Skinny rodents, kala-azar and prostaglandin E(2).

Abstract

What triggers Leishmania parasite dissemination from the site of inoculation to visceral sites is unknown. Evidence suggests that it is dependent upon host and parasite genetic background (e.g. host susceptibility and parasite strain variation). Sandfly vector saliva has been shown to affect the clinical outcome of Leishmania infantum infections 1 – different levels of Lutzomyia longipalpis salivary enzymes appear to determine whether an infection remains localized and produces a cutaneous ulcer, or disseminates to viscera leading to classical kala-azar. Previous epidemiological and experimental studies indicated that malnourishment is a risk factor for visceral leishmaniasis caused by Leishmania donovani and L. infantum. One study demonstrated that moderately to severely malnourished children were 12 times more at risk of developing kala-azar than well-nourished children 2.