The German cockroach (Blattella germanica L.) is a worldwide pest that lives exclusively in human environments. B. germanica threatens human health by producing asthma-triggering allergens, vectoring pathogenic/antibiotic-resistant microbes, and by contributing to unhealthy indoor environments. While insecticides are essential for reducing cockroach populations and improving health outcomes, insecticide resistance has been a consistent barrier to cockroach control since the 1950s. We conducted seminal field studies to compare three insecticide resistance intervention strategies for cockroaches and evaluated resistance evolution across multiple generations. Using pre-treatment resistance assessment to drive decisions, we found that single active ingredient (AI) treatments can successfully eliminate cockroaches if starting resistance levels are low. We further established that rotation treatments intuitively reduce selection pressure, and are effective when insecticides with no/low resistance are used. We also found that mixture products containing thiamethoxam + λ-cyhalothrin AIs were universally ineffective and highly repellent; and finally, evolution of cross-resistance among AIs is a significant, previously unrealized challenge.

Mast cell (MC)-associated diseases, including allergy/anaphylaxis and neuroinflammatory pain disorders, exhibit a sex bias, with females at increase risk. While much attention has been directed toward adult sex hormones as drivers of sex differences, that female sex bias in MC-associated diseases is evident in prepubertal children, suggesting early-life origins of sex differences which have yet to be explored. Utilizing rodent models of MC-mediated anaphylaxis, our data here reveal that, 1) compared with females, males exhibit significantly reduced severity of MC-mediated anaphylactic responses that emerge prior to puberty and persist into adulthood, 2) reduced severity of MC-mediated anaphylaxis in males is linked with the naturally high level of perinatal androgens and can be recapitulated in females by perinatal exposure to testosterone proprionate, 3) perinatal androgen exposure guides bone marrow MC progenitors toward a masculinized tissue MC phenotype characterized by decreased concentration of prestored MC granule mediators (e.g., histamine, serotonin, and proteases) and reduced mediator release upon degranulation, and 4) engraftment of MC-deficient Kit^W-sh/W-sh mice with adult male, female, or perinatally androgenized female MCs results in MC-mediated anaphylaxis response that reflects the MC sex and not host sex. Together, these data present evidence that sex differences in MC phenotype and resulting disease severity are established in early life by perinatal androgens. Thus, factors affecting levels of perinatal androgens could have a significant impact on MC development and MC-associated disease risk across the life span. Significance Mast cell (MC)-associated disorders exhibit a sex bias, with females at increased risk. While attention has been directed to adult sex hormones as a mechanism for disease risk between the sexes, epidemiological evidence clearly shows that these same sex biases also exist in prepubertal children, thus challenging this concept. Here, we show that perinatal, but not adult gonadal, androgens play a protective role in MC-mediated anaphylaxis severity into adulthood. We propose that perinatal androgens mediate their protective effects via programming of bone marrow MC precursors to exhibit reduced granule histamine and release. These findings shift attention to perinatal life as a critical period for potential interventions to mitigate MC-associated disease risk across the lifespan in males and females.

Insecticide resistance in German cockroaches (Blattella germanica (L.)) has been a barrier to effective control since its first documentation in the 1950s. A necessary first step toward managing resistance is to understand insecticide susceptibility profiles in field-collected strains so that active ingredients (AIs) with lowest resistance levels can be identified. As a first step in this study, diagnostic concentrations (DCs) were determined for 14 insecticide AIs based on lethal concentrations that killed 99% or 90% of the individuals from a susceptible lab strain (JWax-S). Next, cockroaches were collected from two low-income multifamily housing complexes in Danville, IL, and Indianapolis, IN, and used to establish laboratory strains. These strains were screened against the 14 AI-DCs in vial bioassays, and susceptibility profiles were determined by comparing percent mortalities between the field strains relative to the JWax-S strain. Results revealed lowest resistance of field strains to boric acid, abamectin, dinotefuran, clothianidin, thiamethoxam, and chlorfenapyr. For the AIs hydramethylnon and imidacloprid, field strains did not display survivorship different than the lab strain, but >90% mortality was never achieved. Lastly, both field strains displayed resistance to indoxacarb, fipronil, acetamiprid, beta-cyfluthrin, bifenthrin, and lambda-cyhalothrin, but at varying levels. These results satisfy two objectives. First, baseline monitoring DCs were established for 14 insecticides presently registered for use against cockroaches, which represents a useful resource. Second, our findings reveal insecticide AIs with lowest resistance levels for use in forthcoming field studies that will investigate impacts of different insecticide deployment strategies on resistance management and evolution in cockroach field populations.