The Disease State Of Chlamydia Essay, Research Paper

A parasite is defined as an being that lives in or on another being, called a host ( 2 ) . If the parasite has the capacity to do disease in the host so 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 endurance in some of the instances. The pathogen divides within or on the host in an effort to maintain its species alive while the host? s defence mechanisms at the same time attempt to extinguish the pathogen. The extent of the & # 8220 ; conflict & # 8221 ; for endurance varies depending on the relationship. This paper discusses the disease province of Chlamydia ; how the being invades its host, evades the host? s defence mechanisms, multiplies within the host, and is released from the host. Certain facets of the chlamydiae will be compared to the other pathogens, Rickettsia and the Herpesviruses as they relate to the disease province.

Bacterias are classified into four classs harmonizing to shared features, these classs are so divided into groups, and the groups are divided further into subgroups. The 9th group of bacterium contains merely two subgroups called the Rickettsias and Chlamydias ( 1 ) . Harmonizing to 16S R RNA sequencing Rickettsias are related to the purple Bacteria and Chlamydias comprise a major subdivision of Bacteria ( 2 ) . Viruss are non grouped among the procaryotes. In fact viruses are non truly organisms by definition. They are familial elements that are replicated by host cells. The herpesvirus group contains over 70 viruses all of which are potentially infective. Merely five of these viruses infect worlds. This group of viruses resemble each other and have biological belongingss in common, peculiarly the latency-reactivation phases in the disease province.

Before discoursing the host-parasite interactions the developmental rhythm of chlamydiae need to be mentioned briefly. Chlamydiae alternate between two cell types called simple organic structures and reticular organic structures. The simple organic structures are released from septic host cells and enter clean host cells. In the freshly infected host cells the simple organic structures transform to reticulate organic structures. The reticulate organic structures divide in the host cell and so transform themselves into new simple organic structures. The simple organic structures ne’er divide and the reticulate organic structures ne’er invade host cells, they are both incapable of making the other? s & # 8220 ; occupation & # 8221 ; .

The morphology and metamorphosis of viruses are wholly different from that of bacteriums. The herpes group of viruses consist of a cardinal nucleus, called a nucleoid, incorporating the viral DNA. The nucleoid is surrounded by a mirid bug made of cannular protein fractional monetary units called capsomeres. The mirid bug is surrounded by an envelope coated with viral antigens. Other viruses have fluctuations of this morphology.

In the sense that chlamydiae alteration signifier between infecting and multiplying they can be compared to viruses. Viruss have extracellular and intracellular signifiers. In the extracellular signifier the virus is in the signifier described in the old paragraph. When the virus infects the host cell it leaves behind its mirid bug and envelope so that merely 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 signifier that attaches to the host cell and an intracellular signifier that replicates or is replicated in the host cell.

The first measure in the host-parasite interaction is the fond regard of the parasite to the host cell. Chlamydial cell walls resemble those of Gram-negative bacteriums except that the chlamydial cell walls lack peptidoglycan. Alternatively of the peptide cross links in the peptidoglycan bed, disulfide bonds between outer membrane proteins provide rigidness to the wall. Interestingly, rickettsiae besides have a Gram-negative type of cell wall and they excessively lack peptidoglycan. The same outer membrane proteins of the chlamydial cell walls have besides been reported in the chaparral typhus rickettsiae. & # 8220 ; It has been suggested [ by Hatch et al. , ( 1981 ) that ] negative chlamydial ligands are neutralized by electrostatic interaction with host ligands, therefore taking to the binding of chlamydiae to host cells by powerful van der Waals forces & # 8221 ; ( 3 ) . It is non yet clear whether chlamydiae enter the host cell by agencies of microfilament-dependent phagocytosis or receptor-mediated endocytosis or if both of these tracts are someway involved together ( 3 ) . The major outer membrane protein ( MOMP ) of the chlamydial cell has been suggested to work as a chlamydial adhesin by advancing the electrostatic and hydrophobic bonding with host cells ( 3 ) . As the chlamydiae enter the host cell they become enclosed in a membrane bounded cyst called a phagosome. The phagosome and the chlamydiae within is called an inclusion.

Once inside the host cell there are two possible destinies for the chlamydiae or any other invading parasite. One destiny is that the parasite

is destroyed by host mechanisms for defence and the other is that the parasite evades the host mechanisms and multiplies. One mechanism of host defence against parasites is the merger of their lysosomes with parasite-containing phagosomes followed by the release of acid hydrolases into the phagosome to destruct the parasites. Chlamydiae have the ability to avoid lysosomal merger. The lysosomes in the cell do non blend with the inclusions. It is non known yet how this is possible. The rickettsiae flight from the phagosome before lysosomal merger. Upon come ining the host cell the chlamydial simple organic structures begin to reorganise into reticular organic structures.

& # 8220 ; Chlamydial generation is the merchandise of structural and metabolic interactions between chlamydiae and host cells & # 8221 ; ( 3 ) . The simple organic structures within the inclusions transform into reticular organic structures by undergoing legion morphological intermediate phases. There is an tremendous addition in size. The reticulate organic structure is ten to one hundred times larger than the simple organic structure. There are besides alterations in the construction of the cell was and the nucleoid. Multiplication occurs in the inclusions by binary fission of the reticulate organic structures. Some of the reticulate organic structures transform to simple organic structures while others remain reticular organic structures and go on spliting. The inclusion membrane enlarges to suit the freshly synthesized cells. The inclusion membrane is highly stable, capable of suiting several hundred reticular organic structures, simple organic structures, and intermediate organic structures.

All of the energy that the chlamydiae usage for growing comes from the host cell. This is an interesting characteristic of the chlamydial-host interaction that is besides seen in rickettsial-host interactions. The host cell contains ATP-ADP translocases which are enzymes in adenylate nucleotide conveyance systems. These enzymes were discovered in chondriosome and chloroplasts by Viginais et. Al. ( 1985 ) . Normally these translocases couple the elimination of ATP, into the cytol, with the consumption of ADP, into the cell organ, across the chondriosome 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 foremost demonstrated in R. prowazekii by Winkler ( 1976 ) . Within host cells the rickettsiae received ATP from their host by interchanging an ADP for it, but if the host ATP was unavailable the rickettsiae would do the ATP on their ain. Chlamydiae exchange ADP for host ATP merely as the rickettsiae but they are unable to synthesise their ain ATP. Viruss, including the Herpesvirus have no metabolic capacity of their ain, they must ever utilize host machinery to acquire energy and for the synthesis of all their supermolecules.

The developmental rhythm ends with the release of the chlamydiae from the host cell. Several manners of release have been proposed but it is ill-defined what really happens ( 3 ) . One manner of release is lysis of the host cells followed by the release of the chlamydiae. In this manner of release the inclusions burst inside the host cell, interrupting host cellular cell organs. Another mechanism of release & # 8220 ; in some host cells is as follows ; the inclusion is extruded through a focal dilatation of the cytoplasmatic membrane of the host cell without seemingly impacting the remainder of the cell surface & # 8221 ; ( 3 ) . Here the host cell continues its normal maps and is non destroyed. The inclusion must someway be opened outside of the cell, possible by lysis caused by the turning organic structures within it. In both instances there is no discriminatory release of simple organic structures and reticulate organic structures and intermediate organic structures are besides released at the same clip. At this point the simple organic structures continue the rhythm anew by infecting new host cells.

All of these pathogens infect epithelial cells specific to the infection location. Rickettsiae and chlamydiae Begin in the cell phagosome and both have mechanisms for hedging host defence mechanisms. The chlamydiae-host interactions discussed in this paper are luxuriant. This paper did non even get down to cover all the inside informations of the events that take topographic point. Further surveies of this interaction should take to more interesting and unexpected events. It is interesting how different beings and non-organisms ( viruses ) portion unusual traits of the host-parasite interactions. One might believe that these traits would be alone to the one being because of their complexness but as seen here they are non.

Mentions Cited:

( 1 ) Holt et Al. Bergey? s Manual of Determinative Bacteriology. Baltimore: Williams and Williams, 1994.

( 2 ) Madigan, Michael et Al. Brock Biology of Microorganisms. Upper Saddle River: Prentice Hall. 1997.

( 3 ) Moulder, James W. Rickettsia species ( as being ) . 1990. Annual Review Microbiology. 44:131-153.

( 4 ) Winkler, Herbert H. Interaction of Chlamydiae and Host Cells In Vitro. 1991. Microbiological Reviews. 55:143-190.