Blood feeding patterns of mosquitoes: random or structured?

<p>Abstract</p> <p>Background</p> <p>The foraging behavior of blood-sucking arthropods is the defining biological event shaping the transmission cycle of vector-borne parasites. It is also a phenomenon that pertains to the realm of community ecology, since blood-feeding patterns of vectors can occur across a community of vertebrate hosts. Although great advances in knowledge of the genetic basis for blood-feeding choices have been reported for selected vector species, little is known about the role of community composition of vertebrate hosts in determining such patterns.</p> <p>Methods & Results</p> <p>Here, we present an analysis of feeding patterns of vectors across a variety of locations, looking at foraging patterns of communities of mosquitoes, across communities of hosts primarily comprised of mammals and birds. Using null models of species co-occurrence, which do not require ancillary information about host abundance, we found that blood-feeding patterns were aggregated in studies from multiple sites, but random in studies from a single site. This combination of results supports the idea that mosquito species in a community may rely primarily on host availability in a given landscape, and that contacts with specific hosts will be influenced more by the presence/absence of hosts than by innate mosquito choices. This observation stresses the importance of blood-feeding plasticity as a key trait explaining the emergence of many zoonotic mosquito transmitted diseases.</p> <p>Discussion</p> <p>From an epidemiological perspective our observations support the idea that phenomena promoting synchronization of vectors and hosts can promote the emergence of vector-borne zoonotic diseases, as suggested by observations on the linkages between deforestation and the emergence of several human diseases.</p

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

Assessing the Effects of Trematode Infection on Invasive Green Crabs in Eastern North America

<div><p>A common signature of marine invasions worldwide is a significant loss of parasites (= parasite escape) in non-native host populations, which may confer a release from some of the harmful effects of parasitism (e.g., castration, energy extraction, immune activation, behavioral manipulation) and possibly enhance the success of non-indigenous species. In eastern North America, the notorious invader <i>Carcinus maenas</i> (European green crab) has escaped more than two-thirds its native parasite load. However, one of its parasites, a trematode (<i>Microphallus similis</i>), can be highly prevalent in the non-native region; yet little is known about its potential impacts. We employed a series of laboratory experiments to determine whether and how <i>M</i>. <i>similis</i> infection intensity influences <i>C</i>. <i>maenas</i>, focusing on physiological assays of body mass index, energy storage, and immune activation, as well as behavioral analyses of foraging, shelter utilization, and conspicuousness. We found little evidence for enduring physiological or behavioral impacts four weeks after experimental infection, with the exception of mussel handling time which positively correlated with cyst intensity. However, we did find evidence for a short-term effect of <i>M</i>. <i>similis</i> infection during early stages of infection (soon after cercarial penetration) via a significant drop in circulating immune cells, and a significant increase in the crabs’ righting response time. Considering <i>M</i>. <i>similis</i> is the only common parasite infecting <i>C</i>. <i>maenas</i> in eastern North America, our results for minimal lasting effects of the trematode on the crab’s physiology and behavior may help explain the crab’s continued prominence as a strong predator and competitor in the region.</p></div

Average (± SE) righting response time (seconds) for uninfected and infected crabs from the 72h (medium) treatment.

<p>This demonstrates the average time it took for crabs to right themselves after being placed on their dorsal side. These trials took place two hours after the 72h induction experiment ended, shortly after cercarial penetration of crab tissues.</p

Life cycle of <i>Microphallus similis</i> in eastern North America with <i>Carcinus maenas</i> as second-intermediate host.

<p><i>Microphallus similis</i> infects multiple hosts to complete its life cycle, starting with (A) two species of <i>Littorina</i> snails (<i>L</i>. <i>saxatilis</i> and <i>L</i>. <i>obtusata</i>), where the trematode asexually reproduces, producing numerous cercariae. (B) These cercariae are shed from the snail into the water column, where they seek out and encyst as a metacercariae within a second-intermediate host, primarily the green crab, <i>Carcinus maenas</i>. To sexually reproduce, (C) the trematode’s crab host must be ingested by a definitive host, often a <i>Larus</i> gull species, where (D) the trematode’s eggs, containing miracidia, are then deposited into the marine environment with the birds’ feces. Grazing snails accidentally ingest these eggs, and the cycle continues.</p

Regression of mussel handling time by metacercarial cyst intensity.

<p>Metacercarial infection intensity represents actual counts. The regression remains significant with (R² = 0.238; p<0.001) or without (R² = 0.123; p = 0.005) the crab with 6500 cysts.</p

Hepatosomatic index (HSI) and gonadosomatic index (GSI) analyses by cyst intensity (estimated metacercarial abundance).

<p>Panel ‘a’ represents HSI for all crabs combined; ‘b’ represents GSI for all crabs combined; ‘c’ represents GSI for females only; ‘d’ represents GSI for males only. Cyst intensity for HSI is lower bound estimated hepatopancreas metacercarial cyst abundance, and cyst intensity for GSI is lower bound estimated gonad metacercarial cyst abundance.</p

Average (± SE) infection intensity of metacercarial cysts in hepatopancreas, gonad, and thoracic ganglion tissues in each treatment and naturally at Appledore Island, ME and metacercarial cyst intensity per gram hepatopancreas tissue by crab carapace width (mm).

<p>(a) Differences in capitalized letters above the bars indicate a significant difference in infection intensity (p<0.05) of counted cysts. Numbers above the control bars indicate the average infection intensities per control (all less than 1). LOW (24) and CONT (24) refer to the 24 hour infection treatment and its associated control; MED (72) and CONT (72) refer to the 72 hour infection treatment and its associated control; HIGH (120) and CONT (120) refer to the 120 hour infection treatment and its associated control; ‘LARUS’ refers to naturally infected crabs collected at Larus Ledge in 2007 and 2012 on Appledore Island, Isles of Shoals, ME. (b) There is a significant exponential relationship between crab size (CW) and cyst intensity per gram hepatopancreas.</p

Average (± SE) hemocyte counts in crabs 72 hours after exposure and after the four week incubation period.

<p>The grey bar is the control and the black bar is the experimental treatment showing circulating hemocytes per μL hemolymph from blood drawn for exposed and control crabs for two exposure periods. *refers to a significant difference (p<0.05) between the treatments.</p