*1.2.4 Invasive cervical carcinoma (ICC)*

Invasive cervical carcinoma (ICC) is most likely caused by the human papillomavirus (HPV). Research investigating the etiology of cervical neoplasia and invasive cervical carcinoma has recently examined factors that may affect susceptibility to or progression of HPV infection [13]. *C. trachomatis* may be a significant HPV cofactor for cervical cancer among sexually transmitted diseases other than HPV. As well as HPV, *C. trachomatis* may play an important role in cervical cancer development. *C. trachomatis* is an obligate intracellular bacterium that infects the genital tract [14]. Genital *C. trachomatous* infection may cause chronic inflammation, damage to epithelial tissues, and pelvic inflammation in some cases. In addition, it has been clinically associated with cervical atypia and metaplasia, increasing women's risk of cervical neoplasia [15].

A case-control study from England and a pooled analysis of cohort studies from Finland, Norway and Sweden have found positive associations between *C. trachomatis* microimmunofluorescence (MIF) seropositivity and ICC [16, 17]. According to a Swedish cohort study, *C. trachomatis* DNA is highly predictive of the development of ICC [18].

Squamous cell ICC may also be increased by infections with *C. trachomatis* by increasing a host's susceptibility to HPV and enhancing its effects. Infection with C trachomatis may lead to inflammation, which can produce reactive oxygen species, which can damage DNA and increase the risk of HPV-associated cancer [19]. According to in vitro experiments, Chlamydia-infected cells are also less likely to undergo the normal process of programmed cell death [19, 20]. The cadherin-catenin junction structure in cervical epithelial cells is altered by C trachomatis, increasing the risk of infection with HPV. As opposed to cellular mechanisms, humoral mechanisms (Th2) may mediate the immune response to a particular antigen [21]. The

symptoms of cervical neoplasia may be difficult to control in women with C trachomatis infection. An increase in HPV persistence after 12 months was associated with a previous history of C trachomatis, according to a study conducted among Swedish women aged 32–38 years old [22].

#### *1.2.5 Infertility*

Worldwide, infertility is becoming an increasingly prevalent health issue [12]. *C. trachomatis* is becoming a more prominent sexually transmitted disease as a result of the increase in cases [23]. Currently, *C. trachomatis* is the most prevalent sexually transmitted pathogen. The symptoms of chlamydial infection are less severe than those of other sexually transmitted diseases. A patient may be unaware of the infection until secondary or tertiary symptoms develop due to these deceptively mild symptoms. Infections such as acute salpingitis and pelvic inflammatory disease that go undetected and untreated can result in not only significant morbidity but also infertility [24].

Infertility associated with *C. trachomatis* can be prevented if detected early [25]. Infertile women are estimated to be infected with chlamydial infections by 18–20%, according to a WHO study [23].

It is reported that infertility is reported to last between 2 and 4 years in chlamydiapositive women [26]. Women with secondary infertility were more likely to contract *C. trachomatis* infection. Due to their long period of active sexual life, they may be more susceptible to chlamydial infections. There was a surprisingly high percentage of infertile women (38%) who were positive for *C. trachomatis*. There was no history of previous upper genital tract infection in the majority of these women [23].

#### *1.2.6 Complications of pregnancy*

Furthermore, the chlamydial genital infection may increase the risk of premature rupture of the membranes during labor, preterm delivery, and low birth weight infants in addition to the risk of future ectopic pregnancy [27]. According to a study of 3913 pregnant Dutch women screened for *C. trachomatis*, those with chlamydial infection had a higher risk of preterm delivery (adjusted odds ratio 4.35, 95% CI 1.3–15.2). However, the chlamydial infection did not predict miscarriage or perinatal death [24].

#### *1.2.7 Perihepatitis (Fitz-Hugh-Curtis syndrome)*

Perihepatitis is an inflammation of the liver capsule and adjacent peritoneal surfaces that may occur in patients with chlamydia infection. An acute PID is more likely to result in perihepatitis, which occurs in 5–15% of cases. In most cases, there is no abnormality in liver enzymes, but there can be a pain in the right upper part of the rig or pleuritic pain. We do not fully understand the pathogenesis of this condition. An immunological mechanism may be involved, or the infected material could be directly transmitted from the cul-de-sac to the lymphatics and peritoneum [28, 29].

### *1.2.8 Reactive arthritis/reactive arthritis triad (RAT)*

STIs can trigger reactive arthritis. There is a small percentage of patients with sexually acquired reactive arthritis who develop the complete reactive arthritis triad,

#### Chlamydia trachomatis*: A Tiny Being beyond the Nature DOI: http://dx.doi.org/10.5772/intechopen.111425*

consisting of arthritis, conjunctivitis, uveitis, and urethritis. It has been shown that *C. trachomatis* causes sexually acquired reactive arthritis most frequently.

Detection of chlamydial nucleic acids in synovial tissue further supports the association between chlamydia and reactive arthritis. Seven out of nine patients with RAT had a positive in situ hybridization for chlamydial RNA in synovial tissue samples compared to three out of thirteen patients without RAT (the cause of arthritis was not otherwise determined). In addition, five of eight sexually acquired reactive arthritis patients and one control patient with another form of arthritis had stored synovial tissues that contained chlamydial DNA found by polymerase chain reaction.
