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| Leprosy seemed to be especially prevalent in the district of Kumaun in the late 1800’s. (23) In a statistical study, the disease was more prominent in the eastern side of the district rather than the western side. (26) Research showed that there would not be an increase in leprosy of the population of Kumaun, as long as the disease was hereditary. (71) | | Leprosy seemed to be especially prevalent in the district of Kumaun in the late 1800’s. (23) In a statistical study, the disease was more prominent in the eastern side of the district rather than the western side. (26) Research showed that there would not be an increase in leprosy of the population of Kumaun, as long as the disease was hereditary. (71) |
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| In a 1852 census, for every four males that had leprosy, only one female had leprosy. In the previous census, the ratio for males to females with leprosy was almost ten to one. For some reason, the leprosy ratio decreased rapidly. (25) However, with more recent studies, it seems that leprosy has been affecting females more than males (53). For ages 20-30, the percentage of males diseased is 20.0% whereas for females the percentage is 26.4% (53). | | In a 1852 census, for every four males that had leprosy, only one female had leprosy. In the previous census, the ratio for males to females with leprosy was almost ten to one. For some reason, the leprosy ratio decreased rapidly. (25) However, with more recent studies, it seems that leprosy has been affecting females more |
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| <h2> <span class="mw-headline"><B>Description of <I>Mycobacterium leprae</i></b></span></h2>
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| <FONT SIZE=4>2.1 Genome<BR></FONT>
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| The complete sequence is 3,268,203 bp in length with a G+C content of 57.8%, and was generated from a combination of cosmid and 6-fold whole-genome shotgun sequencing. The start of the sequence is the first base of the dnaA gene, close to the origin of replication. There are 1,604 protein-coding genes and 1,116 pseudogenes. Both the sequence and annotation have been deposited in the public databases (NCBI) with the accession number AL450380.http://www.ncbi.nlm.nih.gov/nuccore/30407142 The Sanger Institute sequenced Mycobacterium leprae in collaboration with the laboratory of Stewart Cole at the Unit de Genetique Moleculaire Bacterienne, Institut Pasteu. Sequencing was funded by the Heiser Program for Research in Leprosy and Tuberculosis of The New York Community Trust, L'Association Raoul Follereau, The Wellcome Trust, ILEP, and the Institut Pasteur.
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| <BR><BR>
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| <FONT SIZE=4>2.2 Transmission of disease<BR></FONT>
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| Traditionally, mycobacterium leprae was known to infect and affect the
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| skin, mainly through lining containing epithelial cells and also the
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| peripheral nerves such as those contained in the central nervous system.
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| However, recent research attempts to elaborate further into such findings
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| to narrow down a specific mechanism of infection, which to this day, is
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| still unknown. Although a specific method proves lacking, there seems to
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| be various hypotheses surrounding this greatly debatable topic.
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| Thus far, it has been postulated that mycobacterium leprae may gain access
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| to entry through two primary routes- the nasal mucosal membrane or through
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| skin injuries. However, it has been shown that passage through the nasal
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| mucosal membrane may be the primary route of infection. A study, focusing
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| primarily on the mce1A gene in mce1 operon (mammalian cell entry) of
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| mycobacterium tuberculosis which proved to have a similar set of encoded
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| proteins as mycobacterium leprae; experiment was to be done in vitro, to
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| observe the cell uptake activity of polystyrene latex beads which are
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| layered with purified recombinant r proteins expressed by a specific locus
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| within the mce1A gene. The results showed that the r-protein did promote
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| uptake of the polystyrene latex beads into human nasal mucosal cells which
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| concludes that the mce1A gene could mediate the entry of mycobacterium
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| leprae into respiratory mucosal tracts and may possibly be the main mode
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| of transmission of such microbe. Additionally, endothelial cells may
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| perhaps serve as a microbial reservoir, the cause of long-term infections.
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| Unlike many other mycobacteriums, mycobacterium leprae does not only
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| survive in macrophages in vivo, it can also survive in nonmacrophage cells
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| such as epithelial cells (as shown previously) and Schwann cells.
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| Extensive research has revealed that destruction of such nonmacrophage
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| cells is the primary manifestation of the disease, leprosy. It has been
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| found that a mycobacterium leprae gene encoding fibronectin (FN) binding
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| protein is the main mechanism of transmission via epithelial and Schwann
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| cells. The interaction between FAP-L (FN attachment protein) and FN is an
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| important step in the pathogenesis of leprosy; FN acts as an oposinin.
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| <BR>2.3 Symptoms
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| 2.4 Prevention
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| 2.5 Treatment
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| <h2> <span class="mw-headline"><B>Why is this disease a problem in India?</b></span></h2>
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| How is it transmitted? Is there a vector (animal/insect)?
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| Prevention
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| Do lifestyle/environment/economics/political issues play a role?
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| What is being done to address this problem
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| Include anything being done by the local government or groups as well as efforts by non-local groups.
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| What else could be done to address this problem
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| Are there solutions that could be successful but haven't been implemented due to political or economic reasons? Are there successful efforts in other countries? Are there reasons why these efforts may or may not be successful in the country you've focused on? etc. etc.
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| References
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| [Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.
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| Edited by [Katherine Tang, Victor Tran, Natalie Nguyen, Julia Chu, Millie (Mei) Liu, Jason Wang], students of Rachel Larsen
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