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Condom effectiveness for prevention of C trachomatis infection
  1. L Warner1,2,
  2. M Macaluso1,
  3. D Newman1,
  4. H Austin2,
  5. D Kleinbaum2,
  6. M Kamb3,
  7. J Douglas3,
  8. C K Malotte4,
  9. J M Zenilman5
  1. 1Centers for Disease Control and Prevention, Division of Reproductive Health, Atlanta, GA, USA
  2. 2Rollins School of Public Health of Emory University, Department of Epidemiology, Atlanta, GA, USA
  3. 3Centers for Disease Control and Prevention, Division of STD Prevention, Atlanta, GA, USA
  4. 4California State University – Long Beach Department of Health Science, Long Beach, CA, USA
  5. 5Baltimore City Health Department, and Johns Hopkins University School of Medicine, Infectious Diseases Division, Baltimore, MD, USA
  1. Correspondence to:
 Lee Warner
 Centers for Disease Control and Prevention, Division of Reproductive Health, 4770 Bulford Highway NE, Mail Stop K-34, Atlanta, GA 30333, USA; dlw7{at}cdc.gov

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Replicating methods and comparing results across studies are critical for the resolution of scientific controversies. In a recent report, Niccolai et al demonstrated that condoms were effective in preventing chlamydia among STD clinic patients with known exposure to Chlamydia trachomatis.1 We were pleased to see the authors apply the methodology that we first presented for estimating condom effectiveness against chlamydia and gonorrhoea in 20012,3 and published in the American Journal of Epidemiology last year.4 Their findings confirm the importance of restricting the study population to people with known STI exposure (that is, sexual contacts of infected people) to reduce confounding on condom effectiveness estimates against bacterial4 and viral5,6 infections.

By focusing their analysis on chlamydia alone, Niccolai et al underscore the need for disease specific estimates of condom effectiveness. Focusing on a single disease is important because, although condoms should protect against all infections transmitted via the male urethra (including gonorrhoea and chlamydia),7 other factors, such as transmission efficiency, are disease specific and may influence the magnitude of the protective effect. We would like to clarify for readers, however, that the methodology we described will also allow for disease specific estimates of protection when multiple infections are evaluated among people with known exposure. As we noted (Warner et al4 p 243)), the key point is that infections diagnosed among study participants must be identical to those of the participants’ infected partner. (For example, the relation between condom use and risk for gonorrhoea should be assessed only among participants exposed to gonorrhoea, likewise for chlamydia.) Maintaining this algorithm, we combined estimates for chlamydia and gonorrhoea after observing the disease specific point estimates (0.38 and 0.47, respectively) were neither appreciably nor significantly different from each other (Warner et al4 p 245)). Thus, application of this methodology need not be limited to a single infection.

Niccolai et al’s study represents the most recent application of this methodology for estimating condom effectiveness among people with known STI exposure and, encouragingly, provides independent confirmation of the validity of this approach and of our earlier findings. This work adds to an increasing body of evidence4,8,9 suggesting that studies confounded by important differences between consistent users and inconsistent or non-users (for example, degree of STI exposure) tend to underestimate the protective effect of condoms against bacterial STI. Studies limited to individuals with known STI exposure are likely to estimate the protective effect of condom use more accurately. Given that such studies can be conducted using secondary analyses of existing trial data,4,8 as well as routinely collected clinic data,1,9 we encourage investigators to adopt similar methodologies to reduce confounding when evaluating condom effectiveness.

Finally, restricting the study population to sexual contacts of infected people probably has many applications for STI research beyond assessment of condom effectiveness. This methodology for reducing confounding may also provide a clearer insight into an array of potential causative and preventive factors for STI, where studies are subject to the same sources of confounding that have plagued condom effectiveness research.

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Footnotes

  • Disclaimer: The findings and conclusions in this letter are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention.

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