Corrigendum to 'Panton-Valentine Leucocidin (PVL) Staphylococcus aureus a position statement from the International Society of Chemotherapy' [International Journal of Antimicrobial Agents 51/1 (2018) 16-25] (original) (raw)
Related papers
Necrotising pneumonia due to Panton Valentine Leukocidin Staphylococcus aureus
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Culture by two genes, luk-S-PV and luk-F-PV, and transferred between strains of S. aureus by bacteriophage. A heterogeneous mix of MSSA and MRSA strains carrying the genes for PVL production is spreading throughout Europe. Sporadic cases and small outbreaks have been reported in the UK, some spreading within hospitals, as has the emergence of new stains of PVL producing communityassociated MRSA (CA-MRSA) now appearing in animals. Less than 2% of strains of S. aureus from invasive infections submitted to the Health Protection Agency (HPA) produced PVL 5. A bi-component toxin, structurally similar to gamma-haemolysin, PVL comprises two sub-units (F & S) that together are leukocidal and dermonecrotic. Of S. aureus from invasive infections submitted to HPA, 1.6% of strains produced PVL, of which 46% were MRSA 5 .
Journal of Clinical Microbiology, 2005
Staphylococcus aureus isolates carrying the genes that encode for Panton-Valentine leucocidin (PVL), a highly potent toxin, have been responsible for recent outbreaks of severe invasive disease in previously healthy children and adults in the United States of America and Europe. To determine the frequency of PVL-positive isolates sent to the Staphylococcus Reference Unit (United Kingdom) for epidemiological purposes, we tested 515 isolates of S. aureus, and 8 (1.6%) were positive for the PVL locus. A further 470 isolates were selected to explore the association of PVL-positive S. aureus with clinical disease. Of these, 23 (4.9%) were PVL positive and most were associated with skin and soft tissue infections (especially abscesses). The PVL genes were also detected in isolates responsible for community-acquired pneumonia, burn infections, bacteremia, and scalded skin syndrome. Genotyping by pulsed-field gel electrophoresis and multilocus sequence typing revealed that the PVL-positive isolates were from diverse genetic backgrounds, although one prevalent clone of 12 geographically dispersed methicillin-resistant S. aureus (MRSA) isolates was identified (ST80). All 12 isolates were stapylococcal cassette chromosome mec type IVc, had an agr3 allele, and shared a common toxin gene profile (sea-see, seg-sej, eta, etb, and tst negative but etd positive). ST80 strains with similar genetic characteristics have been responsible for community-acquired infections in France and Switzerland. The remaining PVL-positive isolates were mostly methicillin-sensitive S. aureus and belonged to 12 different sequence types, including ST22 and ST30, which are closely related to the most prevalent MRSA clones in United Kingdom hospitals, EMRSA-15 and EMRSA-16, respectively. Staphylococcus aureus is a very successful hospital and community-acquired pathogen. It causes a broad spectrum of disease, from mild skin infections to more serious invasive infections, including septicemia, pneumonia, endocarditis, and deep-seated abscesses. Pathogenicity is related to a number of virulence factors that allow it to adhere to surfaces, invade or avoid the immune system, and cause harmful toxic effects to the host. These factors include cell surface components (e.g., protein A, fibronectin-binding protein, collagen-binding protein, and clumping factor), and exoproteins (e.g., enterotoxins, exfoliatins, toxic shock syndrome toxin, and Panton-Valentine leucocidin [PVL]). PVL is a pore-forming cytotoxin that targets human and rabbit mononuclear and polymorphonuclear cells (37). When injected intradermally into rabbits, it induces severe inflammatory lesions, leading to capillary dilation, chemotaxis, polymorphonuclear karyorrhexis, and skin necrosis (44). Studies have shown that its toxic effect results from the synergistic action of two separate exoproteins, namely, LukS-PV and LukF-PV. These proteins are encoded by two contiguous and cotranscribed genes (lukS-PV and lukF-PV) (36), which are carried on temperate bacteriophages (20). Lysogenic conversion of PVLnegative strains of S. aureus leading to the production of the toxin has been demonstrated (29).
Panton-Valentine leukocidin in community and hospital-acquired Staphylococcus aureus strains
Biotechnology & Biotechnological Equipment, 2014
Staphylococcus aureus causes serious hospital-acquired (HA) and community acquired (CA) infections. Skin and softtissue infections especially are sometimes caused by strains harbouring Panton-Valentine leukocidin (PVL). PVL belongs to a family of bi-component leukocidal toxins produced by staphylococci. It is a pore forming toxin encoded by lukF-PV and lukS-PV. A total of 70 S. aureus strains: 38 (54%) methicillin-resistant (MRSA) and 32 (46%) methicillin-susceptible (MSSA), were isolated from patients admitted to Dicle University Hospital (Turkey). Identification of S. aureus and antibiotics-susceptibility testing were performed with PHOENIX 100. PVL genes and mecA genes were detected by polymerase chain reaction. Of the 70 studied strains, 36 ones (51%) were community acquired and 34 ones (49%) were hospital acquired . A total of 38 (54%) strains were positive for mecA (mecAC), of which 32 ones (84%) were HA. Of the mecA strains, 30 (94%) were CA. Of the 70 studied strains, 12 (17%) strains were PVLC: 8 (22%) of the 36 CA strains and 4 (12%) of the 34 HA strains. Of the 12 PVLC strains, 4 strains were mecAC. The PVL positivity rate was 25% in MSSA, whereas 10.5% in MRSA. Of the overall PVLC strains, seven strains were obtained from wounds; four ones from skin abscess; and one from blood culture. Taken together, the obtained results showed a substantial level of PVL genes in the studied region. Although PVL is known as a common virulence factor of CA MRSA, HA MRSA isolates in our study showed a considerable rate of PVL positivity. Keywords: Staphylococcus aureus; Panton-Valentine leukocidin; MRSA; MSSA
Staphylococcus aureus, Panton-Valentine leukocidin, and necrotising pneumonia
BMJ, 2005
The Staphylococcus aureus Panton Valentine leukocidin (PVL) is a pore-forming toxin secreted by strains epidemiologically associated with the current outbreak of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and with the often lethal necrotizing pneumonia. To investigate the role of PVL in pulmonary disease, we tested the pathogenicity of clinical isolates, isogenic PVL-negative and PVL-positive S. aureus strains, as well as purified PVL, in a mouse acute pneumonia model. Here we show that PVL is sufficient to cause pneumonia and that the expression of this leukotoxin induces global changes in transcriptional levels of genes encoding secreted and cell-wall-anchored staphylococcal proteins, including the lung inflammatory factor staphylococcal protein A (Spa).
Journal of Clinical Microbiology, 2005
Staphylococcus aureus isolates carrying the genes that encode for Panton-Valentine leucocidin (PVL), a highly potent toxin, have been responsible for recent outbreaks of severe invasive disease in previously healthy children and adults in the United States of America and Europe. To determine the frequency of PVL-positive isolates sent to the Staphylococcus Reference Unit (United Kingdom) for epidemiological purposes, we tested 515 isolates of S. aureus, and 8 (1.6%) were positive for the PVL locus. A further 470 isolates were selected to explore the association of PVL-positive S. aureus with clinical disease. Of these, 23 (4.9%) were PVL positive and most were associated with skin and soft tissue infections (especially abscesses). The PVL genes were also detected in isolates responsible for community-acquired pneumonia, burn infections, bacteremia, and scalded skin syndrome. Genotyping by pulsed-field gel electrophoresis and multilocus sequence typing revealed that the PVL-positive isolates were from diverse genetic backgrounds, although one prevalent clone of 12 geographically dispersed methicillin-resistant S. aureus (MRSA) isolates was identified (ST80). All 12 isolates were stapylococcal cassette chromosome mec type IVc, had an agr3 allele, and shared a common toxin gene profile (sea-see, seg-sej, eta, etb, and tst negative but etd positive). ST80 strains with similar genetic characteristics have been responsible for community-acquired infections in France and Switzerland. The remaining PVL-positive isolates were mostly methicillin-sensitive S. aureus and belonged to 12 different sequence types, including ST22 and ST30, which are closely related to the most prevalent MRSA clones in United Kingdom hospitals, EMRSA-15 and EMRSA-16, respectively. Staphylococcus aureus is a very successful hospital and community-acquired pathogen. It causes a broad spectrum of disease, from mild skin infections to more serious invasive infections, including septicemia, pneumonia, endocarditis, and deep-seated abscesses. Pathogenicity is related to a number of virulence factors that allow it to adhere to surfaces, invade or avoid the immune system, and cause harmful toxic effects to the host. These factors include cell surface components (e.g., protein A, fibronectin-binding protein, collagen-binding protein, and clumping factor), and exoproteins (e.g., enterotoxins, exfoliatins, toxic shock syndrome toxin, and Panton-Valentine leucocidin [PVL]). PVL is a pore-forming cytotoxin that targets human and rabbit mononuclear and polymorphonuclear cells (37). When injected intradermally into rabbits, it induces severe inflammatory lesions, leading to capillary dilation, chemotaxis, polymorphonuclear karyorrhexis, and skin necrosis (44). Studies have shown that its toxic effect results from the synergistic action of two separate exoproteins, namely, LukS-PV and LukF-PV. These proteins are encoded by two contiguous and cotranscribed genes (lukS-PV and lukF-PV) (36), which are carried on temperate bacteriophages (20). Lysogenic conversion of PVLnegative strains of S. aureus leading to the production of the toxin has been demonstrated (29).
Clinical Infectious Diseases, 2007
Background. Community-acquired methicillin-resistant Staphylococcus aureus strains have recently been associated with severe necrotizing infections. Greater than 75% of these strains carry the genes for Panton-Valentine leukocidin (PVL), suggesting that this toxin may mediate these severe infections. However, to date, studies have not provided evidence of toxin production. Methods. Twenty-nine community-acquired methicillin-resistant Staphylococcus aureus and 2 community-acquired methicillin-susceptible S. aureus strains were collected from patients with infections of varying severity. Strains were analyzed for the presence of lukF-PV and SCCmecA type. PVL production in lukF-PV gene-positive strains was measured by ELISA, and the amount produced was analyzed relative to severity of infection. Results. Only 2 of the 31 strains tested, 1 methicillin-resistant Staphylococcus aureus abscess isolate and 1 nasal carriage methicillin-susceptible S. aureus isolate, were lukF-PV negative. All methicillin-resistant Staphylococcus aureus strains were SCCmec type IV. PVL was produced by all strains harboring lukF-PV, although a marked strain-to-strain variation was observed. Twenty-six (90%) of 29 strains produced 50-350 ng/mL of PVL; the remaining strains produced PVL in excess of 500 ng/mL. The quantity of PVL produced in vitro did not correlate with severity of infection. Conclusions. Although PVL likely plays an important role in the pathogenesis of these infections, its mere presence is not solely responsible for the increased severity. Factors that up-regulate toxin synthesis in vivo could contribute to more-severe disease and worse outcomes in patients with community-acquired methicillin-resistant Staphylococcus aureus infection. Staphylococcus aureus has re-emerged as a major worldwide threat to human health. Epidemics of S. aureus infection occurred in the 1950s, when strains acquired resistance to penicillin, and again in the 1980s, when strains acquired staphylococcal toxic shock syndrome toxin 1 [1]. Nosocomial infections due to methicillinresistant S. aureus (MRSA) were first reported in the
PLoS Pathogens, 2010
The Staphylococcus aureus Panton Valentine leukocidin (PVL) is a pore-forming toxin secreted by strains epidemiologically associated with the current outbreak of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and with the often lethal necrotizing pneumonia. To investigate the role of PVL in pulmonary disease, we tested the pathogenicity of clinical isolates, isogenic PVL-negative and PVL-positive S. aureus strains, as well as purified PVL, in a mouse acute pneumonia model. Here we show that PVL is sufficient to cause pneumonia and that the expression of this leukotoxin induces global changes in transcriptional levels of genes encoding secreted and cell-wall-anchored staphylococcal proteins, including the lung inflammatory factor staphylococcal protein A (Spa).