**1. Introduction**

*Chlamydia trachomatis* and *Chlamydia pneumoniae* are significant human pathogens that affect people of all ages worldwide. *Chlamydia psittaci* is a cause of zoonosis, and birds are the reservoirs. All are diseases for which there is no effective vaccine.

All members of the family share a lipopolysaccharide antigen and use host resources to synthesize chlamydial protein. They also encode the major outer membrane protein (MOMP or OmpA), which is surface-exposed in *C. trachomatis* and *C. psittaci* but not in *C. pneumoniae*. The MOMP is the major determinant of *C. trachomatis* and *C. psittaci* serologic classification [1, 2].

Chlamydiae are obligate intracellular microorganisms that have a distinct developmental cycle. Understanding this life cycle is important because it underlies the potential problems with laboratory diagnosis, persistent infection, and treatment.

#### **1.1 The biology and life cycle**

The chlamydial life cycle is biphasic, with two functional and morphological forms that alternate: infectious "elementary bodies" (EBs) and replicative, non-infectious

"reticulate bodies" (RB). The metabolically inactive and infectious "Elementary Body" (EB), which is capable of extracellular survival, binds to the surface of host cells via interactions between bacterial ligands and host receptors, resulting in EB endocytosis. The vesicles containing the EBs are referred to as "inclusion." Because multiple EBs can bind to and enter the same host cell, multiple inclusions are formed. EBs differentiate into metabolically active RBs after internalization. RBs are specialized in nutrient acquisition and the expression of proteins required for energy synthesis. RBs replicate by binary fission within inclusion bodies, avoid lysosomes by modifying host cell endocytic pathways by changing or mimicking the inclusion membrane, and transform into EBs with the ability to infect new host cells [3]. Host metabolites are used in this process via interactions with multiple host cell organelles. After 48–72 hours, new EBs are released by cell lysis to infect other cells while leaving the host cell alive. In this one-of-a-kind cycle, RBs, the organism's intracellular form, play a role in disease persistence, while EBs infect new hosts or neighboring host cells [3, 4].
