title: Outbreak of osteomyelitis/septic arthritis caused by Kingella kingae among child care center attendees.
abstract: OBJECTIVE
  Kingella kingae often colonizes the oropharyngeal and respiratory tracts of children but infrequently causes invasive disease. In mid-October 2003, 2 confirmed and 1 probable case of K kingae osteomyelitis/septic arthritis occurred among children in the same 16- to 24-month-old toddler classroom of a child care center. The objective of this study was to investigate the epidemiology of K kingae colonization and invasive disease among child care attendees.
  
  
  METHODS
  Staff at the center were interviewed, and a site visit was performed. Oropharyngeal cultures were obtained from the staff and children aged 0 to 5 years to assess the prevalence of Kingella colonization. Bacterial isolates were subtyped by pulsed-field gel electrophoresis (PFGE), and DNA sequencing of the 16S rRNA gene was performed. A telephone survey inquiring about potential risk factors and the general health of each child was also conducted. All children and staff in the affected toddler classroom were given rifampin prophylaxis and recultured 10 to 14 days later. For epidemiologic and microbiologic comparison, oropharyngeal cultures were obtained from a cohort of children at a control child care center with similar demographics and were analyzed using the same laboratory methods. The main outcome measures were prevalence and risk factors for colonization and invasive disease and comparison of bacterial isolates by molecular subtyping and DNA sequencing.
  
  
  RESULTS
  The 2 confirmed case patients required hospitalization, surgical debridement, and intravenous antibiotic therapy. The probable case patient was initially misdiagnosed; MRI 16 days later revealed evidence of ankle osteomyelitis. The site visit revealed no obvious outbreak source. Of 122 children in the center, 115 (94%) were cultured. Fifteen (13%) were colonized with K kingae, with the highest prevalence in the affected toddler classroom (9 [45%] of 20 children; all case patients tested negative but had received antibiotics). Six colonized children were distributed among the older classrooms; 2 were siblings of colonized toddlers. No staff (n = 28) or children aged <16 months were colonized. Isolates from the 2 confirmed case patients and from the colonized children had an indistinguishable PFGE pattern. No risk factors for invasive disease or colonization were identified from the telephone survey. Of the 9 colonized toddlers who took rifampin, 3 (33%) remained positive on reculture; an additional toddler, initially negative, was positive on reculture. The children of the control child care center demonstrated a similar degree and distribution of K kingae colonization; of 118 potential subjects, 45 (38%) underwent oropharyngeal culture, and 7 (16%) were colonized with K kingae. The highest prevalence again occurred in the toddler classrooms. All 7 isolates from the control facility had an indistinguishable PFGE pattern; this pattern differed from the PFGE pattern observed from the outbreak center isolates. 16S rRNA gene sequencing demonstrated that the outbreak K kingae strain exhibited >98% homology to the ATCC-type strain, although several sequence deviations were present. Sequencing of the control center strain demonstrated more homology to the outbreak center strain than to the ATCC-type strain.
  
  
  CONCLUSIONS
  This is the first reported outbreak of invasive K kingae disease. The high prevalence in the affected toddler class and the matching PFGE pattern are consistent with child-to-child transmission within the child care center. Rifampin was modestly effective in eliminating carriage. DNA sequence analysis suggests that there may be considerable variability within the species K kingae and that different K kingae strains may demonstrate varying degrees of pathogenicity.
authors: Acute Disease Investigation and Control Section, Minnesota Department of Health, 717 Delaware St, SE, Minneapolis, MN 55414, USA.
authors: Karen M
authors: KM
authors: Kiang
authors: Folashade
authors: F
authors: Ogunmodede
authors: Billie A
authors: BA
authors: Juni
authors: David J
authors: DJ
authors: Boxrud
authors: Anita
authors: A
authors: Glennen
authors: Joanne M
authors: JM
authors: Bartkus
authors: Elizabeth A
authors: EA
authors: Cebelinski
authors: Kathleen
authors: K
authors: Harriman
authors: Steven
authors: S
authors: Koop
authors: Ralph
authors: R
authors: Faville
authors: Richard
authors: R
authors: Danila
authors: Ruth
authors: R
authors: Lynfield
mesh_terms: D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D001170:Arthritis, Infectious / Q000188:drug therapy / Q000453:epidemiology / Q000382:microbiology*; D002656:Child Day Care Centers; D002675:Child, Preschool; D004196:Disease Outbreaks; D016521:Electrophoresis, Gel, Pulsed-Field; D006801:Humans; D007223:Infant; D017882:Kingella kingae / Q000145:classification / Q000302:isolation & purification; D008910:Minnesota / Q000453:epidemiology; D016870:Neisseriaceae Infections / Q000188:drug therapy / Q000453:epidemiology* / Q000517:prevention & control / Q000635:transmission; D009960:Oropharynx / Q000382:microbiology; D010019:Osteomyelitis / Q000188:drug therapy / Q000453:epidemiology / Q000382:microbiology*; D012141:Respiratory Tract Infections / Q000150:complications / Q000382:microbiology; D012293:Rifampin / Q000627:therapeutic use; D017422:Sequence Analysis, DNA
chemical_list: D000900:Anti-Bacterial Agents; D012293:Rifampin