title: Marked biological differences between insecticide resistant and susceptible strains of Anopheles funestus infected with the murine parasite Plasmodium berghei.
abstract: BACKGROUND
  Anopheles funestus is one of the major malaria vectors in Africa but research on this species has been restricted due to the lack of viable laboratory colonies. The vectorial capacity of natural populations of An. funestus is well known but its ability to host Plasmodium in the laboratory and the development cycle of the parasite within this mosquito species was, until very recently, unknown. In this study we compared laboratory strains of An. funestus that were resistant and susceptible to pyrethroid insecticides, for their receptiveness to infection with Plasmodium berghei and compared development times with other vector species available in our laboratory.
  
  
  METHODS
  The murine parasite P. berghei was used to infect two base An. funestus colonies (FANG and FUMOZ) and two selected sub-colonies with different degrees of pyrethroid resistance (FUMOZ-BS susceptible and FUMOZ-R resistant). Results were compared with the G3 strain of An. gambiae.
  
  
  RESULTS
  While all colonies were able to support the parasite, the development time in An. funestus was generally longer than that recorded in the laboratory strain of An. gambiae. Infected females were able to initiate new rounds of infection when feeding on healthy mice. The pyrethroid resistant strain FUMOZ-R supported the lowest numbers of oocysts and sporozoites while the insecticide susceptible strain FUMOZ-BS produced one of the highest sporozoite indices ever documented in P. berghei research. The FUMOZ base colony, exhibiting partial insecticide resistance was the median in terms of infection intensity. The oocyst number in all colonies did not fully correlate with the sporozoite index, indicating possible factors influencing the sporozoites' transit from the midgut to the salivary glands.
  
  
  CONCLUSIONS
  The presence of both insecticide resistance and limited parasite infection phenotypes in the same individuals suggests there may be association between the two mechanisms, but further elucidation is required.
authors.affiliation: Wits Research Institute for Malaria, School of Pathology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.
authors.forename: T Mike
authors.initials: TM
authors.lastname: Lo
authors.forename: Maureen
authors.initials: M
authors.lastname: Coetzee
mesh_terms: D000349:Africa; D000818:Animals; D000852:Anopheles / Q000187:drug effects* / Q000469:parasitology*; D002452:Cell Count; D005260:Female; D006801:Humans; D007303:Insect Vectors / Q000187:drug effects / Q000469:parasitology*; D007305:Insecticide Resistance; D051379:Mice; D009865:Oocytes / Q000254:growth & development; D010962:Plasmodium berghei / Q000254:growth & development*