**4.1 Pathogenesis and transmission**

All the included pathogens are highly transmissible, one of the most important features for this is that most of the infected people, mostly women, remain asymptomatic and do not seek treatment. All of these diseases are transmitted during sexual intercourse.

CT can avoid destruction by the host's innate and adaptive immune systems by autophagy, which allows CT to migrate to the upper genital tract for establishing a chronic infection. Without treatment, up to 50% of infected women will continue to be infected for greater than 1 year. CT can be in the semen of infected males or can be released from infected female genital tract epithelial cell. CT can bind to almost all receptors in the epithelial cell (i.e. mannose, mannose-6-phosphate, epidermal growth factor, B1 integrin, platelet-derived growth factor receptor, protein disulfide isomerase, fibroblast growth factor receptor, and ephrin receptor A2). CT induces actin remodeling that facilitates the entry in the cytoplasm. The EBs are internalized in vacuoles and form an intracytoplasmic inclusion, which can evolve to RBs, these RBs are the non-infectious replicative form and use nutrients within the host cytoplasm and replicate by binary fission, when the RB-filled inclusion reaches critical volume, RBs convert back to EBs, and they can be released to the extracellular milieu by two mechanisms: host lysis or extrusion of the cytoplasmic inclusion [4, 14].

Ng affects the urogenital tract, mostly the columnar and transitional epithelia. Ng prevents complement activation, opsonization, and bacterial killing. Ng prevents complement activation, opsonization, and bacterial killing and can survive in and around the macrophages and neutrophils during infection and modulate the immuneactivating properties of dendritic cells. Ng infection does not generate immunological memory, owing to the ability of Ng antigenically and phase vary its surface structures. In men, Ng attaches to sperm, which is easily transmitted from men to their partners through ejaculates with high number of bacteria. In women, bacterial sialidases, which are secreted by the cervicovaginal microbiota of women, must first desialylate Ng lipooligosaccharide to enable efficient transmission [10].

In the case of Tp, the mechanisms of tissue damage by Tp are still not well described. The local inflammation process has been attributed to the spirochete itself; nevertheless, the fragility and low protein content of its outer membrane make it very difficult to well characterize them. A well definition of protective immunity is still unavailable. Transmission of venereal syphilis occurs during sexual contact with an actively infected partner, same as the other three diseases described in this chapter; with only 10 organisms in the exudate, the disease can be transmitted. Tp can penetrate directly the mucous membranes and adhere to the epithelial cells and extracellular matrix components for establishing the infection, fibronectin and laminin are key for Tp interactions with the cell. The infection becomes systemic very fast, once the blood–brain barrier is reached (this happens in as many as 40% of individuals with syphilis), early syphilis without treatment can cause severe neurological complications [12].

*Sexually Transmitted Diseases in Pediatrics DOI: http://dx.doi.org/10.5772/intechopen.107991*

Tv transmission occurs almost exclusively via sexual contact, even some transmission via fomites has been argued, which is highly controversial and lacks strong evidence. During sexual intercourse, Tv in the genital tract of the infected partner is transferred to the uninfected partner, when Tv reaches the epithelial cells, Tv assumes an ameboid form increasing its surface area contact. The five primary surface adhesins responsible for the attachment of the parasite to the epithelia are AP120, AP65, AP51, AP33, and AP23. Iron is the most important mediator of Tv growth [13].
