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A significant amount of work has been devoted towards understanding the cellular and humoral immune responses in arthropod vectors. Although fleas (Siphonaptera) are vectors of numerous bacterial pathogens, few studies have examined how these insects defend themselves from infection. In this study, we investigated the immune defense mechanisms in the hemocoel of cat fleas (Ctenocephalides felis), currently the most important flea pest of humans and many domestic animals. Using model species of bacteria (Micrococcus luteus, Serratia marcescens, and Escherichia coli), we delivered a systemic infection and measured the following: antimicrobial activity of hemolymph, levels of free radicals resulting from the induction of oxidase-based pathways, number of circulating hemocytes, phagocytosis activity of circulating hemocytes, and in vivo bacteria killing efficiency when phagocytosis activity is limited. Our results show that the antimicrobial activity of flea hemolymph increases in response to certain species of bacteria; yet, a systemic infection with the same bacterial species did not influence levels of hydrogen peroxide (H 2 O 2 ), a reactive intermediate of oxygen, at the same time. Additionally, the number of circulating hemocytes increases in response to E. coli infection, and these cells display strong phagocytic activity against this bacterium. Moreover, limiting phagocytosis by injecting polystyrene beads subsequently increases flea susceptibility to E. coli infection when compared to injury controls; however, impairing the cellular immune response itself did not increase flea susceptibility to infection when compared to untreated fleas. Overall, this work yields significant insight into how fleas interact with bacterial pathogens in their hemocoel, and suggests that cellular and humoral immune responses cooperate to combat systemic bacterial infections., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

During all life stages, mosquitoes are exposed to pathogens, and employ an immune system to resist or limit infection. Although much attention has been paid to how adult mosquitoes fight infection, little is known about how an infection during the larval stage affects the biology of the resultant adult. In this study, we investigated whether a bacterial infection in the hemocoel of the African malaria mosquito, Anopheles gambiae, is transstadially transmitted from larvae to adults (both females and males), and whether immune stimulation in the hemocoel as a larva alters development or biological traits of the adult. Specifically, larvae were injected in the hemocoel with either fluorescent microspheres or Escherichia coli, and the following traits were examined: transstadial transmission, larval development to adulthood, adult survival, and adult body size. Our results show that transstadial transmission of hemocoel contents occurs from larvae to pupae and from pupae to adults, but that bacterial prevalence and intensity varies with age. Injury, immune stimulation or infection decreases the proportion of larvae that undergo pupation and eclosion, infection decreases the longevity of adult females, and treatment has complex effects on the body size of the resultant adults. The present study adds larval hemocoelic infection to the known non-genetic factors that reduce overall fitness by negatively affecting development and adult biological traits that influence mosquito vector competence., (Copyright © 2017 Elsevier Inc. All rights reserved.)