Archive for December 22, 2016

Epidemiology of Chikungunya in the Americas

Journal of Infectious Diseases December 15, 2016 V.214 Suppl 5 S441-S44

Sergio Yactayo, J. Erin Staples, Véronique Millot, Laurence Cibrelus, and Pilar Ramon-Pardo

1Department of Pandemic and Epidemic Diseases, World Health Organization, Geneva, Switzerland

2Division of Vector-Borne Diseases, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado

3Department of International Health Regulations, Pan American Health Organization/World Health Organization, Washington D.C.

Abstract

Chikungunya virus (CHIKV) emerged in the Americas in late 2013 to cause substantial acute and chronic morbidity.

About 1.1 million cases of chikungunya were reported within a year, including severe cases and deaths.

The burden of chikungunya is unclear owing to inadequate disease surveillance and underdiagnosis. Virus evolution, globalization, and climate change may further CHIKV spread.

No approved vaccine or antiviral therapeutics exist. Early detection and appropriate management could reduce the burden of severe atypical and chronic arthritic disease.

Improved surveillance and risk assessment are needed to mitigate the impact of chikungunya.

PDF

http://jid.oxfordjournals.org/content/214/suppl_5/S441.full.pdf+html

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December 22, 2016 at 8:20 am

Genomic Epidemiology of Gonococcal Resistance to Extended-Spectrum Cephalosporins, Macrolides, and Fluoroquinolones in the United States, 2000–2013

Journal of Infectious Diseases November 15, 2016 V.214 N.10 P.1579-1587

Yonatan H. Grad, Simon R. Harris, Robert D. Kirkcaldy, Anna G. Green, Debora S. Marks, Stephen D. Bentley, David Trees, and Marc Lipsitch

1Department of Immunology and Infectious Diseases

2Center for Communicable Disease Dynamics, Department of Epidemiology, Harvard T. H. Chan School of Public Health

3Division of Infectious Diseases, Brigham and Women’s Hospital and Harvard Medical School

4Department of Systems Biology, Harvard Medical School, Boston, Massachusetts

5Centers for Disease Control and Prevention, Atlanta, Georgia

6Wellcome Trust Sanger Institute, Hinxton

7Department of Medicine, University of Cambridge and Addenbrookes Hospital, Cambridge, United Kingdom

Background

Treatment of Neisseria gonorrhoeae infection is empirical and based on population-wide susceptibilities. Increasing antimicrobial resistance underscores the potential importance of rapid diagnostic tests, including sequence-based tests, to guide therapy. However, the usefulness of sequence-based diagnostic tests depends on the prevalence and dynamics of the resistance mechanisms.

Methods

We define the prevalence and dynamics of resistance markers to extended-spectrum cephalosporins, macrolides, and fluoroquinolones in 1102 resistant and susceptible clinical N. gonorrhoeae isolates collected from 2000 to 2013 via the Centers for Disease Control and Prevention’s Gonococcal Isolate Surveillance Project.

Results

Reduced extended-spectrum cephalosporin susceptibility is predominantly clonal and associated with the mosaic penA XXXIV allele and derivatives (sensitivity 98% for cefixime and 91% for ceftriaxone), but alternative resistance mechanisms have sporadically emerged. Reduced azithromycin susceptibility has arisen through multiple mechanisms and shows limited clonal spread; the basis for resistance in 36% of isolates with reduced azithromycin susceptibility is unclear. Quinolone-resistant N. gonorrhoeae has arisen multiple times, with extensive clonal spread.

Conclusions

Quinolone-resistant N. gonorrhoeae and reduced cefixime susceptibility appear amenable to development of sequence-based diagnostic tests, whereas the undefined mechanisms of resistance to ceftriaxone and azithromycin underscore the importance of phenotypic surveillance. The identification of multidrug-resistant isolates highlights the need for additional measures to respond to the threat of untreatable gonorrhea.

PDF

http://jid.oxfordjournals.org/content/214/10/1579.full.pdf+html

December 22, 2016 at 8:18 am

Editor’s Choice: No Evidence That HIV-1 Subtype C Infection Compromises the Efficacy of Tenofovir-Containing Regimens: Cohort Study in the United Kingdom

Journal of Infectious Diseases November 1, 2016 V.214 N.9 P.1302-1308

Ellen White, Erasmus Smit, Duncan Churchill, Simon Collins, Clare Booth, Anna Tostevin, Caroline Sabin, Deenan Pillay, and David T. Dunn on behalf of the UK HIV Drug Resistance Database and UK Collaborative HIV Cohort Study

1MRC Clinical Trials Unit at UCL

2Department of Infection and Population Health

3Division of Infection and Immunity, University College London

4HIV i-Base

5Health Service Laboratories, Royal Free Hospital, London

6Public Health England, Birmingham Heartlands Hospital

7Brighton and Sussex Hospitals NHS Trust, United Kingdom

8Africa Centre for Population Health, University of KwaZulu-Natal, Durban, South Africa

Concern has been expressed that tenofovir-containing regimens may have reduced effectiveness in the treatment of human immunodeficiency virus type 1 (HIV-1) subtype C infections because of a propensity for these viruses to develop a key tenofovir-associated resistance mutation.

We evaluated whether subtype influenced rates of virological failure in a cohort of 8746 patients from the United Kingdom who received a standard tenofovir-containing first-line regimen and were followed for a median of 3.3 years.

In unadjusted analyses, the rate of failure was approximately 2-fold higher among patients infected with subtype C virus as compared to those with subtype B virus (hazard ratio [HR], 1.86; 95% confidence interval [CI], 1.50–2.31; P < .001). However, the increased risk was greatly attenuated in analyses adjusting for demographic and clinical factors (adjusted HR, 1.14; 95% CI, .83–1.58; P = .41).

There were no differences between subtypes C and subtypes non-B and non-C in either univariate or multivariate analysis. These observations imply there is no intrinsic effect of viral subtype on the efficacy of tenofovir-containing regimens.

PDF

http://jid.oxfordjournals.org/content/214/9/1302.full.pdf+html

 

J Infect Dis. (2016) 214 (9): 1289-1291

Editor’s Choice: HIV-1 Subtype C, Tenofovir, and the Relationship With Treatment Failure and Drug Resistance

Huldrych F. Günthard and Alexandra U. Scherrer

Division of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, University of Zurich and Institute of Medical Virology, Switzerland

Tenofovir disoproxil fumarate (TDF) has emerged as a cornerstone of initial antiretroviral therapy (ART) [1, 2].

However, human immunodeficiency virus type 1 (HIV) subtype C, the most prevalent worldwide subtype, accounting for >50% of all HIV infections, harbors polymorphisms in reverse transcriptase codons 64, 65, and 66, which lead to more-rapid in vitro selection of the K65R mutation [3], the signature mutation conferring resistance to TDF [4].

Subtype C viruses may only require a single point mutation at position 65 to select for K65R.

Several clinical studies have suggested that this mechanism may contribute to higher treatment failure rates and higher rates of the emergence of the K65R mutations observed in HIV subtype C–infected, compared with subtype B–infected, individuals treated with TDF-containing regimens [5–9], although others could not confirm different response rates between subtype B and C [10–12].

In this issue of The Journal of Infectious Diseases, White et al report a comprehensive study on this issue [13].

They analyzed data from the UK Collaborative HIV Cohort (CHIC) Study (available at: http://www.ukchic.org.uk) and included 8746 patients who had initiated ART containing TDF, plus lamivudine or emtricitabine and either a nonnucleoside reverse transcriptase inhibitor (NNRTI; efavirenz or nevirapine) or a ritonavir-boosted protease inhibitor (lopinavir, atazanavir, or darunavir), and were followed for a median of 3.3 years.

Unadjusted analyses indicated an approximately 2-fold higher virological failure rate for subtype C–infected individuals as compared to subtype B–infected individuals. However, when they adjusted …

PDF

http://jid.oxfordjournals.org/content/214/9/1289.full.pdf+html

December 22, 2016 at 8:17 am


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