**1. Introduction**

The order Chlamydiales, family Chlamydiaceae comprises obligate intracellular bacteria, classified as Gram-negative bacteria due to the cell wall structure but are difficult to stain. The cell wall has no peptidoglycan but contains an outer lipopolysaccharide membrane. Instead of peptidoglycan it contains proteins which confer the same functional properties as peptidoglycan. Those proteins are rich in cysteine. Due to this unique cell wall structure, the microorganism can divide intracellularly and survive extracellularly. The shape is coccoid or rod-shaped. Both survive intracellularly in aerobic conditions and are not able to synthesize its own ATP or grow on an artificial medium [1, 2].

*Chlamydiae* are not metabolically active outside the host cell. This is a unique characteristic of *Chlamydiae* and in contrast with other intracellular bacteria [3]. The life cycle of *Chlamydia* is biphasic and is characterized by a succession between the infectious inactive elementary body which does not replicate and represents the dispersal form of the microorganism, and the noninfectious reticulate body which can replicate [1]. Upon contact with the host cell, the bacterium provokes endocytosis by injecting chlamydial proteins into the epithelial cell it attacks. Those injected proteins force the epithelial cells to endocytose particles they would never do otherwise [4].

Once inside the host cell, the interaction with glycogen drives the elementary body to germinate and take its reticulate form [4]. The microorganism survives intracellularly into a protective parasitophorous vacuole [1]. To do so, the microorganisms act on host cell cytoskeletal structures and endocytic pathways so as not to fuse the parasitophorous vacuole with the infected cell lysosomes [4]. In those vacuoles, the microbe uptake nutrients and energy and simultaneously alter host cell transcriptional pathways to prevent apoptosis and hide from host defense mechanisms [4]. Some proteins of the bacterium are secreted into the inclusion membrane. Those proteins are called inclusion membrane proteins and their role as virulence factors still needs to be elucidated [4]. The reticulate form has an incubation period of about 7–21 days in its host as it divides every 2–3 hours. When division is complete, in about 48 hours, it takes the elementary form and is released from the host cell via exocytosis to infect new cells [1].

*Chlamydophila (Chlamydia) pneumoniae* is a main culprit of communityacquired pneumonia, bronchitis, and adult-onset asthma. They are also linked in the literature to atherosclerosis and multiple sclerosis [2, 5]. *Chlamydia psittaci* causes infection in birds and can cause severe pneumonia in humans who inhale the feces of those birds [1].

*Chlamydia trachomatis*, depending on the disease they induce and different tissue tropisms, are divided into biovars. Depending on the humoral response they provoke are divided into serovars (genovars) [1, 4, 6]. Based on antigenic variation of the major outer membrane protein (MOMP), *C. trachomatis* is classified into 15 serovars [6]. The genital strains of *C. trachomatis* serovars D through K cause the sexually transmitted disease chlamydia (cervicitis in women and urethritis in men) [1, 6]. The microbe infects squamocolumnar or transitional epithelial cells. Ascending infection causes Pelvic Inflammatory Disease in women and epididymitis and reactive arthritis in men. In women, infection may lead to infertility, ectopic pregnancy, and chronic pelvic pain [6]. Serovars L1–L3 cause the invasive lymphoma granuloma venereum (LGV), also sexually transmitted infection [1, 6]. The ocular biovar that causes Trachoma includes the serovars A through C [1]. Trachoma is a state directly linked with blindness. The disease is transmitted via infected secretions of the genital urinary tract or through ocular discharge or contact with eye-seeking flies. The microorganism binds to the mucosal membranes of the cervix, rectum, urethra, throat, and conjunctiva [1].

*Chlamydia gallinacea* is an obligate intracellular bacterium and an opportunistic human pathogen. In human, it is known to cause pneumonia in poultry slaughterhouse workers [7].

The genome of *Chlamydial* microorganisms has significant similarities that make it difficult to comprehend the way they provoke so diverse diseases [1]. Comparing the genome structure of *C. trachomatis* to *Chlamydia pneumoniae* may lead to better understanding of the ways those microorganisms act. The genome of *C. trachomatis* is described to be 1,042,519, while the respective of *C. pneumoniae* is 1,230,230 base pairs long. There are clear differences between the two: 186 genes on the *C. pneumoniae* genome are not present on the *C. trachomatis* genome, and seventy genes on the *C. trachomatis* genome are not represented on the *C. pneumoniae* genome [8]. The *C. trachomatis* genome is considered small. Nonetheless, there have been specified 900 coding sequences on the chromosome and the plasmid of the microbe. The over 200 open reading frames encode proteins their function still needs to be elucidated and are all responsible for the virulence, intracellular survival, and replication of the bacterium [9].
