Posts filed under ‘Infecciones emergentes’

2007 LEGIONELLA and the Prevention of LEGIONELLOSIS – WHO MANUAL 276 pags

World Health Organization 2007

Edited by:

Jamie Bartram, Yves Chartier, John V Lee,

Kathy Pond and Susanne Surman-Lee



November 20, 2017 at 11:31 am

High Rate of MCR-1–Producing Escherichia coli and Klebsiella pneumoniae among Pigs, Portugal

Emerging Infectious Diseases December 2017 V.23 N.12 P.2023-2029


Nicolas Kieffer, Marta Aires-de-Sousa, Patrice Nordmann, and Laurent Poirel

Author affiliations: Université de Fribourg, Fribourg, Switzerland (N. Kieffer, P. Nordmann, L. Poirel); Escola Superior de Saúde da Cruz Vermelha Portuguesa, Lisbon, Portugal (M. Aires-de-Sousa); University of Lausanne and University Hospital Centre, Lausanne, Switzerland (P. Nordmann)

The mcr-1 (mobile colistin resistance 1) gene, which encodes phosphoethanolamine transferase, has been recently identified as a source of acquired resistance to polymyxins in Escherichia coli.

Using the SuperPolymyxin selective medium, we prospectively screened 100 pigs at 2 farms in Portugal for polymyxin-resistant Enterobacteriaceae and recovered 98 plasmid-mediated MCR-1–producing isolates.

Most isolates corresponded to nonclonally related E. coli belonging to many sequence types; we also found 2 Klebsiella pneumoniae sequence types. The mcr-1 gene was carried on IncHI2 or IncP plasmid backbones.

Our finding of a high rate of MCR-1 producers on 2 pig farms in Portugal highlights the diffusion of that colistin-resistance determinant at the farm level.

The fact that the pigs received colistin as metaphylaxis in their feed during the 6 weeks before sampling suggests selective pressure.


November 19, 2017 at 1:02 pm

LEPTOSPIROSIS – Guia para el Equipo de Salud – Ministerio Salud de la Nación Argentina


Guia para el Equipo de Salud – Ministerio Salud de la Nación Argentina

Abril 2014

  1. Introducción
  2. Manifestaciones clínicas
  3. ¿Cuándo sospechar leptospirosis?
  4. ¿Cómo confirmar leptospirosis?
  5. ¿Cómo notificar el caso de leptospirosis?
  6. ¿Cómo se trata el paciente con leptospirosis?
  7. Flujograma de manejo de casos sospechosos de leptospirosis
  8. Diagnóstico diferencial
  9. ¿Qué hacer si se confirma?
  10. ¿Cómo se tratan los casos caninos de leptospirosis?
  11. Prevención de la leptospirosis en la familia y la comunidad


November 18, 2017 at 10:05 am

LEPTOSPIROSIS – Puesta al día

Revista Chilena de Infectología Junio 2007 V.24 N.3 P.220-226

Zunino, P. Pizarro

We review epidemiological, clinical, laboratory and therapeutic aspects of leptospirosis. In relation to the epidemiology it is worth noting the importance of recreational and occupational risk factors, as well as the lack of date available in Chile before the year 2000, when leptospirosis became the object of epidemiological surveillance. There are many forms of clinical presentations for this disease and often signs and symptoms may be nonspecific. Thus, differential diagnosis must include many clinical entities. Laboratory diagnosis, on the other hand, is complex and not widely available. Although still controversial, a literature review supports antimicrobial treatment, with different antibiotics to choose from.


November 18, 2017 at 10:04 am


Clinical Microbiology Reviews April 2001 V.14 N.2 P.296-326


Paul N. Levett

University of the West Indies, School of Clinical Medicine & Research, and Leptospira Laboratory, Ministry of Health, Barbados

Leptospirosis is a worldwide zoonotic infection with a much greater incidence in tropical regions and has now been identified as one of the emerging infectious diseases. The epidemiology of leptospirosis has been modified by changes in animal husbandry, climate, and human behavior. Resurgent interest in leptospirosis has resulted from large outbreaks that have received significant publicity. The development of simpler, rapid assays for diagnosis has been based largely on the recognition that early initiation of antibiotic therapy is important in acute disease but also on the need for assays which can be used more widely. In this review, the complex taxonomy of leptospires, previously based on serology and recently modified by a genotypic classification, is discussed, and the clinical and epidemiological value of molecular diagnosis and typing is also evaluated.



November 18, 2017 at 10:02 am

Follow-up brain imaging of 37 children with congenital Zika syndrome: Case series study

BMJ 2017 Oct 13; 359:j4188

Calheiros de Lima Petribu N et al.



To compare initial brain computed tomography (CT) scans with follow-up CT scans at one year in children with congenital Zika syndrome, focusing on cerebral calcifications.


Case series study.


Barão de Lucena Hospital, Pernambuco state, Brazil.


37 children with probable or confirmed congenital Zika syndrome during the microcephaly outbreak in 2015 who underwent brain CT shortly after birth and at one year follow-up.

Main outcome measure

Differences in cerebral calcification patterns between initial and follow-up scans.


37 children were evaluated. All presented cerebral calcifications on the initial scan, predominantly at cortical-white matter junction. At follow-up the calcifications had diminished in number, size, or density, or a combination in 34 of the children (92%, 95% confidence interval 79% to 97%), were no longer visible in one child, and remained unchanged in two children. No child showed an increase in calcifications. The calcifications at the cortical-white matter junction which were no longer visible at follow-up occurred predominately in the parietal and occipital lobes. These imaging changes were not associated with any clear clinical improvements.


The detection of cerebral calcifications should not be considered a major criterion for late diagnosis of congenital Zika syndrome, nor should the absence of calcifications be used to exclude the diagnosis.




November 16, 2017 at 8:12 am

An update on Zika virus infection.  

Lancet  November 4, 2017 V.390 N.10.107 P.2099-2109


Prof David Baud, MD, Prof Duane J Gubler, ScD, Bruno Schaub, MD, Marion C Lanteri, PhD, Didier Musso, MD


The epidemic history of Zika virus began in 2007, with its emergence in Yap Island in the western Pacific, followed in 2013–14 by a larger epidemic in French Polynesia, south Pacific, where the first severe complications and non-vector-borne transmission of the virus were reported.

Zika virus emerged in Brazil in 2015 and was declared a national public health emergency after local researchers and physicians reported an increase in microcephaly cases.

In 2016, WHO declared the recent cluster of microcephaly cases and other neurological disorders reported in Brazil a global public health emergency. Similar clusters of microcephaly cases were also observed retrospectively in French Polynesia in 2014.

In 2015–16, Zika virus continued its spread to cause outbreaks in the Americas and the Pacific, and the first outbreaks were reported in continental USA, Africa, and southeast Asia.

Non-vector-borne transmission was confirmed and Zika virus was established as a cause of severe neurological complications in fetuses, neonates, and adults. This Review focuses on important updates and gaps in the knowledge of Zika virus as of early 2017.


November 3, 2017 at 8:20 am

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