Journal
INFECTION AND IMMUNITY
Volume 68, Issue 5, Pages 2880-2887Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.68.5.2880-2887.2000
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Funding
- NIAID NIH HHS [R01-AI-28944] Funding Source: Medline
- NIAMS NIH HHS [P30-AR-041942, P30 AR041942] Funding Source: Medline
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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,uas 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 hare a strong tendency to cause impetigo, whereas pattern A-C strains are more likely to cause pharyngitis.
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