Archive for September 22, 2014

Antimicrobial activity of a novel adhesive containing chlorhexidine gluconate (CHG) against the resident microflora in human volunteers

Journal of Antimicrobial Chemotherapy AUG 2014 V.69 N.8 P.2224-2229

Neal Carty1,*, Anne Wibaux1, Colleen Ward1, Daryl S. Paulson2 and Peter Johnson1

1Vancive Medical Technologies™, 20 N. Wacker Drive Suite 2240, Chicago, IL 60606, USA

2BioScience Laboratories, Inc., 1765 S. 19th Avenue, Bozeman, MT 59718, USA

*Corresponding author. Tel: +1-440-534-3515; Fax: +1 440 534 2955; E-mail:


To evaluate the antimicrobial activity of a new, transparent composite film dressing, whose adhesive contains chlorhexidine gluconate (CHG), against the native microflora present on human skin.


CHG-containing adhesive film dressings and non-antimicrobial control film dressings were applied to the skin on the backs of healthy human volunteers without antiseptic preparation. Dressings were removed 1, 4 or 7 days after application. The bacterial populations underneath were measured by quantitative cultures (cylinder-scrub technique) and compared with one another as a function of time.


The mean baseline microflora recovery was 3.24 log10 cfu/cm2. The mean log reductions from baseline measured from underneath the CHG-containing dressings were 0.87, 0.78 and 1.30 log10 cfu/cm2 on days 1, 4 and 7, respectively, compared with log reductions of 0.67, −0.87 and −1.29 log10 cfu/cm2 from underneath the control film dressings. There was no significant difference between the log reductions of the two treatments on day 1, but on days 4 and 7 the log reduction associated with the CHG adhesive was significantly higher than that associated with the control adhesive.


The adhesive containing CHG was associated with a sustained antimicrobial effect that was not present in the control. Incorporating the antimicrobial into the adhesive layer confers upon it bactericidal properties in marked contrast to the non-antimicrobial adhesive, which contributed to bacterial proliferation when the wear time was ≥4 days.


September 22, 2014 at 2:41 pm

Pitfalls in evidence assessment: the case of chlorhexidine and alcohol in skin antisepsis

Journal of Antimicrobial Chemotherapy AUG 2014 V.69 N.8 P.2017-2021

Matthias Maiwald1,2,3,* and Edwin S.-Y. Chan3,4,5

1Department of Pathology and Laboratory Medicine, KK Women’s and Children’s Hospital, Singapore

2Department of Microbiology, National University of Singapore, Singapore

3Duke-NUS Graduate Medical School, Singapore

4Singapore Clinical Research Institute, Singapore

5Singapore Branch, Australasian Cochrane Centre, Singapore

*Corresponding author. Department of Pathology and Laboratory Medicine, KK Women’s and Children’s Hospital, 100 Bukit Timah Road, Singapore 229899, Singapore. Tel: +65 6394 8725; Fax: +65 6394 1387; E-mail:

Chlorhexidine has attracted increasing attention for its role in skin antisepsis in recent years.

It was tested in several prominent clinical trials and subsequently recommended in important guidelines for blood culture collection, vascular catheter insertion and surgical skin preparation.

We noticed and subsequently reported a widespread misinterpretation of evidence surrounding chlorhexidine and its role in skin antisepsis.

Multiple clinical trial reports and systematic reviews that had assessed the clinical efficacy of chlorhexidine/alcohol combinations for skin antisepsis had attributed efficacy solely to the chlorhexidine component.

This misinterpretation was carried over into the tertiary literature, including evidence-based guidelines.

Here we discuss some of the scientific, ethical, patient safety and infection control implications of this misinterpretation, as well as broader implications for evidence-based medicine.


September 22, 2014 at 2:37 pm

Infrequent Recovery of HIV from but Robust Exogenous Infection of Activated CD4+ T Cells in HIV Elite Controllers

Clin Infect Dis. July 15, 2010 V.51 N.2P.233-238

Julg1, F. Pereyra1, M. J. Buzón3, A. Piechocka-Trocha1,2, M. J. Clark1, B. M. Baker1, J. Lian1, T. Miura1,2,5, J. Martinez-Picado3,4, M. M. Addo1, and B. D. Walker1,2

1Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard, Boston, Massachusetts

2Howard Hughes Medical Institute, Chevy Chase, Maryland

3irsiCaixa Foundation, Hospital Universitari Germans Trias i Pujol, Badalona, Spain

4Institució Catalana de Recerca i Estudis Avançats, Barcelona, Spain

5Institute of Medical Science, University of Tokyo, Tokyo, Japan

Reprints or correspondence: Dr Bruce D. Walker, Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, 149 Thirteenth St, Charlestown, MA 02129 (



Human immunodeficiency virus (HIV) elite controllers are able to control infection with HIV-1 spontaneously to undetectable levels in the absence of antiretroviral therapy, but the mechanisms leading to this phenotype are poorly understood. Although low frequencies of HIV-infected peripheral CD4+ T cells have been reported in this group, it remains unclear to what extent these are due to viral attenuation, active immune containment, or intracellular host factors that restrict virus replication.


We assessed proviral DNA levels, autologous viral growth from and infectability of in vitro activated, CD8+ T cell—depleted CD4+ T cells from HIV elite controllers (mean viral load, <50 copies/mL), viremic controllers (mean viral load, <2000 copies/mL), chronic progressors, and individuals receiving highly active antiretroviral therapy.


Although we successfully detected autologous virus production in ex vivo activated CD4+ T cells from all chronic progressors and from most of the viremic controllers, we were able to measure robust autologous viral replication in only 2 of 14 elite controllers subjected to the same protocol. In vitro activated autologous CD4+ T cells from elite controllers, however, supported infection with both X4 and R5 tropic HIV strains at comparable levels to those in CD4+ T cells from HIV-uninfected subjects. Proviral DNA levels were the lowest in elite controllers, suggesting that extremely low frequencies of infected cells contribute to difficulty in isolation of virus.


These data indicate that elite control is not due to inability of activated CD4+ T cells to support HIV infection, but the relative contributions of host and viral factors that account for maintenance of low-level infection remain to be determined.


September 22, 2014 at 2:31 pm

How Do HIV Elite Controllers Do What They Do?

Clin Infect Dis. July 15, 2010 V.51 N.2P.239-241

Editorial Commentary

Michael Saag1 and Steven G. Deeks2

1University of Alabama at Birmingham, Birmingham, Alabama

2San Francisco General Hospital, University of California, San Francisco, California

Reprints or correspondence: Dr Michael Saag, Center for AIDS Research, University of Alabama at Birmingham, 845 19th St South, BBRB 256, Birmingham, AL 35294-2170 (

Soon after the initial discovery of human immunodeficiency virus (HIV) as the cause of AIDS, a small group of HIV-infected patients were identified who did not seem to progress immunologically toward AIDS.

These “long-term nonprogressors” were initially defined on the basis of their ability to maintain high CD4 cell counts over many years in the absence of antiretroviral therapy [1].

Over the past decade, many of the long-term nonprogressors exhibited slow progression to lower CD4 cell counts, a process that was predicted in part by their level of viremia.

This prompted further refinement of the “nonprogressor” phenotype into one that was based primarily on viral load, with most studies now focusing on those who have undetectable viremia using conventional assays (HIV RNA <50 copies/mL, “elite controllers”) and those who have low but detectable viremia (HIV RNA <2000 copies/mL, “viremic controllers”) [2, 3].

It is widely hoped that knowledge gained regarding the mechanism of virus control could informboth the vaccine and the HIV eradication efforts…


September 22, 2014 at 2:30 pm


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