IndexSymptoms of ChlamydiaLife Cycle of ChlamydiaFuture Alternatives to Relieve Chlamydia trachomatis InfectionReferencesChlamydia is a common sexually transmitted disease caused by the gram-negative bacterium Chlamydia trachomatis through sexual contact and is treated with antibiotics. Having numerous sexual partners and a past history of chlamydia infection, as well as inconsistent condom use, increase the risk of receiving a chlamydia diagnosis. Chlamydial infection begins when the elementary body comes into contact with the apical epithelial surface of a target cell. This triggers a series of early events that aid in chlamydial programming and prepare the host cell for productive infection. (Beatty, Morrison, & Byrne, 1994) Studies show that there is a higher rate of chlamydia infection in young women than men, especially between 15 and 24 years of age. Furthermore, the risk is markedly increased in men and women infected with Chlamydia trachomatis in the last 12 months and there is great concern that approximately 65-70% of infected women and 50% of infected men are asymptomatic. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an Original Essay Symptoms of Chlamydia Symptoms of chlamydia infection depend on the site of the infection. Infection of the lower genital tract and urethra can cause abnormal vaginal discharge and dysuria, while infection of the upper genital tract can cause abdominal or pelvic discomfort. If left untreated, chlamydia can cause late complications including pelvic inflammatory disease, ectopic pregnancy, subfertility, and infertility in women. In males, chlamydial infection causes acute epididymitis, nongonococcal urethritis, and may also be associated with male infertility. (Peipert, 2003) Not only that, chlamydia also facilitates the transmission of HIV. (Ozolins, 2011) Despite having convenient and effective treatments, it is still a difficult challenge to control chlamydia as most people are asymptomatic and infections can persist for several months. Therefore, it is difficult to determine the prevalence of chlamydia because even if someone has the infection, they won't know it until they get checked out. Not forgetting that it is also difficult to control the spread of Chlamydia infection since it can be transmitted if the partner does not use contraceptives. Chlamydia Life Cycle Chlamydia alternates between two forms: the infectious, non-replicating, extracellular elementary body that shows zero activity, as well as the non-infectious, replicating, intracellular reticulate body. Infection occurs when the small elementary body comes into contact with the surface of the epithelial cell. (AbdelRahman and Belland, 2005) After chlamydia reaches the endoplasmic reticulum, the elementary body begins to transform into the larger, metabolically active reticular body. Subsequently the DNA of the elementary body relaxes, signals for DNA, RNA and protein synthesis are activated and cell division of the reticulate body occurs. (Belland et al., 2003) This intracellular microcolony of Chlamydia, together with the depletion of nutrition and removal of ATP from the infected host, gives a signal for the transformation of the non-infectious reticulate body into the infectious elementary body, which are then exocytosed from the host cell to infect neighboring epithelial cells in order to perpetuate the infection process. EB enters the host cell via endocytosis and once inside, it converts into the metabolically active RB, which replicates within a vaculolar compartment known asinclusion. Towards the end of the developmental cycle, RBs differentiate back into EBs, stimulating host cell lysis and release of infectious EBs into the extracellular space. These EBs then move on to infect new host cells. Before entering host cells, antigen-presenting cells engulf the EBS. Antibodies also bind to EBs, neutralizing their ability to enter epithelial cells. Cytokines can also directly inhibit both the replication and development of Chlamydia trachomatis within cells. (Roan and Starnbach, 2007) Host cells in which Chlamydia trachomatis replication is underway will be lysed by CD8+ T cells. Over the years, Chlamydia infection has been a major public health problem as it increases genital Chlamydia infection such as pelvic inflammatory disease and decreases in reproductive rates if left untreated. Beyond that, it also imposes a significant economic burden on healthcare systems due to the complications they cause. Subfertility treatment is expensive as is IVF. In addition to this, chlamydia is also difficult to treat due to the immune evasion mechanisms it possesses. Due to the presence of major outer membrane and polymorphic membrane proteins, Chlamydia trachomatis has the ability to avoid being detected by antibodies, which leads to increased survival outside of host cells. Subsequently, mitochondrial release of cytochrome C inhibition is another factor contributing to the enhanced survival of Chlamydia trachomatis outside host cells as it leads to inhibition of infected host cells. In addition to all this, Chlamydia trachomatis also has the ability to thrive as alternative intracellular forms. Gene expression encoding tryptophan synthase and a tryptophan repressor by genital Chlamydia trachomatis strains suppresses the growth inhibitory effect of interferon-γ. The production of interferon-γ by T cells results in the expression of the enzyme indolemainin-2,3-dioxygenase, which in turn leads to the degradation of tryptophan. (Beatty et al., 1994) Thus, insufficient tryptophan leads to the death of Chlamydia trachomatis due to tryptophan deficiency. After removal of interferon-γ and replenishment of tryptophan, persistent forms of Chlamydia trachomatis begin to rapidly differentiate into infectious elementary bodies (EBs). Some Chlamydia trachomatis strains carry a functional tryptophan synthase that has the ability to synthesize tryptophan, allowing them to escape the growth inhibition mechanism. Chlamydia transmission can be reduced with the use of antibiotics. Without antibiotics, this bacterium can normally survive for several months. The antibiotics azithromycin and doxycucline are widely used to treat chlamydia infection, where the former should be taken orally in a single dose, while the latter should be taken orally twice a day for a week. Azithromycin is said to be more effective than doxycucline as it is a single dose, so compliance is improved. However, Chlamydia trachomatis is becoming resistant to antibiotics, with some clinical isolates exhibiting both single and multiple resistance when cultured in vitro. Furthermore, screening is also widely used to prevent the prevalence of Chlamydia infection. It identifies apparently healthy people who may be at risk of chlamydia infection, who will then be offered some information about the infection, further testing and appropriate treatment to reduce the risk of complications. The screening aims respectively atcontrol and reduce the transmission and frequency of chlamydia. At the same time, it reduces the risk of complications, especially reproductive tract complications in women. However, because some affected people are symptomatic, screening adolescents who have sexual intercourse very often is the only way to detect most chlamydial infections. Although screening programs are widely used, they have not proven to be very effective after all because repeated screening further reduces baseline frequency of Chlamydia trachomatis, which in turn leads to inaccurate statistical evaluation. Besides that, screening for Chlamydia infection in asymptomatic patients with a long history of inability to conceive is not recommended since the consequences are already evident and a high percentage of subfertile males have been infected with Chlamydia trachomatis. Future alternatives for alleviating Chlamydia trachomatis infection Since multi-subunit vaccines are more effective than single antigen-based vaccines, Chlamydia trachomatis vaccine candidates are likely to include various antigens in the future. It is important to focus on identifying additional Chlamydia trachomatis antigens that induce protective T cell responses and also on mechanisms that promote protective immunity in the female genital tract, including the role of dendritic cells in antigen uptake and presentation as well such as the role of proinflammatory cytokines in influencing T-helper cell response distortion. Nucleic acid amplification tests (NATTs) should also be considered in one of the tests of choice for the diagnosis of Chlamydia trachomatis infection as they provide diagnostic tests for Chlamydia trachomatis that are more sensitive than antigen or culture tests. Nucleotide sequences will be targeted by polymerase chain reaction and ligase chain reaction in the cryptic chlamydial plasmid. The plasmid measures approximately 10 copies per elementary body, thus being advantageous in terms of sensitivity compared to a chromosomal DNA target. Both PCR and LCR provide sensitivities above 90% and NAAT have only some specificities of false positive results reaching 100%. Please note: this is just a sample. Get a custom paper from our expert writers now. Get a Custom Essay All in all, despite the current control mechanisms used to combat chlamydia infection, they are still not sufficient to significantly alleviate it. Since our immune response to Chlamydia infection involves both innate and adaptive immunity, further research is needed to develop a vaccine and antibiotics that are strong enough and even more effective in relieving Chlamydia infection. More importantly, it would be best for people with Chlamydia trachomatis to avoid engaging in any sexual activity for a week after taking antibiotics. References MD, H. (2017). Screening for Chlamydia trachomatis infections in women. New England Journal of Medicine, [online] 376(22), pp.2197-2198. Available at: https://www-nejm-org.ez.library.latrobe.edu.au/doi/pdf/10.1056%2FNEJMcp1412935.Workowski, K., and Bolan, G. (2019). Guidelines for the Treatment of Sexually Transmitted Diseases, 2015. [online] 64(RR-03), pp.1-137. Available at: https://www.cdc.gov/mmwr/preview/mmwrhtml/rr6403a1.htm?s_cid=rr6403a1_w.Torrone, E., Papp, J., & Weinstock, H. (2014). Prevalence of genital Chlamydia trachomatis infection among persons aged 14 to 39 years - United States, 2007-2012. Morbidity and Mortality Weekly Report (MMWR) Weekly, [online] 63(38), pp.834-838.Available at: https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6338a3.htm.Cohen, C. R., & Brunham, R. C. (1999). The pathogenesis of chlamydia induced pelvic inflammatory disease. Sexually Transmitted Infections, 75(1), 21-24. Available at: https://www.researchgate.net/publication/12852162_Pathogenesis_of_Chlamydia_activated_pelvic_inflammatorya_diseaseCarey, A., & Beagley, K. (2010). Chlamydia trachomatis, a hidden epidemic: effects on female reproduction and treatment options. American Journal of Reproductive Immunology, [online] 63(6), pp.576-586. Available at: https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1600-0897.2010.00819.x.Peipert, J. (2003). Genital chlamydial infections. New England Journal of Medicine, [online] 349(25), pp.2424-2430. Available at: https://www.researchgate.net/publication/8953388_Genital_Chlamydial_Infections.Ozolins D. (2011). Why are chlamydia and HPV important public health problems?. EJIFCC, 22(1), 36-8. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4975330/AbdelRahman, Y., & Belland, R. (2005). The developmental cycle of chlamydia: Figure 1. FEMS Microbiology Reviews, [online] 29(5), pp.949-959. Available at:https://pdfs.semanticscholar.org/cf3c/e8fdfd0d45036a0e7b332dd75083a726b9c3.pdf.Belland, R., Zhong, G., Crane, D., Hogan, D., Sturdevant, D., Sharma, J., Beatty , W., & Caldwell, H. (2003). Genomic transcriptional profiling of the Chlamydia trachomatis developmental cycle. Proceedings of the National Academy of Sciences, [online] 100(14), pp.8478-8483. Available at: https://www.researchgate.net/publication/10701106_Genomic_transcriptional_profiling_of_the_developmental_cycle_of_Chlamydia_trachomatis.Redgrove, K., & McLaughlin, E. (2014). The role of the immune response in Chlamydia trachomatis infection of the male genital tract: a double-edged sword. Frontiers in Immunology, [online] 5. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4209867/.Shaw, K., Coleman, D., O'Sullivan, M ., & Stephens, N. (2011). Public health policies and management strategies for genital Chlamydia trachomatis infection. Risk Management and Health Policy, 4, 57-65. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270924/#b8-rmhp-4-057Horner, P. (2006). The case for further studies on the treatment of uncomplicated genital Chlamydia trachomatis infection. Sexually Transmitted Infections, [online] 82(4), pp.340-343. Available at: https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1600-0897.2010.00819.x.Jones, R., Van Der Pol, B., Martin, D., and Shepard, M. (1990). Partial characterization of Chlamydia trachomatis isolates resistant to multiple antibiotics. Journal of Infectious Diseases, [online] 162(6), pp.1309-1315. Available at: https://www.ncbi.nlm.nih.gov/pubmed/2230260.Roan, N., & Starnbach, M. (2007). Immune-mediated control of Chlamydial infection. Cellular Microbiology, [online] 0(0), p.071103031556005-???. Available at: https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1462-5822.2007.01069.xBrunham, R.,Plummer, F., & Stephens, R. (1993). Bacterial antigenic variation, host immune response and pathogen-host coevolution. [online] 61(6), pp.2273-2276. Available at: https://iai-asm-org.ez.library.latrobe.edu.au/content/iai/61/6/2273.full.pdf.Fan, T., Lu, H., Hu, H ., Shi, L., McClarty, G., Nance, D., Greenberg, A., & Zhong, G. (1998). Inhibition of apoptosis in chlamydial-infected cells: blockade of mitochondrial cytochrome release and caspase activation. The Journal of Experimental Medicine, [online] 187(4), pp.487-496. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212145Beatty, W.,Belanger, T., Desai, A., Morrison, R., & Byrne, G. (1994) . Role of tryptophan in interferon gamma-mediated chlamydial persistence. Annals. (2018,.