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Fleas (Siphonaptera) are holometabolous insects with larval and adult stages that exhibit vastly different ecologies from each other. Adult fleas are parasitic and feed exclusively on the blood of a vertebrate host, whereas flea larvae do not live on hosts and consume dried faecal blood from adult fleas. Because flea larvae rely on adult flea faeces for food, excrement and eggs must fall in the same location; thus, larval density is likely high in these restricted habitats. However, the influence of larval density on the subsequent adult stage has not been examined. In the present study, we utilized egg density to investigate density‐dependent effects on larval development and adult body size in the cat flea (Ctenocephalides felis Bouché) (Siphonaptera: Pulicidae). Specifically, eggs were collected to create three different larval densities (n = 50, 100 and 150 per 56.7 cm2), and hatched larvae from all groups were fed an excess amount of adult faecal pellets. Larval development was measured by recording the proportion of eggs that developed to the pupal stage and the proportion of eggs that reached adulthood (eclosion). The body size of eclosed adults was quantified for both sexes using head length and length of the total body. We found that the number of eggs had no effect on the proportion of larvae that pupated or the proportion of larvae that eclosed; however, higher egg densities resulted in larger body sizes for both sexes. Overall, these data yield significant insight into how the ecology of larval fleas impacts the biology of the resultant adults. [ABSTRACT FROM AUTHOR]

Background: Fleas are insect vectors that transmit several Gram-negative bacterial pathogens acquired by ingesting infected vertebrate blood. To combat foodborne illness, insect midgut epithelial cells are armed with efficient microbial recognition and control systems, such as the immune deficiency (IMD) pathway that regulates the expression of antimicrobial peptides (AMPs). However, despite their medical and veterinary importance, relatively little is known about the IMD signaling pathway and production of AMPs in the digestive tract of cat fleas (Ctenocephalides felis). Methods: In the present study, we measured the expression of target genes comprising the IMD pathway, as well as corresponding AMP transcripts, in the digestive tract of C. felis following exposure to three different species of bacteria: Gram-negative Bartonella henselae (a flea-borne pathogen), Gram-negative Serratia marcescens (a model laboratory species), and Gram-positive Micrococcus luteus (a model laboratory species). Additionally, we examined the antibacterial activity of proteins isolated from the flea digestive tract in vitro following bacterial challenge and at different days post adult emergence to determine if feeding-induced antibacterial activity varies with age. Results: In our analysis of C. felis, we observed an increase in the expression of representative IMD pathway genes and associated AMP transcripts, indicating the activation of the IMD pathway. Furthermore, our results revealed that different bacterial species elicit distinct transcriptional profiles of IMD pathway genes, suggesting a species-specific response to bacterial invasion. We found that the gut of C. felis produces antibacterial molecules as a localized defense mechanism. Additionally, we observed that proteins with antimicrobial properties are synthesized as part of local defense mechanisms in the gut, with differential patterns of antibacterial activity related to infection status and age. Conclusions: Our findings provide essential insights into the potential mechanisms by which cat fleas regulate immune responses in their digestive tract against different bacterial species. [ABSTRACT FROM AUTHOR]

The immune response of arthropod vectors plays a key role in the spread and transmission of vector-borne diseases. Although fleas transmit several human pathogens (e.g. , Bartonella henselae , Rickettsia felis , R. typhi , and Yersinia pestis), few studies have examined how these vectors respond to infection. In hematophagous arthropods, imbibed pathogens must survive the hostile environment of blood meal digestion, which includes proteolytic digestive enzymes, protease inhibitors and expression of genes associated with protection of epithelial linings. Additionally, insect epithelial cells exhibit local immune defense against ingested pathogens by producing antimicrobial peptides and reactive oxygen species. This review details these and other aspects of insect immunity as it relates to fleas, with an emphasis on the gut immune response to two blood-borne pathogens, R. typhi and Y. pestis. • The first barrier faced by a pathogen acquired with a blood meal is attachment to the gut to avoid excretion. • Infection modulates the transcription of digestive proteases. • Infection influences the transcription of serine protease inhibitors. • Defense mechanisms in the gut includes local production of AMPs and ROS. • The hemocoel can also be inhabited by pathogens and contains additional immune factors. [ABSTRACT FROM AUTHOR]

Larval and adult mosquitoes mount immune responses against pathogens that invade their hemocoel. Although it has been suggested that a correlation exists between immune processes across insect life stages, the influence that an infection in the hemocoel of a larva has on the immune system of the eclosed adult remains unknown. Here, we used Anopheles gambiae to test whether a larval infection influences the adult response to a subsequent bacterial or malaria parasite infection. We found that for both female and male mosquitoes, a larval infection enhances the efficiency of bacterial clearance following a secondary infection in the hemocoel of adults. The adults that emerge from infected larvae have more hemocytes than adults that emerge from naive or injured larvae, and individual hemocytes have greater phagocytic activity. Furthermore, mRNA abundance of immune genes—such as cecropin A, Lysozyme C1, Stat‐A, and Tep1—is higher in adults that emerge from infected larvae. A larval infection, however, does not have a meaningful effect on the probability that female adults will survive a systemic bacterial infection, and increases the susceptibility of females to Plasmodium yoelii, as measured by oocyst prevalence and intensity in the midgut. Finally, immune proficiency varies by sex; females exhibit increased bacterial killing, have twice as many hemocytes, and more highly express immune genes. Together, these results show that a larval hemocoelic infection induces transstadial immune activation—possibly via transstadial immune priming—but that it confers both costs and benefits to the emerged adults. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background: Vector-borne pathogens must overcome arthropod infection and escape barriers (e.g. midgut and salivary glands) during the extrinsic incubation period (EIP) before subsequent transmission to another host. This particular timespan is undetermined for the etiological agent of flea-borne spotted fever (Rickettsia felis). Artificial acquisition of R. felis by blood-feeding cat fleas revealed dissemination to the salivary glands after seven days; however, this length of time is inconsistent with co-feeding studies that produced infectious cat fleas within 24 h of infection. In the current study, we demonstrated that an alternative mechanism is responsible for the early-phase transmission that typifies flea-borne R. felis spread. Methods: Co-feeding transmission bioassays were constructed to assess temporal dynamics of R. felis amongst cat fleas, including exposure time to produce infectious fleas and association time to transmit infection to naïve fleas. Additional experiments examined the proportion of R. felis-exposed cat fleas with contaminated mouthparts, as well as the likelihood for cat fleas to release R. felis from their mouthparts following exposure to an infectious bloodmeal. The potential for mechanical transmission of R. felis by co-feeding cat fleas was further examined using fluorescent latex beads, as opposed to a live pathogen, which would not require a biological mechanism to achieve transmission. Results: Analyses revealed that R. felis-infected cat fleas were infectious to naïve fleas less than 24 h after exposure to the pathogen, but showed no rickettsial dissemination to the salivary glands during this early-phase transmission. Additionally, the current study revealed that R. felis-infected cat fleas must co-feed with naïve fleas for more than 12 h in order for early-phase transmission to occur. Further evidence supported that contaminated flea mouthparts may be the source of the bacteria transmitted early, and demonstrated that R. felis is released from the mouthparts during brief probing events. Moreover, the use of fluorescent latex beads supports the notion that early-phase transmission of R. felis is a mechanical mechanism. Conclusions: Determination of the transmission mechanisms utilized by R. felis is essential to fully understand the vulnerability of susceptible vertebrate hosts, including humans, to this pathogen. [ABSTRACT FROM AUTHOR]

Cat fleas ( Ctenocephalides felis) are known as the primary vector and reservoir of Rickettsia felis, the causative agent of flea-borne spotted fever; however, field surveys regularly report molecular detection of this infectious agent from other blood-feeding arthropods. The presence of R. felis in additional arthropods may be the result of chance consumption of an infectious bloodmeal, but isolation of viable rickettsiae circulating in the blood of suspected vertebrate reservoirs has not been demonstrated. Successful transmission of pathogens between actively blood-feeding arthropods in the absence of a disseminated vertebrate infection has been verified, referred to as cofeeding transmission. Therefore, the principal route from systemically infected vertebrates to uninfected arthropods may not be applicable to the R. felis transmission cycle. Here, we show both intra- and interspecific transmission of R. felis between cofeeding arthropods on a vertebrate host. Analyses revealed that infected cat fleas transmitted R. felis to naïve cat fleas and rat fleas ( Xenopsylla cheopis) via fleabite on a nonrickettsemic vertebrate host. Also, cat fleas infected by cofeeding were infectious to newly emerged uninfected cat fleas in an artificial system. Furthermore, we utilized a stochastic model to demonstrate that cofeeding is sufficient to explain the enzootic spread of R. felis amongst populations of the biological vector. Our results implicate cat fleas in the spread of R. felis amongst different vectors, and the demonstration of cofeeding transmission of R. felis through a vertebrate host represents a novel transmission paradigm for insect-borne Rickettsia and furthers our understanding of this emerging rickettsiosis. [ABSTRACT FROM AUTHOR]

The Alberta oil sands contain one of the world’s largest reserves of oil – over 169 billion barrels of bitumen are economically recoverable with current extraction technologies. Surface mining and subsequent hot water extraction of bitumen from the ore generates about nine cubic meters of raw tailings per cubic meter of oil. Oil sands facilities are required to operate under a policy of zero water discharge, resulting in ponds containing more than one billion cubic meters of tailings, a mixture of sand, fines and process-affected water. Process-affected water contains numerous organic compounds, including naphthenic acids (NAs), which have been identified as the primary source of acute toxicity of process-affected water. Developments in analytical techniques, aerobic biodegradability, and treatment via chemical oxidation (ozone) of NAs are reviewed. The field continues to be challenged by the lack of a cost-effective, accurate analytical technique for NAs or an understanding of all the organic constituents in process-affected water that may be contributing to observed toxicity and thus requiring treatment. [ABSTRACT FROM AUTHOR]

Highlights: [•] 50mgL−1 utilized ozone dose improves biodegradability of dissolved organic carbon. [•] Indigenous oil sands microbial community survive moderate ozone exposure. [•] Microbial community exposed to ozone performs as well as unexposed community. [•] Aged oil sands process-affected waters contain <1mgL−1 naphthenic acids. [•] Naphthenic acids are removed with light ozone treatment. [Copyright &y& Elsevier]

Two Ca2+-dependent signaling pathways, mediated by the Ca2+-activated phosphatase calcineurin and by the Ca2+-activated kinase Ca2+/calmodulin- dependent kinase (CaMK), are both believed to function in fast-to-slow skeletal muscle fiber type transformation, but questions about the relative importance of the two pathways still remain. Here, the differential gene expression during fast-to-slow fiber type transformation was studied using cultured adult flexor digitorum brevis (FDB) fibers and a custom minimicroarray system containing 21 fiber type-specific marker genes. After 3 days of culture, unstimulated fibers showed a generally slower gene expression profile; 3 days of electric field stimulation of cultured FDB fibers with a slow fiber-type pattern transformed the fibers to an even slower gene expression profile. Unstimulated FDB fibers overexpressing constitutively active calcineurin featured a slower gene expression profile, except four genes, indicating that transformation occurred, but was incomplete with activation of the calcineurin pathway alone. In both unstimulated FDB fibers and slow-type electrically stimulated FDB fibers, blocking of CaMK pathway with KN93 generated a faster gene expression profile compared with the negative control KN92, indicating that CaMK pathway functions during the transformation induced by both unstimulated culturing and slow fiber-type electrical stimulation. Moreover, neither the calcineurin nor the CaMK pathway alone could maximally activate the transformation, and coordination of the two pathways is required to accomplish a complete fast-to-slow fiber type transformation. [ABSTRACT FROM AUTHOR]

Ca+ sparks are rare in healthy adult mammalian skeletal muscle but may appear when adult fiber integrity is compromised, and occur in embryonic muscle but decline as the animal develops. Here we used cultured adult mouse flexor digitorum brevis muscle fibers to monitor occurrence of Ca2+ sparks during maintenance of adult fiber morphology and during eventual fiber morphological dedifferentiation after various times in culture. Fibers cultured for up to 3 days retain normal morphology and striated appearance. Ca2+ sparks were rare in these fibers. At 5-7 days in culture, many of the original muscle fibers exhibit sprouting and loss of striations, as well as the occurrence of spontaneous Ca2+ sparks. The average rate of occurrence of Ca2+ sparks is >10-fold higher after 5-7 days in culture than in days 1-3. With the use of fibers cultured for 7 days, application of the Ca2+ channel blockers Co2+ or nifedipine almost completely suppressed the occurrence of Ca2+ sparks, as previously shown in embryonic fibers, suggesting that Ca2+ sparks may be generated by similar mechanisms in dedifferentiating cultured adult fibers and in embryonic fibers before final differentiation. The sarcomeric disruption observed under transmitted light microscopy in dedifferentiating fibers was accompanied by morphological changes in the transverse (T) tubular system, as observed by fluorescence confocal imaging of both an extracellular marker dye and membrane staining dyes. Changes in T tubule morphology coincided with the appearance of Ca2+ sparks, suggesting that Ca2+ sparks may either be a signal for, or the result of, disruption of DHPR-ryanodine receptor 1 coupling. [ABSTRACT FROM AUTHOR]

Presents a study which asserted that New Mexico's Middle Rio Grande Conservancy District's protection is unconstitutional and contrary to public welfare values. Analysis of the constitutional provisions governing New Mexico's water; Implications of New Mexico's constitutional declaration that water is a public resource to be managed by the state; Emphasis on equal protection law; Conclusion.

Fleas (Order Siphonaptera) transmit numerous bacterial pathogens that cause severe human diseases (e.g. , cat scratch disease, flea-borne spotted fever, murine typhus, plague). Because initial entry of these infectious agents occurs while blood feeding, the immune response in the flea gut is considered to be the first line of defense against invading microbes. However, relatively few studies have identified the flea immune molecules that effectively resist or limit infection in the gut. In other hematophagous insects, an immediate immune response to imbibed pathogens is the generation of reactive oxygen species (ROS). In this study, we utilized cat fleas (Ctenocephalides felis) to investigate whether oral infection with a well-known insect bacterial pathogen (Serratia marcescens) induces ROS synthesis in the flea gut, and whether production of ROS provides a defense mechanism against microbial colonization. Specifically, we treated fleas with an antioxidant to limit the number of free radicals in the digestive tract prior to infection, and then measured the following: S. marcescens infection loads, hydrogen peroxide (ROS) levels, and mRNA abundance of ROS signaling pathway genes. Overall, our data shows that ROS levels increase in response to infection in the flea gut, and that this increase helps to strengthen the flea immune response through the microbicidal activity of ROS. [Display omitted] • Bacterial load in the flea gut increases with exposure time to a Serratia marcescens -infected bloodmeal. • Suppression of ROS levels increases bacterial survival in the flea gut. • Peroxide levels in the flea gut increase in response to bacterial infection. • Select genes in the DUOX expression pathway are differentially expressed in infected flea guts. [ABSTRACT FROM AUTHOR]

The article focuses on the Morgan State University's participation in the Association of American Colleges and Universities' (AAC&U's) Committing to Equity and Inclusive Excellence: Campus-Based Strategies for Student Success project. It highlights key aspects of Morgan's data-driven action plan for student success.

[Display omitted] • Systemic infection has mixed effects on flea humoral immune responses. • Systemic infection increases the number of flea phagocytic hemocytes. • Suppression of cellular immunity increases flea susceptibility to infection. • Tissue injury increases flea resistance to infection. 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. [ABSTRACT FROM AUTHOR]