Archive for February 23, 2017

The Brief Case: A Reactive HIV Rapid Antibody Test in a Pregnant Woman

Journal of Clinical Microbiology April 2016 V.54 N.4 P.826-828

Melanie L. Yarbrough and Neil W. Anderson

A 32-year-old pregnant woman presented to her obstetrician for routine prenatal care during her 3rd month of pregnancy. She reported no major health concerns, with the exception of mild morning sickness that had been gradually improving. Upon physical examination, she appeared healthy and her vitals were stable and within normal limits.

Abdominal ultrasound revealed reassuring fetal heart tones, and her remaining physical exam was unremarkable.

She was counseled regarding the need for several routine prenatal laboratory tests, including testing for human immunodeficiency virus (HIV), to which she agreed.

A rapid HIV test performed in the obstetrician’s office was positive for antibodies against HIV.

The positive rapid antibody result was shared with the patient. She denied any risk factors for HIV infection, including intravenous drug use and sex with multiple partners.

The obstetrician stressed that the results were only preliminary and required confirmatory testing. Prior to sending the patient home, a blood sample was drawn for submission to the local clinical laboratory for additional testing. The obstetrician called the laboratory asking how long it would take for the Western blot confirmatory test to be performed.

A representative from the testing laboratory informed him that they now used the fourth-generation algorithm and therefore no longer performed confirmatory testing by Western blot assay….

PDF

http://jcm.asm.org/content/54/4/826.full.pdf

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February 23, 2017 at 7:54 am

Selective Conditions for a Multidrug Resistance Plasmid Depend on the Sociality of Antibiotic Resistance

Antimicrobial Agents and Chemotherapy April 2016 V.60 N.4 P.2524-2527

Michael J. Bottery, A. Jamie Wood, and Michael A. Brockhurst

aDepartment of Biology, University of York, York, United Kingdom

bDepartment of Mathematics, University of York, York, United Kingdom

Multidrug resistance (MDR) plasmids frequently carry antibiotic resistance genes conferring qualitatively different mechanisms of resistance.

We show here that the antibiotic concentrations selecting for the RK2 plasmid in Escherichia coli depend upon the sociality of the drug resistance: the selection for selfish drug resistance (efflux pump) occurred at very low drug concentrations, just 1.3% of the MIC of the plasmid-free antibiotic-sensitive strain, whereas selection for cooperative drug resistance (modifying enzyme) occurred at drug concentrations exceeding the MIC of the plasmid-free strain.

PDF

http://aac.asm.org/content/60/4/2524.full.pdf

February 23, 2017 at 7:52 am

Rapid Emergence and Evolution of Staphylococcus aureus Clones Harboring fusC-Containing Staphylococcal Cassette Chromosome Elements

Antimicrobial Agents and Chemotherapy April 2016 V.60 N.4 P.2359-2365

Sarah L. Baines, Benjamin P. Howden, Helen Heffernan, Timothy P. Stinear, Glen P. Carter, Torsten Seemann, Jason C. Kwong, Stephen R. Ritchie, and Deborah A. Williamson

aDoherty Applied Microbial Genomics, Department of Microbiology & Immunology, The University of Melbourne at The Doherty Institute for Infection and Immunity, Melbourne, Australia

bMicrobiological Diagnostic Unit Public Health Laboratory, Department of Microbiology & Immunology, The University of Melbourne at The Doherty Institute for Infection and Immunity, Melbourne, Australia

cInfectious Diseases Department, Austin Health, Melbourne, Australia

dInstitute of Environmental Science and Research, Wellington, New Zealand

eVictorian Life Sciences Computation Initiative, The University of Melbourne, Melbourne, Australia

fSchool of Medical Sciences, University of Auckland, Auckland, New Zealand

The prevalence of fusidic acid (FA) resistance among Staphylococcus aureus strains in New Zealand (NZ) is among the highest reported globally, with a recent study describing a resistance rate of approximately 28%.

Three FA-resistant S. aureus clones (ST5 MRSA, ST1 MSSA, and ST1 MRSA) have emerged over the past decade and now predominate in NZ, and in all three clones FA resistance is mediated by the fusC gene. In particular, ST5 MRSA has rapidly become the dominant MRSA clone in NZ, although the origin of FA-resistant ST5 MRSA has not been explored, and the genetic context of fusC in FA-resistant NZ isolates is unknown.

To better understand the rapid emergence of FA-resistant S. aureus, we used population-based comparative genomics to characterize a collection of FA-resistant and FA-susceptible isolates from NZ. FA-resistant NZ ST5 MRSA displayed minimal genetic diversity and represented a phylogenetically distinct clade within a global population model of clonal complex 5 (CC5) S. aureus.

In all lineages, fusC was invariably located within staphylococcal cassette chromosome (SCC) elements, suggesting that SCC-mediated horizontal transfer is the primary mechanism of fusC dissemination.

The genotypic association of fusC with mecA has important implications for the emergence of MRSA clones in populations with high usage of fusidic acid. In addition, we found that fusC was colocated with a recently described virulence factor (tirS) in dominant NZ S. aureus clones, suggesting a fitness advantage.

This study points to the likely molecular mechanisms responsible for the successful emergence and spread of FA-resistant S. aureus.

PDF

http://aac.asm.org/content/60/4/2359.full.pdf

February 23, 2017 at 7:51 am

Infectious complications in chronic lymphocytic leukemia.

Mediterr J Hematol Infect Dis. 2012;4(1):e2012070. doi: 10.4084/MJHID.2012.070. Epub 2012 Nov 5.

Nosari A1.

Author information

1Divisione di Ematologia, Niguarda Ca’ Granda Hospital, Piazza Ospedale Maggiore 3 – 20162 Milano, Italy. Tel: 39-02-64442668.

Abstract

Infectious complications have been known to be a major cause of morbidity and mortality in Chronic Lymphocytic Leukemia (CLL) patients who are prone to infections because of both the humoral immunodepression inherent to the hematologic disease and to the immunosuppression related to the therapy.

The majority of infections in CLL patients treated with alkilating agents is of bacterial origin. The immunodeficiency and natural infectious history of alkylator-resistant, corticosteroid-treated patients appears to have changed with the administration of purine analogs, which has been complicated by very severe and unusual infections and also more viral infections due to sustained reduction of CD4-positive T lymphocytes.

The subsequent introduction of monoclonal antibodies in therapies, in particular alemtuzumab, further increased the immunodepression, increasing also infections which appeared more often in patients with recurrent neutropenia due to chemotherapy cycles.

Epidemiological data regarding fungal infections in lymphoproliferative disorders are scarce.

Italian SEIFEM group in a retrospective multicentre study regarding CLL patients reported an incidence of mycoses 0.5%; however, chronic lymphoproliferative disorders emerged as second haematological underlying disease after acute leukemia in a French study on aspergillosis; in particular CLL with aspergillosis accounted for a third of these chronic lymphoproliferative diseases presenting mould infection.

PDF

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507529/pdf/mjhid-4-1-e2012070.pdf

February 23, 2017 at 7:49 am


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