Current Molecular Epidemiology of Methicillin-Resistant Staphylococcus aureus in Elderly French People: Troublesome Clones on the Horizon.

In 2015, we conducted at 44 healthcare facilities (HCFs) and 21 nursing homes (NHs) a 3-month bloodstream infection (BSI) survey, and a 1-day prevalence study to determine the rate of carriage of methicillin-resistant Staphylococcus aureus (MRSA) in 891 patients and 470 residents. We investigated the molecular characteristics of the BSI-associated and colonizing MRSA isolates, and assessed cross-transmission using double-locus sequence typing and pulsed-field gel electrophoresis protocol. The incidence of MRSA-BSI was 0.040/1000 patient-days (19 cases). The prevalence of MRSA carriage was 4.2% in patients (n = 39) and 8.7% in residents (n = 41) (p < 0.001). BSI-associated and colonizing isolates were similar: none were PVL-positive; 86.9% belonged to clonal complexes 5 and 8; 93.9% were resistant to fluoroquinolones. The qacA/B gene was carried by 15.8% of the BSI-associated isolates [3/3 BSI cases in intensive care units (ICUs)], and 7.7% of the colonizing isolates in HCFs. Probable resident-to-resident transmission was identified in four NHs. Despite generally reassuring results, we identified two key concerns. First, a worryingly high prevalence of the qacA/B gene in MRSA isolates. Antisepsis measures being crucial to prevent healthcare-associated infections, our findings raise questions about the potential risk associated with chlorhexidine use in qacA/B(+) MRSA carriers, particularly in ICUs. Second, NHs are a weak link in MRSA control. MRSA spread was not controlled at several NHs; because of their frequent contact with the community, conditions are favorable for these NHs to serve as reservoirs of USA300 clone for local HCFs

Human Origin for Livestock-Associated Methicillin-Resistant Staphylococcus aureus

ABSTRACT Methicillin-resistant Staphylococcus aureus (MRSA) is a major cause of human morbidity and mortality worldwide. The emergence in the last decade of a livestock-associated MRSA (LA-MRSA) clone which also has the capacity to cause zoonotic infections in humans has raised important questions regarding its origin and its potential to cause human epidemics. An important study by L. B. Price et al. [mBio 3(1):e00305-11, 2012] provides evidence for a human ancestral origin for LA-MRSA, raising concerns about agricultural practices that may have contributed to its emergence and expansion. The study highlights the potential for comparative whole-genome sequencing of closely related strains to provide valuable insights into the evolutionary history of bacterial pathogens. The emergence in the last decade of a livestock-associated methicillin-resistant clone of Staphylococcus aureus (LA-MRSA) that can cause zoonotic disease in humans has been a major public health concern. A paper published by Price et al. addresses the evolutionary origin of the LA-MRSA multilocus sequence type 398 (ST398) strains (1). ST398 strains were first identified in France in 2005 but subsequently came to prominence in the Netherlands as a common component of the skin microbiom

phiD12-Like Livestock-Associated Prophages Are Associated With Novel Subpopulations of Streptococcus agalactiae Infecting Neonates

Group B Streptococcus (GBS) is a major cause of invasive disease in neonates worldwide. Monitoring data have revealed a continuing trend toward an increase in neonatal GBS infections, despite the introduction of preventive measures. We investigated this trend, by performing the first ever characterization of the prophage content for 106 GBS strains causing neonatal infections between 2002 and 2018. We determined whether the genome of each strain harbored prophages, and identified the insertion site of each of the prophages identified. We found that 71.7% of the strains carried at least one prophage, and that prophages genetically similar to livestock-associated phiD12, carrying genes potentially involved in GBS pathogenesis (e.g., genes encoding putative virulence factors and factors involved in biofilm formation, bacterial persistence, or adaptation to challenging environments) predominated. The phiD12-like prophages were (1) associated with CC17 and 1 strains (p = 0.002), (2) more frequent among strains recovered during the 2011–2018 period than among those from 2002–2010 (p < 0.001), and (3) located at two major insertion sites close to bacterial genes involved in host adaptation and colonization. Our data provide evidence for a recent increase in lysogeny in GBS, characterized by the acquisition, within the genome, of genetic features typical of animal-associated mobile genetic elements by GBS strains causing neonatal infection. We suggest that lysogeny and phiD12-like prophage genetic elements may have conferred an advantage on GBS strains for adaptation to or colonization of the maternal vaginal tract, or for pathogenicity, and that these factors are currently playing a key role in the increasing ability of GBS strains to infect neonates

Marked increase in incidence for bloodstream infections due to Escherichia coli, a side effect of previous antibiotic therapy in the elderly.

We conducted a survey including 3334 bloodstream infections (BSIs) due to E. coli diagnosed in 2005-2014 at a stable cohort of hospitals. Marked increases in incidence were observed for community-acquired (CA) BSIs in patients aged >75 years, CA-BSIs of digestive origin in patients aged 60-74 years, healthcare-associated BSIs, and BSIs associated with ESBL (extended-spectrum B-lactamase)-producing E. coli (ESBLEc). Using MLST, we studied the genetic diversity of 412 BSI isolates recovered during the 2014 survey: 7 major sequence type complexes (STCs) were revealed in phylogenetic group B2, 3 in group A/B1 and 2 in group D. Among the 31 ESBLEc isolates, 1/3 belonged to STC 131. We searched for possible associations between clonal groups, clinical determinants and characteristics of BSIs: isolates from groups B2 (except STC 131) and D were susceptible to antibiotics and associated with BSIs of urinary origin in patients <60 years. STC 131 and group A/B1 isolates were multi-drug resistant and associated with CA-BSIs of digestive origin in patients aged 60-74 with a recent history of antibiotic treatment. STC 131 isolates were associated with HCA-BSIs in patients with recent/present hospitalization in a long-stay unit. We provide a unique population-based picture of the epidemiology of E. coli BSI. The aging nature of the population led to an increase in the number of cases caused by the B2 and D isolates generally implicated in BSIs. In addition, the association of a trend toward increasing rates of gut colonization with multi drug-resistant isolates revealed by the rise in the incidence of BSIs of digestive origin caused by STC 131 and A/B1 (STCs 10, 23, and 155) isolates, and a significant increase in the frequency of BSIs in elderly patients with recent antibiotic treatment suggested that antibiotic use may have contributed to the growing incidence of BSI

Methicillin-Susceptible ST398 Staphylococcus aureus Responsible for Bloodstream Infections: An Emerging Human-Adapted Subclone?

In the course of an annual 3-month bloodstream infections (BSI) survey conducted during a four-year period in 31 healthcare institutions located in three noncontiguous French regions, we report 18 ST398 Staphylococcus aureus BSI. ST398 BSI incidence showed a seven-fold increase during the study period (0.002 per 1,000 patient days in 2007 vs. 0.014 in 2010). ST398 BSI isolates differed from the pig-borne multiresistant clone: 17/18 BSI isolates were methicillin susceptible and none was of t011, t034 or t108 pig-borne spa-types. ST398 BSI isolates had homogenous resistance patterns (15/18 with only Eryr) and prophagic content (all harboured the hlb-converting Sau3int phage). The clustering of BSI and pig-borne isolates by spa-typing and MLVA, the occurrence of Sau3int phage in BSI isolates and the lack of this phage in pig-borne isolates suggest that the emergence of BSI isolates could have arisen from horizontal transfer, at least of the Sau3int phage, in genetically diverse MSSA ST398 isolates. The acquisition of the phage likely plays a role in the increasing ability of the lysogenic ST398 isolates to colonize human. The mode of acquisition of the non pig-borne ST398 isolates by our 18 patients remains unclear. ST398 BSI were diagnosed in patients lacking livestock exposure and were significantly associated with digestive portals of entry (3/18 [16.7%] for ST398 vs. 19/767 [2.5%] for non ST398 BSI; p = .012). This raises the question of possible foodborne human infections. We suggest the need for active surveillance to study and control the spread of this human-adapted subclone increasingly isolated in the hospital setting

Methicillin-resistant Staphylococcus aureus Toxic Shock Syndrome

Case ReportsLetterSCOPUS: le.jinfo:eu-repo/semantics/publishe

Temperate Prophages Increase Bacterial Adhesin Expression and Virulence in an Experimental Model of Endocarditis Due to Staphylococcus aureus From the CC398 Lineage.

Until 2007, Staphylococcus aureus from clonal complex 398 (CC398) was exclusively associated with livestock species and companion animals. Recently, several studies described the emergence of S. aureus CC398 as etiologies of severe infections in humans living in an animal-free environment. Recent sequencing efforts showed that the mobile genetic elements found in CC398 isolates were specific for each population and enabled differentiation of strains responsible for asymptomatic colonization from strains involved in bloodstream infections. We mobilized prophages from a human CC398 isolate and introduced them into two naïve ancestral isolates devoid of prophages that exclusively colonize animals. These lysogenized ancestral CC398 isolates acquired features related to virulence, such as an increased capacity to adhere to human extracellular matrix proteins and the ability to invade and survive within non-phagocytic cells. Pathogenicity of several clinical isolates from the CC398 lineage as well as ancestral and in vitro lysogenized ancestral counterparts was assessed in a model of infectious endocarditis in rats. Natural and artificial lysogens were not only more invasive than their prophage-free parent but also showed an increased capacity to multiply within aortic vegetations. This study identified prophages as mediators of bacterial virulence in a model of infectious endocarditis, probably through promotion of interaction with extracellular matrix components. Further studies are needed to identify mechanisms leading to promotion of intrinsic virulence