Chlamydia trachomatis is a bacterium responsible for one of the most common sexually transmitted infections (STIs) globally. While known for causing conditions like pelvic inflammatory disease (PID), the question of whether this infection can also lead to cancer is complex and a major focus of ongoing research. Examining the scientific data reveals that while it is not a direct cause, the chronic nature of the infection may significantly increase cancer risk, particularly in specific tissues.
Chlamydia and the Current Scientific Consensus on Cancer Risk
Major international health organizations have not classified Chlamydia trachomatis as a direct, standalone carcinogen, meaning it does not cause cancer on its own in the same way that Human Papillomavirus (HPV) directly causes cervical cancer. The current scientific consensus points to the bacterium acting as a co-factor or risk enhancer rather than an independent carcinogenic agent. While the infection is statistically correlated with certain cancers in epidemiological studies, this distinction is important because it does not demonstrate a direct cause-and-effect relationship.
The association found in many studies suggests that a prior or persistent Chlamydia infection significantly increases the likelihood of developing certain cancers, but often only in the presence of other established risk factors. For example, in cervical cancer, Chlamydia is thought to promote the progression of disease initiated by high-risk HPV. This relationship indicates that the infection creates a more favorable environment for cancer development without being the sole trigger.
The Role of Chronic Inflammation and Cellular Change
The proposed mechanism linking Chlamydia to an increased cancer risk centers on the long-term inflammatory state it can induce. If the infection remains untreated, it can persist for months or years, leading to chronic inflammation in reproductive organs like the cervix or fallopian tubes. This prolonged inflammation recruits immune cells that release reactive oxygen species, which damage the DNA of nearby host cells through oxidative stress.
The bacteria also possess mechanisms that actively interfere with the body’s natural defense processes against malignant changes. Chlamydia infection has been shown to block the function of the tumor-suppressing protein p53, which normally detects and stops damaged cells from multiplying. By breaking down this protein, the bacterium prevents the host cell from initiating programmed cell death. This allows cells with genetic damage to survive, increasing their vulnerability to malignant transformation over time.
Specific Cancers Under Investigation
Research has most consistently investigated the link between Chlamydia infection and cervical cancer, where it is strongly supported as a co-factor with HPV. Women with a history of Chlamydia infection have an increased risk for invasive squamous cell carcinoma of the cervix. Some meta-analyses show the risk of co-infection with HPV is four times higher than with HPV alone, suggesting the infection increases the persistence of oncogenic HPV types.
Evidence also suggests a link with ovarian cancer, as women with antibodies indicating a past Chlamydia infection have shown an approximately two-fold increased risk in some studies. This association is plausible because PID, a complication of untreated Chlamydia, is a known risk factor for ovarian cancer, linking the disease to chronic inflammation. Studies examining prostate cancer have yielded mixed results, with some finding no association and others suggesting a connection based on bacterial DNA detection in tissue samples.
Reducing Risk Through Testing and Prompt Treatment
Since chronic, untreated infection drives the theorized cancer risk, the most effective preventative measure is early detection and complete treatment. Chlamydia is easily cured with a short course of antibiotics, which eliminates the source of damaging, long-term inflammation. Prompt antibiotic treatment prevents progression to complications like PID, thereby removing the inflammatory risk factor that contributes to cell changes.
Regular STI screening is recommended for sexually active individuals, especially women under the age of 25, who are at a higher risk of infection. Screening for Chlamydia should be based on risk factors, not solely tied to cervical cancer screening schedules like Pap tests. Adhering to screening guidelines and ensuring immediate and complete treatment eliminates this potential long-term health risk.