There are currently 18 serovars of C. trachomatis, each associated with specific diseases affecting mucosal cells in the lungs, genital tracts, and ocular systems.

[3] Infections are often asymptomatic, but can lead to severe complications such as pelvic inflammatory disease in women and epididymitis in men.

[10] Currently, no vaccines are available, largely due to the complexity of the immunological pathways involved in C. trachomatis, which remain poorly understood.

[11][12] Chlamydia trachomatis is a gram-negative bacterium that replicates exclusively within a host cell, making it an obligate intracellular pathogen.

Elementary bodies (EBs) are 200 to 400 nanometers across and are surrounded by a rigid cell wall that enables them to survive in an extracellular form.

[10] Several important metabolic functions are not encoded in the C. trachomatis genome and are instead scavenged from the host cell.

[3][13] The bacterium is largely dependent on the host cell for metabolic intermediates and energy, particularly in the form of adenosine triphosphate (ATP).

[13] C. trachomatis lacks several enzymes necessary for independent glucose metabolism, and instead utilizes two ATP/ADP translocases (Npt1 and Npt2) to import ATP from the host cell.

[17] The reticulate body substantially modifies the inclusion, making it a more hospitable environment for rapid replication of the bacteria, which occurs over the following 30 to 72 hours.

[17] The massive number of intracellular bacteria then transition back to resistant elementary bodies before causing the cell to rupture and being released into the environment.

[20] Serovars D through K infect the genital tract, causing pelvic inflammatory disease, ectopic pregnancies, and infertility.

This genus contains a total of nine species: C. trachomatis, C. muridarum, C. pneumoniae, C. pecorum, C. suis, C. abortus, C. felis, C. caviae, and C. psittaci.

[3] The chlamydial plasmid, a DNA molecule existing separately from the genome of C. trachomatis, functions to enhance genetic diversity via the genes encoded.

[22] The plasmid gene protein 3 (pgp3) has been linked to the establishment of persistent infection within the genital tract by suppressing the host immune response.

[25] CPAF (Chlamydia Protease-like Activity Factor) functions by preventing the host from triggering the proper immune response.

[7] Genitourinary cases can include genital discharge, vaginal bleeding, itchiness (pruritus), painful urination (dysuria), among other symptoms.

[6] C. trachomatis may latently infect the chorionic villi tissues of pregnant women, thereby impacting pregnancy outcome.

Risk factors for genitourinary infections include unprotected sex with multiple partners, lack of condom use, and low socioeconomic status living in urban areas.

[9] Trachoma is the primary source of infectious blindness in some parts of rural Africa and Asia and is a neglected tropical disease that has been targeted by the World Health Organization for elimination by 2020.

[11] If the infection has progressed, ascending the reproductive tract and pelvic inflammatory disease develops, damage to the fallopian tubes may have already occurred.

Mutations in the 23S rRNA gene, including A2057G and A2059G, have been identified as significant contributors to resistance against azithromycin, a commonly used treatment.

This resistance is linked to treatment failures and persistent infections, necessitating ongoing research into alternative antibiotics, such as moxifloxacin, as well as non-antibiotic approaches like bacteriophage therapy.

NAATs have facilitated broader screening programs, particularly in high-risk populations, and are integral to public health initiatives aimed at controlling the spread of C. trachomatis.

Research continues into point-of-care diagnostic tools, which promise faster results and greater accessibility, especially in low-resource settings.

While these vaccines show promise in inducing partial immunity in murine models, further research is needed to evaluate their efficacy in humans.

[17] Over the next several decades, "Chlamydozoa" was thought to be a virus as it was small enough to pass through bacterial filters and unable to grow on known laboratory media.

It was originally believed that Chlamydia lacked peptidoglycan because researchers were unable to detect muramic acid in cell extracts.

[41] Subsequent studies determined that C. trachomatis synthesizes both muramic acid and peptidoglycan, but relegates it to the microbe's division septum and does not utilize it for construction of a cell wall.

[49] It is now known that C. trachomatis comprises 19 serovars which are identified by monoclonal antibodies that react to epitopes on the major outer-membrane protein (MOMP).

[51] Furthermore, there have been over 220 Chlamydia vaccine trials done on mice and other non-human host species to target C. muridarum and C. trachomatis strains.