The Epidemiology of Chlamydia trachomatis within a Sexually Transmitted
Diseases Core Group
Robert C. Brunham, Joshua Kimani, Job Bwayo,
Gregory Maitha, Ian Maclean, Chunlin Yang,
Caixia Shen, Susan Roman, Nico J. D. Nagelkerke,
Mary Cheang, and Francis A. Plummer
Departments ofMedical Microbiology and Community Health Sciences,
University ofManitoba, Winnipeg, Canada; Department ofMedical
Microbiology, University ofNairobi, Nairobi, Kenya
Female sex workers in Nairobi were prospectively evaluated for risk factors ofincident Chlamydia
trachomatis infection. Independent risk factors included cervical ectopy (P = .007), gonococcal
infection (P = .002), human immunodeficiency virus (HIV) seropositivity (P = .003), HIV serocon-
version (P = .001), and duration of prostitution (P = .002). Eighteen different C. trachomatis outer
membrane protein (ompl) genotypes were identified, with the allelic composition of the C. tracho-
matis population changing significantly over time (P = .005). Seventeen of 19 reinfections ~
months apart were with different C. trachomatis ompi genotypes. Women with HIV infection had
an increased proportion of visits with C. trachomatis infection (P = .001) and an increased risk of
reinfection (P = .008). Overall, the data demonstrate significant fluctuations in the genotypecomposi-
tion of the C. trachomatis population and a reduced rate of same-genotype reinfection consistent
with the occurrence of strain-specific immunity.
Strains of Chlamydia trachomatis are antigenically variant
and classifiable into stable serologic variants or serovars .
The major outer membrane protein (MOMP) of the organism
is the predominant surface protein and determines the serologic
properties for individual C. trachomatis serovars . The sin-
gle-copy MOMP gene is termed omp], and the DNA sequence
for the entire open-reading frame is known for at least 7 differ-
ent C. trachomatis serovars [3, 4]. The genetic basis for C.
trachomatis serovar classification is due to allelic variation of
the single-copy gene, with 15 different omp] alleles recognized
for the 15 prototype serovars of C. trachomatis [5, 6]. The
omp] gene is >80% identical in DNA sequence among differ-
ent serovars, with most DNA sequence polymorphism concen-
trated into four regularly spaced variable gene segments. Com-
parison of DNA sequences among closely related serovars
shows that nucleotide variation within variable segments results
in nonsynonymous codons, and thus amino acid differences
among MOMP proteins are clustered into four variable domains
(VDs) [5, 7]. In general, the four VDs are exposed on the
chlamydial cell surface and recognizable by monoclonal anti-
bodies that are capable of neutralizing the organism in animal
models of experimental infection . Thus, MOMP displays
Received 12 September 1995; revised 22 November 1995.
Informed consent was obtained from all study participants at their enrollment
visit after review of the protocol by the Institutional Review Boards of the
University of Nairobi and the University of Manitoba.
Grant support: Medical Research Council ofCanada (SP27); Nationallnsti-
tutes of Health (955920).
Reprints or correspondence: Dr. Robert C. Brunham, Dept. ofMedical Mi-
crobiology, University of Manitoba, Room 543,730 William Ave., Winnipeg,
Manitoba, R3E OW3, Canada.
The Journal of Infectious Diseases
© 1996 by The University of Chicago. All rights reserved.
immunobiologic attributes that should playa role in the epide-
miology of C. trachomatis infection.
We previously suggested that antigenic (allelic) variation of
the C. trachomatis MOMP allows C. trachomatis strains to
persist in sexually transmitted disease (STD) core groups be-
cause ofthe occurrence ofserovar- or strain-specific immunity
[9, 10]. The genetic diversity at the omp] locus was proposed
to be maintained by frequency-dependent immune selection in
the STD core group members. This hypothesis was derived
from earlier observations ofexperimental C. trachomatis infec-
tion of humans, which showed that persons infected with a
given serovar of C. trachomatis were resistant to reinfection
with the same serovar but susceptible to infection with a heter-
ologous serovar . However, this finding has been more
difficult to demonstrate epidemiologically after natural human
infection, in part because ofthe difficulty in identifying a popu-
lation in which the incidence of infection is high enough that
episodes of reinfection with a variety of strains can be com-
pared. To obtain such data, we prospectively followed a cohort
ofurban sex workers in Nairobi for episodes of C. trachomatis
infection and characterized chlamydial strains by DNA se-
quencing ofvariable segments from the polymerase chain reac-
tion-amplified omp] gene.
sex workers in the Pumwani district ofNairobi was established in
April 1991 and prospectively followed for incident C. trachomatis
infection. Enrollment into the cohort was stratified to achieve about
equal numbers of women with and without human immunodefi-
ciency virus (HIV) infection. The stratification was purposefully
chosen after we reasoned that if C. trachomatis infection induces
immunity, it may be less evident among women with HIV infec-
As described previously , a cohort of
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956Brunham et al.
lID 1996; 173 (April)
fection to reinfection with same or different C. trachomatis strain as
determined by omp1 genotyping.
Relationship ofhuman immunodeficiency virus (HIV) in-
trachomatis occurring ;;:: I month apart; 97 episodes of infection represent 40
reinfections and 57 single infections. NR, not reinfected; S, reinfected with
same omp] genotype; D, reinfectedwith different omp] genotype. -, negative.
* HIV-negative vs. HIV-positive (HIV-seropositive and -seroconverting):
rate ratio, 11.0; 95% confidence interval, 1.2-98.0; P = .03 (per positive
Episode of reinfection was defined as ;;::2 positive tests for C.
nity to C. trachomatis infection, IgAl protease production by
gonococci may explain the association we and others  have
observed for gonococcal infection as a risk factor for chlamyd-
ial infection . Future study of the relationship between C.
trachomatis infection, omp] genotypes, MOMP-specific secre-
tory IgA, IgAl protease, and local interferon-'}'  as well as
other T cell cytokines will be required to adequately evaluate
the immunobiologic basis for host resistance to chlamydial
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s u b s p e c i e s ~ r e a c t i v e
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