title: Panton-Valentine Leukocidin-positive methicillin-resistant Staphylococcus aureus lung infection in patients with cystic fibrosis.
abstract: BACKGROUND
  Panton-Valentine Leukocidin-expressing (PVL+) methicillin-resistant Staphylococcus aureus (MRSA) is an emerging pathogen worldwide causing fatal necrotizing pneumonias in otherwise healthy individuals but has not been described in patients with cystic fibrosis (CF). Following two cases of patients with CF admitted with lung abscesses in association with PVL+ MRSA, we examined the incidence and the clinical characteristics of MRSA acquisition in our CF patient population.
  
  
  METHODS
  Newly acquired MRSA isolates from patients with CF followed up at St. Louis Children's Hospital were analyzed for the presence of Panton-Valentine leukocidin coding region, clindamycin susceptibility, staphylococcal cassette chromosome (SCC) mec type, and multilocus sequence type. Medical records and pulmonary function studies at the time of MRSA isolation were reviewed.
  
  
  RESULTS
  MRSA isolates from 40 CF patients were available for analysis. Six children (15%) had PVL+ MRSA infection. All PVL+ organisms were clindamycin susceptible. Patients who acquired a PVL+ organism were more likely to have a focal pulmonary infiltrate on chest radiograph, including cavitary lung lesions in two patients (p = 0.04), a markedly greater decline in FEV1 at the time of MRSA detection (p = 0.01), and a significantly higher WBC count (p = 0.04) and absolute neutrophil count (p = 0.04). These patients were more likely to be admitted for IV antibiotic therapy for respiratory illnesses (p < 0.01).
  
  
  CONCLUSIONS
  We describe the emergence of PVL+ MRSA in our CF population in association with development of invasive lung infections including lung abscesses. Early identification and treatment of CF patients with newly acquired PVL+ MRSA may be crucial.
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, Campus Box 8116, 660 S Euclid Ave, Saint Louis, MO 63110, USA. Elizur_A@kids.wustl.edu
authors.forename: Arnon
authors.initials: A
authors.lastname: Elizur
authors.forename: Rachel C
authors.initials: RC
authors.lastname: Orscheln
authors.forename: Thomas W
authors.initials: TW
authors.lastname: Ferkol
authors.forename: Jeffrey J
authors.initials: JJ
authors.lastname: Atkinson
authors.forename: W Michael
authors.initials: WM
authors.lastname: Dunne
authors.forename: Richard S
authors.initials: RS
authors.lastname: Buller
authors.forename: Jon R
authors.initials: JR
authors.lastname: Armstrong
authors.forename: Elaine R
authors.initials: ER
authors.lastname: Mardis
authors.forename: Gregory A
authors.initials: GA
authors.lastname: Storch
authors.forename: Carolyn L
authors.initials: CL
authors.lastname: Cannon
mesh_terms: D000038:Abscess / Q000188:drug therapy / Q000209:etiology / Q000473:pathology; D000293:Adolescent; D000328:Adult; D000900:Anti-Bacterial Agents / Q000494:pharmacology / Q000627:therapeutic use; D001427:Bacterial Toxins / Q000378:metabolism*; D002648:Child; D002675:Child, Preschool; D002981:Clindamycin / Q000494:pharmacology / Q000627:therapeutic use; D003550:Cystic Fibrosis / Q000150:complications* / Q000503:physiopathology; D005098:Exotoxins / Q000378:metabolism*; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D015994:Incidence; D007223:Infant; D007956:Leukocidins / Q000378:metabolism*; D008297:Male; D008712:Methicillin / Q000494:pharmacology / Q000627:therapeutic use; D016106:Methicillin Resistance; D015995:Prevalence; D012141:Respiratory Tract Infections / Q000188:drug therapy / Q000209:etiology / Q000473:pathology*; D012307:Risk Factors; D013203:Staphylococcal Infections / Q000188:drug therapy / Q000209:etiology / Q000473:pathology*; D013211:Staphylococcus aureus / Q000187:drug effects / Q000378:metabolism*
chemical_list: D000900:Anti-Bacterial Agents; D001427:Bacterial Toxins; D005098:Exotoxins; D007956:Leukocidins; C078284:Panton-Valentine leukocidin; D002981:Clindamycin; D008712:Methicillin