The Disease State Of Chlamydia Essay Research — страница 2

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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 suggested to function as a chlamydial adhesin by promoting

the electrostatic and hydrophobic bonding with host cells (3). As the chlamydiae enter the host cell they become enclosed in a membrane bounded vesicle called a phagosome. The phagosome and the chlamydiae within is called an inclusion. Once inside the host cell there are two possible fates for the chlamydiae or any other invading parasite. One fate is that the parasite is destroyed by host mechanisms for defense and the other is that the parasite evades the host mechanisms and multiplies. One mechanism of host defense against parasites is the fusion of their lysosomes with parasite-containing phagosomes followed by the release of acid hydrolases into the phagosome to destroy the parasites. Chlamydiae have the ability to avoid lysosomal fusion. The lysosomes in the cell do not

fuse with the inclusions. It is not known yet how this is possible. The rickettsiae escape from the phagosome before lysosomal fusion. Upon entering the host cell the chlamydial elementary bodies begin to reorganize into reticulate bodies. “Chlamydial multiplication is the product of structural and metabolic interactions between chlamydiae and host cells” (3). The elementary bodies within the inclusions transform into reticulate bodies by undergoing numerous morphological intermediate stages. There is an enormous increase in size. The reticulate body is ten to one hundred times larger than the elementary body. There are also changes in the structure of the cell was and the nucleoid. Multiplication occurs in the inclusions by binary fission of the reticulate bodies. Some of

the reticulate bodies transform to elementary bodies while others remain reticulate bodies and continue dividing. The inclusion membrane enlarges to accommodate the newly synthesized cells. The inclusion membrane is extremely stable, capable of accommodating several hundred reticulate bodies, elementary bodies, and intermediate bodies. All of the energy that the chlamydiae use for growth comes from the host cell. This is an interesting feature of the chlamydial-host interaction that is also seen in rickettsial-host interactions. The host cell contains ATP-ADP translocases which are enzymes in adenylate nucleotide transport systems. These enzymes were discovered in mitochondria and chloroplasts by Viginais et. al. (1985). Normally these translocases couple the excretion of ATP,

into the cytoplasm, with the uptake of ADP, into the organelle, across the mitochondria or chloroplast membrane. However, translocase activity in the presence of these intracellular parasites is reversed, ATP is taken in, to the inclusion, and ADP is excreted, out of the inclusion, across the inclusion membrane. Translocase activity in intracellular parasites was first demonstrated in R. prowazekii by Winkler (1976). Within host cells the rickettsiae received ATP from their host by exchanging an ADP for it, but if the host ATP was unavailable the rickettsiae would make the ATP on their own. Chlamydiae exchange ADP for host ATP just as the rickettsiae but they are unable to synthesize their own ATP. Viruses, including the Herpesvirus have no metabolic capacity of their own, they

must always use host machinery to get energy and for the synthesis of all their macromolecules. The developmental cycle ends with the release of the chlamydiae from the host cell. Several modes of release have been proposed but it is unclear what actually happens (3). One mode of release is lysis of the host cells followed by the release of the chlamydiae. In this mode of release the inclusions burst inside the host cell, disrupting host cellular organelles. Another mechanism of release “in some host cells is as follows; the inclusion is extruded through a focal distention of the cytoplasmic membrane of the host cell without apparently affecting the rest of the cell surface” (3). Here the host cell continues its normal functions and is not destroyed. The inclusion must