Posts filed under ‘Infecciones emergentes’

Identification of a PVL-negative SCCmec-IVa sublineage of the methicillin-resistant Staphylococcus aureus CC80 lineage: understanding the clonal origin of CA-MRSA

Clinical Microbiology and Infection March 2018 V.24 N.3 P.273-278

S.M. Edslev, H. Westh, P.S. Andersen, R. Skov, N. Kobayashi, M.D. Bartels, F. Vandenesch, A. Petersen, P. Worning, A.R. Larsen, M. Stegger

Objetivos

Los aislados de MRSA adquiridos en la comunidad (CA) que pertenecen al complejo clonal 80 (CC80) se reconocen como el CA-MRSA europeo. El clon de CA-MRSA europeo prevalente contiene un cromosoma de cassette estafilocócico de tipo IVc mec (SCCmec) y expresa leucocidina Panton-Valentine (PVL). Recientemente, se ha observado un aumento significativo de CCL-CC80 MRSA negativo en Dinamarca. El objetivo de este estudio fue examinar su genética y epidemiología, y compararlos con el clon de CA-MRSA europeo con el fin de comprender la aparición de CCL-MR negativo MRSA.

Métodos

El análisis filogenético del linaje CC80 S. aureus se realizó a partir de secuencias de genoma completo de 217 aislados (23 SAMS y 194 MRSA) de 22 países. Todos los aislamientos se caracterizaron genéticamente con respecto a los determinantes de resistencia y el transporte de PVL, y se obtuvieron datos epidemiológicos para aislados seleccionados.

Resultados

El análisis filogenético reveló la existencia de tres clados distintos del linaje CC80: (a) un clado de SAMS que abarca aislados del África subsahariana (n = 13); (b) un derivado que abarca el clon europeo CA-MRSA SCCmec-IVc (n = 185); y (c) un nuevo y genéticamente distinto clado que abarca SARM SCCmec-IVa aislados (n = 19). Todos los aislamientos en el nuevo clado eran negativos para PVL, pero portaban partes remanentes (8-12 kb) del profago ΦSa2 que codificaba PVL y eran susceptibles a ácido fusídico y kanamicina/amikacina. El mapeo geo-espacial podría vincular estos aislamientos a las regiones de Medio Oriente, Asia y el Pacífico Sur.

Conclusiones

Este estudio informa sobre la aparición de un sublineage CC80 CA-MRSA novedoso, que muestra que el linaje CC80 es más diverso de lo que se suponía anteriormente.

 

PDF

http://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(17)30346-4/pdf

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April 24, 2018 at 7:57 am

Global emergence of the widespread Pseudomonas aeruginosa ST235 clone

Clinical Microbiology and Infection March 2018 V.24 N.3 P.258-266

Treepong, V.N. Kos, C. Guyeux, D.S. Blanc, X. Bertrand, B. Valot, D. Hocquet

Objetivos

A pesar de la estructura poblacional epidémica no clonal de Pseudomonas aeruginosa (PAE), varios tipos de secuencias multilocales se distribuyen en todo el mundo y se asocian frecuentemente con epidemias en las que la resistencia a múltiples fármacos confunde el tratamiento. ST235 es el más frecuente de estos clones generalizados. En este estudio, intentamos comprender el origen de ST235 y las bases moleculares de su éxito.

Métodos

Se examinaron los genomas de 79 aislados de PAE ST235 recolectados en todo el mundo durante un período de 27 años. Se construyó una red filogenética, que utiliza un enfoque bayesiano para encontrar el ancestro común más reciente, e identificamos los determinantes de la resistencia a los ATB y los genes específicos de ST235.

Resultados

Nuestros datos sugieren que el sublineaje ST235 surgió en Europa alrededor de 1984, coincidiendo con la introducción de fluoroquinolonas como tratamiento anti-PAE. El sublineage ST235 aparentemente se extendió desde Europa a través de dos clones independientes. Luego, los aislamientos de ST235 parecieron adquirir determinantes de resistencia a aminoglucósidos, β-lactamas y carbapenémicos localmente. Además, encontramos que todos los genomas ST235 contenían la exotoxina codificada por exoU e identificaban 22 genes específicos de ST235 que se agrupaban en bloques e implicaban eflujo transmembrana, procesamiento de ADN y transformación bacteriana. Estas combinaciones únicas de genes pueden haber contribuido al mal resultado asociado con las infecciones por PAE ST235 y aumentar la capacidad de este clon internacional para adquirir elementos de resistencia móvil.

Conclusión

Nuestros datos sugieren que PAE ST235 (a) se ha vuelto prevalente en todo el mundo potencialmente debido a la presión selectiva de las fluoroquinolonas y (b) se volvió fácilmente resistente a los aminoglucósidos, β-lactámicos y carbapenémicos a través de la mutación y adquisición de elementos de resistencia entre las poblaciones locales .

PDF

http://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(17)30342-7/pdf

April 24, 2018 at 7:56 am

REVIEW – Emerging infections—an increasingly important topic: review by the Emerging Infections Task Force

Clinical Microbiology and Infection April 2018 V.24 N.4 P.369-375

Petersen, N. Petrosillo, M. Koopmans, the ESCMID Emerging Infections Task Force Expert Panel

Objetivos

Este artículo revisa las tendencias en infecciones emergentes y la necesidad de una mayor vigilancia clínica y de laboratorio.

Métodos

Se han revisado los factores que contribuyeron a la aparición de brotes recientes. Se revisaron los principales brotes conocidos durante las últimas dos décadas.

Resultados

Identificamos al menos cuatro causas principales de infecciones emergentes: (i) aumento de la densidad de la población humana; (ii) el estrés de la expansión de las tierras de cultivo en el medio ambiente; (iii) globalización del mercado y la fabricación de alimentos; (iv) contaminación ambiental. Los factores que crean nuevas oportunidades para infecciones emergentes incluyen: (i) crecimiento de la población; (ii) propagación en instalaciones de atención médica; (iii) una población que envejece; (iv) viajes internacionales; (v) cambiar y expandir los hábitats de vectores.

Conclusiones

Las infecciones emergentes son impredecibles. En esta revisión, argumentamos que para descubrir nuevas tendencias en enfermedades infecciosas, los médicos deben buscar lo inusual e inesperado y garantizar diagnósticos adecuados y que la vigilancia sindrómica debe ser respaldada por servicios de laboratorio altamente especializados. El modelado matemático no ha sido capaz de predecir los brotes. Se necesita más énfasis en la biología de la evolución. El EID rara vez se destaca por ser inusual, y la presión continua sobre los presupuestos de atención médica obliga a los médicos y los laboratorios a priorizar su diagnóstico hasta condiciones comunes y tratables. La Sociedad Europea de Enfermedades Infecciosas y Microbiología Clínica, ESCMID, ha establecido un Grupo de Trabajo sobre Infecciones Emergentes, EITaF, para fortalecer las actividades de la sociedad sobre infecciones emergentes y garantizar que las infecciones emergentes se incluyan en las consideraciones diagnósticas diferenciales en la práctica clínica diaria.

PDF

http://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(17)30641-9/pdf

April 24, 2018 at 7:54 am 1 comment

Wound healing: Natural history and risk factors for delay in Australian patients treated with antibiotics for Mycobacterium ulcerans disease.

PLoS Negl Trop Dis. 2018 Mar 19;12(3):e0006357.

O’Brien DP1,2,3, Friedman ND1, McDonald A4, Callan P4, Hughes A1, Walton A1, Athan E1.

Author information

1 Department of Infectious Diseases, Barwon Health, Geelong, Australia.

2 Department of Medicine and Infectious Diseases, Royal Melbourne Hospital, University of Melbourne, Melbourne, Australia.

3 Manson Unit, Médecins Sans Frontières, London, United Kingdom.

4 Department of Plastic Surgery, Barwon Health, Geelong, Australia.

Abstract

BACKGROUND:

Healing times following treatment with antibiotics, and factors that influence healing, have not been reported in Australian patients with Mycobacterium ulcerans.

METHODOLOGY/PRINCIPAL FINDINGS:

Healing times were determined for all M. ulcerans cases treated by a single physician with antibiotics at Barwon Health, Victoria, from 1/1/13-31/12/16. Lesions were categorised by induration size: category A ≤ 400mm2, Category B 401-1600mm2 and Category C ≥1601mm2. A logistic regression analysis was performed to determine risk factors for prolonged wound healing (>150 days from antibiotic commencement). 163 patients were included; 92 (56.4%) were male and median age was 58 years (IQR 39-73 years). Baseline lesion size [available in 145 (89.0%) patients] was categorised as A in 46 (31.7%), B in 67 (46.2%) and C in 32 (22.1%) patients. Fifty (30.7%) patients had surgery. In those treated with antibiotics alone, 83.0% experienced a reduction in induration size after 2 weeks, then 70.9% experienced an increase in induration size from the lowest point, and 71.7% experienced an increase in ulceration size. A linear relationship existed between the time induration resolved and wound healing began. Median time to heal was 91 days (IQR 70-148 days) for category A lesions; significantly shorter than for category B lesions (128 days, IQR 91-181 days, p = 0.05) and category C lesions (169 days, IQR 159-214 days, p<0.001). Fifty-seven (35.0%) patients experienced a paradoxical reaction. Of those treated with antibiotics alone, lesions experiencing a paradoxical reaction had longer healing times [median time to heal 177 days (IQR 154-224 days) compared to 107 days (IQR 79-153 days), p<0.001]. On multivariable logistic regression, lesion size at baseline (p<0.001) and paradoxical reactions (p<0.001) were independently associated with prolonged healing times. For category A and B lesions, healing time was significantly shorter with antibiotics plus excision and direct closure compared with antibiotics alone [Category A lesions median 55 days (IQR 21-63 days) compared with 91 days (IQR 70-148 days), p<0.001; Category B lesions median 74 days (IQR 21-121 days) compared to 128 days (IQR 97-181 days), p<0.001].

CONCLUSIONS:

In Australian patients treated with antibiotics M. ulcerans lesions usually initially improve, then clinically deteriorate with increased induration and ulceration, before healing after the inflammation associated with lesions resolves. The time to complete healing of lesions is generally long, and is further prolonged in those with larger initial lesion size or who develop paradoxical reactions. For small lesions (<4cm2), excisional surgery may reduce healing times.

PDF

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5875894/pdf/pntd.0006357.pdf

April 23, 2018 at 7:22 pm

The incubation period of Buruli ulcer (Mycobacterium ulcerans infection) in Victoria, Australia – Remains similar despite changing geographic distribution of disease

PLoS Negl Trop Dis. 2018 Mar 19;12(3):e0006323.

Loftus MJ1,2, Trubiano JA1,3, Tay EL2, Lavender CJ4, Globan M4, Fyfe JAM4, Johnson PDR1,3.

Author information

1 Department of Infectious Diseases, Austin Health, Heidelberg, Victoria, Australia.

2 Victorian Department of Health and Human Services, Melbourne, Victoria, Australia.

3 Department of Medicine, Melbourne University, Parkville, Victoria, Australia.

4 Victorian Infectious Diseases Reference Laboratory, North Melbourne, Victoria, Australia.

Abstract

BACKGROUND:

Buruli ulcer (BU) is a geographically-restricted infection caused by Mycobacterium ulcerans; contact with an endemic region is the primary risk factor for disease acquisition. Globally, efforts to estimate the incubation period of BU are often hindered as most patients reside permanently in endemic areas. However, in the south-eastern Australian state of Victoria, a significant proportion of people who acquire BU are visitors to endemic regions. During a sustained outbreak of BU on the Bellarine peninsula we estimated a mean incubation period of 4.5 months. Since then cases on the Bellarine peninsula have declined but a new endemic area has developed centred on the Mornington peninsula.

METHOD:

Retrospective review of 443 cases of BU notified in Victoria between 2013 and 2016. Telephone interviews were performed to identify all cases with a single visit to an endemic region, or multiple visits within a one month period. The incubation period was defined as the time between exposure to an endemic region and symptom onset. Data were subsequently combined with those from our earlier study incorporating cases from 2002 to 2012.

RESULTS:

Among the 20 new cases identified in short-term visitors, the mean incubation period was 143 days (4.8 months), very similar to the previous estimate of 135 days (4.5 months). This was despite the predominant exposure location shifting from the Bellarine peninsula to the Mornington peninsula. We found no association between incubation period and age, sex, location of exposure, duration of exposure to an endemic region or location of BU lesion.

CONCLUSIONS:

Our study confirms the mean incubation period of BU in Victoria to be between 4 and 5 months. This knowledge can guide clinicians and suggests that the mode of transmission of BU is similar in different geographic regions in Victoria.

PDF

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5875870/pdf/pntd.0006323.pdf

 

April 23, 2018 at 7:21 pm

Risk factors for Mycobacterium ulcerans infection (Buruli Ulcer) in Togo ─ a case-control study in Zio and Yoto districts of the maritime region.

BMC Infect Dis. 2018 Jan 19;18(1):48.

Maman I1,2, Tchacondo T3, Kere AB4, Piten E5, Beissner M6, Kobara Y7, Kossi K4, Badziklou K4, Wiedemann FX8, Amekuse K8, Bretzel G6, Karou DS3.

Author information

1 Institut National d’Hygiène (INH), National Reference Laboratory for Buruli ulcer disease in Togo, 26 QAD Rue Nangbeto, 1BP, 1396, Lomé, Togo. mamanissaka@yahoo.fr.

2 Ecole Supérieure des Techniques Biologiques et Alimentaires (ESTBA), Laboratoire des Sciences Biologiques et des Substances Bioactives, Université de Lomé, Lomé, Togo. mamanissaka@yahoo.fr.

3 Ecole Supérieure des Techniques Biologiques et Alimentaires (ESTBA), Laboratoire des Sciences Biologiques et des Substances Bioactives, Université de Lomé, Lomé, Togo.

4 Institut National d’Hygiène (INH), National Reference Laboratory for Buruli ulcer disease in Togo, 26 QAD Rue Nangbeto, 1BP, 1396, Lomé, Togo.

5 Centre National de Référence pour le Traitement de l’Ulcère de Buruli (CNRT-UB), Centre Hospitalier Régional (CHR) de Tsévié, Lomé, Togo.

6 Department for Infectious Diseases and Tropical Medicine (DITM), Medical Center of the University of Munich (LMU), Munich, Germany.

7 Programme National de Lutte Contre l’Ulcère de Buruli, la Lèpre et le Pian (PNLUB-LP), Lomé, Togo.

8 German Leprosy and Tuberculosis Relief Association (DAHW-T), Togo office, Lomé, Togo.

Abstract

BACKGROUND:

Buruli ulcer (BU) is a neglected mycobacterial skin infection caused by Mycobacterium ulcerans. This disease mostly affects poor rural populations, especially in areas with low hygiene standards and sanitation coverage. The objective of this study was to identify these risk factors in the districts of Zio and Yoto of the Maritime Region in Togo.

METHODS:

We conducted a case-control study in Zio and Yoto, two districts proved BU endemic from November 2014 to May 2015. BU cases were diagnosed according to the WHO clinical case definition at the Centre Hospitalier Régional de Tsévié (CHR Tsévié) and confirmed by Ziehl-Neelsen (ZN) microscopy and IS2404 polymerase chain reaction (PCR). For each case, up to two controls matched by sex and place of residence were recruited. Socio-demographic, environmental or behavioral data were collected and conditional logistic regression analysis was used to identify and compare risk factors between BU cases and controls.

RESULTS:

A total of 83 cases and 128 controls were enrolled. The median age was 15 years (range 3-65 years). Multivariate conditional logistic regression analysis after adjustment for potential confounders identified age (< 10 years (OR =11.48, 95% CI = 3.72-35.43) and 10-14 years (OR = 3.63, 95% CI = 1.22-10.83)), receiving insect bites near a river (OR = 7.8, 95% CI = 1.48-41.21) and bathing with water from open borehole (OR = 5.77, (1.11-29.27)) as independent predictors of acquiring BU infection.

CONCLUSIONS:

This study identified age, bathing with water from open borehole and receiving insect bites near a river as potential risk of acquiring BU infection in Zio and Yoto districts of the Maritime Region in south Togo.

PDF

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5775556/pdf/12879_2018_Article_2958.pdf

April 23, 2018 at 7:20 pm

Mycobacterium ulcerans DNA in Bandicoot Excreta in Buruli Ulcer-Endemic Area, Northern Queensland, Australia.

Emerg Infect Dis. 2017 Dec;23(12):2042-2045.

Röltgen K, Pluschke G, Johnson PDR, Fyfe J.

Abstract

To identify potential reservoirs/vectors of Mycobacterium ulcerans in northern Queensland, Australia, we analyzed environmental samples collected from the Daintree River catchment area, to which Buruli ulcer is endemic, and adjacent coastal lowlands by species-specific PCR. We detected M. ulcerans DNA in soil, mosquitoes, and excreta of bandicoots, which are small terrestrial marsupials.

FULL TEXT

https://wwwnc.cdc.gov/eid/article/23/12/17-0780_article

PDF

https://wwwnc.cdc.gov/eid/article/23/12/pdfs/17-0780.pdf

April 23, 2018 at 7:19 pm

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