Papenburg Jesse, Fontela Patricia, Raynal Lélia, Jetté Louise, Ismail Johanne, Bekal Sadjia, Al-Zahrani Ibrahim, Quach Caroline
Department of Pediatrics, Montreal Children's Hospital, McGill University Health Centre, Montreal, Quebec, Canada.
Clin Invest Med. 2009 Oct 1;32(5):E352-9. doi: 10.25011/cim.v32i5.6923.
Panton-Valentine Leukocidin (PVL) is an exotoxin produced by strains of Staphylococcus aureus (SA). Its importance as a virulence factor is controversial. We aim to further characterize the role of PVL in pediatric community-acquired SA infections.
In a cohort study conducted from July to November 2006, we prospectively collected all strains of SA isolated at the Montreal Children's Hospital causing community-acquired infections in children aged 18 years or younger. The strains were analyzed for the presence of the PVL encoding genes by PCR and were phage typed. Strains resistant to methicillin or pvl+ were analyzed by pulsed-field gel electrophoresis. A medical chart review blinded to patient pvl status was performed to retrieve demographic and clinical data. Data were analyzed by logistic regression.
We identified 74 pediatric community-acquired SA infections. Nineteen strains (25.7%) were positive for the pvl genes. Four isolates (5.4%) were resistant to methicillin and three of these were pvl+. No predominant clone was identified by phage typing or pulsed field gel electrophoresis. Pvl+ and pvl- infections were statistically similar for patient age, hospital admission, length of hospital stay, invasive disease, intravenous antibiotics and outcomes. Pvl+ strains were more likely to cause abscesses (OR 20.79; 95% CI 4.93 - 87.58), less likely to cause superficial skin infections (OR 0.18; 95% CI 0.05 - 0.64) and less likely to be resistant to erythromycin (OR 0.048; 95% CI 0.004 - 0.52).
In a clonally heterogeneous population of pediatric community-acquired SA infections, pvl+ strains were associated with abscess formation and erythromycin susceptibility, but not invasive disease.
杀白细胞素（PVL）是金黄色葡萄球菌（SA）菌株产生的一种外毒素。其作为毒力因子的重要性存在争议。我们旨在进一步明确PVL在儿童社区获得性SA感染中的作用。
在2006年7月至11月进行的一项队列研究中，我们前瞻性收集了蒙特利尔儿童医院分离出的所有SA菌株，这些菌株导致18岁及以下儿童发生社区获得性感染。通过聚合酶链反应（PCR）分析菌株中PVL编码基因的存在情况，并进行噬菌体分型。对耐甲氧西林或pvl+菌株进行脉冲场凝胶电泳分析。对患者pvl状态不知情的情况下进行病历审查，以获取人口统计学和临床数据。通过逻辑回归分析数据。
我们确定了74例儿童社区获得性SA感染。19株（25.7%）pvl基因呈阳性。4株（5.4%）对甲氧西林耐药，其中3株为pvl+。通过噬菌体分型或脉冲场凝胶电泳未鉴定出主要克隆。pvl+和pvl-感染在患者年龄、住院、住院时间、侵袭性疾病、静脉使用抗生素及转归方面在统计学上相似。pvl+菌株更易引起脓肿（比值比[OR]20.79；95%可信区间[CI]4.93 - 87.58），较少引起浅表皮肤感染（OR 0.18；95%CI 0.05 - 0.64），且较少对红霉素耐药（OR 0.048；95%CI 0.004 - 0.52）。
在儿童社区获得性SA感染的克隆异质性群体中，pvl+菌株与脓肿形成及对红霉素敏感相关，但与侵袭性疾病无关。
