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Chlamydia Trachomatis - Essay Example

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It is an obligate intracellular, nonmotile, gram-negative organism that is about 0.3-1 micrometer in diameter. This bacterium is the world’s…
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Chlamydia Trachomatis
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Chlamydia trachomatis Chlamydia trachomatis Chlamydia trachomatis is a bacterium belonging to the Chlamydiaceae family that causes genital and ocular tract infections in humans. It is an obligate intracellular, nonmotile, gram-negative organism that is about 0.3-1 micrometer in diameter. This bacterium is the world’s leading cause of preventable blindness. Preventable blindness (trachoma) currently infects more than 150 million people worldwide. More than 92 million people are infected with trachomatis in the urogenital tract annually. In the United States, more than one million cases are reported every year (CDC, 2014). However, the actual rates are approximated to be 2.8 million due to deficiencies in reporting and screening. The species has a complex and unique biphasic life cycle and are infectious in only a single life stage. Moreover, they have an elementary body form that enables them to cope with the extracellular environment as well as a reticulate body form that is involved in intracellular replication and growth. The species has eighteen serovars of which four of them cause trachoma, five cause lymph granuloma venereum and the rest cause several other sexually transmitted infections. According to the American Family Physician, (2006), Chlamydia trachomatis exists as a reticulate body as well as an elementary body. The elementary body is an infectious, non-replicating particle that has a rigid cell wall, a genome of about 600 genes, and a plasmid with 7,498 base pairs. The rigid cell wall is extensively cross-linked by disulfide bonds. It makes the organism be resistant to harsh environmental conditions that it encounters when the organism is outside its eukaryotic host cells. The elementary body has an open reading frame for a gene serving the role of DNA replication, and also has a Ribonucleic Acid polymerase that transcripts the DNA genome upon invading a host cell. Moreover, elementary bodies attach to receptors on host cells and initiate infection. Most infect columnar epithelial cells while some infect macrophages. Weir, (2004) asserts that the reticulate body houses the DNA genome, ribosomes and proteins during the development cycle. The American Family Physician emphasizes that the reticulate bodies are the non-infectious intracellular form of the chlamydia. Chlamydia trachomatis has 894 protein coding sequences that are 135 – 5,358 nucleotides long. In the production of energy, Chlamydia trachomatis uses a form of electron transport. The synthesis of glycogen and the utilization of glucose by-products influence the chlamydial metabolism. Chlamydia trachomatis is the worlds leading cause of preventable blindness. An estimated 150 million people who live in trachoma epidemic areas have the bacterium that infects the inner eyelid. It makes the eyelid turn inward thus damaging the cornea. After a series of infections, blindness commences when the victims are in their 50’s or 60’s. It is the main source of preventable blindness because trachoma cases have been treated successfully with antibiotics (CDC, 2014). The commonest way to be infected by the organism is through having intercourse with an infected individual. Affected mothers can infect their newborns during birth. In women, it causes pelvic inflammatory disease as a result of their bodies trying to react to the organism’s invasion. Other infections include ocular infections such as blindness and conjunctivitis. Lympho granuloma venereum, on the other hand, causes wounds in the genital mucosa of the host’s body. Furthermore, people infected with gonorrhea are vulnerable for chlamydial infections. Females between 15-24 years in the United States are most susceptible to chlamydia. Prevalence incidence rates are usually highest among blacks (CDC, 2014). As an intracellular organism, Chlamydia trachomatis only replicates inside eukaryotic host cells. It has an exceptional developmental cycle, with metabolically inert, spore-like elementary bodies that poison host cells before developing into active, replicative reticulate bodies within a membrane-bound inclusion. Reticulate bodies redifferentiate into elementary bodies 24–48 hours after infection. The host body then releases elementary bodies through the lysis process (Weir, 2004). The organism is usually unable to manufacture their own energy and completely rely on their host for energy. The organism encounters its host in the elementary stage of its life cycle and is taken up by phagocytosis. It prevents the fusion of the lysosome and the phagosome, a process that usually kills pathogens. Preventing the fusion of the lysosome and phagosome allows it to secrete glycogen and transform into the reticulate body. Reticulate bodies divide by binary fusion and get their energy through sending “straw-like” structures into the host cell cytoplasm (Weir, 2004). The cell wall of Chlamydia is gram negative and lacks muramic acid that is found in the cell walls of most bacteria. The gram negative feature makes it resistant to lactam antibiotics because such antibiotics target to disrupt the cell wall. It also contains LPS a feature that enables them cause damage to the body of the host mainly because of the immune response of the host. When it gets into the body of the host it binds sialic acid receptors that are usually situated in mucous-rich environments (Novak, Kovalski, et al, 1995). The elementary bodies bind to receptors on susceptible cells and are internalized by phagocytosis and endocytosis. In the host cell endosome, elementary bodies reorganize and become reticulate bodies. The chlamydia prevents the merging of the endosome with lysosomes hence resist intracellular killing. The rigid cell membrane is extensively cross-linked by disulfide bonds and this feature makes the organism resistant to harsh environmental conditions it encounters when it is outside its eukaryotic host cells. The elementary body has an open reading frame for a gene serving the role of DNA replication, and also has a ribonucleic acid polymerase that transcripts the DNA genome after it invades a host cell. Moreover, elementary bodies attach to receptors on host cells and initiate infection. Most infect columnar epithelial cells while some infect macrophages (Somani, Bhuller et al). Chlamydia trachomatis causes damage to the host by infecting the epithelial cells. The infection of epithelial cells leads to activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) and secretion of pro-inflammatory cytokines. The activation of NF-kappaB is inhibited when RNA is interfered with during chlamydial infection. NF-kappaB plays a major role in controlling the response of the immune system to infection. Incorrect control of NF-kappaB is linked to cancer, viral infection, improper development of the immune system and septic shock (Black, 2013). In conclusion, Chlamydia trachomatis has a broad spectrum of effects to the human body. It causes various diseases to human beings such as blindness, cancer and sexually transmitted infections. In facilitating an intracellular developmental cycle, it has developed features to change the regulatory mechanisms of the host cell. It has also caused effects that are undesired to the host. The bacterium has recently become an issue of concern due to the increased incidences of spread of diseases associated with it. References American Family Physician (2006). Diagnosis and Treatment of Chlamydia trachomatis Infection. Retrieved from http://www.aafp.org/afp/2006/0415/p1411.html. Black, C.M. (2013). Chlamydial Infection: A Clinical and Public Health Perspective. Issues in Infectious Diseases. 7: 25-77. C.D.C (2014). Recommendations for the Laboratory-Based Detection of Chlamydia trachomatis and Neisseria gonorrhea. Retrieved from http://www.cdc.gov/std/laboratory/2014LabRec/default.htm. Novak, K. D., Kowalski, R. P., Karenchak, L. M., & Gordon, Y. J. (1995). Chlamydia trachomatis can be transmitted by a nonporous plastic surface in vitro-cornea. 14(5), 523-526. Somani, J., Bhullar, V. B., Workowski, K. A., Farshy, C. E., & Black, C. M. (2000). Multiple drug-resistant Chlamydia trachomatis associated with clinical treatment failure. The Journal of Infectious Diseases, 181(4): 1421-1427 Weir, E. (2004). Upsurge of genital Chlamydia trachomatis infection. Canadian Medical Association Journal, 171(8), 855. Read More
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