Selection for insecticide resistance can promote Plasmodium falciparum infection in Anopheles.

Insecticide resistance is under strong selective pressure in Anopheles mosquitoes due to widespread usage of insecticides in vector control strategies. Resistance mechanisms likely cause changes that profoundly affect mosquito physiology, yet it remains poorly understood how selective pressures imposed by insecticides may alter the ability of the mosquito to host and transmit a Plasmodium infection. From pyrethroid-resistant field-derived Anopheles gambiae s.l. mosquitoes, we established resistant (RES) and susceptible (SUS) colonies by either selection for, or loss of insecticide resistance. We show increased oocyst intensity and growth rate as well as increased sporozoite prevalence and intensity in RES compared to SUS females infected with Plasmodium falciparum. The increase in infection intensity in RES females was not associated with the presence of the kdrL1014F mutation and was not impacted by inhibition of Cytochrome P450s. The lipid transporter lipophorin (Lp), which was upregulated in RES compared to SUS, was at least partly implicated in the increased intensity of P. falciparum but not directly involved in the insecticide resistance phenotype. Interestingly, we observed that although P. falciparum infections were not affected when RES females were exposed to permethrin, these females had decreased lipid abundance in the fat body following exposure, pointing to a possible role for lipid mobilization in response to damage caused by insecticide challenge. The finding that selection for insecticide resistance can increase P. falciparum infection intensities and growth rate reinforces the need to assess the overall impact on malaria transmission dynamics caused by selective pressures mosquitoes experience during repeated insecticide challenge.

Levels of Serum Phosphorylated Neurofilament Heavy Subunit in Clinically Healthy Standardbred Horses.

Neurofilaments heavy chain proteins (pNF-H) have been identified as useful serum biomarkers for humans and animals with neurologic conditions, some of which can lead to poor performance, and athletic injuries. However, there are no published reports that describe a reference range for serum pNF-H levels in healthy racehorses. This cross-sectional study was carried out to determine the serum concentration of pNF-H in 1,349 samples collected from 1,291 clinically healthy standardbred (SB) racehorses. Data on age, time of sampling (pre-race or post-race), and finishing position during a race were collected. The concentration of pNF-H in serum samples was determined using an enzyme-linked immunosorbent assay (ELISA). The appropriate statistical techniques were used to determine the median serum concentration of pNF-H in these horses, if the serum concentration of pNF-H changed with age, if there were changes in the serum concentration of pNF-H during a race, and if there was an association between serum concentration of pNF-H, and the finishing position for the horse. The median serum concentration of pNF-H in this group of clinically healthy SB horses was 0.0 ng/mL. The concentration of pNF-H in serum was not associated with the age of the horses in this study as was determined by regression analysis. There was no significant change in the serum concentration of pNF-H before and after a race in paired samples. There was no association of serum concentration of pNF-H and the finishing position of the horses after the race. The data from this study supports use of <0.412 ng/mL as a reference interval for measurement of serum levels of pNF-H in SB racehorses as 95% of the collected samples fell into the range 0.0-0.412 ng/mL.

Wolbachia cifB induces cytoplasmic incompatibility in the malaria mosquito vector.

Wolbachia, a maternally inherited intracellular bacterial species, can manipulate host insect reproduction by cytoplasmic incompatibility (CI), which results in embryo lethality in crosses between infected males and uninfected females. CI is encoded by two prophage genes, cifA and cifB. Wolbachia, coupled with the sterile insect technique, has been used in field trials to control populations of the dengue vector Aedes albopictus, but CI-inducing strains are not known to infect the malaria vector Anopheles gambiae. Here we show that cifA and cifB can induce conditional sterility in the malaria vector An. gambiae. We used transgenic expression of these Wolbachia-derived genes in the An. gambiae germline to show that cifB is sufficient to cause embryonic lethality and that cifB-induced sterility is rescued by cifA expression in females. When we co-expressed cifA and cifB in male mosquitoes, the CI phenotype was attenuated. In female mosquitoes, cifB impaired fertility, which was overcome by co-expression of cifA. Our findings pave the way towards using CI to control malaria mosquito vectors.