Matias Reyes-Lugo’s research while affiliated with Pedro Kourí Tropical Medicine Institute and other places

In this brief note we wish to report the finding of the Crabhole Mosquito (Deinocerites magnus Theobald, 1901), in order to report its presence on a Venezuelan beach (Chuao beach, Aragua state, Venezuela), since it is a species incriminated in the transmission of Venezuelan Equine Encephalitis. KEY WORDS: Culicidae, crabs, Venezuelan Equine Encephalitis. RESUMEN En esta sucinta nota deseamos reportar el hallazgo del mosquito de cueva de cangrejos (Deinocerites magnus Theobald, 1901), con el objeto de informar su presencia en una playa venezolana (playa de Chuao, estado Aragua, Venezuela), ya que se trata de una especie incriminada en la transmisión de la Encefalitis Equina Venezolana.

Panstrongylus geniculatus es un triatomino, vector del Trypanosoma cruzi, agente etiológico de la Enfermedad de Chagas, propio de los corredores biológicos que se dan entre ciclos de transmisión urbano y periurbano en Venezuela. Los modelos de nicho ecológico y distribución potencial de especies permiten conocer la relación entre los factores climáticos y la presencia real de las especies. El modelo de distribución geográfica potencial para P. geniculatus, generado mediante MAXENT, mostró áreas con condiciones bioclimáticas próximas a su nicho ecológico; así, definió una amplia distribución potencial con énfasis en la zona norte costera de Venezuela (estados Lara, Yaracuy, Carabobo, Aragua, Miranda, Distrito Capital, Vargas, Monagas y Sucre) con probabilidades de media a muy altas (0,56 - 1). También predijo áreas con condiciones de idoneidad en estados occidentales y orientales a pesar de que los registros reales son escasos. La isotermalidad y temperatura máxima del mes más caliente contribuyeron en 43,4 % al establecimiento del modelo, en tanto que variables relacionadas con la precipitación, contribuyeron en 56,6 %. Esto coincide con el hecho de que los triatominos son termo-tolerantes y se distribuyen en función de la temperatura, la cual también condiciona el número de triatominos infectados. Las áreas geográficas idóneas del país serían zonas de riesgo para la infestación triatomínica y la transmisión de T. cruzi, por coincidencia con la zona de mayor densidad de la poblacional humana, lo cual requeriría afinar estrategias de vigilancia entomológica y control epidemiológico.

Historically known as the yellow fever mosquito, Aedes aegypti invaded Madeira Island in 2005 and was the vector of the island's first dengue outbreak in 2012. We have studied genetic variation at 16 microsatellites and two mitochondrial DNA genes in temporal samples of Madeira Island, in order to assess the origin of the invasion and the population structure of this mosquito vector. our results indicated at least two independent colonization events occurred on the island, both having a south American source population. In both scenarios, Venezuela was the most probable origin of these introductions, a result that is in accordance with the socioeconomic relations between this country and Madeira Island. once introduced, Ae. aegypti has rapidly expanded along the southern coast of the island and reached a maximum effective population size (N e) in 2012, coincident with the dengue epidemic. After the outbreak, there was a 10-fold reduction in N e estimates, possibly reflecting the impact of community-based vector control measures implemented during the outbreak. These findings have implications for mosquito surveillance not only for Madeira Island, but also for other european regions where Aedes mosquitoes are expanding.

The increasing population of Aedes aegypti mosquitoes on Madeira Island (Portugal) resulted in the first autochthonous dengue outbreak, which occurred in October 2012. Our study establishes the first genetic evaluation based on the mitochondrial DNA (mtDNA) genes [cytochrome oxidase subunit I (COI) and NADH dehydrogenase subunit 4 (ND4)] and knockdown resistance ( kdr ) mutations exploring the colonisation history and the genetic diversity of this insular vector population. We included mosquito populations from Brazil and Venezuela in the analysis as putative geographic sources. The Ae. aegypti population from Madeira showed extremely low mtDNA genetic variability, with a single haplotype for COI and ND4. We also detected the presence of two important kdr mutations and the quasi-fixation of one of these mutations (F1534C). These results are consistent with a unique recent founder event that occurred on the island of Ae. aegypti mosquitoes that carry kdr mutations associated with insecticide resistance. Finally, we also report the presence of the F1534C kdr mutation in the Brazil and Venezuela populations. To our knowledge, this is the first time this mutation has been found in South American Ae. aegypti mosquitoes. Given the present risk of Ae. aegypti re-invading continental Europe from Madeira and the recent dengue outbreaks on the island, this information is important to plan surveillance and control measures.

SDS-PAGE profiles of both sexes of the haemolymphs of Panstrongylus geniculatus from different Venezuelan regions (savannas, piedmont, tropical forest and urban areas) were compared. It was determined that the haemolymphs showed a different electrophoretic profile, with proteins that ranged from 14 to 164 kDa. The most representative protein band in the profile of females was observed in two sectors: between 164 and 46 kDa and between 33 and 30 kDa. The main illustrative protein band in males was observed in one region: from 46 to 35 kDa. The Haemolymph composition of P. geniculatus from populations evaluated in this work expressed high homogeneity of this species with a clear difference between males and females. This similarity may be useful for control of these insects, taking into account that the genetic stability may be very important, since the use of an insecticide in a population with these characteristics is always more successful. According to the bibliographic review, this is the first study of haemolymph from Panstrongylus geniculatus.

Brown widow spider (BrWS) (Latrodectus geometricus) venom produces intense systemic reactions such as cramps, harsh muscle nociceptive, nauseas, vomiting and hypertension. The proposed pathogenic mechanisms resulting in these accidents have principally been damages occurring at the nervous system. However, it is suspected that there is also damage of the adrenal glands, as a result of the experimental animal's clinical manifestations, which developed symptoms compatible with acute adrenal insufficiency. We have currently found that the adrenal gland is damaged by this venom gland homogenates (VGH) producing severe alterations on cortex cells resulting in death by acute adrenal insufficiency. In general, the ultrastructural study on the glands of mice under transmission electronic microscopy observations showed alterations in the majority of the intracellular membranes within 3 to 24h. BrWSVGH also showed specific actions on extracellular matrix proteins such as fibronectin, laminin and fibrinogen. In addition, zymogram experiments using gelatin as substrates detected gelatinolytic activity. The molecular exclusion fractionation of crude BrWSVGH resulted in 15 fractions, of which F1 and F2 presented alpha/beta-fibrinogenase and fibronectinolytic activities. Fractions F6, F14 and F15 showed only alpha-fibrinogenase activity; in contrast, the gelatinolytic action was only observed in fraction F11. Only metalloproteinase inhibitors abolished all these proteolytic activities. Our results suggest that adrenal cortex lesions may be relevant in the etiopathogenesis of severe brown widow spider envenoming. To our knowledge, this is the first report on adrenal gland damages, fibrinogenolytic activity and interrelations with cell-matrix adhesion proteins caused by L.geometricus VGH. The venom of this spider could be inducing hemostatic system damages on envenomed patients.

El veneno de la araña viuda marrón (Latrodectus geometricus) produce pocas lesiones locales pero intensas reacciones sistémicas, tales como calambres, dolores musculares severos, nauseas, vómitos e hipertensión arterial. Se observaron ~ 16 bandas de proteina bajo condiciones reducidas y ~14 bandas bajo condiciones no reducidas en electroforesis en geles de poliacrilamida al 12.5%. Las manifestaciones neurotóxicas clínicas fueron confirmadas in vivo, mientras que la actividad proteolítica fue demostrada en una placa de gelatina. Los músculos de ratón se estudiaron durante las 3, 6, 12 y 24 horas después de ser inyectados con 45 µg de proteina de veneno. Los músculos fueron seriamente dañados por este veneno. Se demostró una infiltracción de células eosinofílicas y rupturas de membranas celulares en tejido muscular, al mismo tiempo un fuerte incremento de la membrana nuclear y una interrupción de la periodicidad del colágeno. Se observaron daños en la mitocondria y sin cristaes, vacuolas autofágicas e indentación nuclear. Se notó un aumento de la luz de los espacios intermiofibrilares y subsarcolemicos. En los capilares fue visible un desdoblamiento de la membrana endotelial hacia el lúmen vascular. Del mismo modo, fue visto un hinchamiento del sistema sarcotubular con lisis de las membranas; intensa autofagia de mitocondrias y áreas sin vesículas pinocíticas. Fue además observado, glucogenosomas con glucogeno particulado. Se observaron vacuolas autofágicas (autofagolisosomas) y áreas de necrosis. Estos daños podrían ser atribuídos a los efectos interactivos de una acción multifactorial de los componentes del veneno.