TY - JOUR
T1 - Risk factors for Chlamydia trachomatis pelvic inflammatory disease among sex workers in Nairobi, Kenya
AU - Kimani, Joshua
AU - Maclean, Ian W.
AU - Bwayo, Job J.
AU - MacDonald, Kelly
AU - Oyugi, Julius
AU - Maitha, Gregory M.
AU - Peeling, Rosanna W.
AU - Cheang, Mary
AU - Nagelkerke, Nicolaas J.D.
AU - Plummer, Francis A.
AU - Brunham, Robert C.
N1 - Funding Information:
Received 11 May 1995; revised 29 January 1996. Informed consent was obtained from study participants. Financial support: National Institutes of Health (subcontract with University of Washington, 483731). F. A. Plummer is the recipient of a Scientist Award from the Medical Research Council of Canada. Work was done in the departments of medical microbiology at the universities of Manitoba and Nairobi. Reprints or correspondence: Dr. Robert C. Brunham, Dept. of Medical Microbiology, University of Manitoba, Room 543,730 William Ave., Winnipeg, Manitoba R3E OW3, Canada.
PY - 1996
Y1 - 1996
N2 - Among 302 female sex workers in Nairobi, Kenya, who were followed for 17.6 ± 11.1 months, 146 had one or more infections with Chlamydia trachomatis; 102 had uncomplicated cervical infection only, 23 had C. trachomatis pelvic inflammatory disease (PID), and 21 had combined C. trachomatis and Neisseria gonorrhoeae PID. As determined by multivariate logistic regression analysis, risk factors for C. trachomatis PID included repeated C. trachomatis infection (odds ratio [OR], 1.8; 95% confidence interval [CI], 1.3-2.4; P = .0004), antibody to C. trachomatis heat-shock protein 60 (OR, 3.9; CI, 1.04-14.5; P = .04), oral contraceptive use (OR, 0.28; 95% CI, 0.08-0.99; P = .048), and number of episodes of nongonococcal nonchlamydial PID (OR, 1.7; 95% CI, 1.1-2.7; P = .02). Among human immunodeficiency virus (HIV)-seropositive women, a CD4 lymphocyte count of <400/mm3 was an additional independent risk factor for C. trachomatis PID (OR, 21.7; 95% CI, 1.2-383; P = .036); among HLA-typed women, HLA-A31 was independently associated with C. trachomatis PID (OR, 5.6; 95% CI, 1.1- 29.4; P = .043). The results suggest an immune-mediated pathogenesis for C. trachomatis PID.
AB - Among 302 female sex workers in Nairobi, Kenya, who were followed for 17.6 ± 11.1 months, 146 had one or more infections with Chlamydia trachomatis; 102 had uncomplicated cervical infection only, 23 had C. trachomatis pelvic inflammatory disease (PID), and 21 had combined C. trachomatis and Neisseria gonorrhoeae PID. As determined by multivariate logistic regression analysis, risk factors for C. trachomatis PID included repeated C. trachomatis infection (odds ratio [OR], 1.8; 95% confidence interval [CI], 1.3-2.4; P = .0004), antibody to C. trachomatis heat-shock protein 60 (OR, 3.9; CI, 1.04-14.5; P = .04), oral contraceptive use (OR, 0.28; 95% CI, 0.08-0.99; P = .048), and number of episodes of nongonococcal nonchlamydial PID (OR, 1.7; 95% CI, 1.1-2.7; P = .02). Among human immunodeficiency virus (HIV)-seropositive women, a CD4 lymphocyte count of <400/mm3 was an additional independent risk factor for C. trachomatis PID (OR, 21.7; 95% CI, 1.2-383; P = .036); among HLA-typed women, HLA-A31 was independently associated with C. trachomatis PID (OR, 5.6; 95% CI, 1.1- 29.4; P = .043). The results suggest an immune-mediated pathogenesis for C. trachomatis PID.
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U2 - 10.1093/infdis/173.6.1437
DO - 10.1093/infdis/173.6.1437
M3 - Article
C2 - 8648217
AN - SCOPUS:19244363174
SN - 0022-1899
VL - 173
SP - 1437
EP - 1444
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 6
ER -