Leishmania’s infectious form – metacyclic promastigotes – is resistant to complement lysis but not opsonization. How is this efficacious for the parasite? We know that changes in LPG accompany the transition from procyclic promastigote to metacyclic promastigote. Do you think that the LPG molecule is involved in the resistance to complement lysis? What other factors might govern complement resistance?
Since Leishmaniasis is a disease of poverty, would eliminating poverty eliminate the disease? What else might need to be considered when trying to eliminate the spread of Leishmania spp? How would you accomplish the elimination of Leishmaniasis? What characteristics of the disease vector need to be considered in order to effectively eliminate disease transmission? What factors might be involved in the recent move of the disease to more urban areas?
Vaccination has proven effective as a means of disease prevention. Do you think a vaccine could be developed for Leishmania? What are some barriers to the development of a vaccine?
MHC Class II is expressed on the surface of the compartments in which Leishmania replicates within the macrophage. This protein is usually only expressed by activated macrophages. How might the parasite be interfering with the normal function of MHC II? Why would this be good strategy?
Why are their so few drugs available to treat Leishmaniasis? Why is it hard to find and develop a drug for treatment?