5. How does Leishmania tropica evade the immune system?
Leishmania tropica surface molecule glycoprotein 63 (gp36) is found throughout the parasite surface and has the potential to degrade immunoglobulins, complement factors, and lysosomal proteins (Olivier et al. 2005). Gp36 can cleave C3b into an inactivated form and C3bi will appear on the surface of the membrane and hinders the formation of C5 convertase (Gupta et al. 2013). It is also able to use C3bi to bind to complement receptor 3 (CR3); which is advantageous to the as binding restricts the production of IL-12, which thus limits the Th1 response and it allows the amastigote parasite to enter the macrophage without detection (Marth and Kelsall 1997, Gupta et al. 2013). Macrophages are the main cell targeted for survival and proliferation of L. Tropica as it replicates in the …show more content…
tropica according to the Center for Disease Control and Prevention (CDC, 2015). The best way to prevent yourself from acquiring the disease is to limit exposure to sandfly bites, wear protective clothing, and apply bug spray to exposed skin. Bug nets can limit the amount of sandflies able to get inside houses, and sleeping with a bed net is highly advised. While cutaneous leishmaniasis caused by L. tropica can heal on their own, treatment can prevent the development of other infections (Sharma 2015) Options to treat L. tropica, vary depending on location. Many studies using L. tropica are usually small, informal, or partially representative which can lead to inaccurate findings. One treatment option involves local infiltration with animonials of sodium stiboglucoante and meglumine antimoniate. The lesion must be treated once to twice a week and be blanched to be effective (Blum et al, 2004). Another treatment is a combination of 15% paromomycin and 12% methylbenzethonium chloride ointment which should be treated twice a day for 10-20 days (Blum et al,
Leishmania tropica surface molecule glycoprotein 63 (gp36) is found throughout the parasite surface and has the potential to degrade immunoglobulins, complement factors, and lysosomal proteins (Olivier et al. 2005). Gp36 can cleave C3b into an inactivated form and C3bi will appear on the surface of the membrane and hinders the formation of C5 convertase (Gupta et al. 2013). It is also able to use C3bi to bind to complement receptor 3 (CR3); which is advantageous to the as binding restricts the production of IL-12, which thus limits the Th1 response and it allows the amastigote parasite to enter the macrophage without detection (Marth and Kelsall 1997, Gupta et al. 2013). Macrophages are the main cell targeted for survival and proliferation of L. Tropica as it replicates in the …show more content…
tropica according to the Center for Disease Control and Prevention (CDC, 2015). The best way to prevent yourself from acquiring the disease is to limit exposure to sandfly bites, wear protective clothing, and apply bug spray to exposed skin. Bug nets can limit the amount of sandflies able to get inside houses, and sleeping with a bed net is highly advised. While cutaneous leishmaniasis caused by L. tropica can heal on their own, treatment can prevent the development of other infections (Sharma 2015) Options to treat L. tropica, vary depending on location. Many studies using L. tropica are usually small, informal, or partially representative which can lead to inaccurate findings. One treatment option involves local infiltration with animonials of sodium stiboglucoante and meglumine antimoniate. The lesion must be treated once to twice a week and be blanched to be effective (Blum et al, 2004). Another treatment is a combination of 15% paromomycin and 12% methylbenzethonium chloride ointment which should be treated twice a day for 10-20 days (Blum et al,