivity of trachoma-inclusion conjunctivitis (TRIC) organisms (TW-5) was enhanced by pretreatment of HeLa cell monolayers before inoculation with diethylaminoethyl (DEAE)-dextran (30 mug/ml) and poly-l-lysine (10 mug/ml) and inhibited by dextran sulphate (250 mug/ml), fetuin (4%), ovomucoid (5%), N-acetyl neuraminic acid (0.5%), and Cholera vibrio neuraminidase (100 U/ml). The infectivity of lymphogranuloma venereum organisms (434) was not affected by DEAE-dextran, fetuin, and neuraminidase, was slightly inhibited by poly-l-lysine, and was inhibited by dextran-sulphate, ovomucoid, and N-acetyl neuraminic acid. The study suggested that sialic acid residues on the cell surface may be specific receptors for TRIC organisms. The receptors for TRIC organisms (TW-5 and TW-3) could be specifically blocked with inactivated (56 C for 30 min) TRIC organisms at the ratio of one live to 100 inactivated TRIC organisms, but not by inactivated lymphogranuloma venereum (434) or influenza virus (A(2)/Jap 305).
Female guinea pigs infected in the genital tract with the chlamydial agent of guinea pig inclusion conjunctivitis were selectively immunosuppressed by varying regimens of cyclophosphamide (Cy) treatment. Temporary suppression of both humoral and cell-mediated immunity by daily treatment of Cy (25 mg/kg) for 13 days resulted in a prolonged infection, whereas daily treatment for the duration of the experiment totally prevented the development of humoral and cell-mediated responses and produced an intense and prolonged infection which did not resolve. When humoral immunity alone was suppressed by treatment with Cy (250 and 150 mg/kg) at 9-day intervals, the infection again did not resolve. Treatment with 100 mg of Cy per kg at 9-day intervals resulted in an extended infection which resolved concomitantly with the development of antibody to guinea pig inclusion conjunctivitis. These data indicate that humoral immunity is essential for the recovery of female guinea pigs from guinea pig inclusion conjunctivitis genital infection. A market weight loss was observed which could not be attributed to Cy treatment alone. Edematous and ulcerative changes of the external genitalia were also noted.
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