Archive for May, 2017

Increase in travel-associated Legionnaires’ disease among European travellers returning from Dubai since 1 October 2016.

Europa

Aumento de casos de legionelosis en viajeros que retornan de Dubai

24/05/2017 – El sistema de vigilancia ELDSNet del Centro Europeo para la Prevención y el Control de Enfermedades (ECDC) ha observado un aumento en el número de casos de legionelosis asociados a viajes a Dubai, Emiratos Árabes Unidos, desde el comienzo del último trimestre de 2016, en comparación con 2014-2015.

El número de casos reportados en febrero y abril de 2017 sigue siendo significativamente superior al observado en los últimos años.

Entre el 1/10/2016 y el 23/05/2017, los Estados miembros de la Unión Europea (UE) y un país perteneciente a la Asociación Europea de Libre Comercio (AELC) han notificado al ECDC 60 casos de legionelosis asociados a viajes a Dubai dentro de los 2-10 días previos al inicio de los síntomas. La fecha de inicio de los síntomas del caso informado más reciente fue el 11 de mayo de 2017.

Los casos fueron reportados por:

Gran Bretaña (29 casos),

Suecia (8),

Países Bajos (6),

Dinamarca (4),

Francia (3),

Alemania (3),

Austria (1),

Bélgica (1),

España (1),

Hungría (1),

Irlanda (1),

República Checa (1) y

Suiza (1).

El retraso entre la semana de inicio de la enfermedad y la semana de notificación del caso al ELDSNet es de alrededor de dos semanas (rango: 1-6 semanas).

Por lo tanto, el número de casos notificados en las últimas seis semanas es probable que esté subestimado

De los 60 casos reportados, 54 se estuvieron en alojamientos comerciales (hoteles o departamentos) y seis en alojamientos privados.

Dieciocho casos utilizaron un hotel que estuvo asociado con otro caso que enfermó posteriormente al 1/10/2016.

Doce casos estuvieron alojados en otro sitio en los Emiratos Árabes Unidos o en otro país distinto de su país de origen durante el período de incubación. Uno de los casos fue reportado como fatal.

Trece casos se habían alojado en Dubai durante todo su período de incubación.

Todos los casos fueron confirmados por laboratorio. Tres de los casos fueron infectados por Legionella pneumophila serogrupo 1 tipo de secuencia basal 616, y uno por L. pneumophila serogrupo 1 tipo de secuencia basal 2382.

El tipo de secuencia basal 616 es poco común en Europa y se ha asociado con casos de legionelosis en viajeros que retornan de Dubai en años anteriores, mientras que el tipo de secuencia basal 2382 es el primero identificado en todo el mundo y parece estar estrechamente relacionado con el tipo 616. Un caso fue caracterizado como L. pneumophila serogrupo 13 tipo de secuencia basal 1327.

Las autoridades de los Emiratos Árabes Unidos han informado al ECDC que no han observado un aumento en los casos de neumonía de declaración obligatoria en Dubai durante el período de octubre a diciembre de 2016.

Investigaciones ambientales

Las autoridades de salud pública de los Emiratos Árabes Unidos han informado al ECDC que se llevaron a cabo  investigaciones ambientales en los hoteles notificados y que los conteos de Legionella dentro del municipio de Dubai mostraron niveles aceptables en los sistemas de agua (inferiores a 1.000 unidades formadoras de colonias/litro).

El umbral aceptable es el mismo que el indicado en las directrices técnicas europeas por la Red de Vigilancia Europea para Infecciones por Legionella (EWGLI).

Según las autoridades de los Emiratos Árabes Unidos, se ha llevado a cabo en Dubai la evaluación de riesgos de todos los hoteles notificados a través del ELDSNet y de posibles sitios de alto riesgo, tales como plantas de refrigeración y grandes fuentes, y ninguna ha sido identificada hasta la fecha.

También se ha informado de que el Municipio de Dubai continúa con la investigación de cualquier nuevo caso notificado por el ELDSNet, como así también con la supervisión y vigilancia, de acuerdo con las leyes y reglamentos de Dubai.

Fuente:

Reporte Epidemiológico de Córdoba- Argentina 31/05/2017

European Centre for Disease Prevention and Control

Epidemiological update: Legionella in Dubai

24/May/2017

Increase in travel-associated Legionnaires’ disease among European travellers returning from Dubai since 1 October 2016.

The ECDC surveillance scheme (ELDSNet) for travel-associated Legionnaires’ disease (TALD) [1] has observed an increase in the number of cases associated with travel to Dubai, United Arab Emirates (UAE) since the beginning of the last quarter of 2016 compared to 2014-2015 (Figure 1).

Case numbers reported in February and April 2017 continue to be significantly above that observed in recent years.

This epidemiological update is the third since a rapid risk assessment was published by ECDC on 23 December 2016.

FULL TEXT

http://ecdc.europa.eu/en/press/news/_layouts/forms/News_DispForm.aspx?ID=1624&List=8db7286c-fe2d-476c-9133-18ff4cb1b568

PDF

http://ecdc.europa.eu/en/press/news/_layouts/forms/News_DispForm.aspx?ID=1624&List=8db7286c-fe2d-476c-9133-18ff4cb1b568&preview=yes&pdf=yes

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May 31, 2017 at 8:49 am

Impact of simultaneous exposure to arboviruses on infection and transmission by Aedes aegypti mosquitoes

Nature Communications May 19, 2017

Claudia Rückert, James Weger-Lucarelli, Selene M. Garcia-Luna, Michael C. Young, Alex D. Byas, Reyes A. Murrieta, Joseph R. Fauver & Gregory D. Ebel

The recent emergence of both chikungunya and Zika viruses in the Americas has significantly expanded their distribution and has thus increased the possibility that individuals may become infected by more than one Aedes aegypti-borne virus at a time. Recent clinical data support an increase in the frequency of coinfection in human patients, raising the likelihood that mosquitoes could be exposed to multiple arboviruses during one feeding episode. The impact of coinfection on the ability of relevant vector species to transmit any of these viruses (that is, their vector competence) has not been determined. Thus, we here expose Ae. aegypti mosquitoes to chikungunya, dengue-2 or Zika viruses, both individually and as double and triple infections. Our results show that these mosquitoes can be infected with and can transmit all combinations of these viruses simultaneously. Importantly, infection, dissemination and transmission rates in mosquitoes are only mildly affected by coinfection.

FULL TEXT (CLIC en PDF para el DOWNLOAD)

https://www.nature.com/articles/ncomms15412

May 31, 2017 at 8:46 am

Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration

Así se propaga el virus de la varicela por el organismo

Un grupo de investigadores de la Escuela de Medicina de Hannover, Alemania, ha demostrado en laboratorio que el virus se sirve de la glicoproteína C para secuestrar a los glóbulos blancos y extenderse por el cuerpo.

26/05/2017 – El virus de la varicela zóster (VZV) posee una proteína que podría mejorar su capacidad de manipular a los glóbulos blancos y propagarse por todo el cuerpo, según un estudio liderado por el investigador español Víctor González-Motos de la Escuela de Medicina de Hannover.

Los resultados del trabajo se han publicado en el último número de la revista PLOS Pathogens. (VER MAS ABAJO)

El hallazgo proporciona una nueva visión del hasta ahora poco entendido mecanismo por el cual el virus de la varicela se extiende, tras una infección inicial en el tracto respiratorio.

El VZV causa varicela en niños y puede reactivarse más tarde para producir herpes zóster en adultos. Después de infectar las vías respiratorias, el virus secuestra a los glóbulos blancos del sistema inmunológico, usándolos para esparcirse por el cuerpo –incluyendo la piel– para causar la varicela.

Para entender mejor este proceso, los autores investigaron si el VZV influye en la función de las quimiocinas, pequeña proteínas del sistema inmune que atraen a los glóbulos blancos a las zonas donde está la infección y guían su movimiento dentro del cuerpo.

Manipular el sistema inmunitario

Los científicos se centraron en una proteína del virus, conocida como glicoproteína C, ya que una investigación previa indicaba que podía desempeñar un papel importante en el ciclo de la infección.

En el laboratorio, realizaron experimentos de quimiotaxis –un proceso por el cual las bacterias y otras células dirigen sus movimientos de acuerdo con la concentración de ciertas sustancias químicas–. Los expertos encontraron que la adición de glicoproteína C mejoraba la capacidad de las quimiocinas para atraer los glóbulos blancos, incluyendo los de las amígdalas, que son un objetivo principal de VZV durante la infección inicial.

Los resultados indican que la glicoproteína C puede interactuar con las quimiocinas para atraer más glóbulos blancos al sitio de la infección por VZV, donde el virus puede manipularlos para extenderse a otras partes del cuerpo. Los autores señalan que se necesita más investigación para comprobar si esta hipótesis se mantiene en tejido humano.

Source

PLoS Pathogens 2017

Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration

Víctor González-Motos, Carina Jürgens, Birgit Ritter, Kai A. Kropp, Verónica Durán, Olav Larsen, Anne Binz, Werner J. D. Ouwendijk, Tihana Lenac Rovis, Stipan Jonjic, Georges M. G. M. Verjans, Beate Sodeik, Thomas Krey,….

1 Institute of Virology, Hannover Medical School, Hannover, Germany,

2 University of Veterinary Medicine Hannover, Foundation, Hannover, Germany,

3 Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover, Germany,

4 Department of Biomedical Sciences, Faculty of Health and Medical Science, University of Copenhagen, Copenhagen, Denmark,

5 Department of Viroscience, Erasmus MC, Rotterdam, The Netherlands,

6 Center for Proteomics and Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, Rijeka, Croatia,

7 Research Center for Emerging Infections and Zoonoses, University of Veterinary Medicine Hannover, Hannover, Germany,

8 German Center for Infection Research (DZIF), Hannover-Braunschweig, Germany,

9 Research Core Unit for Laser Microscopy, Hannover Medical School, Hannover, Germany,

10 Institute for Virology, Freie Universita¨t Berlin, Berlin, Germany,

11 NovImmune, Geneva, Switzerland

Varicella zoster virus (VZV) is a highly prevalent human pathogen that establishes latency in neurons of the peripheral nervous system. Primary infection causes varicella whereas reactivation results in zoster, which is often followed by chronic pain in adults. Following infection of epithelial cells in the respiratory tract, VZV spreads within the host by hijacking leukocytes, including T cells, in the tonsils and other regional lymph nodes, and modifying their activity. In spite of its importance in pathogenesis, the mechanism of dissemination remains poorly understood. Here we addressed the influence of VZV on leukocyte migration and found that the purified recombinant soluble ectodomain of VZV glycoprotein C (rSgC) binds chemokines with high affinity. Functional experiments show that VZV rSgC potentiates chemokine activity, enhancing the migration of monocyte and T cell lines and, most importantly, human tonsillar leukocytes at low chemokine concentrations. Binding and potentiation of chemokine activity occurs through the C-terminal part of gC ectodomain, containing predicted immunoglobulin-like domains. The mechanism of action of VZV rSgC requires interaction with the chemokine and signalling through the chemokine receptor. Finally, we show that VZV viral particles enhance chemokine-dependent T cell migration and that gC is partially required for this activity. We propose that VZV gC activity facilitates the recruitment and subsequent infection of leukocytes and thereby enhances VZV systemic dissemination in humans.

PDF

http://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1006346&type=printable

May 30, 2017 at 3:33 pm

Updated Recommendations for Use of MenB-FHbp Serogroup B Meningococcal Vaccine — Advisory Committee on Immunization Practices, 2016

Morb Mortal Wkly Rep. 2017;66:509-513.

PDF

https://www.cdc.gov/mmwr/volumes/66/wr/pdfs/mm6619a6.pdf

May 29, 2017 at 8:09 am

Rifabutin Is Active against Mycobacterium abscessus Complex

Antimicrob. Agents Chemother. June 2017 V.61 N.6

Dinah Binte Aziz, Jian Liang Low, Mu-Lu Wu, Martin Gengenbacher, Jeanette W. P. Teo, Véronique Dartois, and Thomas Dick

aDepartment of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore

bDepartment of Laboratory Medicine, National University Hospital, Singapore

cPublic Health Research Institute, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, New Jersey, USA

Lung infections caused by Mycobacterium abscessus are emerging as a global threat to individuals with cystic fibrosis and to other patient groups. Recent evidence for human-to-human transmission worsens the situation. M. abscessus is an intrinsically multidrug-resistant pathogen showing resistance to even standard antituberculosis drugs, such as rifampin. Here, our objective was to identify existing drugs that may be employed for the treatment of M. abscessus lung disease. A collection of more than 2,700 approved drugs was screened at a single-point concentration against an M. abscessus clinical isolate. Hits were confirmed with fresh solids in dose-response experiments. For the most attractive hit, growth inhibition and bactericidal activities against reference strains of the three M. abscessus subspecies and a collection of clinical isolates were determined. Surprisingly, the rifampin derivative rifabutin had MICs of 3 ± 2 μM (3 μg/ml) against the screening strain, the reference strains M. abscessus subsp. abscessus ATCC 19977, M. abscessus subsp. bolletii CCUG 50184-T, and M. abscessus subsp. massiliense CCUG 48898-T, as well as against a collection of clinical isolates. Furthermore, rifabutin was active against clarithromycin-resistant strains. In conclusion, rifabutin, in contrast to rifampin, is active against the Mycobacterium abscessus complex bacteria in vitro and may be considered for treatment of M. abscessus lung disease.

PDF

http://aac.asm.org/content/61/6/e00155-17.full.pdf+html

May 28, 2017 at 4:54 pm

The Race To Find Antivirals for Zika Virus

Antimicrob. Agents Chemother. June 2017 V.61 N.6

Juan-Carlos Saiz and Miguel A. Martín-Acebes

Department of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Madrid, Spain

Zika virus (ZIKV), a flavivirus transmitted by mosquitoes, was an almost neglected pathogen until its introduction in the Americas in 2015 and its subsequent explosive spread throughout the continent, where it has infected millions of people. The virus has caused social and sanitary alarm, mainly due to its association with severe neurological disorders (Guillain-Barré syndrome and microcephaly in fetuses and newborns). Nowadays, no specific antiviral therapy against ZIKV is available. However, during the past months, a great effort has been made to search for antiviral candidates using different approaches and methodologies, ranging from testing specific compounds with known antiviral activity to the screening of libraries with hundreds of bioactive molecules. The identified antiviral candidates include drugs targeting viral components as well as cellular ones. Here, an updated review of what has been done in this line is presented.

PDF

http://aac.asm.org/content/61/6/e00411-17.full.pdf+html

May 28, 2017 at 4:52 pm

Epidemiological and Molecular Characterization of an Invasive Group A Streptococcus emm32.2 Outbreak

J. Clin. Microbiol. June 2017 V.55 N.6

Jennifer E. Cornick, Anmol M. Kiran, Roberto Vivancos, Jon Van Aartsen, Jenny Clarke, Edward Bevan, Mansoor Alsahag, Maaike Alaearts, Laura Bricio Moreno, Howard F. Jenkinson, Angela H. Nobbs, James Anson, Aras Kadiolgu, Neil French, and Dean B. Everett

aMalawi Liverpool Wellcome Trust Clinical Research Programme, Blantyre, Malawi

bInstitute of Infection & Global Health, University of Liverpool, Liverpool, United Kingdom

cField Epidemiology Service, Public Health England, London, United Kingdom

dNIHR Health Protection Research Unit in Emerging and Zoonotic Infections, University of Liverpool, Liverpool, United Kingdom

eHeart of England NHS Foundation Trust, Birmingham Heartlands Hospital, Birmingham, United Kingdom

fSchool of Oral and Dental Sciences, University of Bristol, Bristol, United Kingdom

gLiverpool Clinical Laboratories, Royal Liverpool & Broadgreen University Hospitals Trust, Liverpool, United Kingdom

An emm32.2 invasive group A streptococcus (iGAS) outbreak occurred in Liverpool from January 2010 to September 2012. This genotype had not previously been identified in Liverpool, but was responsible for 32% (14/44) of all iGAS cases reported during this time period. We performed a case-case comparison of emm32.2 iGAS cases with non-emm32.2 control iGAS cases identified in the Liverpool population over the same time period to assess patient risk factors for emm32.2 iGAS infection. The emm32.2 iGAS cases were confined to the adult population. We show that homelessness, intravenous drug use, and alcohol abuse predisposed patients to emm32.2 iGAS disease; however, no obvious epidemiological linkage between the patients with emm32.2 iGAS could be identified. Comparative whole-genome sequencing analysis of emm32.2 iGAS and non-emm32.2 control isolates was also performed to identify pathogen factors which might have driven the outbreak. We identified 19 genes, five of which had previously been implicated in virulence, which were present in all of the emm32.2 iGAS isolates but not present in any of the non-emm32.2 control isolates. We report that a novel emm32.2 genotype emerged in Liverpool in 2010 and identified a specific subset of genes, which could have allowed this novel emm32.2 genotype to persist in a disadvantaged population in the region over a 3-year period.

PDF

http://jcm.asm.org/content/55/6/1837.full.pdf+html

May 28, 2017 at 4:51 pm

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