Information on the prevalence, incidence, and geographical distribution of malaria in Zimbabwe is reviewed. Malaria control operations carried out during the last 30 years are briefly described together with available information of their impact on malaria. From 1972 to 1981, 51,962 positive blood slides were submitted to Blair Research Laboratory from health institutions, of which 97.8% were Plasmodium falciparum, 1.8% P. malariae and 0.3% P. ovale. Blood slide surveys undertaken from 1969 to 1981 during which time 156,194 slides were examined showed P. falciparum to constitute 92.5% of malaria infections, P. malariae 8.3% and P. ovale 0.7%. The data from active and passive case finding are used to describe the seasonal and geographical pattern of malaria in Zimbabwe. The seasonal peak of transmission occurs from February to May each year with very low transmission from July to October. Endemicity of malaria is shown to be markedly influenced by altitude varying from hyperendemic in the low altitude areas to hypoendemic or absent on the central watershed.

Costly resistance mechanisms have been cited as an explanation for the widespread occurrence of parasitic infections, yet few studies have examined these costs in detail. A malaria-mosquito model has been used to test this concept by making a comparison of the fitness of highly susceptible lines of mosquitoes with lines that are resistant to infection. Malaria infection is known to cause a decrease in fecundity and fertility of mosquitoes; resistant mosquitoes were thus predicted to be fitter than susceptible ones. Anopheles gambiae were selected for refractoriness/resistance or for increased susceptibility to infection by Plasmodium yoelii nigeriensis. Additional lines that acted as controls for inbreeding depression were raised in parallel but not exposed to selection pressure. Selections were made in triplicate so that founder effects could be detected. Resistance mechanisms that were selected included melanotic encapsulation of parasites within 24 h postinfection and the complete disappearance of parasites from the gut. Costs of immune surveillance were assessed after an uninfected feed, and costs of immune deployment were assessed after exposure to infection and to infection and additional stresses. Mosquito survivorship was unaffected by either resistance to infection or by an increased burden of infection when compared with low levels of infection. In most cases reproductive fitness was equally affected by refractoriness or by infection. Resistant mosquitoes did not gain a fitness advantage by eliminating the parasites. Costs were consistently associated with larval production and egg hatch rate but rarely attributed to changes in blood feeding and never to changes in mosquito size. No advantages appeared to be gained by the offspring of resistant mosquitoes. Furthermore, we were unable to select for refractoriness in groups of mosquitoes in which 100% or 50% of the population were exposed to infection every generation for 22 generations. Under these selection pressures, no population had become completely refractory and only one became more resistant. Variations in fitness relative to control lines in different groups were attributed to founder effects. Our conclusion from these findings is that refractoriness to malaria is as costly as tolerance of infection. KeywordsAnopheles gambiae; fitness costs; innate immunity; malaria; mosquito; Plasmodium; refractoriness Despite their detrimental effects on the host, parasitic infections are extremely common (Esch and Fernandez 1993). This observation has led evolutionary ecologists to evoke life-history theories to explain why host traits for parasite resistance are not always selected. Immune defense is deemed to be costly, and thus supposed trade-offs exist with other fitness 2 E-mail: h.hurd@keele.ac.uk 3 E-mail: p.j.taylor@keele.ac.uk 4 E-mail: bia13@keele.ac.uk 5 E-mail: bia50@keele.ac.uk 6 E-mail: p.eggleston@keele.ac.uk UKPMC Funders Group Author Manuscript UKPMC Funders Group Author Manuscript UKPMC Funders Group Author Manuscriptcomponents. Th...

No abstract

Costly resistance mechanisms have been cited as an explanation for the widespread occurrence of parasitic infections, yet few studies have examined these costs in detail. A malaria-mosquito model has been used to test this concept by making a comparison of the fitness of highly susceptible lines of mosquitoes with lines that are resistant to infection. Malaria infection is known to cause a decrease in fecundity and fertility of mosquitoes; resistant mosquitoes were thus predicted to be fitter than susceptible ones. Anopheles gambiae were selected for refractoriness/resistance or for increased susceptibility to infection by Plasmodium yoelii nigeriensis. Additional lines that acted as controls for inbreeding depression were raised in parallel but not exposed to selection pressure. Selections were made in triplicate so that founder effects could be detected. Resistance mechanisms that were selected included melanotic encapsulation of parasites within 24 h postinfection and the complete disappearance of parasites from the gut. Costs of immune surveillance were assessed after an uninfected feed, and costs of immune deployment were assessed after exposure to infection and to infection and additional stresses. Mosquito survivorship was unaffected by either resistance to infection or by an increased burden of infection when compared with low levels of infection. In most cases reproductive fitness was equally affected by refractoriness or by infection. Resistant mosquitoes did not gain a fitness advantage by eliminating the parasites. Costs were consistently associated with larval production and egg hatch rate but rarely attributed to changes in blood feeding and never to changes in mosquito size. No advantages appeared to be gained by the offspring of resistant mosquitoes. Furthermore, we were unable to select for refractoriness in groups of mosquitoes in which 100% or 50% of the population were exposed to infection every generation for 22 generations. Under these selection pressures, no population had become completely refractory and only one became more resistant. Variations in fitness relative to control lines in different groups were attributed to founder effects. Our conclusion from these findings is that refractoriness to malaria is as costly as tolerance of infection. KeywordsAnopheles gambiae; fitness costs; innate immunity; malaria; mosquito; Plasmodium; refractoriness Despite their detrimental effects on the host, parasitic infections are extremely common (Esch and Fernandez 1993). This observation has led evolutionary ecologists to evoke life-history theories to explain why host traits for parasite resistance are not always selected. Immune defense is deemed to be costly, and thus supposed trade-offs exist with other fitness 2 E-mail: h.hurd@keele.ac.uk 3 E-mail: p.j.taylor@keele.ac.uk 4 E-mail: bia13@keele.ac.uk 5 E-mail: bia50@keele.ac.uk 6 E-mail: p.eggleston@keele.ac.uk UKPMC Funders Group Author Manuscript UKPMC Funders Group Author Manuscript UKPMC Funders Group Author Manuscriptcomponents. Th...

Two studies were carried out to determine the effect of the rodent malaria Plasmodium yoelii nigeriensis on the blood feeding success of Anopheles stephensi. Initially, pairs of mice with similar packed cell volume (PCV) (measured by haematocrit) were selected. Following infection of one of the pair its PCV gradually fell. At various times post-infection, a comparison was made of the bloodmeal size (haemoglobin content) of mosquitoes feeding on these mice. The bloodmeal sizes increased with parasite-induced fall in PCV down to a haematocrit of 43-44%, which occurred approximately 48 h post-infection. Bloodmeals were significantly reduced, however, when mosquitoes fed on mice with higher parasitaemias and a haematocrit of 15-35%. Thus, at early stages of infection, mosquitoes ingested a bloodmeal significantly greater than did the mosquitoes feeding on the control mice. However, mosquitoes were not able to compensate for severe infection-associated anaemia. To compensate for variation due to innate differences in the mice, a second experiment was performed. Mosquitoes were fed on the same mice before (control) and after infection. Again, the bloodmeal size increased with decreasing PCV down to haematocrits of 42-45%, but declined thereafter. In this host-parasite-vector system, haematocrits that maximized erythrocyte intake were produced when gametocytes, capable of exflagellation, were present.