BackgroundBlood-meal sources of malaria vectors affect their capacity to transmit the disease. Most efficient malaria vectors prefer human hosts. However, with increasing personal protection measures it becomes more difficult for them to find human hosts. Here recent malaria vector blood-meal sources in western Kenya highlands were investigated.MethodsAdult mosquitoes resting indoors, outdoors and exiting through windows were collected in three study areas within the western Kenya highlands from June 2011 to June 2013. A census of people, livestock and of insecticide-treated nets was done per house. Mosquito blood-meal sources were determined as human, goat, bovine or chicken using enzyme-linked-immunosorbent assays.ResultsMost (86.3 %) households possessed at least one bed net, 57.2 % had domesticated animals and 83.6 % had people sharing houses with livestock at night. Most (94.9 %) unfed malaria vectors were caught exiting through windows. Overall, 53.1 % of Anopheles gambiae sensu stricto obtained blood-meals from humans, 26.5 % from goats and 18.4 % from bovines. Single blood-meal sources by An. gambiae s.s. from humans were 26.5 %, 8.2 % from bovines and 2.0 % from goats. Mixed blood-meal sources by An. gambiae s.s. identified included: 24.5 % human/goat, 10.2 % human/bovine, 8.2 % human/bovine/goat and also 8.2 % bovine/goat. One An. arabiensis mosquito obtained blood-meal only from humans.ConclusionAn unusually high frequency of animal and mixed human-animal blood meals in the major malaria vector An. gambiae s.s. was revealed in the western Kenya highlands where bed net coverage is above the WHO target. The shift in blood-meal sources from humans to livestock is most likely the vectors’ response to increased bed net coverage and the close location of livestock frequently in the same house as people at night. Livestock-targeted interventions should be considered under these circumstances to address residual malaria transmission.

From 1975–2009, the WHO guidelines classified symptomatic dengue virus infections as dengue fever, dengue hemorrhagic fever, and dengue shock syndrome. In 2009 the case definition was changed to a clinical classification after concern the original criteria was challenging to apply in resource-limited settings and not inclusive of a substantial proportion of severe dengue cases. Our goal was to examine how well the current WHO definition identified new dengue cases at our febrile surveillance sites in Kenya. Between 2014 and 2019 as part of a child cohort study of febrile illness in our four clinical study sites (Ukunda, Kisumu, Msambweni, Chulaimbo) we identified 369 dengue PCR positive symptomatic cases and characterized whether they met the 2009 revised WHO diagnostic criteria for dengue with and without warning signs and severe dengue. We found 62% of our PCR-confirmed dengue cases did not meet criteria per the guidelines. Our findings also correlate with our experience that dengue disease in children in Kenya is less severe as reported in other parts of the world. Although the 2009 clinical classification has recently been criticized for being overly inclusive and non-specific, our findings suggest the 2009 WHO dengue case definition may miss more than 50% of symptomatic infections in Kenya and may require further modification to include the African experience.