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Chlamydia
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Chlamydia
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Chlamydia
Other namesChlamydia infection
Pap smear showing C. trachomatis (H&E stain)
Pronunciation
SpecialtyInfectious disease, gynecology, urology
SymptomsNone, vaginal discharge, discharge from the penis, burning with urination[1]
ComplicationsPain in the testicles, pelvic inflammatory disease, infertility, ectopic pregnancy[1][2]
Usual onsetFew weeks following exposure[1]
CausesChlamydia trachomatis spread by sexual intercourse or childbirth[3]
Diagnostic methodUrine or swab of the cervix, vagina, or urethra[2]
PreventionNot having sex, condoms, sex with only one non–infected person[1]
TreatmentAntibiotics (azithromycin or doxycycline)[2]
Frequency4.2% (women), 2.7% (men)[4][5]
Deaths~200 (2015)[6]

Chlamydia, or more specifically a chlamydia infection, is a sexually transmitted infection caused by the bacterium Chlamydia trachomatis.[3] Most people who are infected have no symptoms.[1] When symptoms do appear, they may occur only several weeks after infection;[1] the incubation period between exposure and being able to infect others is thought to be on the order of two to six weeks.[7] Symptoms in women may include vaginal discharge or burning with urination.[1] Symptoms in men may include discharge from the penis, burning with urination, or pain and swelling of one or both testicles.[1] The infection can spread to the upper genital tract in women, causing pelvic inflammatory disease, which may result in future infertility or ectopic pregnancy.[2]

Chlamydia infections can occur in other areas besides the genitals, including the anus, eyes, throat, and lymph nodes. Repeated chlamydia infections of the eyes that go without treatment can result in trachoma, a common cause of blindness in the developing world.[8]

Chlamydia can be spread during vaginal, anal, oral, or manual sex and can be passed from an infected mother to her baby during childbirth.[1][9] The eye infections may also be spread by personal contact, flies, and contaminated towels in areas with poor sanitation.[8] Infection by the bacterium Chlamydia trachomatis only occurs in humans.[10] Diagnosis is often by screening, which is recommended yearly in sexually active women under the age of 25, others at higher risk, and at the first prenatal visit.[1][2] Testing can be done on the urine or a swab of the cervix, vagina, or urethra.[2] Rectal or mouth swabs are required to diagnose infections in those areas.[2]

Prevention is by not having sex, the use of condoms, or having sex with only one other person, who is not infected.[1] Chlamydia can be cured by antibiotics, with typically either azithromycin or doxycycline being used.[2] Erythromycin or azithromycin is recommended in babies and during pregnancy.[2] Sexual partners should also be treated, and infected people should be advised not to have sex for seven days and until symptom free.[2] Gonorrhea, syphilis, and HIV should be tested for in those who have been infected.[2] Following treatment, people should be tested again after three months.[2]

Chlamydia is one of the most common sexually transmitted infections, affecting about 4.2% of women and 2.7% of men worldwide.[4][5] In 2015, about 61 million new cases occurred globally.[11] In the United States, about 1.4 million cases were reported in 2014.[3] Infections are most common among those between the ages of 15 and 25 and are more common in women than men.[2][3] In 2015, infections resulted in about 200 deaths.[6] The word chlamydia is from the Greek χλαμύδα, meaning 'cloak'.[12][13]

Signs and symptoms

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Genital disease

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Inflammation of the cervix from chlamydia infection characterized by mucopurulent cervical discharge, redness, and inflammation
A white, cloudy or watery discharge may emerge from the tip of the penis.

Women

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Chlamydial infection of the cervix (neck of the womb) is a sexually transmitted infection which has no symptoms for around 70% of women infected. The infection can be passed through vaginal, anal, oral, or manual sex. Of those who have an asymptomatic infection that is not detected by their doctor, approximately half will develop pelvic inflammatory disease (PID), a generic term for infection of the uterus, fallopian tubes, and/or ovaries. PID can cause scarring inside the reproductive organs, which can later cause serious complications, including chronic pelvic pain, difficulty becoming pregnant, ectopic (tubal) pregnancy, and other dangerous complications of pregnancy.[14]

Chlamydia is known as the "silent epidemic", as at least 70% of genital C. trachomatis infections in women (and 50% in men) are asymptomatic at the time of diagnosis,[15] and can linger for months or years before being discovered. Signs and symptoms may include abnormal vaginal bleeding or discharge, abdominal pain, painful sexual intercourse, fever, painful urination or the urge to urinate more often than usual (urinary urgency).[14]

For sexually active women who are not pregnant, screening is recommended in those under 25 and others at risk of infection.[16] Risk factors include a history of chlamydial or other sexually transmitted infection, new or multiple sexual partners, and inconsistent condom use.[17] Guidelines recommend all women attending for emergency contraceptive are offered chlamydia testing, with studies showing up to 9% of women aged under 25 years had chlamydia.[18]

Men

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In men, those with a chlamydial infection show symptoms of infectious inflammation of the urethra in about 50% of cases.[15] Symptoms that may occur include: a painful or burning sensation when urinating, an unusual discharge from the penis, testicular pain or swelling, or fever. If left untreated, chlamydia in men can spread to the testicles causing epididymitis, which in rare cases can lead to sterility if not treated.[15] Chlamydia is also a potential cause of prostatic inflammation in men, although the exact relevance in prostatitis is difficult to ascertain due to possible contamination from urethritis.[19]

Eye disease

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Main article: Trachoma
Conjunctivitis due to chlamydia

Trachoma is a chronic conjunctivitis caused by Chlamydia trachomatis.[20] It was once the leading cause of blindness worldwide, but its role diminished from 15% of blindness cases by trachoma in 1995 to 3.6% in 2002.[21][22] The infection can be spread from eye to eye by fingers, shared towels or cloths, coughing and sneezing and eye-seeking flies.[23] Symptoms include mucopurulent ocular discharge, irritation, redness, and lid swelling.[20] Newborns can also develop chlamydia eye infection through childbirth (see below). Using the SAFE strategy (acronym for surgery for in-growing or in-turned lashes, antibiotics, facial cleanliness, and environmental improvements), the World Health Organization aimed (unsuccessfully) for the global elimination of trachoma by 2020 (GET 2020 initiative).[24][25] The updated World Health Assembly neglected tropical diseases road map (2021–2030) sets 2030 as the new timeline for global elimination.[26]

Joints

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Chlamydia may also cause reactive arthritis—the triad of arthritis, conjunctivitis and urethral inflammation—especially in young men. About 15,000 men develop reactive arthritis due to chlamydia infection each year in the U.S., and about 5,000 are permanently affected by it. It can occur in both sexes, though is more common in men.[citation needed]

Infants

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As many as half of all infants born to mothers with chlamydia will be born with the disease. Chlamydia can affect infants by causing spontaneous abortion; premature birth; conjunctivitis, which may lead to blindness; and pneumonia.[27] Conjunctivitis due to chlamydia typically occurs one week after birth (compared with chemical causes (within hours) or gonorrhea (2–5 days)).[28]

Other conditions

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A different serovar of Chlamydia trachomatis is also the cause of lymphogranuloma venereum, an infection of the lymph nodes and lymphatics. It usually presents with genital ulceration and swollen lymph nodes in the groin, but it may also manifest as rectal inflammation, fever or swollen lymph nodes in other regions of the body.[29]

Transmission

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Chlamydia can be transmitted during vaginal, anal, oral, or manual sex or direct contact with infected tissue such as conjunctiva. Chlamydia can also be passed from an infected mother to her baby during vaginal childbirth.[27] It is assumed that the probability of becoming infected is proportionate to the number of bacteria one is exposed to.[30]

Recent research using droplet digital PCR and viability assays found evidence of high-viability C. trachomatis in the gastrointestinal tract of women who abstained from receptive anal intercourse. Rectal C. trachomatis appeared independent of cervical infection—with distinct MLST types detected in rectal versus endocervical samples—suggesting persistent gastrointestinal colonization likely acquired through prior vaginorectal or oral routes, rather than direct anal exposure.[31]

Pathophysiology

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Chlamydia bacteria have the ability to establish long-term associations with host cells. When an infected host cell is starved for various nutrients such as amino acids (for example, tryptophan),[32] iron, or vitamins, this has a negative consequence for chlamydia bacteria since the organism is dependent on the host cell for these nutrients. Long-term cohort studies indicate that approximately 50% of those infected clear within a year, 80% within two years, and 90% within three years.[33]

The starved chlamydia bacteria can enter a persistent growth state where they stop cell division and become morphologically aberrant by increasing in size.[34] Persistent organisms remain viable as they are capable of returning to a normal growth state once conditions in the host cell improve.[35]

There is debate as to whether persistence has relevance: some believe that persistent chlamydia bacteria are the cause of chronic chlamydial diseases. Some antibiotics such as β-lactams have been found to induce a persistent-like growth state.[36][37]

Diagnosis

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Chlamydia trachomatis inclusion bodies (brown) in a McCoy cell culture

The diagnosis of genital chlamydial infections evolved rapidly from the 1990s through 2006. Nucleic acid amplification tests (NAAT), such as polymerase chain reaction (PCR), transcription mediated amplification (TMA), and the DNA strand displacement amplification (SDA) now are the mainstays. NAAT for chlamydia may be performed on swab specimens sampled from the cervix (women) or urethra (men), on self-collected vaginal swabs, or on voided urine.[38] NAAT has been estimated to have a sensitivity of approximately 90% and a specificity of approximately 99%, regardless of sampling from a cervical swab or by urine specimen.[39] In women seeking treatment in a sexually transmitted infection clinic where a urine test is negative, a subsequent cervical swab has been estimated to be positive in approximately 2% of the time.[39]

At present, the NAATs have regulatory approval only for testing urogenital specimens, although rapidly evolving research indicates that they may give reliable results on rectal specimens.

Because of improved test accuracy, ease of specimen management, convenience in specimen management, and ease of screening sexually active men and women, the NAATs have largely replaced culture, the historic gold standard for chlamydia diagnosis, and the non-amplified probe tests. The latter test is relatively insensitive, successfully detecting only 60–80% of infections in asymptomatic women, and often giving falsely-positive results. Culture remains useful in selected circumstances and is currently the only assay approved for testing non-genital specimens. Other methods also exist including: ligase chain reaction (LCR), direct fluorescent antibody resting, enzyme immunoassay, and cell culture.[40]

The swab sample for chlamydial infections does not show difference whether the sample was collected in home or in clinic in terms of numbers of patient treated. The implications in cured patients, reinfection, partner management, and safety are unknown.[41]

Rapid point-of-care tests are, as of 2020, not thought to be effective for diagnosing chlamydia in men of reproductive age and non-pregnant women because of high false-negative rates.[42]

Prevention

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Prevention is by not having sex, the use of condoms, or having sex only in a long-term monogamous relationship with someone who has been tested and confirmed not to be infected.[1]

Screening

[edit]

For sexually active women who are not pregnant, screening is recommended in those under 25 and others at risk of infection.[16] Risk factors include a history of chlamydial or other sexually transmitted infection, new or multiple sexual partners, and inconsistent condom use.[17] For pregnant women, guidelines vary: screening women with age or other risk factors is recommended by the U.S. Preventive Services Task Force (USPSTF) (which recommends screening women under 25) and the American Academy of Family Physicians (which recommends screening women aged 25 or younger). The American College of Obstetricians and Gynecologists recommends screening all at risk, while the Centers for Disease Control and Prevention recommend universal screening of pregnant women.[16] The USPSTF acknowledges that in some communities there may be other risk factors for infection, such as ethnicity.[16] Evidence-based recommendations for screening initiation, intervals and termination are currently not possible.[16] For men, the USPSTF concludes evidence is currently insufficient to determine if regular screening of men for chlamydia is beneficial.[17] They recommend regular screening of men who are at increased risk for HIV or syphilis infection.[17] A Cochrane review found that the effects of screening are uncertain in terms of chlamydia transmission but that screening probably reduces the risk of pelvic inflammatory disease in women.[43]

In the United Kingdom the National Health Service (NHS) aims to:

  1. Prevent and control chlamydia infection through early detection and treatment of asymptomatic infection;
  2. Reduce onward transmission to sexual partners;
  3. Prevent the consequences of untreated infection;
  4. Test at least 25 percent of the sexually active under 25 population annually.[44]
  5. Retest after treatment.[45]

Treatment

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C. trachomatis infection can be effectively cured with antibiotics. Guidelines recommend azithromycin, doxycycline, erythromycin, levofloxacin, or ofloxacin.[46] In men, doxycycline (100 mg twice a day for 7 days) is probably more effective than azithromycin (1 g single dose) but evidence for the relative effectiveness of antibiotics in women is very uncertain.[47] Agents recommended during pregnancy include erythromycin or amoxicillin.[2][48]

An option for treating sexual partners of those with chlamydia or gonorrhea includes patient-delivered partner therapy (PDT or PDPT), which is the practice of treating the sex partners of index cases by providing prescriptions or medications to the patient to take to his/her partner without the health care provider first examining the partner.[49]

Following treatment people should be tested again after three months to check for reinfection.[2] Test of cure may be false-positive due to the limitations of NAAT in a bacterial (rather than a viral) context, since targeted genetic material may persist in the absence of viable organisms.[50]

Epidemiology

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Disability-adjusted life year (DALY) for chlamydia per 100,000 inhabitants in 2004[51]
  no data
  ≤10
  10–20
  20–30
  30–40
  40–50
  50–60
  60–70
  70–80
  80–90
  90–100
  100–110
  more than 110

Globally, as of 2015, sexually transmitted chlamydia affects approximately 61 million people.[11] It is more common in women (3.8%) than men (2.5%).[52] In 2015 it resulted in about 200 deaths.[6]

In the United States about 1.6 million cases were reported in 2016.[53] The CDC estimates that if one includes unreported cases there are about 2.9 million each year.[53] It affects around 2% of young people.[54] Chlamydial infection is the most common bacterial sexually transmitted infection in the UK.[55]

Chlamydia causes more than 250,000 cases of epididymitis in the U.S. each year. Chlamydia causes 250,000 to 500,000 cases of PID every year in the United States. Women infected with chlamydia are up to five times more likely to become infected with HIV, if exposed.[27]

See also

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Chlamydia

View on Grokipedia
from Grokipedia
Chlamydia is a common and curable sexually transmitted infection (STI) caused by the bacterium Chlamydia trachomatis, which primarily infects the mucous membranes of the genital tract, rectum, throat, and eyes. It affects both men and women and is often asymptomatic, with an estimated 70–80% of infections in women and 50% in men showing no symptoms, leading to undetected spread. Globally, chlamydia is one of the most prevalent bacterial STIs, with an estimated 129 million new cases among adults aged 15–49 years in 2020. Transmission occurs mainly through unprotected vaginal, anal, or oral sex with an infected partner, and it can also be passed from mother to child during childbirth, potentially causing neonatal conjunctivitis or pneumonia. When symptoms do appear, typically 1–3 weeks after exposure, they may include unusual genital discharge, pain or burning during urination, lower abdominal pain in women, or testicular pain in men. In women, untreated infections can ascend to the upper reproductive tract, causing pelvic inflammatory disease (PID). Complications from untreated chlamydia are significant, including infertility, ectopic pregnancy, and chronic pelvic pain in women, as well as epididymitis and reactive arthritis in men; chlamydia infection also increases the risk of acquiring and transmitting HIV, with studies reporting relative risks (RR) or odds ratios (OR) typically ranging from 1.5 to 5, depending on population, gender, site of infection, and study design. Non-ulcerative STIs like chlamydia are often associated with a 1.5-3 fold increase in risk, while some prospective studies report higher estimates (up to 4-5 fold) in specific groups such as MSM with rectal chlamydia or heterosexual women with genital infection. In the United States, chlamydia remains the most frequently reported notifiable infectious disease, with prevalence highest among individuals aged 15–24 years and cases declining by 8% from 2023 to 2024. Diagnosis relies on nucleic acid amplification tests (NAATs) using urine or swab samples from affected sites, which are highly sensitive and specific. Effective treatment involves antibiotics such as doxycycline (100 mg orally twice daily for 7 days) as the preferred regimen for non-pregnant adults, or azithromycin (1 g single oral dose) as an alternative; expedited partner therapy is recommended to prevent reinfection. Prevention strategies emphasize consistent and correct condom use during sexual activity, routine screening for at-risk populations (e.g., sexually active women under 25), and prompt treatment of partners. No vaccine is currently available, but global health targets aim to reduce new chlamydia cases by 50% by 2030 through improved access to testing and care.

Microbiology

Genus Chlamydia

The genus Chlamydia comprises obligate intracellular bacteria belonging to the phylum Chlamydiota, class Chlamydiia, order Chlamydiales, and family Chlamydiaceae. These Gram-negative pathogens are characterized by their dependence on eukaryotic host cells for replication and survival. Three primary species are pathogenic to humans: Chlamydia trachomatis, which causes a range of infections including sexually transmitted diseases; Chlamydia pneumoniae, associated with respiratory illnesses; and Chlamydia psittaci, linked to zoonotic infections from birds and mammals. A defining feature of the genus is its unique biphasic developmental cycle, alternating between two distinct morphological forms within host cells. Elementary bodies (EBs) are small (0.25–0.3 μm), infectious, and metabolically inert, serving as the extracellular transmission form that attaches to and enters host cells via endocytosis. Once inside, EBs differentiate into larger (0.5–1.0 μm), replicative reticulate bodies (RBs) within a membrane-bound inclusion, where they undergo binary fission every 2–3 hours over 18–24 hours. RBs are non-infectious but metabolically active, eventually reorganizing into new EBs over 24–36 hours before host cell lysis releases them to infect new cells. This cycle ensures efficient propagation while evading host defenses. Genomically, Chlamydia species possess a compact chromosome of approximately 1 megabase (Mb), encoding around 900 genes, alongside a small cryptic plasmid of about 7.5 kilobases that aids in replication and virulence. Due to genome reduction, they lack key biosynthetic pathways, including the ability to independently synthesize ATP via oxidative phosphorylation or a complete tricarboxylic acid cycle, instead importing ATP from the host through a specialized ADP/ATP translocase. This metabolic parasitism underscores their obligate intracellular lifestyle, relying on host nucleotides, amino acids, and lipids for energy and growth. The genus was formally named Chlamydia in 1945 by Jones, Rake, and Stearns, deriving from the Greek "chlamys" (cloak), reflecting the pathogens' intracellular seclusion. However, infections caused by these bacteria, such as trachoma, have been documented since ancient times, with evidence from Egyptian papyri dating to around 1550 BCE describing ocular symptoms consistent with the disease. Early microbiological studies in the early 20th century initially classified chlamydiae as viruses due to their filterability and host dependence, but ribosomal and cell wall analyses later confirmed their bacterial nature.

Chlamydia trachomatis

Chlamydia trachomatis is an obligate intracellular bacterium that primarily infects humans and is responsible for a range of mucosal infections. It belongs to the genus Chlamydia and shares the characteristic biphasic developmental cycle of the genus. Unlike other species in the genus, C. trachomatis is adapted to human hosts and targets epithelial cells in the ocular and urogenital tracts. The species is classified into 15 serovars based on antigenic variations in the major outer membrane protein (MOMP), which is encoded by the ompA gene and determines tissue tropism and disease presentation. Serovars A, B, Ba, and C are associated with trachoma, a leading cause of infectious blindness; serovars D through K cause urogenital infections; and serovars L1 through L3 are linked to lymphogranuloma venereum (LGV), a more invasive form of disease. Serotyping relies on the immunogenic epitopes of MOMP, which exhibit sequence variability in four hypervariable domains while conserving structural regions. Additionally, C. trachomatis harbors a 7.5 kb cryptic plasmid present in 7-10 copies per bacterium, which plays a role in plasmid maintenance and is a common target for molecular detection assays due to its stability and conservation across strains. The host range of C. trachomatis is largely restricted to humans, with no established natural reservoirs in animals, though limited experimental infections in non-human primates have been reported. This contrasts with Chlamydia psittaci, which has a broad zoonotic potential infecting birds and mammals, often causing psittacosis in humans via inhalation. Similarly, Chlamydia pneumoniae primarily causes respiratory infections in humans but can spread person-to-person without zoonotic involvement, differing from C. trachomatis' focus on sexually and perinatally transmitted mucosal diseases. Genomic studies have identified key virulence factors in C. trachomatis, including a type III secretion system (T3SS) that enables direct injection of effector proteins into host cells to manipulate cellular processes and evade immune responses. This system, conserved across chlamydiae, is crucial for invasion and intracellular survival, with ongoing genomic analyses through 2025 highlighting its role in serovar-specific pathogenesis through sequencing of clinical isolates. Recent advances as of 2025 include improved genome assembly pipelines, direct sequencing from clinical swabs, core-genome MLST schemes for surveillance, and enhanced genetic manipulation tools to study T3SS and other effectors.

Clinical Manifestations

Urogenital Infections

Urogenital infections caused by Chlamydia trachomatis serovars D-K are the most common form of chlamydial disease and primarily affect the urethra, cervix, and upper genital tract. These infections are frequently asymptomatic, with estimates indicating that at least 70% of cases in women and 50% in men lack noticeable symptoms at diagnosis, contributing to silent transmission and delayed detection. When symptoms occur, they typically manifest 1-3 weeks after exposure and vary by sex, often mimicking other sexually transmitted infections. In men, symptomatic urogenital chlamydia usually presents as urethritis, characterized by dysuria, urethral pruritus, and a mucoid or purulent discharge from the penis. These signs can be mild and intermittent, leading some individuals to overlook them. In women, the infection often causes cervicitis, with symptoms including abnormal vaginal discharge, postcoital or intermenstrual bleeding, and lower abdominal or pelvic pain. Dysuria may also occur due to urethral involvement, though many cases progress unnoticed to the upper genital tract. Untreated urogenital chlamydia can lead to serious complications, particularly in women, where ascending infection may result in pelvic inflammatory disease (PID), affecting up to 10-15% of cases and causing tubal scarring that increases risks of ectopic pregnancy and infertility. In men, complications are less frequent but include epididymitis, presenting as unilateral testicular pain and swelling, and rare cases of prostatitis. A more invasive form of urogenital chlamydia is lymphogranuloma venereum (LGV), caused by C. trachomatis serovars L1, L2, or L3, which can disseminate beyond the mucosa. LGV typically begins with a transient genital ulcer or papule, followed by regional lymphadenopathy—often painful and suppurative in the inguinal or femoral nodes—and, in cases of rectal involvement, proctocolitis with symptoms like anal pain, discharge, and bleeding. Recent surveillance data indicate a notable rise in LGV cases among men who have sex with men (MSM), with a 41% increase from 2022 to 2023 in the EU/EEA (from 1,302 cases in 2021 to 2,059 in 2022, continuing upward), highlighting ongoing challenges in prevention and screening within this population.

Ocular Infections

Ocular infections caused by Chlamydia trachomatis primarily manifest as trachoma and adult inclusion conjunctivitis, distinct forms of keratoconjunctivitis that can lead to significant visual impairment if untreated. Trachoma represents a chronic form of keratoconjunctivitis resulting from repeated infections with C. trachomatis serovars A, B, Ba, and C. These serovars target the conjunctival epithelium, initiating an inflammatory response that progresses through distinct stages as defined by the World Health Organization's simplified grading system. The initial active stage, trachomatous follicular inflammation (TF), features five or more follicles at least 0.5 mm in diameter on the central upper tarsal conjunctiva, commonly observed in preschool-aged children in endemic areas. This advances to trachomatous intense inflammation (TI), characterized by pronounced inflammatory thickening of the upper tarsal conjunctiva obscuring more than half of the deep tarsal vessels. Over time, chronic inflammation leads to trachomatous scarring (TS), visible as scarring in the tarsal conjunctiva, followed by trachomatous trichiasis (TT), where two or more lashes touch the eyeball, causing corneal abrasion. The final stage, corneal opacity (CO), involves easily visible scarring in the central cornea that blurs the pupil's margin, resulting in irreversible blindness. Adult inclusion conjunctivitis arises from ocular exposure to genital serovars D through K of C. trachomatis, often through direct contact or autoinoculation. It typically presents as a unilateral condition with chronic hyperemia, marked tarsal follicular response, and mucopurulent discharge, accompanied by symptoms such as lid swelling, irritation, and foreign body sensation persisting for weeks to months. Unlike trachoma, it rarely progresses to scarring but may involve superior corneal subepithelial opacities and preauricular lymphadenopathy. Globally, trachoma remains the leading infectious cause of blindness, affecting approximately 1.9 million people with visual impairment or blindness as of 2025. This burden is concentrated in approximately 38 endemic countries, where poor sanitation facilitates transmission via fomites such as infected eye secretions on hands or towels. As of November 2025, 27 countries have been validated by WHO as having eliminated trachoma as a public health problem, including recent validations for Fiji (October 2025) and Egypt (November 2025). A pathognomonic sign of active chlamydial ocular infection in both trachoma and adult inclusion conjunctivitis is the presence of characteristic inclusion bodies—intracellular vacuoles containing chlamydial reticulate bodies—visible in Giemsa-stained conjunctival scrapings from epithelial cells.

Extragenital and Systemic Manifestations

Chlamydia trachomatis infections can manifest in extragenital sites beyond the urogenital tract, particularly in the rectum and pharynx, often acquired through receptive anal or oral intercourse. Rectal infections may be asymptomatic or present with proctitis, characterized by rectal pain, bleeding, discharge, and tenesmus, while pharyngeal infections are typically asymptomatic but can cause pharyngitis or lymphadenitis in symptomatic cases. These extragenital infections are notably prevalent among men who have sex with men (MSM), with rectal chlamydia detection rates ranging from 2.1% to 23.0% (median 8.9%) and pharyngeal rates from 0% to 3.6% (median 1.7%). Detection relies on nucleic acid amplification tests (NAATs) at anatomic exposure sites, which are the most sensitive method despite not being FDA-approved for extragenital use without validation. A significant systemic complication of C. trachomatis infection is reactive arthritis, formerly known as Reiter's syndrome, which arises as a post-infectious autoimmune response typically 1-4 weeks after urogenital infection. It is characterized by the classic triad of asymmetric oligoarthritis (affecting lower extremities), sterile urethritis, and conjunctivitis, though not all patients exhibit the full triad. The condition is strongly associated with the HLA-B27 genotype, present in 30-50% of cases and up to 80% in severe forms, predisposing individuals to chronicity and sacroiliitis. Evidence of C. trachomatis infection is found in 36-50% of posturethritic reactive arthritis cases, involving molecular mimicry where bacterial antigens trigger T-lymphocyte-mediated synovial inflammation. Rarer systemic manifestations include perihepatitis, known as Fitz-Hugh-Curtis syndrome, which involves inflammation of the liver capsule and affects 4-14% of women with pelvic inflammatory disease caused by C. trachomatis ascent. Symptoms include acute right upper quadrant pain, fever, and chills, often mimicking other abdominal conditions. Adult pneumonia due to C. trachomatis is uncommon outside immunocompromised states, presenting with respiratory symptoms and detectable bacterial elements in lung tissue. Other infrequent associations encompass endocarditis and erythema nodosum. Recent expansions in extragenital screening have led to increased detections of C. trachomatis infections, with CDC surveillance noting that broader testing at rectal and pharyngeal sites in 2023 identified more cases, particularly among high-risk groups like MSM. This rise reflects improved NAAT accessibility and guideline adherence rather than a true epidemic surge.

Neonatal Infections

Neonatal infections with Chlamydia trachomatis primarily occur through perinatal transmission during passage through an infected birth canal, with a transmission risk of 50-60% to the infant if the mother is infected. These infections manifest most commonly as conjunctivitis or pneumonia in the neonate. Chlamydial conjunctivitis, also known as inclusion blennorrhea, typically develops 5-14 days after birth and presents with mucopurulent or purulent ocular discharge, conjunctival injection, and eyelid edema. This condition is the leading infectious cause of neonatal conjunctivitis in many regions. Pneumonia due to C. trachomatis usually appears between 4 and 12 weeks of age, often following or concurrent with conjunctivitis in up to 50% of cases. It is characterized by an afebrile illness with a distinctive staccato or paroxysmal cough, tachypnea, and rales on auscultation, without significant fever or leukocytosis. Chest radiographs commonly show bilateral hyperinflation and interstitial infiltrates, reflecting the subacute nature of the infection. In addition to ocular and pulmonary involvement, neonates may develop nasopharyngeal carriage of C. trachomatis, which can lead to nasopharyngitis or otitis media as secondary complications. This carriage contributes to the respiratory tract involvement seen in affected infants.

Transmission

Sexual Transmission

Chlamydia trachomatis, the primary causative agent of bacterial sexually transmitted infections, is transmitted through direct mucosal contact during vaginal, anal, or oral sexual activity with an infected partner. The bacterium adheres to and infects columnar epithelial cells in the genital tract, with transmission occurring via exposure to infected secretions such as semen or cervical mucus. Per-partnership transmission probabilities are estimated at approximately 32% from male to female and 25% from female to male, highlighting the high infectivity within ongoing sexual relationships. A significant proportion of C. trachomatis infections, particularly in women, are asymptomatic, with 70-95% of cases showing no symptoms, enabling prolonged shedding of the pathogen from genital sites without detection. This asymptomatic carriage facilitates silent transmission, as infected individuals can unknowingly spread the bacteria during sexual contact, contributing to its high prevalence. Serovars D through K are the predominant strains responsible for these urogenital infections, targeting the endocervix in women and urethra in men. Key risk factors for sexual acquisition include having multiple sexual partners, which increases exposure opportunities, and inconsistent or incorrect condom use, which reduces protection against mucosal transmission. A 2024 study (using data from 2017-2022) found a high prevalence of high-risk HPV co-infection (70.2%) in individuals with rectal Chlamydia trachomatis or Neisseria gonorrhoeae infections among men who have sex with men, potentially exacerbating transmission and complications.

Perinatal Transmission

Perinatal transmission of Chlamydia trachomatis occurs via vertical spread from an infected mother to her infant during childbirth, primarily through direct contact with cervical or vaginal secretions as the infant traverses the birth canal. This exposure can affect the neonate's mucous membranes, including the eyes, nasopharynx, rectum, and urogenital tract. Ascending infection from the lower genital tract to the amniotic fluid may also contribute, particularly in cases of prolonged rupture of membranes. In the absence of maternal treatment or prophylaxis, the vertical transmission rate ranges from 30% to 50%. Transmission can occur even with cesarean delivery if membranes have ruptured prior to surgery, though rates are lower compared to vaginal birth. Maternal urogenital infections, often asymptomatic, serve as the primary reservoir for this exposure. Key risk factors include untreated maternal cervicitis, which heightens bacterial load in genital secretions, and premature rupture of membranes, which facilitates pathogen ascent and prolongs exposure. Infants born to mothers without prenatal care or those at high risk for sexually transmitted infections face elevated transmission probabilities. Prevention relies on antenatal screening of pregnant individuals, typically at the first prenatal visit and in the third trimester for those at ongoing risk, followed by prompt treatment with antibiotics such as azithromycin to reduce maternal infection and thereby transmission. Unlike group B streptococcal disease, no routine intrapartum antibiotic prophylaxis is recommended for C. trachomatis, emphasizing the importance of early detection over labor-time interventions. This mode of transmission commonly results in neonatal conjunctivitis or pneumonia, with manifestations addressed in the Neonatal Infections section.

Other Routes

Chlamydia is mainly transmitted through unprotected sexual contact or from mother to child during birth; it is not spread through air, sharing items like towels or toilets, or common surfaces unless there is immediate direct contact with fresh secretions, which is rare. For urogenital infections caused by Chlamydia trachomatis, spread through household items or public bathrooms is unlikely because the bacterium dies quickly on dry surfaces, in air, or when secretions dry. Any theoretical risk from immediate contact with fresh infected secretions contacting skin or mucosa is minimal and does not occur in practice. In addition to the primary modes of transmission, Chlamydia trachomatis can spread through rare indirect routes, particularly affecting the eyes in cases of trachoma and inclusion conjunctivitis. For trachoma, caused by specific ocular serovars of C. trachomatis, transmission often involves fomites such as contaminated towels, clothing, or other shared objects, as well as eye-seeking flies like Musca sorbens that carry infectious discharge from infected individuals' eyes to others in close proximity, especially in endemic areas with poor sanitation. These vectors facilitate spread in hyperendemic communities, where the "three Fs"—fingers, fomites, and flies—play a key role in sustaining infection cycles, distinguishing this from the negligible fomite risk in urogenital infections. Autoinoculation represents another infrequent pathway, where individuals with genital C. trachomatis infections inadvertently transfer bacteria to their own eyes via contaminated hands or fingers, leading to adult inclusion conjunctivitis. This self-transfer of infected genital secretions to the ocular surface underscores the importance of hygiene in preventing such secondary infections. Historically, eye-to-eye transmission has been documented in household settings for inclusion conjunctivitis, often through direct contact with ocular secretions or shared personal items among family members, contributing to outbreaks before widespread recognition of the pathogen in the mid-20th century. Laboratory-acquired infections, though exceedingly rare, have occurred via accidental exposure to aerosols or contaminated materials during research, resulting in cases of conjunctivitis or trachoma-like ocular infections among workers handling C. trachomatis cultures. Unlike other chlamydial species such as C. psittaci, C. trachomatis is not considered zoonotic and lacks evidence of natural transmission from animals to humans. As of 2025, these alternative routes are negligible in developed countries due to improved hygiene, sanitation, and infection control measures, but they remain critical for global trachoma elimination efforts, particularly in endemic regions where vector control and fomite reduction are integral to the World Health Organization's SAFE strategy.

Pathophysiology

Infection Cycle

Chlamydia trachomatis exhibits a biphasic developmental cycle characterized by two distinct forms: the infectious, extracellular elementary body (EB) and the non-infectious, intracellular reticulate body (RB). This cycle enables the bacterium to invade host cells, replicate, and disseminate while evading degradation. The infection begins with the attachment of EBs to the surface of host epithelial cells, primarily mediated by binding to heparan sulfate-like glycosaminoglycans on the bacterial surface and host cell receptors. This interaction facilitates entry via endocytosis into a membrane-bound vacuole, potentially involving clathrin- and dynamin-dependent pathways as well as actin polymerization. Once inside, the EB differentiates into an RB within the nascent inclusion, a modified vacuole that actively avoids fusion with lysosomes through the action of type III secretion system effectors, ensuring the pathogen's survival. Within the inclusion, RBs replicate by binary fission, expanding the bacterial population over approximately 24-48 hours. As the inclusion matures, RBs asynchronously revert to EBs, completing the developmental cycle in 48-72 hours. New EBs are released either by host cell lysis, which disrupts the plasma membrane, or by extrusion, where the entire inclusion is pinched off and expelled intact, allowing dissemination to adjacent cells. In chronic or stress-induced conditions, such as exposure to antibiotics or nutrient deprivation, C. trachomatis can enter a persistent state characterized by aberrant bodies—enlarged, non-dividing forms that maintain viability but halt the standard replicative cycle. These aberrant forms contribute to long-term infection by evading host clearance mechanisms, potentially reactivating upon resolution of the stressor.

Host Immune Response

The innate immune response to Chlamydia trachomatis infection primarily involves recognition of bacterial components by Toll-like receptors (TLRs), particularly TLR2 and TLR4, expressed on epithelial cells and other mucosal surfaces. These receptors detect chlamydial lipopolysaccharide (LPS) and heat shock proteins, triggering signaling pathways that lead to the activation of nuclear factor kappa B (NF-κB) and the release of pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α). This cytokine production promotes local inflammation, recruiting neutrophils and natural killer (NK) cells that release reactive oxygen species and additional cytokines to contain the infection. However, C. trachomatis actively suppresses these responses by blocking TLR4/MD-2 dimerization and inhibiting TRIF/MyD88 pathways, thereby reducing NF-κB activation and limiting cytokine production. The adaptive immune response is predominantly Th1-mediated, with CD4+ T cells playing a central role in host defense through the secretion of interferon-gamma (IFN-γ), which inhibits chlamydial replication by depleting intracellular tryptophan via indoleamine 2,3-dioxygenase induction and promoting nitric oxide production. CD8+ T cells also contribute by producing IFN-γ and exerting cytolytic effects on infected cells. In contrast, humoral immunity via antibodies, such as IgG and IgA, provides limited protection; while they can neutralize elementary bodies in vitro, B cell-deficient models demonstrate infection resolution without them, indicating that antibodies do not prevent reinfection or persistence effectively. This Th1 bias helps clear acute infections but often fails to eradicate persistent forms, leading to incomplete resolution. C. trachomatis employs multiple evasion strategies to subvert both innate and adaptive immunity, facilitating chronic infection. It inhibits host cell apoptosis through the chlamydial protease-like activity factor (CPAF), which degrades pro-apoptotic BH3-only proteins like BIM and PUMA, and activates anti-apoptotic pathways such as PI3K/Akt and ERK1/2, allowing intracellular persistence for extended periods. Additionally, CPAF downregulates major histocompatibility complex (MHC) class I and II expression by degrading transcription factors like RFX5 and USF-1, impairing antigen presentation to T cells and inducing T-cell exhaustion via upregulated PD-L1. These mechanisms, combined with entry into a non-replicative persistent state under immune pressure (e.g., IFN-γ exposure), result in incomplete bacterial clearance and recurrent or chronic infections. Recent research highlights the role of the cervicovaginal microbiota in modulating the host immune response to C. trachomatis. Lactobacillus-dominated microbiomes (e.g., L. crispatus) produce lactic acid that lowers pH and suppresses pro-inflammatory cytokines like IL-6, IL-8, and TNF-α, enhancing epithelial barrier integrity and promoting spontaneous clearance rates of 11-44%. In contrast, dysbiotic communities (e.g., CST IV with anaerobes) elevate short-chain fatty acids and tryptophan levels, exacerbating inflammation and prolonging infection persistence. Studies from 2024-2025 emphasize that microbial composition influences chlamydial load and upper genital tract ascension, with indole-producing bacteria countering IFN-γ effects by supporting bacterial tryptophan synthesis via nutrient provision.

Tissue Damage Mechanisms

Chlamydia trachomatis infection initiates tissue damage primarily through the activation of inflammatory cascades that recruit neutrophils to infected mucosal sites, leading to direct epithelial cell injury via the release of reactive oxygen species, proteases, and other cytotoxic mediators. This neutrophil influx, driven by chemokines such as IL-8 produced by infected epithelial cells, disrupts the epithelial barrier and exacerbates local inflammation, contributing to the progression of pathology in the genital tract. In pelvic inflammatory disease (PID), chronic inflammation promotes fibrosis through the upregulation of transforming growth factor-beta (TGF-β), which induces epithelial-to-mesenchymal transition (EMT) in fallopian tube cells, resulting in excessive extracellular matrix deposition and scar tissue formation. TGF-β signaling synergizes with other pathways, such as epidermal growth factor receptor activation, to perpetuate myofibroblast differentiation and fibrotic remodeling in the upper genital tract. Serovar-specific differences in invasiveness further dictate the extent of tissue destruction; lymphogranuloma venereum (LGV) serovars (L1-L3) exhibit enhanced lymphotropism, enabling systemic dissemination and direct invasion of lymphatic tissues, which leads to granulomatous inflammation, lymphatic vessel occlusion, and eventual destruction of regional lymph nodes. In contrast, urogenital serovars (D-K) primarily cause localized mucosal damage but can ascend to the upper reproductive tract, where repeated infections trigger salpingitis and subsequent tubal occlusion through hydrosalpinx formation and adhesions that block ovum transport. Long-term sequelae include the loss of ciliated epithelial cells in the fallopian tubes, as Chlamydia infection disrupts ciliary assembly and function by activating disassembly machinery, impairing mucociliary clearance and contributing to ectopic pregnancy risk. Recent investigations as of 2025 have highlighted oxidative stress as a key mediator of chlamydial complications, with infection elevating intracellular iron levels and reactive oxygen species production, inducing ferroptosis in host cells via p53/SLC7A11 pathway dysregulation that amplifies lipid peroxidation and mitochondrial damage, sustaining chronic inflammation. Additionally, cervicovaginal microbiome disruption during Chlamydia infection alters bacterial community composition, reducing Lactobacillus dominance and promoting dysbiosis that facilitates bacterial ascension, enhances pro-inflammatory cytokine release, and predicts severe outcomes like endometritis through impaired epithelial barrier integrity. These mechanisms underscore how initial host immune responses, such as neutrophil recruitment, evolve into pathological consequences including fibrosis and structural damage.

Diagnosis

Clinical Evaluation

Clinical evaluation of chlamydia begins with a thorough history to identify risk factors and potential exposure, as the infection is often asymptomatic but prevalent among sexually active individuals, particularly those under 25 years of age. Key elements include assessing the number and gender of recent sex partners, types of sexual practices (vaginal, anal, or oral), condom use, and any history of prior STIs or partner diagnoses, using frameworks like the CDC's "Five Ps" (partners, practices, protection, past history, pregnancy plans). Pregnancy status should be determined in women of reproductive age, as infection can lead to complications like preterm birth. Suspicion is heightened in adolescents, individuals with multiple or new partners, or those whose partners have concurrent sexual contacts or known STIs. Physical examination focuses on genital sites relevant to symptoms or risk, though findings are frequently absent or nonspecific. In women, speculum examination may reveal cervical friability (easy bleeding upon manipulation), mucopurulent endocervical discharge, or edema, particularly in cases of cervicitis. For men, urethral discharge—often mucopurulent and elicited by gentle stripping of the urethra—may be observed in urethritis, alongside potential prostatic tenderness on palpation. Extragenital sites, such as the rectum or pharynx, warrant consideration in high-risk groups like men who have sex with men or women reporting anal intercourse, per CDC STI Treatment Guidelines emphasizing behavioral history to guide evaluation. Differential diagnosis for suspected chlamydia includes other causes of urethritis or cervicitis, such as gonorrhea (Neisseria gonorrhoeae), trichomoniasis, herpes simplex virus (HSV), and Mycoplasma genitalium, which may present with overlapping symptoms like discharge or dysuria. Noninfectious etiologies, including vaginal candidiasis (yeast infections) or allergic reactions, should also be considered based on exam characteristics. In resource-limited settings, a syndromic approach is often employed, treating presumptively for chlamydia and gonorrhea in patients with urethral or cervical syndromes without immediate etiologic testing, as recommended by WHO guidelines. Urogenital symptoms, if present, such as abnormal discharge or pain during urination, further raise suspicion but do not confirm the diagnosis.

Laboratory Testing

Laboratory testing for Chlamydia trachomatis infection primarily relies on direct detection methods to confirm the presence of the bacterium in clinical specimens, with nucleic acid amplification tests (NAATs) serving as the cornerstone due to their high sensitivity and specificity. NAATs detect C. trachomatis genetic material, such as ribosomal RNA or DNA, and are recommended by the Centers for Disease Control and Prevention (CDC) as the preferred diagnostic approach for urogenital, rectal, pharyngeal, and conjunctival specimens. These tests can utilize first-void urine, vaginal, endocervical, urethral, or extragenital swabs, offering non-invasive options that improve patient compliance. NAATs demonstrate sensitivities exceeding 95% for urine and swab specimens from symptomatic and asymptomatic individuals, outperforming older methods in detecting low-burden infections. For instance, assays like the Aptima Combo 2 and Xpert CT/NG have been cleared by the U.S. Food and Drug Administration (FDA) for extragenital sites, including rectal and oropharyngeal samples, addressing the need for comprehensive screening in high-risk populations. Specificity approaches 99%, minimizing false positives, though confirmatory testing may be required in low-prevalence settings to account for positive predictive value. These platforms are FDA-approved for self-collected samples in some cases, facilitating broader access. Cell culture remains the historical gold standard for isolating viable C. trachomatis, requiring inoculation of clinical specimens onto McCoy or HeLa cells followed by detection via immunofluorescence or staining, but its clinical utility is limited by low yield and technical demands. Culture sensitivity ranges from 70% to 90%, often underdetecting infections compared to NAATs, due to the bacterium's obligate intracellular nature and specimen transport challenges. It is primarily reserved for research purposes, such as strain typing or assessing antibiotic susceptibility, rather than routine diagnosis. Serologic tests, which measure antibodies like immunoglobulin M (IgM) for acute infection or IgG for past exposure, have limited diagnostic value for acute genital C. trachomatis infections due to poor specificity and the bacterium's intracellular lifecycle, which delays seroconversion. These assays, often enzyme immunoassays or microimmunofluorescence, cannot reliably distinguish current from prior infections and are prone to cross-reactivity with other Chlamydia species. They are not recommended for routine use in uncomplicated urogenital cases but may support diagnosis in neonates, reactive arthritis, or lymphogranuloma venereum. As of 2025, advancements include point-of-care (POC) NAATs, such as the binx io platform, which provides results in approximately 30 minutes using simple swab or urine inputs, enhancing rapid diagnosis in resource-limited settings. Multiplex STI panels, like those detecting C. trachomatis alongside Neisseria gonorrhoeae and other pathogens, are increasingly integrated into clinical workflows for efficient syndromic testing. However, routine antibiotic resistance testing is not yet standard, as C. trachomatis shows no widespread resistance to azithromycin or doxycycline, though molecular methods for susceptibility assessment are emerging in research contexts.

Treatment

The recommended first-line treatment for uncomplicated genital, rectal, or oropharyngeal chlamydia infections in adolescents and adults is doxycycline 100 mg orally twice daily for 7 days, as endorsed by both the 2021 CDC STI Treatment Guidelines and the 2025 European guideline on Chlamydia trachomatis infections. This regimen is preferred over single-dose azithromycin due to superior microbiological cure rates, particularly for rectal infections where doxycycline achieves approximately 100% efficacy compared to 74% with azithromycin in men who have sex with men. Alternative regimens include azithromycin 1 g orally as a single dose, which may be considered for patients with compliance concerns despite its lower efficacy for extragenital sites. For pregnant individuals, azithromycin 1 g orally as a single dose is recommended, with amoxicillin 500 mg orally three times daily for 7 days as an alternative; doxycycline is contraindicated due to potential fetal risks. For lymphogranuloma venereum (LGV), the recommended regimen is doxycycline 100 mg orally twice daily for 21 days, applicable to both CDC and European guidelines. Both doxycycline and azithromycin demonstrate high overall cure rates exceeding 95% for uncomplicated infections, with test-of-cure testing not routinely required except in pregnancy (at 4 weeks post-treatment) or neonatal cases to confirm eradication. Recent guidelines reflect a shift away from azithromycin as first-line due to efficacy limitations and growing concerns over macrolide resistance in co-occurring pathogens like Mycoplasma genitalium, driven by widespread azithromycin use.

Management of Complications and Special Populations

Management of pelvic inflammatory disease (PID) associated with Chlamydia trachomatis infection requires a broader antibiotic regimen to address potential co-pathogens, including anaerobes implicated in tubal damage. The recommended parenteral regimen consists of ceftriaxone 1 g intravenously every 24 hours, combined with doxycycline 100 mg orally or intravenously every 12 hours and metronidazole 500 mg orally or intravenously every 12 hours; after clinical improvement within 24–48 hours, transition to oral doxycycline 100 mg twice daily plus metronidazole 500 mg twice daily to complete a 14-day course. An alternative intramuscular/oral regimen is ceftriaxone 500 mg intramuscularly as a single dose (1 g if patient weight exceeds 150 kg), followed by doxycycline 100 mg orally twice daily for 14 days and metronidazole 500 mg orally twice daily for 14 days. Metronidazole specifically targets anaerobes such as Bacteroides fragilis, which contribute to PID sequelae like infertility and ectopic pregnancy. In pregnant individuals, azithromycin 1 g orally as a single dose is the preferred treatment for chlamydial infection to avoid the teratogenic risks of doxycycline, which is contraindicated in the second and third trimesters. An alternative is amoxicillin 500 mg orally three times daily for 7 days. Universal screening for chlamydia is recommended at the first prenatal visit, with retesting in the third trimester for those at continued risk, to prevent vertical transmission and complications such as preterm birth. A test of cure is advised approximately 4 weeks post-treatment, followed by routine retesting at 3 months. For neonates exposed to chlamydia during birth, erythromycin ophthalmic ointment is applied to prevent or treat conjunctivitis (ophthalmia neonatorum). If pneumonia develops, oral erythromycin at 50 mg/kg/day divided into four doses for 14 days is the standard regimen, with azithromycin 20 mg/kg/day for 3 days as an alternative; a test of cure is recommended due to the approximately 80% efficacy of erythromycin. Maternal treatment during pregnancy can prevent transmission to the neonate. Among exposed infants born to untreated infected mothers, 30–50% develop conjunctivitis and 10–20% develop pneumonia. In individuals with HIV co-infection, chlamydial treatment follows the same regimens as for HIV-negative patients, with no specific adjustments required, though extragenital screening is emphasized to detect asymptomatic infections. As of 2025, expedited partner therapy (EPT) has expanded in several U.S. states and aligns with federal implementation plans, allowing providers to prescribe or dispense antibiotics (typically azithromycin 1 g single dose) directly to partners without examination, thereby reducing reinfection rates. Routine follow-up for all treated cases includes retesting approximately 3 months post-treatment to detect reinfection, particularly in high-risk groups such as sexually active individuals under 25 years, without a routine test of cure unless symptoms persist or adherence is uncertain.

Prevention

Behavioral and Barrier Methods

Barrier methods, particularly the consistent and correct use of male latex condoms during vaginal, anal, or oral sex, significantly reduce the risk of chlamydia transmission by providing a physical barrier that prevents contact with infected genital fluids. Studies indicate that consistent condom use can lower the risk of chlamydia acquisition by 50% to 90%. For oral sex, dental dams—thin latex or polyurethane sheets placed over the genitals—offer similar protection by covering the area and preventing direct contact with infectious secretions, as recommended by public health guidelines. However, these methods are not 100% effective due to potential breakage, slippage, or incomplete coverage of all potentially infected areas. Behavioral strategies play a crucial role in preventing chlamydia by modifying sexual practices to minimize exposure opportunities. Abstinence from vaginal, anal, or oral sex eliminates the risk of transmission entirely, serving as the most reliable personal prevention method. Limiting the number of sexual partners and engaging in mutual monogamy with a tested, uninfected partner further reduces transmission risk, as fewer partners mean fewer potential sources of infection. Education on the asymptomatic nature of chlamydia infections—where many individuals show no symptoms yet remain contagious—empowers people to adopt proactive behaviors, such as discussing STI status with partners before sexual activity. Incorporating regular testing into one's routine, even without symptoms, allows individuals to maintain awareness of their infection status and make informed decisions about sexual behavior. Doxycycline post-exposure prophylaxis (Doxy-PEP) is an additional prevention strategy recommended by the Centers for Disease Control and Prevention (CDC) for certain high-risk groups, including gay, bisexual, and other men who have sex with men (MSM) and transgender women who have had a bacterial sexually transmitted infection in the past 12 months. It involves taking 200 mg of doxycycline orally within 72 hours (ideally within 24 hours) after condomless sex. Clinical trials have shown Doxy-PEP reduces the incidence of chlamydia by over 70%, as well as syphilis and gonorrhea. As of 2025, no vaccine is available for chlamydia prevention, despite ongoing research efforts targeting chlamydial antigens like major outer membrane protein (MOMP). Several vaccine candidates are in early-stage clinical development, including mRNA-based formulations in phase I/II trials evaluating safety, immunogenicity, and efficacy in reducing infection incidence. These trials, such as those testing low, medium, and high doses of chlamydia mRNA vaccines, represent promising steps but have not yet progressed to widespread use. Public health approaches to chlamydia prevention often center on debates between abstinence-only education and comprehensive sex education programs. Abstinence-only programs emphasize delaying sexual debut as the primary strategy to avoid STIs, including chlamydia, but evidence shows they are less effective at reducing overall infection rates compared to no education in some contexts. In contrast, comprehensive sex education, which includes information on abstinence alongside condom use, partner communication, and risk reduction, has been associated with delayed sexual initiation, increased condom use, and lower STI rates among youth. These programs address the asymptomatic spread of chlamydia by promoting multifaceted behavioral changes, though their implementation varies by region and faces political challenges.

Screening and Partner Notification

Screening for chlamydia is recommended annually for all sexually active women under 25 years of age, as well as for older women at increased risk, such as those with new or multiple sex partners or a history of sexually transmitted infections. The Centers for Disease Control and Prevention (CDC) recommends annual screening for sexually active women under 25 years, as well as for those at increased risk, including high-risk men such as men who have sex with men (MSM), to address transmission in young adults and vulnerable populations. For high-risk men, including men who have sex with men (MSM), annual screening is advised due to elevated infection rates and asymptomatic cases. Screening sites should include genital areas for all individuals, with extragenital testing—such as rectal and pharyngeal swabs—recommended for MSM to detect infections missed by urine-based tests alone, as up to 20-30% of cases in this population occur at extragenital sites. Pregnant women under 25 years should be screened at the first prenatal visit, with retesting in the third trimester for those under 25 or at increased risk, to prevent adverse outcomes like preterm birth or neonatal infection. Nucleic acid amplification tests (NAATs) are the preferred method for screening, as referenced in diagnostic guidelines, enabling detection at multiple anatomical sites with high sensitivity. Partner notification is a key strategy to interrupt transmission, with clinicians encouraging patients diagnosed with chlamydia to inform their recent sex partners—typically those from the past 60 days or the most recent partner if longer—and urge them to seek testing and treatment. Expedited partner therapy (EPT) is endorsed by the CDC for chlamydia, allowing providers to prescribe or dispense antibiotics like azithromycin or doxycycline directly to partners without an in-person evaluation, improving treatment rates and reducing reinfection risk. Anonymous digital tools, such as text or email notification services (e.g., TellYourPartner.org or STDcheck.com), facilitate partner tracing by allowing users to alert contacts without revealing their identity, enhancing privacy and uptake in stigma-sensitive contexts. Modeled studies demonstrate the cost-effectiveness of chlamydia screening combined with partner notification, with one analysis estimating costs at approximately $9,700 per quality-adjusted life year (QALY) gained compared to no intervention, primarily by averting pelvic inflammatory disease (PID) and related sequelae. Seminal trials, such as a 1996 randomized controlled study, showed that screening reduced PID incidence by about 56% in screened women versus controls, supporting broader program implementation to prevent long-term complications like infertility. Despite these benefits, significant gaps persist, including low screening uptake among men—often below 10-20% in primary care settings—and limited access in resource-poor settings due to infrastructure barriers and low awareness. Targeted efforts are needed to address these disparities and optimize transmission control.

Epidemiology

Global Burden and Prevalence

Chlamydia trachomatis infection imposes a significant global health burden, manifesting as both a major sexually transmitted infection (STI) and the leading infectious cause of blindness through trachoma. In 2020, the World Health Organization (WHO) estimated 129 million new cases of chlamydia among adults aged 15-49 years worldwide, accounting for a substantial portion of the 374 million incident cases of four curable STIs that year. This burden is particularly concentrated in the 15-24 age group, where incidence rates are highest due to behavioral and biological factors. Regionally, sub-Saharan Africa bears the heaviest load, representing approximately 40% of the global STI burden, with chlamydia prevalence among women estimated at 6.6% (95% CI: 5.0–8.2%) in 2020. In the United States, the Centers for Disease Control and Prevention (CDC) reported 1,515,985 provisional cases of chlamydia in 2024, reflecting an 8% decline from the previous year but underscoring ongoing challenges in surveillance and control. Trachoma, caused by ocular infection with Chlamydia trachomatis, affects vulnerable populations in 42 countries, primarily in Africa, Asia, and the Middle East. As of April 2025, approximately 103 million people reside in trachoma-endemic areas and are at risk of blindness from the disease. An estimated 1.9 million individuals are blind or visually impaired due to trachoma, with women disproportionately affected owing to their roles in childcare and increased exposure. Progress toward elimination as a public health problem has been driven by the WHO-endorsed SAFE strategy—surgery for advanced cases, antibiotics, facial cleanliness, and environmental improvements—which has led to 27 countries achieving elimination status as of November 2025. The true global burden of chlamydia is likely underestimated due to its predominantly asymptomatic nature, with up to 70-95% of infections in women and 50% in men lacking symptoms, resulting in underdiagnosis and underreporting. Surveillance variations across regions further exacerbate this issue, as routine screening is limited in many low-resource settings, leading to incomplete data on prevalence and incidence. As of 2025, global incidence estimates remain based on 2020 WHO data, with no updated comprehensive figures available. Risk factors for Chlamydia trachomatis infection primarily involve sexual behaviors and social determinants that facilitate transmission. Young age, particularly among sexually active individuals under 25 years, significantly elevates risk due to higher rates of new or multiple sexual partners and inconsistent condom use. Inconsistent barrier methods, such as condoms during vaginal, anal, or oral sex, further compound vulnerability, as unprotected contact with an infected partner is the main transmission route. Incarceration represents another key risk, with persons in correctional facilities exhibiting elevated STI rates linked to pre-incarceration behaviors like substance misuse, transactional sex, and limited healthcare access. Co-infection with other STIs, such as gonorrhea or HIV, acts as a cofactor by increasing susceptibility to chlamydia through genital inflammation or immune modulation. The relationship is bidirectional, as chlamydia infection increases the risk of HIV acquisition, with studies reporting relative risks (RR) or odds ratios (OR) typically ranging from 1.5 to 5, depending on population, gender, site of infection, and study design. Demographic patterns reveal disparities influenced by screening practices and social inequities. Infections are more frequently diagnosed in women than men, partly attributable to routine screening guidelines targeting sexually active females under 25, though this may reflect detection bias rather than true incidence differences. Among men who have sex with men (MSM), risk is heightened for lymphogranuloma venereum (LGV), a severe form of chlamydia, due to prevalent anal transmission networks. In the United States, racial disparities are pronounced, with chlamydia rates among Black or African American individuals approximately 6.4 times higher than among White individuals in 2023, driven by structural factors like healthcare access barriers and socioeconomic inequities affecting youth aged 15-24 most severely. Epidemiological trends indicate stability in high-income countries alongside emerging challenges. In the US, chlamydia cases remained relatively stable through 2023 before declining 8% to approximately 1.5 million in 2024, following a post-COVID screening dip in 2020 and subsequent rebound, with youth continuing to bear the highest burden. In Europe, LGV cases surged 41% to 3,075 in 2023, predominantly among HIV-negative MSM, signaling ongoing transmission in key populations. Antibiotic resistance is emerging, particularly to tetracyclines like doxycycline, with minimum inhibitory concentrations (MICs) rising due to widespread post-exposure prophylaxis (doxyPEP) use among MSM, potentially complicating treatment efficacy. By 2025, telehealth expansions have boosted testing access, enabling remote STI screening and mitigating post-pandemic disruptions, though youth surges persist amid behavioral shifts like increased partner concurrency.

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