Clinical Correlates of Panton‐Valentine Leukocidin (PVL), PVL Isoforms, and Clonal Complex in theStaphylococcus aureusPopulation of Northern Australia

Abstract

PVL(+) and PVL(-) infections are clearly distinct. MSSA contributes a large but underrecognized burden of PVL(+) disease. Compared with elsewhere in the world, there is a relative abundance of the clade that contains CC93 and CC121 in both northern Australia and Asia.

Presence of Genes Encoding Panton-Valentine Leukocidin Is Not the Primary Determinant of Outcome in Patients with Hospital-Acquired Pneumonia Due to Staphylococcus aureus

“…Less than 10% of the S. aureus HAP isolates in this study contained pvl. This relatively low prevalence stands in sharp contrast to trends seen in soft tissue infections (1,45) as well as in a pneumonia study in children (6).…”

Molecular Characterization and Panton-Valentine Leucocidin Typing of Community-Acquired Methicillin-Sensitive Staphylococcus aureus Clinical Isolates

“…These strains are genetically similar in susceptibility and toxin profile, as well as spa type, to the recently described ST22 PVL-MRSA United Kingdom strains, rather than the predominant hospital-acquired MRSA (HA-MRSA) ST22 EMRSA-15 clone (5). This study observed the previously noted geographical and clonal bias in the distribution of the PVL haplotypes, with the R haplotype limited to a few lineages, predominantly in the United States and more recently Australia (22,29). Due to previous reports of R haplotypes being found in the United Kingdom in significant numbers of MRSA strains (4,24), the dearth of R haplotypes in this small study population may reflect more on the methicillin susceptibility of the isolates rather than geographical location.…”

“…Represented among the MSSA isolates in this study were major sequence types (ST22, ST88, ST30, and ST1) associated with PVL-MRSA clones (21,27,29). Though the majority of PVL-MRSA clones circulating in the United Kingdom belong to either ST8, ST30, or ST80 (13, 17, 23), the predominant group described in this study, ST22, also constitute a significant burden of infection (13).…”

“…With clinical and epidemiological characteristics similar to those of CA-MRSA (9,25), PVL-MSSA may represent a hitherto-unrecognized, overlooked emerging public health threat. Several studies have recently attempted to address this information imbalance (7,21,27,29); however, only two of these reported on PVL gene polymorphisms and their implications (7,29). In addition to contributing to the limited molecular typing data on PVL-MSSA strains, this study sought to explore PVL gene polymorphisms and phage distribution in this group and how this relates with those previously observed in PVL-MRSA strains.…”

“…A nonsynonymous mutation at position 527, however, serves as the basis of the H and R isoforms (2,12,22,28). Currently, though most research is focused on PVL-positive MRSA (PVL-MRSA), a rising incidence of PVL-positive, methicillin-sensitive S. aureus (PVL-MSSA) infections reported recently is the main contributing factor in the increased incidence of PVL-positive strains in some locales, with approximately 60% of total PVL-positive S. aureus isolates in England in the past 5 years found to be susceptible to methicillin (6,16,29). With clinical and epidemiological characteristics similar to those of CA-MRSA (9,25), PVL-MSSA may represent a hitherto-unrecognized, overlooked emerging public health threat.…”