Epidemiology

Chlamydia is the most commonly reported curable bacterial sexually transmitted infection (STI) in the United Kingdom. In 2019 there were 229 411 cases of chlamydia, accounting for 49% of all new STI diagnoses [1]. The number of genital chlamydia infections in the United Kingdom and United States is highest in women aged 16–19 and in men aged 20–24. A pilot study for the UK National Chlamydia Screening Programme between 1999 and 2000 showed a prevalence of 10.5% in women in the 16–19 age group [2]. The burden of disease of genital chlamydial infection is high, with important consequential disease including pelvic inflammatory disease (PID), ectopic pregnancy, and tubal infertility. This incurs an annual cost to the UK Department of Health of £100 million.

Pathophysiology

Non‐LGV serovars of C. trachomatis mainly infect transitional and columnar epithelial cells, which explains the cervix, urethra, rectum, and conjunctiva being the main sites of infection. The organism attaches as an infectious, but metabolically inert, form called the elementary body (EB), which then enters the cell via a membrane‐bound vesicle called an inclusion body. Differentiation and further replication occur within the inclusion body, following which reorganisation takes place, resulting in the formation of further infectious EBs. The EBs are released by cytolysis and go on to infect new cells [3]. Infection with C. trachomatis is known to be associated with the establishment of persistent low‐grade infection that may be present for years. However, the mechanisms for this are poorly defined. In cell culture, interferon gamma (IFN‐γ) induces the production of non‐infectious, atypical organisms which remain viable for over 1 month [4]. These atypical forms of chlamydia differentiate into infectious EBs when IFN‐γ is removed from the cell culture system [5].

The clinical effects of chlamydia infection are likely to result from tissue damage caused by the organism and the inflammatory response induced by infected host cells. The inflammatory response may be caused by hypersensitivity induced by chlamydial heat shock proteins (HSPs). Women with ectopic pregnancy and tubal infertility have been found to have high levels of antibody to chlamydial HSP‐60 [6,7].

Clinical features

The incubation period of C. trachomatis is approximately 11 days for men [8], but it is not known for women, although it is inferred at about 20 days in women in rural Uganda [9]. Up to 80% of women with genital chlamydia are asymptomatic [10]. In those who do experience symptoms, these include postcoital or intermenstrual bleeding, lower abdominal pain, vaginal discharge, or dysuria. Examination may be normal or reveal a mucopurulent cervicitis or contact bleeding from the cervix. Women with PID may have adnexal or cervical tenderness.

Diagnosis

Testing using nucleic acid amplification technique (NAAT) is the standard of care, with NAATs being 90–95% sensitive and 99–100% specific [11]. These demonstrate superior performance to culture and enzyme immunoassay (EIA) [12,13], and can be done on non‐invasive samples such as urine tests or vulvovaginal swabs taken by the patient. Suitable samples for chlamydia testing include endocervical, urethral, and vulvovaginal swabs as well as first‐catch urine samples.

Complications

Chlamydial disease may be associated with infection of Bartholin’s glands [14]. Infection may also spread upwards from the cervix into the endometrium and along the fallopian tubes, resulting in PID. Seronegative reactive arthritis (sexually associated reactive arthritis) is rare in women, but may occur as a consequence of genital chlamydial infection and can manifest as circinate vulvitis [15], a condition clinically similar to circinate balanitis seen in men with Reiter’s syndrome. Other complications include Fitz‐Hugh–Curtis syndrome (chlamydial perihepatitis associated with PID) and adult conjunctivitis. Neonatal transmission can also occur, resulting in neonatal conjunctivitis and pneumonia.