Stephen J.LurieMD, PhD, Senior EditorIndividualAuthorJody W.ZylkeMD, Contributing EditorIndividualAuthor
Copyright 2001 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2001
To the Editor: Dr Anttila and colleagues1 described a serological correlation between past C trachomatis infection and the development of cervical SCC. They also described a potential clinical relevance for C trachomatis serovar typing since certain serovars, in particular serovar G, were associated with SCC. We previously described C trachomatis serovar number 19, serovar Ga.2,3 Serovar G (prototype strain UW-57) and Ga (prototype strain IOL-238) can be distinguished by using specific monoclonal antibodies (8.2C4 and 8.3H8) and by genotyping due to an additional BstU1 site in VS4 of the omp1 gene. A statistical difference in the clinical course of infection between the serovars G and Ga has been described: serovar Ga was associated with symptoms in both men and women and specifically with dysuria in men.4 As discussed by Anttila et al, some C trachomatis serovars may be more virulent than others, are perhaps less sensitive to certain antibiotics and could play a role in carcinogenesis. In the light of differences in virulence among serovars, it would be interesting to investigate whether the serological responses to the serovar G identified by Anttila et al are really responses to serovar G or, in fact, to serovar Ga.
Morré SA, Ossewaarde JM. Chlamydia trachomatis and Cervical Squamous Cell Carcinoma. JAMA. 2001;285(13):1703-1706. doi:10.1001/jama.285.13.1703