Severity of nonbullous Staphylococcus aureus impetigo in children is associated with strains harboring genetic markers for exfoliative toxin B, Panton-Valentine leukocidin, and the multidrug resistance plasmid pSK41.
Nonbullous impetigo is a common skin infection in children and is frequently caused by Staphylococcus aureus. Staphylococcal toxins and especially exfoliative toxin A are known mediators of bullous impetigo in children. It is not known whether this is also true for nonbullous impetigo. We set out to analyze clonality among clinical isolates of S. aureus from children with nonbullous impetigo living in a restricted geographical area in The Netherlands. We investigated whether staphylococcal nasal carriage and the nature of the staphylococcal strains were associated with the severity and course of impetigo. Bacterial isolates were obtained from the noses and wounds of children suffering from impetigo. Strains were genetically characterized by pulsed-field gel electrophoresis-mediated typing and binary typing, which was also used to assess toxin gene content. In addition, a detailed clinical questionnaire was filled in by each of the participating patients. Staphylococcal nasal carriage seems to predispose the patients to the development of impetigo, and 34% of infections diagnosed in the Rotterdam area are caused by one clonal type of S. aureus. The S. aureus strains harbor the exfoliative toxin B (ETB) gene as a specific virulence factor. In particular, the numbers (P = 0.002) and sizes (P < 0.001) of the lesions were increased in patients infected with an ETB-positive strain. Additional predictors of disease severity and development could be identified. The presence of a staphylococcal plasmid encoding multiple antibiotic resistance traits, as detected by binary typing, was associated with a reduction in the cure rate. Our results recognize that a combination of staphylococcal virulence and resistance genes rather than a single gene determines the development and course of nonbullous impetigo. The identification of these microbial genetic markers, which are predictive of the severity and the course of the disease, will facilitate guided individualized antimicrobial therapy in the future.
Koning
Sander
S
Department of General Practice, Erasmus MC University Medical Center Rotterdam, 3015 GD Rotterdam, The Netherlands.
van Belkum
Alex
A
Snijders
Susan
S
van Leeuwen
Willem
W
Verbrugh
Henri
H
Nouwen
Jan
J
Op 't Veld
Mariet
M
van Suijlekom-Smit
Lisette W A
LW
van der Wouden
Johannes C
JC
Verduin
Cees
C
D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D001427:Bacterial Toxins; D002648:Child; D002675:Child, Preschool; D024901:Drug Resistance, Multiple, Bacterial / Q000235:genetics; D005083:Exfoliatins / Q000235:genetics; D005098:Exotoxins; D005672:Fusidic Acid / Q000627:therapeutic use; D005819:Genetic Markers; D006801:Humans; D007169:Impetigo / Q000188:drug therapy / Q000382:microbiology / Q000503:physiopathology*; D007956:Leukocidins / Q000235:genetics; D009666:Nose / Q000382:microbiology; D010957:Plasmids; D012720:Severity of Illness Index; D013203:Staphylococcal Infections / Q000188:drug therapy / Q000382:microbiology / Q000503:physiopathology; D013211:Staphylococcus aureus / Q000145:classification* / Q000235:genetics* / Q000302:isolation & purification / Q000472:pathogenicity; D014774:Virulence / Q000235:genetics
D000900:Anti-Bacterial Agents; D001427:Bacterial Toxins; D005083:Exfoliatins; D005098:Exotoxins; D005819:Genetic Markers; D007956:Leukocidins; C078284:Panton-Valentine leukocidin; D005672:Fusidic Acid