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Infection and Immunity, May 2000, p. 2880-2887, Vol. 68, No. 5
Departments of Epidemiology and Public
Health1 and
Dermatology,2 Yale University School
of Medicine, New Haven, Connecticut
Received 29 October 1999/Returned for modification 9 December
1999/Accepted 1 February 2000
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.
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Humanized In Vivo Model for Streptococcal
Impetigo
*
Corresponding author. Mailing address: Yale University
School of Medicine, Dept. of Epidemiology & Public Health, 60 College St., Box 208034, New Haven, CT 06520. Phone: (203) 785-4480. Fax: (203)
737-4285. E-mail: debra.bessen{at}yale.edu.
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