Humanized in vivo model for streptococcal impetigo.
An in vivo model for group A streptococcal (GAS) impetigo was developed, whereby human neonatal foreskin engrafted onto SCID mice was superficially damaged and bacteria were topically applied. Severe infection, indicated by a purulent exudate, could be induced with as few as 1,000 CFU of a virulent strain. Early findings (48 h) showed a loss of stratum corneum and adherence of short chains of gram-positive cocci to the external surface of granular keratinocytes. This was followed by an increasing infiltration of polymorphonuclear leukocytes (neutrophils) of mouse origin, until a thick layer of pus covered an intact epidermis, with massive clumps of cocci accumulated at the outer rim of the pus layer. By 7 days postinoculation, the epidermis was heavily eroded; in some instances, the dermis contained pockets (ulcers) filled with cocci, similar to that observed for ecthyma. Importantly, virulent GAS underwent reproduction, resulting in a net increase in CFU of 20- to 14,000-fold. The majority of emm pattern D strains had a higher gross pathology score than emm pattern A, B, or C (A-C) strains, consistent with epidemiological findings that pattern D strains have a strong tendency to cause impetigo, whereas pattern A-C strains are more likely to cause pharyngitis.
Scaramuzzino
D A
DA
Departments of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut.
McNiff
J M
JM
Bessen
D E
DE
D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D007169:Impetigo / Q000382:microbiology* / Q000473:pathology; D051379:Mice; D016513:Mice, SCID; D012867:Skin / Q000473:pathology; D013290:Streptococcal Infections / Q000382:microbiology* / Q000473:pathology; D013297:Streptococcus pyogenes / Q000254:growth & development / Q000472:pathogenicity*; D014774:Virulence