**2. General information:** *C. trachomatis*

Chlamydial species have been described as gram-negative, aerobic, and obligate intracellular pathogens. Molecular studies have shown that they are unable to synthesize their ATP, and therefore they need to use their host cell's energy resources [1]. Due to this scientific fact, previously chlamydial species have been considered as viruses. *C. trachomatis* and Chlamydia pneumonia are pathogens causing infections in human. *C. trachomatis* has been divided into 19 serovars, according to the specificity of major outer protein membrane protein (MOPM) epitopes [4, 5]. It has been reported that while serovars A, B, Ba, and C are pathogens causing trachoma, serovars D, Da, E, F, G, Ga, H, I, Ia, J, and K are the most commonly encountered sexually transmitted agents. Furthermore, serovars L1, L2, L2a, and L3 are described as the bacteria, which are the pathogens of transmission of lymphogranuloma venereum (LGV) [4, 6].

Microbiological investigations provided that the chlamydial life cycle includes two different phases. The first phase is called the infectious phase, which occurs outside the target cells. During this phase, *chlamydia trachomatis* forms elementary forms, which cause the transmission of infection. After its transmission to the target cells, chlamydia forms the so-called reticulate forms, which are capable of replication. Basically, once the chlamydial elementary bodies infect non-ciliated columnar cells and macrophages, chlamydia induces its own endocytosis. Inside the host cell, the elementary bodies convert to reticulate bodies, which begin to replicate every 3 hours after an incubation of 7 to 21 days. Finally, after a certain production, the reticulate bodies change again into elementary bodies and shed off the cell membrane through exocytosis. It has been reported that because of its unique cell-wall structure chlamydial pathogens are able to survive against phagocytosis and destruction by lysosomal enzymes [4–6].
