**2. Pathophysiology**

Chlamydia affects columnar epithelium, so adolescent women are particularly at risk since the squamocolumnar junction is located on the ectocervix until early adulthood. Chlamydia has extraordinary features regarding its life cycle. It has two different forms in the course of infection in both intracellular and extracellular environments. The elementary body (EB) is the infectious form existing in the extracellular space; it is a spore-like, inactive structure that enters the host cell. Inside the cell, it turns into an active form called a reticulate body (RB). The RB uses the host cell's amino acids and the energy sources in the form of ATP to synthesize its own DNA, RNA, and proteins to replicate and after enough RBs have formed, some of them turn back to the EB form, which can then exit the initial host cell and infect others. This cycle is then repeated in the adjacent cells [14, 15]. Thus, this process creates an immunogenic environment around the infection. However, there are ways for *C. trachomatis* to escape and evade the immune system. For example, by preventing T-cell immune recognition, it down-regulates the major histocompatibility complexes I and II; it modulates some specific cytokines, such as beta interferon, type 1 interferons, interleukin 18 and, inhibits apoptosis by the secretion of Chlamydial protease-like activity factor proteins and enhancing cell survival signals. By this way, it creates a chronic inflammation that allows the infection to become persistent. Replication mechanisms that adapt to the environment during the biphasic development cycle and evolutionary defense mechanisms that allow to escape from the immune system and environmental inflammatory stress are also challenging obstacles to infection treatment and vaccine development [16]. Still, with advances *in silico* studies using bioinformatics tools and machine learning-based modeling, Shiragannavar and his colleagues, have succeeded in developing a candidate vaccine that stimulates T and B cells in a way that provides long-term immunity [17]. There are also other vaccine candidates that use immune and proteomic approaches as well as *in silico* methods [18].

The bacterium is usually transmitted through sexual activity. The risk of an infected man infecting an uninfected woman with each sexual contact is 25%. Chlamydia can also spread vertically. The risk of transmission from the infected mother to the newborn is around 50–60%, and in most cases, the neonatal infection is in the form of conjunctivitis or pneumonia. (In 10–20% of cases, in the form of Afebrile Pneumonia Syndrome).

Genital tract infection is the most common clinical picture. The incubation period is around 1–3 weeks. In total, 50% of infected men and 80% of infected women are asymptomatic. But the infection can cause mucopurulent cervicitis in women, and

*Chlamydia: The Female Reproductive System and Infertility DOI: http://dx.doi.org/10.5772/intechopen.111756*

it can lead to urethritis in men [19]. Ascending infection can result in the development of PID in women and is the most common cause of epididymitis in men under 35 years of age. In total, 5–10% of women who have had PID may progress to perihepatitis also known as Fitz-Hugh-Curtis syndrome.

Although the presence of any STD in one patient increases the likelihood of coinfection with another STD, the most common coinfection in such a case is the combination of Chlamydia and Gonorrhea. In total, 40% of women and 20% of men with chlamydia infection are coinfected with gonorrhea [20, 21]. Other pathogens that can cause coinfection with Chlamydia are *Mycoplasma genitalium* [22, 23] and HPV [24, 25] possibly causing an association between cervical intraepithelial neoplasia and Chlamydia [26]. The frequency of Reiter's syndrome (reactive arthritis, conjunctivitis, and urethritis) in patients with chlamydia is also increased compared to the normal population. LGV cases are the reason for 10% of genital ulcers in tropical countries. In the course of a LGV case, localized inguinal lymphadenopathy and ulceration develop within 2–12 hf after exposure to infection. In untreated cases, proctitis, rectal strictures, and elephantiasis secondary to lymphatic obstruction may occur.
