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Infection prevention and control
Published in Nicola Neale, Joanne Sale, Developing Practical Nursing Skills, 2022
Another important feature of S. aureus is its ability to produce toxins, which, in turn, can have the ability to cause significant tissue damage. One of the most significant of these are the Panton-Valentine Leukocidin (PVL) toxin-producing strains that can cause septic arthritis and necrotising pneumonia. These may also be MRSA but commonly meticillin-sensitive strains are also isolated. Due to the serious nature of these infections, specific guidance in relation to the identification and management of PVL S. aureus has been published (HPA 2008).
Bacterial Skin and Soft Tissue Infections
Published in Firza Alexander Gronthoud, Practical Clinical Microbiology and Infectious Diseases, 2020
Community-acquired MRSA tends to be more virulent than hospital-acquired MRSA, may carry genes that encode the Panton–Valentine leucocidin (PVL) and is more common in the United States than in Europe. Gram-negative and anaerobic bacteria can be found in surgical-site infections and SSTIs in the perianal and inguinal area. Polymicrobial flora can be found in diabetic ulcers. In immunocompromised patients, Gram-negative bacteria should also be considered in cellulitis/erysipelas.
Genetic Engineering of Clostridial Strains for Cancer Therapy
Published in Ananda M. Chakrabarty, Arsénio M. Fialho, Microbial Infections and Cancer Therapy, 2019
Maria Zygouropoulou, Aleksandra Kubiak, Adam V. Patterson, Nigel P. Minton
Panton valentine leucocidin (PVL) is a p-pore-forming toxin from Staphylococcus aureus that causes leukocyte destruction and has an overall immunosuppressive action [110]. PVL was engineered in a strain of C. perfringens with the aim of diminishing host inflammatory responses and facilitating unhindered microbial replication in the tumors. This approach, although entirely opposite to the concept of cancer immunotherapy discussed previously, may be rational in light of the strain employed. C. perfringens is a highly pathogenic and phospholipase-C secreting strain with a residual oxygen tolerance that would allow it to germinate in tissues other than tumors [111]. It follows that C. perfringens is probably more visible to the immune system than other clostridial strains, eliciting an inflammatory response against itself and therefore minimizing the potential oncolytic benefit of the treatment.
Recent updates in the development of molecular assays for the rapid identification and susceptibility testing of MRSA
Published in Expert Review of Molecular Diagnostics, 2023
Masako Mizusawa, Karen C Carroll
The spread of MRSA occurred initially through healthcare contact only. The very first epidemic MRSA clone (archaic clone or phage type 83A) circulated in hospitals throughout Europe until the 1970s [18,19]. The rest of the world was largely spared except for isolated reports of MRSA from hospitals in the U.S.A. [19]. MRSA began to decline in Europe in the 1970s and early 1980s with disappearance of the archaic clone for unclear reasons [20]. This decline was followed by emergence of novel MRSA lineages and those strains became endemic worldwide [19]. In the early 1990s MRSA infections started to emerge in the community among those with no history of prior hospitalization [20]. The community-associated MRSA (CA-MRSA) strains were predominantly isolated from skin and soft infections [21]. Although infections caused by CA-MRSA were commonly mild, it has also caused severe infections such as necrotizing fasciitis and necrotizing pneumonia [21]. This observation was associated with presence of the lukSF genes encoding a toxin called Panton-Valentine leukocidin (PVL), a cytotoxin that causes tissue necrosis and leukocyte destruction [21].
A case report: septic shock due to (tropical) pyomyositis and multiple metastatic embolisms caused by Panton Valentine Leukocidin-positive methicillin-sensitive staphylococcus aureus in a 12-year-old boy
Published in Acta Clinica Belgica, 2022
Valérie Vanbiervliet, Ignace Demeyer, Filip Claus, Kristien Van Vaerenbergh
Staphylococcus aureus (S. aureus) is an important human pathogen and it causes various types of infections, both in nosocomial and community setting. Based on methicillin susceptibility, it is divided into two major groups: methicillin-susceptible S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA). Numerous virulence factors enable the organism to be a successful pathogen through different mechanisms of action. An important virulence factor is Panton-Valentine Leukocidin toxin (PVL). PVL is a membrane pore-forming protein responsible for cell leakage and cell death. PVL producing S. aureus causes more severe infections. Although commonly associated with community-acquired methicillin-resistant S. aureus (CA-MRSA), several outbreaks due to methicillin-susceptible S. aureus have been reported [1].
Prevalence, clinical expression, invasiveness and outcome of Staphylococcus aureus containing Panton-Valentine leukocidin in children treated in a university hospital of Lithuania
Published in Infectious Diseases, 2020
Birute Petraitiene, Pablo Rojo Conejo, Lina Jankauskaite, Rimantas Kevalas, Giedre Trumpulyte, Ausra Snipaitiene, Astra Vitkauskiene, Vaidotas Gurskis
Staphylococcus aureus (S. aureus) is a significant cause of purulent infections, prevalent in both community and hospital acquired settings. It can produce several types of exotoxins differing in their effect [1]. Panton-Valentine leukocidin (PVL) is one of the S. aureus’s synergohymenotropic exotoxin belonging to pore-forming toxin family [2]. PVL consists of two subunits; LukF-PV and LukS-PV proteins, that act synergistically to induce a strong lytic effect on host defence cells, notably with polymorphonuclear leucocytes but especially on neutrophils [2]. Research shows that the pvl gene can be transmitted via bacteriophages from one strain to another [3,4]. PVL positive S. aureus [SA-PVL(+)] is most commonly isolated strain from previously immunocompetent older children and young adults [5,6]. SA-PVL(+) is the predominant causes of skin and soft tissue infections (SSTIs) [7–9], but can also cause severe invasive conditions such as osteoarthritis [10], pyomyositis [11], necrotizing fasciitis [12], necrotizing pneumonia [13] and sepsis [14]. PVL’s impact in respect to invasiveness and infection severity is complex [15,16]. An increasing body of research demonstrates that SA-PVL(+) strains are associated with less invasive infections [7,17]. However, in case of invasive SA-PVL(+) infections, clinical manifestation is more severe [10–14,18].