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

Abstract

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.

Staphylococcus aureus Isolates Carrying Panton-Valentine Leucocidin Genes in England and Wales: Frequency, Characterization, and Association with Clinical Disease

“…Phage group II strains and strains carrying an agr4 allele have been associated with exfoliatin-related diseases and typically carry eta and/or etb (18,19,24). Interestingly, the three phage group II, PVL-positive strains detected in this study did not harbor either of these genes, which may explain why they were not associated with a blistering disease, such as impetigo or SSS.…”

Natural population dynamics and expansion of pathogenic clones of Staphylococcus aureus

“…The distribution is shown in Figures 1 and 5. Compared to pediatric carriage strains, impetigo isolates were more frequently found in cluster IVb (Fisher's exact test, P < 0.0001) and less frequently in cluster II (Fisher's exact test, P = 0.01) ( Figure 5), suggesting clonal expansion of a certain genotype associated with impetigo (22).…”

“…An explanation for this clonal expansion in impetigo could be the facile spread of this disease. A recent study by Koning et al concerning nonbullous S. aureus impetigo concluded that a combination of staphylococcal virulence and resistance genes determines the development and course of nonbullous impetigo (22).…”

Overcoming antibiotic resistance in treatment of pyoderma

“…У CA-MRSA определяется PVL-ген (Panton-Valentin leukocidin), который кодирует выработку лейкоток-сина, обусловливает его вирулентность и вызывает гнойничковые поражения кожи и подкожной жиро-вой клетчатки, синдром токсического шока, а также некротизирующую пневмонию. У многих людей при колонизации отмечается бессимптомное бакте-рионосительство (около 30%), и не до конца понят-но, почему у одних формируются поверхностные пиодермии, а у других при наличии того же штамма -синдром токсического шока и сепсис [17][18][19].…”