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Chlamydia

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.^[1] 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.^[2] 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.^[1] 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.^[1] 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.^[1] In women, untreated infections can ascend to the upper reproductive tract, causing pelvic inflammatory disease (PID).^[3] 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; it also increases the risk of acquiring or transmitting HIV.^[1] 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.^[3]^[4] Diagnosis relies on nucleic acid amplification tests (NAATs) using urine or swab samples from affected sites, which are highly sensitive and specific.^[1] 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.^[3] 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.^[1] 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.^[1]

Microbiology

Genus Chlamydia

The genus Chlamydia comprises obligate intracellular bacteria belonging to the phylum Chlamydiota, class Chlamydiia, order Chlamydiales, and family Chlamydiaceae.^[5] 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.^[6] 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.^[6] 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.^[6] 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.^[7] This cycle ensures efficient propagation while evading host defenses.^[6] 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.^[8] 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.^[9] This metabolic parasitism underscores their obligate intracellular lifestyle, relying on host nucleotides, amino acids, and lipids for energy and growth.^[6] The genus was formally named Chlamydia in 1945 by Jones, Rake, and Stearns, deriving from the Greek "chlamys" (cloak), reflecting the pathogens' intracellular seclusion.^[10] 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.^[11] 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.^[6]

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.^[12]^[6] 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.^[13]^[14] Serotyping relies on the immunogenic epitopes of MOMP, which exhibit sequence variability in four hypervariable domains while conserving structural regions.^[15] 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.^[16]^[17] 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.^[12]^[6]^[18] 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.^[19]^[20]^[21] 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.^[22]^[23]

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.^[24] 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.^[25] 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.^[26] 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.^[3] In men, complications are less frequent but include epididymitis, presenting as unilateral testicular pain and swelling, and rare cases of prostatitis.^[25] 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.^[27] 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.^[28]

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.^[29] Trachoma represents a chronic form of keratoconjunctivitis resulting from repeated infections with C. trachomatis serovars A, B, Ba, and C.^[29] 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.^[30] 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.^[30] 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.^[30] The final stage, corneal opacity (CO), involves easily visible scarring in the central cornea that blurs the pupil's margin, resulting in irreversible blindness.^[30] Adult inclusion conjunctivitis arises from ocular exposure to genital serovars D through K of C. trachomatis, often through direct contact or autoinoculation.^[31] 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.^[31] Unlike trachoma, it rarely progresses to scarring but may involve superior corneal subepithelial opacities and preauricular lymphadenopathy.^[31] Globally, trachoma remains the leading infectious cause of blindness, affecting approximately 1.9 million people with visual impairment or blindness as of 2025.^[32] 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.^[32] 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).^[32]^[33] 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.^[29]

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.^[34] 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.^[35]^[36] 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.^[37]^[38] 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.^[39]

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.^[40] 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.^[41]^[42] This condition is the leading infectious cause of neonatal conjunctivitis in many regions.^[43] 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.^[44] It is characterized by an afebrile illness with a distinctive staccato or paroxysmal cough, tachypnea, and rales on auscultation, without significant fever or leukocytosis.^[45]^[44] Chest radiographs commonly show bilateral hyperinflation and interstitial infiltrates, reflecting the subacute nature of the infection.^[45]^[46] 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.^[47]^[48] 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.^[49] 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.^[13] 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.^[50] 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.^[1] This asymptomatic carriage facilitates silent transmission, as infected individuals can unknowingly spread the bacteria during sexual contact, contributing to its high prevalence.^[13] Serovars D through K are the predominant strains responsible for these urogenital infections, targeting the endocervix in women and urethra in men.^[14] 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.^[49] 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.^[51]

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.^[3]^[52] 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.^[52]^[53]^[3] 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.^[3]^[52]^[54] 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.^[3]^[52] This mode of transmission commonly results in neonatal conjunctivitis or pneumonia, with manifestations addressed in the Neonatal Infections section.^[3]

Other Routes

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. 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.^[55] 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.^[56] 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.^[57] 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.^[58]^[59]^[60] 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.^[61]^[62]

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.^[63]^[64] 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.^[65] 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.^[66]^[67] This Th1 bias helps clear acute infections but often fails to eradicate persistent forms, leading to incomplete resolution.^[68] 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.^[69]^[70]^[65] 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.^[71]^[72]^[73]^[74]

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.^[75] 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.^[76] 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.^[77] 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.^[78] 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.^[79] 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.^[80] 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.^[81] 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.^[82] These mechanisms underscore how initial host immune responses, such as neutrophil recruitment, evolve into pathological consequences including fibrosis and structural damage.^[83]

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.^[3] 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).^[84] Pregnancy status should be determined in women of reproductive age, as infection can lead to complications like preterm birth.^[3] Suspicion is heightened in adolescents, individuals with multiple or new partners, or those whose partners have concurrent sexual contacts or known STIs.^[85] 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.^[86] 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.^[86] 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.^[87] 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.^[25] Noninfectious etiologies, including vaginal candidiasis (yeast infections) or allergic reactions, should also be considered based on exam characteristics.^[88] 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.^[1] Urogenital symptoms, if present, such as abnormal discharge or pain during urination, further raise suspicion but do not confirm the diagnosis.^[3]

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.^[3]^[89] 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.^[89]^[90]^[91] 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.^[92]^[93]^[94] 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.^[95]^[96]^[97] 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.^[98] 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.^[99]^[100]^[101]

Treatment

Recommended Regimens

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.^[3]^[102] 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.^[3]^[103] 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.^[3]^[102] 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.^[3] For lymphogranuloma venereum (LGV), the recommended regimen is doxycycline 100 mg orally twice daily for 21 days, applicable to both CDC and European guidelines.^[3]^[102] 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.^[3]^[102] 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.^[102]^[104]

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.^[105] 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.^[105] Metronidazole specifically targets anaerobes such as Bacteroides fragilis, which contribute to PID sequelae like infertility and ectopic pregnancy.^[105] 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.^[3] An alternative is amoxicillin 500 mg orally three times daily for 7 days.^[3] 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.^[3] A test of cure is advised approximately 4 weeks post-treatment, followed by routine retesting at 3 months.^[3] For neonates exposed to chlamydia during birth, erythromycin ophthalmic ointment is applied to prevent or treat conjunctivitis (ophthalmia neonatorum).^[3] 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.^[3] 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.^[104] 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.^[3] 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.^[106]^[3] 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.^[3]^[104]

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.^[107] 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.^[85] 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.^[49] For high-risk men, including men who have sex with men (MSM), annual screening is advised due to elevated infection rates and asymptomatic cases.^[85] 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.^[85]^[108] 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.^[109] 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.^[110] 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.^[111] 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.^[112]^[113] 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.^[114]^[115] 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.^[116] 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.^[117] 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.^[118]^[119] 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.^[120] This burden is particularly concentrated in the 15-24 age group, where incidence rates are highest due to behavioral and biological factors.^[121] 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.^[122]^[123] 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.^[4] 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.^[32] 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.^[124] 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.^[125] 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.^[1] 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.^[3] As of 2025, global incidence estimates remain based on 2020 WHO data, with no updated comprehensive figures available.^[120]

Risk Factors and Trends

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.^[49] 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.^[49] 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.^[126] Co-infection with other STIs, such as gonorrhea or HIV, acts as a cofactor by increasing susceptibility through genital inflammation or immune modulation.^[3] 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.^[85] 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.^[127] 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.^[39] 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.^[4] In Europe, LGV cases surged 41% to 3,075 in 2023, predominantly among HIV-negative MSM, signaling ongoing transmission in key populations.^[127] 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.^[128] 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.^[106]

References

[1]
Chlamydia - World Health Organization (WHO)
Nov 21, 2024 · Chlamydia is a common sexually transmitted infection that can occur in both men and women. It is caused by a bacterium called Chlamydia trachomatis.
[2]
Chlamydial Infections - STI Treatment Guidelines - CDC
Jul 22, 2021 · Chlamydial infection is the most frequently reported bacterial infectious disease in the United States, and prevalence is highest among persons aged ≤24 years.Special Considerations · Ophthalmia Neonatorum Caused... · Infant Pneumonia Caused By C...
[3]
Chlamydia - Medical Microbiology - NCBI Bookshelf - NIH
The group consists of a single genus, Chlamydia (order Chlamydiales, class Chlamydiaceae). This genus contains the species C trachomatis and C psittaci, as ...
[4]
chlamydial developmental cycle | FEMS Microbiology Reviews
Chlamydia alternates between two morphological forms, the elementary body (EB) and the reticulate body (RB) [11]. EBs are extra-cellular, metabolically inert ...Introduction · Elementary body · Primary differentiation · Reticulate body
[5]
Chlamydia trachomatis: Genome sequence analysis of ...
The genome of C. trachomatis strain L2 is composed of a single circular chromosome of 1.039 Mb and a plasmid of 7499 bp, predicted to encode 889 and eight ...
[6]
Why the SAFE—S Strategy for Trachoma? Are Musca sorbens or ...
Dec 4, 2023 · Chlamydia is an obligate intracellular parasite as it is unable to synthesize ATP; it has long been considered a virus or rickettsia [21] or ...
[7]
In Chlamydia veritas | Pathogens and Disease - Oxford Academic
Chlamydia provides a rich taxonomic history from one of its early scientific descriptions in 1945 when it was known as Miyagawanella (Jones et al. , 1945 ), ...
[8]
Trachoma: A Very Brief History
Reference to trachoma in China date back to 2700 BCE, Sumer in 2000 BCE, Egypt in 1550 BCE, India between 1000 and 500 BCE, Arab authors in the ninth century ...
[9]
Chlamydia trachomatis: the Persistent Pathogen - PubMed Central
Aug 23, 2017 · Chlamydia trachomatis is an obligate intracellular bacterium whose only natural host is humans. Although presenting as asymptomatic in most women, genital ...
[10]
Chlamydia trachomatis Genital Infections - PMC - NIH
Sep 5, 2016 · C. trachomatis can be classified into 15 serovars (genovars) 1 based on antigenic variation in the major outer membrane protein (MOMP) encoded ...
[11]
Pathogenicity and virulence of Chlamydia trachomatis: Insights into ...
Trachomatis is comprised of 15 serovars classified into two distinct biovars: the trachoma biovar (serovars A-K) and the lymphogranuloma venereum (LGV) ...Adhesins · Figure 2 · Figure 3<|control11|><|separator|>
[12]
Nucleotide and deduced amino acid sequences for the four variable ...
The amino acid sequences of major outer membrane proteins (MOMPs) from Chlamydia trachomatis serovars A, B, C, L1, and L2 are predominantly conserved but have ...
[13]
The Chlamydia trachomatis Plasmid Is a Transcriptional Regulator ...
Chlamydia trachomatis possesses a cryptic 7.5-kb plasmid of unknown function. Here, we describe a comprehensive molecular and biological characterization of the ...
[14]
The plasmids of Chlamydia trachomatis and Chlamydophila ...
A 7.5 kbp cryptic plasmid is found in almost all isolates of Chlamydia trachomatis. Real-time PCR assays, using TaqMan chemistry, were set up to quantify ...
[15]
Chlamydia Pneumonia - StatPearls - NCBI Bookshelf - NIH
Three species of Chlamydia namely, C. pneumoniae, C. psittaci, and C. trachomatis are known to cause respiratory infections in humans.Etiology · Epidemiology · Evaluation · Treatment / Management
[16]
Genetic variation in Chlamydia trachomatis and their hosts
Chlamydia trachomatis is divided into the oculogenital and LGV biovars. The ocular (A–C) and genital (D–K) serovars infect conjuctival and genital epithelia, ...Table 1 · Type Iii Secretion System · The Chlamydial Cytotoxin
[17]
Chlamydia trachomatis—An Emerging Old Entity? - PMC - NIH
May 14, 2023 · The trachoma biovar is subdivided into serovars A–C, leading to trachoma, the most common cause of infectious blindness in developing countries ...
[18]
Factsheet about chlamydia - ECDC - European Union
At least 70% of genital C. trachomatis infections in women and 50% in men are asymptomatic at the time of diagnosis. The natural course of genital chlamydia ...Chlamydia infections (genital) · Clinical features and sequelae · Diagnosis
[19]
Urethritis and Cervicitis - STI Treatment Guidelines - CDC
Symptoms, if present, include dysuria, urethral pruritis, and mucoid, mucopurulent, or purulent discharge. Signs of urethral discharge on examination can also ...
[20]
CDC Grand Rounds: Chlamydia Prevention: Challenges and ...
Apr 1, 2011 · Chlamydia, a sexually transmitted infection caused by the bacterium Chlamydia trachomatis, is the most commonly reported nationally notifiable disease.
[21]
Lymphogranuloma Venereum (LGV) - STI Treatment Guidelines - CDC
Jul 22, 2021 · Clinical manifestations of LGV can include GUD, lymphadenopathy, or proctocolitis. Rectal exposure among MSM or women can result in ...
[22]
[PDF] 2023 STI Surveillance Report - CDC
Sep 24, 2025 · Despite these glimpses of hope, we still have a long way to go. There were more than 2.4 million STIs reported across the country last year; ...Missing: global | Show results with:global
[23]
Trachoma - StatPearls - NCBI Bookshelf
Apr 20, 2024 · Trachoma is primarily associated with infections by serovars A, B, Ba, and C of the C trachomatis bacterium, while serovars D to K are typically ...
[24]
Diagnosis of trachoma - Control of Neglected Tropical Diseases
Conjunctival Chlamydia trachomatis infection and the associated signs of ... The WHO simplified grading system for trachoma has 5 signs: Trachomatous ...Missing: serovars AC
[25]
Adult Inclusion Conjunctivitis - Eye Disorders - Merck Manuals
Adult inclusion conjunctivitis is caused by sexually transmitted Chlamydia trachomatis. Symptoms include chronic unilateral hyperemia and mucopurulent discharge ...
[26]
Trachoma - World Health Organization (WHO)
Jul 18, 2025 · Trachoma is the leading infectious cause of blindness worldwide. It is caused by an obligate intracellular bacterium called Chlamydia trachomatis.
[27]
Extragenital Infections Caused by Chlamydia trachomatis and ... - NIH
Gonorrhea and chlamydia infection in the rectum can cause rectal pain, bleeding, and discharge, as well as proctitis. In the pharynx, these infections can cause ...
[28]
Reactive Arthritis - StatPearls - NCBI Bookshelf
Patients who are HLA-B27 positive have a higher risk of recurrence of ReA. 15-30% of patients with ReA can develop long-term arthritis or other joint ...Continuing Education Activity · Introduction · Pathophysiology · Evaluation
[29]
HLA-B27-Associated Reactive Arthritis: Pathogenetic and Clinical ...
Evidence of urogenital C. trachomatis infection is found in 36 to 50% of the posturethritic cases of Reiter's syndrome and in 69% of the patients who have signs ...
[30]
Fitz Hugh Curtis Syndrome - Symptoms, Causes, Treatment | NORD
May 12, 2009 · Fitz-Hugh-Curtis syndrome is a rare disorder that occurs almost exclusively in women. It is characterized by inflammation of the membrane lining the stomach.
[31]
Unusual manifestations of Chlamydia trachomatis infections - PubMed
Endocarditis, pneumonia in adults, otitis media, choroiditis and erythema nodosum are unusual manifestations of C. trachomatis infections that may be seen.Missing: hepatitis rare
[32]
Chlamydia (Chlamydial Genitourinary Infections)
Apr 23, 2025 · The transmission rate from infected mother to newborn is 50-60%, causing conjunctivitis (in most cases) or pneumonia (in 10-20% of cases; see ...
[33]
Ophthalmia Neonatorum - StatPearls - NCBI Bookshelf - NIH
Jul 7, 2025 · Chlamydial conjunctivitis: typically develops insidiously over days 5 to 14, presenting with mucoid or mucopurulent discharge and eyelid ...Missing: afebrile staccato cough carriage
[34]
Neonatal Conjunctivitis - StatPearls - NCBI Bookshelf - NIH
Chlamydia is the most common infectious agent that causes ophthalmia neonatorum in the United States, where 2% to 40% of neonatal conjunctivitis cases are ...Missing: perinatal | Show results with:perinatal
[35]
Chlamydial Infections in Children and Adolescents - AAP Publications
Jul 1, 2009 · C trachomatis is the most frequently identified infectious cause of neonatal conjunctivitis; it is transmitted perinatally by infected mothers.
[36]
AFEBRILE PNEUMONIA IN INFANTS - PMC - PubMed Central
Infants with chlamydial pneumonia typically present between 3 and 16 weeks ... weeks of age, afebrile with a staccato cough, with or without conjunctivitis.Cause And Clinical... · Chlamydia Trachomatis · Viral PneumoniaMissing: ray | Show results with:ray
[37]
Infants Born to Chlamydia-Positive Mothers - Page 5 - Medscape
Symptoms of chlamydial pneumonia are a repetitive staccato cough, tachypnea, and hyperinflation and bilateral diffuse infiltrates on chest x-ray (CXR).
[38]
Acute Chlamydia Trachomatis Respiratory Infection in Infants - NIH
... Chlamydia positive infants had paroxysm of staccato coughing. ... Besides that minimal infiltrates and hyperinflation were also found in the chest X-rays.
[39]
Chlamydial Pneumonias: Overview, Pathophysiology, Epidemiology
Mar 3, 2025 · Chest pain is common, but pleuritic pain is rare. Auscultatory findings may be sparse and may underestimate the extent of pneumonia. Photophobia ...
[40]
Otitis Externa, Otitis Media, and Mastoiditis - PMC - PubMed Central
Chlamydia trachomatis is associated with acute respiratory infections in infants younger than 6 months and is a cause of acute infection of the middle ear in ...
[41]
About Chlamydia - CDC
Jan 31, 2025 · Chlamydia is a common STI that can cause infection among men and women. It can cause permanent damage to a woman's reproductive system.
[42]
Per-partnership transmission probabilities for Chlamydia ... - PubMed
May 17, 2021 · Methods: We have developed a new model for estimating per-partnership chlamydia transmission probabilities from infected to uninfected ...Missing: act | Show results with:act
[43]
Chlamydia - StatPearls - NCBI Bookshelf - NIH
These bacteria are gram-negative, anaerobic, intracellular obligates that replicate within eukaryotic cells. C. trachomatis differentiates into 18 serovars ( ...
[44]
Chlamydia trachomatis and Neisseria gonorrhoeae rectal infections
Apr 5, 2024 · We found a high prevalence of HR-HPV rectal infections (61%), especially in subjects with a concurrent CT/NG rectal infection (70.2%) and in ...<|control11|><|separator|>
[45]
Chlamydia trachomatis Screening and Treatment in Pregnancy to ...
This review evaluates existing literature to determine potential benefits of antenatal screening and treatment of C. trachomatis in preventing adverse outcomes.
[46]
Chlamydia trachomatis | Red Book - AAP Publications
Acquisition occurs in approximately 50% of infants born vaginally to infected individuals and in some infants born by cesarean delivery with membranes intact.
[47]
prevalence, risk factors, and perinatal outcomes | Reproductive Health
Jun 26, 2021 · Prevalence of STI was low among pregnant women and male partners in midwifery practices, except for CT among young women.
[48]
Chlamydia trachomatis: Cell biology, immunology and vaccination
May 21, 2021 · The lymphogranuloma venereum biovar, serovars L1-3, causes invasive urogenital and anorectal infection and has become particularly ...
[49]
Mechanisms of Chlamydia trachomatis Entry into Nonphagocytic Cells
Key structural and regulatory factors associated with clathrin-mediated endocytosis were found to be involved in Chlamydia entry, whereas those for caveola- ...
[50]
Restricted Fusion of Chlamydia trachomatis Vesicles with Endocytic ...
The chlamydial developmental cycle takes place within a vacuole, termed an inclusion, that does not fuse with lysosomes. Inhibition of lysosomal fusion is not ...<|control11|><|separator|>
[51]
Replication-dependent size reduction precedes differentiation in ...
Jan 3, 2018 · Our approach reveals that C. trachomatis RBs replicate by binary fission and decrease in size with successive rounds of replication prior to RB ...
[52]
Mechanisms of host cell exit by the intracellular bacterium Chlamydia
In cells infected with C. trachomatis L2, a maximal amount of lysis occurred at 72 h (Fig. 2D). The amount released at 48 h was 46% of that measured at 72 h, ...
[53]
The multiple functions of the numerous Chlamydia trachomatis ...
Aug 21, 2019 · These proteins interfere with a wide diversity of host cell processes to promote chlamydial invasion, survival, growth, development and dissemination.
[54]
Chlamydia trachomatis Persistence In Vitro: An Overview
EBs released from the extruded inclusion and/or lysis of the host cell can then infect neighboring epithelial cells to perpetuate the infectious process [1, 2].
[55]
Aberrant Bodies: An Alternative Metabolic Homeostasis Allowing ...
Feb 29, 2024 · The Chlamydiae phylum is comprised of obligate intracellular bacteria including human pathogens such as Chlamydia trachomatis and lesser-known ...
[56]
The Role of the Immune Response in Chlamydia trachomatis ...
This review will focus on the ability of the immune system to recognize and clear acute and persistent chlamydial infections in the male genital tract.
[57]
https://pmc.ncbi.nlm.nih.gov/articles/PMC145390/
[58]
Insights into innate immune cell evasion by Chlamydia trachomatis
This review focuses on the recent advances in how C. trachomatis evades various innate immune cells, which contributes to vaccine development.
[59]
T lymphocyte immunity in host defence against Chlamydia ...
New data show that protective immunity to C trachomatis infection centrally involves T cell populations.
[60]
http://microbialcell.com/researcharticles/2019a-bugalhao-microbial-cell/
[61]
https://academic.oup.com/jid/article/201/Supplement_2/S88/808164
[62]
Chlamydia and Its Many Ways of Escaping the Host Immune System
Aug 6, 2019 · This review provides insight into the molecular means utilized by chlamydial species to the evade immune response.
[63]
https://pmc.ncbi.nlm.nih.gov/articles/PMC4209867/
[64]
Influence of cervicovaginal microbiota on Chlamydia trachomatis ...
This review examines the complex interplay between the CVM, C. trachomatis infection, and host immune responses.
[65]
https://pmc.ncbi.nlm.nih.gov/articles/PMC10850350/
[66]
https://pmc.ncbi.nlm.nih.gov/articles/PMC3307538/
[67]
Pathology after Chlamydia trachomatis infection is driven by ... - PNAS
Feb 9, 2018 · We demonstrate that a mucosal influx of neutrophils and CXCR3-driven CD4 + and CD8 + T cells is required for C. trachomatis pathology and does not contribute ...
[68]
Pathogenesis of Genital Tract Disease due to Chlamydia trachomatis
In vitro and mouse data indicate infected host epithelial cells not only drive influx of inflammatory cells, but release tissue-damaging molecules directly.
[69]
Epidermal Growth Factor Receptor and Transforming Growth ... - NIH
Chlamydia also upregulates transforming growth factor beta (TGF-β) expression, whose signaling pathway synergizes with the EGFR cascade, but its role in ...
[70]
Lymphogranuloma Venereum (LGV) - Medscape Reference
Jan 3, 2025 · LGV is a sexually transmitted infection caused by specific serovars of Chlamydia trachomatis that have the ability to invade and replicate in regional lymph ...Missing: destruction | Show results with:destruction
[71]
Pathogenesis of fallopian tube damage caused by Chlamydia ...
Chlamydia can ascend to the upper FGT and infect the fallopian tubes (FTs) causing salpingitis that may lead to functional damage of the FTs and tubal factor ...
[72]
Chlamydia trachomatis induces disassembly of the primary cilium to ...
Jun 17, 2024 · We found that Chlamydia infection caused loss of the primary cilium by activating the cellular cilia disassembly machinery and induced a quiescent host cell to ...
[73]
Chlamydia trachomatis infection induces ferroptosis and enhances ...
Chlamydia trachomatis infection increases intracellular iron levels, oxidative stress and mitochondrial damage.
[74]
Disrupted Cervicovaginal Microbiota: Its Role in Chlamydia ... - MDPI
This microbial imbalance leads to elevated pH, epithelial barrier disruption, and increased expression of pro-inflammatory cytokines (e.g., IL-1β, TNF-α), r ...
[75]
The role of infected epithelial cells in Chlamydia-associated fibrosis
Chronic inflammation or repeated injury leads to persistent myofibroblast activation. This in turn promotes excessive deposition of ECM components ...
[76]
Guide to Taking a Sexual History | STI - CDC
Jun 26, 2024 · A sexual history should be taken as part of routine health care, as well as when there are symptoms or physical exam findings suggestive of STIs ...Clinical Environment · The Five ``p''s · Protection From Stis
[77]
STI Screening Recommendations - CDC
Extragenital Gonorrhea and Chlamydia Among Men and Women According to Type of Sexual Exposure. ... Chlamydia trachomatis Positivity Rates Among Men Tested ...Missing: urogenital | Show results with:urogenital
[78]
Chlamydia (Chlamydial Genitourinary Infections) Clinical Presentation
Apr 23, 2025 · Physical Examination · Cervical friability (easy bleeding on manipulation) · Intermenstrual bleeding · Mucopurulent cervical or vaginal discharge.
[79]
https://pubmed.ncbi.nlm.nih.gov/25592078/
[80]
Urogenital Chlamydial Infections - Infectious Diseases
Chlamydiae may also cause salpingitis, pelvic inflammatory disease, epididymitis, perihepatitis, neonatal conjunctivitis, and infant pneumonia. Untreated ...Missing: hepatitis | Show results with:hepatitis
[81]
Recommendations for the Laboratory-Based Detection of Chlamydia ...
Mar 14, 2014 · C. trachomatis infections of the rectum can result from unprotected anal intercourse and are typically asymptomatic but might progress to ...
[82]
FDA clears first diagnostic tests for extragenital testing for chlamydia ...
May 23, 2019 · The Aptima Combo 2 Assay and the Xpert CT/NG are the first devices cleared for extragenital diagnostic testing of these infections via the throat and rectum.
[83]
[PDF] GEN-PROBE® APTIMA® Assay for Chlamydia trachomatis
Jan 2, 2025 · The APTIMA Assay for Chlamydia trachomatis is a target amplification nucleic acid probe test that utilizes target capture for the in vitro ...
[84]
008565: Chlamydia trachomatis Culture - Labcorp
Although culture is the legal standard, it is not the gold standard for the detection of C trachomatis. The sensitivity of culture is only 70% to 90% because C ...
[85]
Diagnostic Procedures to Detect Chlamydia trachomatis Infections
Therefore, NAATs are generally considered the test of choice for chlamydia and have replaced culture as the diagnostic gold standard [14,17]. Antigen tests ...
[86]
Sensitivity of the Standard Chlamydia trachomatis Culture Method Is ...
The results of this study support the use of a three‐passage Chlamydia culture procedure to increase the detection sensitivity of this method.
[87]
Limitations of serodiagnosis in chlamydial genital tract infections
For these reasons, serology alone is inadequate for the diagnosis of uncomplicated lower genital tract infections. In upper genital tract infections, however, ...
[88]
The laboratory diagnosis of Chlamydia trachomatis infections - NIH
Most invasive specimens, such as cervical or urethral swabs, may be collected for culture, antigen or nucleic acid detection.
[89]
The serodiagnositic value of Chlamydia trachomatis antigens in ...
Feb 26, 2024 · Microimmunofluorescence (MIF), which is the “gold standard” for serodiagnosis of chlamydial infection, is affected by the cross-reactivity of ...
[90]
Increasing Access to Sexually Transmitted Infection Testing - NIH
Aug 6, 2025 · ... screening for extragenital chlamydial and gonococcal infections amongst men who have sex with men. BMC infectious diseases. 2024;24(Suppl 1):224 ...
[91]
STI point-of care tests: a call for quality-assured evaluation ...
Jun 17, 2025 · The design of near-patient POCTs to both detect pathogens and predict antimicrobial susceptibility, based on known antimicrobial resistance ...
[92]
STD Diagnostics Market Size & Share | Industry Report, 2030
It is a multiplex test that can detect and differentiate four common STDs simultaneously-Neisseria gonorrhoeae (NG), Chlamydia trachomatis (CT), Mycoplasma ...
[93]
2025 European guideline on the management of Chlamydia ...
Mar 4, 2025 · The 2025 European C. trachomatis guideline provides up-to-date guidance regarding indications for testing and treatment of C. trachomatis infections.
[94]
Azithromycin versus Doxycycline for Urogenital Chlamydia ...
Dec 24, 2015 · We conducted a randomized trial comparing oral azithromycin with doxycycline for the treatment of urogenital chlamydia infection among adolescents in youth ...Azithromycin Versus... · Study Participants · Discussion
[95]
[PDF] 2025 European guideline on the management of Chlamydia ... - IUSTI
Routine universal testing versus selective or incidental testing for oropharyngeal Chlamydia trachomatis in women in The Netherlands: a retrospective cohort ...
[96]
Pelvic Inflammatory Disease (PID) - STI Treatment Guidelines - CDC
Screening and treating sexually active women for chlamydia and gonorrhea reduces their risk for PID (1162,1163). Although BV is associated with PID, whether PID ...
[97]
[PDF] STI Federal Implementation Plan 2021-2025 - HHS.gov
2021-2025 CDC. Publish an update to the 2015 STD Treatment Guidelines, which provides guidance to health care providers on the evaluation, diagnosis ...
[98]
Extragenital Gonorrhea and Chlamydia Testing and Infection Among ...
The Centers for Disease Control and Prevention recommends that men who have sex with men (MSM) be screened for urogenital GC/CT, rectal GC/CT, and pharyngeal GC ...
[99]
Pregnant Women - CDC
Jul 22, 2021 · Pregnant women identified as having chlamydia should be treated immediately and have a test of cure to document chlamydial eradication by a ...Screening Recommendations · Hiv Infection · Hepatitis BMissing: PID 2025
[100]
Recommendation: Chlamydia and Gonorrhea: Screening - uspstf
Sep 14, 2021 · The USPSTF recommends screening for chlamydia in all sexually active women 24 years or younger and in women 25 years or older who are at ...Missing: physical | Show results with:physical
[101]
Partner Services - CDC
Jul 22, 2021 · Therefore, clinicians should encourage all persons with STIs to notify their sex partners and urge them to seek medical evaluation and treatment ...
[102]
Expedited Partner Therapy | STI - CDC
Jul 16, 2024 · Expedited Partner Therapy (EPT) is the clinical practice of treating the sex partners of patients diagnosed with chlamydia or gonorrhea.STI Treatment Guidelines... · Clinical Treatment of Gonorrhea<|control11|><|separator|>
[103]
Expedited Partner Therapy - CDC
Jul 22, 2021 · If the patient has not had sex during the 60 days before diagnosis, providers should offer EPT for the patient's most recent sex partner.
[104]
TellYourPartner.org |
Oct 17, 2019 · Anonymously text or email a sexual partner that they might be at risk of an STD. If you text a partner, it will ALWAYS be anonymous. (Keep in ...
[105]
Anonymous STD Text Notification | STDcheck.com
If you have recently tested positive for an STD, you can notify your partner that they should get tested by using our free Anonymous STD Text Notification tool.Send Anonymous Notification... · Anonymous Std Text · Send A Text Message Or Email...
[106]
Costs, Health Benefits, and Cost-Effectiveness of Chlamydia ... - NIH
We estimated that chlamydia screening and PN cost $9700 per QALY gained compared with no screening and no PN.
[107]
Prevention of Pelvic Inflammatory Disease by Screening for Cervical ...
May 23, 1996 · A strategy of identifying, testing, and treating women at increased risk for cervical chlamydial infection was associated with a reduced incidence of pelvic ...
[108]
Gaps in Sexually Transmitted Infection Screening Among Men who ...
Substantial gaps exist between CDC recommendations for STI screening during PrEP care and current clinical practice, particularly for rectal and pharyngeal ...
[109]
Facilitators and barriers to point-of-care testing for sexually ...
Jun 20, 2022 · The aim of this review is to explore how point-of-care testing for STIs has been implemented into healthcare systems in LMIC and the facilitators and barriers ...
[110]
Sexually transmitted infections (STIs)
Sep 10, 2025 · More than 30 different bacteria, viruses and parasites are known to be transmitted through sexual contact, including vaginal, anal and oral sex.Chlamydia · Global health sector strategies · Syndromic management · SyphilisMissing: trachomatis | Show results with:trachomatis
[111]
Adolescents - CDC
Jul 22, 2021 · ... rates of certain STIs are highest among adolescents and young adults (141). For example, reported rates of chlamydia and gonorrhea are highest ...Screening Recommendations · Chlamydia · Gonorrhea
[112]
Healthcare-Seeking behavior for sexually transmitted infections ...
May 22, 2025 · Sub-Saharan Africa accounts for approximately 40% of the global burden STI [2]. Thus, prevention and control of STIs have widespread benefits ...
[113]
Sexually Transmitted Infections Surveillance, 2024 (Provisional) - CDC
Sep 24, 2025 · Chlamydia cases declined for the second year in a row, down 8% since 2023. Gonorrhea cases declined for the third year in a row, down 10% since ...
[114]
Key statistics | International Coalition for Trachoma Control
As of April 2025, Ethiopia, accounted for 64% of the global burden of trachoma, with 66 million people at risk - Source: WHO Weekly Epidemiological Record.
[115]
Trachoma - ScienceDirect.com
May 24, 2025 · Trachoma, the leading infectious cause of blindness worldwide, is one of several neglected tropical diseases targeted by WHO for elimination by 2030.
[116]
Public Health Considerations for Correctional Health - CDC
Jul 3, 2024 · Persons who are justice system-involved are more likely to experience risk factors for HIV, viral hepatitis, sexually transmitted infections ( ...
[117]
Lymphogranuloma venereum - Annual Epidemiological Report for ...
Feb 10, 2025 · In 2023, 22 EU/EEA countries reported 3 075 cases of LGV, an increase of 41% compared with 2022. • Two countries (the Netherlands and Spain) ...
[118]
Health Disparities in Black or African American People - CDC
Jan 17, 2024 · The rate of reported chlamydia cases among African American/Black males was 6.8 times the rate among White males (952.3 and 140.4 cases per ...
[119]
Antimicrobial Susceptibility Testing in Chlamydia trachomatis - MDPI
This narrative review synthesizes on a molecular basis the current evidence of C. trachomatis resistance and available AST methods.