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J Clin Pathol 2004;57:657-659 doi:10.1136/jcp.2003.013086
  • Short report

Chlamydia trachomatis serovar E isolates from patients with different clinical manifestations have similar courses of infection in a murine model: host factors as major determinants of C trachomatis mediated pathogenesis

  1. J M Lyons1,
  2. J I Ito, Jr1,
  3. S A Morré2
  1. 1Department of Infectious Diseases, City of Hope National Medical Center and Beckman Research Institute, Duarte, California 91010, USA
  2. 2Laboratory of Immunogenetics, Section Immunogenetics of Infectious Diseases, VU University Medical Centre, 1081 HV Amsterdam, The Netherlands
  1. Correspondence to:
 J M Lyons
 Department of Infectious Diseases, City of Hope National Medical Center and Beckman Research Institute, Duarte, California 91010, USA; jlyonscoh.org
  • Accepted 3 December 2003

Abstract

Background: Some investigators have proposed an association between certain Chlamydia trachomatis serovars and the clinical course of infection in humans. A recent study of over 1100 patients with culture confirmed and serotyped C trachomatis urogenital infection detected no such association.

Aims: To corroborate these results using a murine model of female genital tract infection.

Methods: Various parameters of infection were assessed in mice intravaginally infected with human genital isolates of C trachomatis serovar E from four cases with either a clear symptomatic or asymptomatic clinical course in both the patient and their partner.

Results: No differences were seen among the strains in the incidence or duration of infection, polymorphonuclear granulocyte responses, or upper genital tract progression.

Conclusions: An investigation to determine the correlation between the clinical manifestations of different isolates of C trachomatis serovar E in humans and certain parameters of microbial pathogenesis in a mouse model failed to reveal an association between the measured parameters and the tendency of serovar E to produce symptomatic versus asymptomatic infections in humans. These findings suggest that differences in the clinical course of infection in humans seen with these strains may be more related to host factors than to genetic variation among strains.

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