Author:
Krishna Misra Saurabh,Pundir Ankita
Abstract
Chlamydia was discovered in 1907 by Halberstaedter and Von Prowazek in conjunctival scrapings from an experimentally infected orangutan. Once being thought of as symbiont in plant like unicellular amoebae to intracellular parasites of vertebrates to viruses to currently as obligate intracellular bacteriae. Chlamydia is able to survive indefinitely as viable but non cultivable altered forms being a bacteria. It’s a supremely adaptable microorganism as seen with the emergence of it’s Swedish New variant (nvCT) in 2006, which was not a product of mutation or recombination but due to losing a short segment of DNA from it’s plasmid. The disease expression of Chlamydia is due to the interplay between the differences in the plasticity zone of it’s genome and the host factors. Despite the recombination of genes and emergence of new variants there is no evidence of circulating genomic resistance in Chlamydia trachomatis. The ‘seek and treat’ Chlamydia control strategy shortens the genital infection yet it’s rising sequelae of tubal infertility, the evidence of neoplastic change in cervix via modulation of caveolin-1 and c-myc RNA expression and it’s under investigated role in pathogenesis of atherosclerosis and ischemic heart disease is a sign of how exponentially this organism is evolving.