A parasite is defined as an organism that lives in or on another organism, called a host (2). If the parasite has the capacity to cause disease in the host then the parasite is called a pathogen. Disease in the host is caused by the infection of the parasite. The interaction between the host and parasite is complex. Both the pathogen and the host strive for survival in some of the cases. The pathogen divides within or on the host in an attempt to keep its species alive while the hostís defense mechanisms simultaneously attempt to eliminate the pathogen. The extent of the battle for survival varies depending on the relationship. This paper discusses the disease state of Chlamydia; how the organism invades its host, evades the hostís defense mechanisms, multiplies within the host, and is released from the host. Certain aspects of the chlamydiae will be compared to the other pathogens, Rickettsia and the Herpesviruses as they relate to the disease state.

Bacteria are classified into four categories according to shared characteristics, these categories are then divided into groups, and the groups are divided further into subgroups. The ninth group of bacteria contains only two subgroups called the Rickettsias and Chlamydias (1). According to 16S r RNA sequencing Rickettsias are related to the purple Bacteria and Chlamydias comprise a major branch of Bacteria (2). Viruses are not grouped among the prokaryotes. In fact viruses are not really organisms by definition. They are genetic elements that are replicated by host cells. The herpesvirus group contains over seventy viruses all of which are potentially pathogenic. Only five of these viruses infect humans. This group of viruses resemble each other and have biological properties in common, particularly the latency-reactivation stages in the disease state.

Before discussing the host-parasite interactions the developmental cycle of chlamydiae need to be mentioned briefly. Chlamydiae alternate between two cell types called elementary bodies and reticulate bodies. The elementary bodies are released from infected host cells and enter uninfected host cells. In the newly infected host cells the elementary bodies transform to reticulate bodies. The reticulate bodies divide in the host cell and then transform themselves into new elementary bodies. The elementary bodies never divide and the reticulate bodies never invade host cells, they are both incapable of doing the otherís job.

The morphology and metabolisms of viruses are completely different from that of bacteria. The herpes group of viruses consist of a central core, called a nucleoid, containing the viral DNA. The nucleoid is surrounded by a capsid made of tubular protein subunits called capsomeres. The capsid is surrounded by an envelope coated with viral antigens. Other viruses have variations of this morphology.

In the sense that chlamydiae change form between infecting and multiplying they can be compared to viruses. Viruses have extracellular and intracellular forms. In the extracellular form the virus is in the form described in the previous paragraph. When the virus infects the host cell it leaves behind its capsid and envelope so that only its nucleic acid enters the host cell. The viral nucleic acid is replicated by host cell machinery. So both chlamydiae and viruses, including the herpesviruses, have an extracellular form that attaches to the host cell and an intracellular form that replicates or is replicated in the host cell.

The first step in the host-parasite interaction is the attachment of the parasite to the host cell. Chlamydial cell walls resemble those of gram-negative bacteria except that the chlamydial cell walls lack peptidoglycan. Instead of the peptide cross links in the peptidoglycan layer, disulfide bonds between outer membrane proteins provide rigidity to the wall. Interestingly, rickettsiae also have a gram-negative type of cell wall and they too lack peptidoglycan. The same outer membrane proteins of the chlamydial cell walls have also been reported in the scrub typhus rickettsiae. It has been suggested [by Hatch et al.,(1981) that] negative chlamydial ligands are neutralized by electrostatic interaction with host ligands, thus leading to the binding of chlamydiae to host cells by powerful van der Waals forces (3). It is not yet clear whether chlamydiae enter the host cell by means of microfilament-dependent phagocytosis or receptor-mediated endocytosis or if both of these pathways are somehow involved together (3). The major outer membrane protein (MOMP) of the chlamydial cell has been