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Infection and Immunity, April 1999, p. 1871-1877, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Risk Factors in the Pathogenesis of Invasive Group
A Streptococcal Infections: Role of Protective Humoral
Immunity
Hesham
Basma,1,2
Anna
Norrby-Teglund,1
Yajaira
Guedez,2
Allison
McGeer,3
Donald E.
Low,3
Omar
El-Ahmedy,1
Benjamin
Schwartz,4 and
Malak
Kotb1,2,*
Veterans Affairs Medical Center, Research
Service, Memphis, Tennessee 381041;
Departments of Surgery and of Microbiology and Immunology,
University of Tennessee, Memphis, Tennessee
381632; Department of Microbiology,
Mount Sinai Hospital, and the University of Toronto, Toronto, Ontario,
Canada M5G 1X53; and
Centers for Disease Control and Prevention, Atlanta, Georgia
303334
Received 1 October 1998/Returned for modification 29 October
1998/Accepted 10 January 1999
An impressive change in the epidemiology and severity of invasive
group A streptococcal infections occurred in the 1980s, and the
incidence of streptococcal toxic shock syndrome cases continues to
rise. The reason for the resurgence of severe invasive cases remains a
mystery
has there been a change in the pathogen or in host protective
immunity? To address these questions, we have studied 33 patients with
invasive infection caused by genotypically indistinguishable M1T1
strains of Streptococcus pyogenes who had different disease
outcomes. Patients were classified as having severe (n = 21) and nonsevere (n = 12) invasive infections based on the presence or absence of shock and organ failure. Levels of
anti-M1 bactericidal antibodies and of anti-streptococcal superantigen neutralizing antibodies in plasma were significantly lower in both
groups than in age- and geographically matched healthy controls (P < 0.01). Importantly, the levels of these
protective antibodies in plasma samples from severe and nonsevere
invasive cases were not different. Together the data suggest that low
levels of protective antibodies may contribute to host susceptibility
to invasive streptococcal infection but do not modulate disease
outcome. Other immunogenetic factors that regulate superantigen
responses may influence the severity of systemic manifestations
associated with invasive streptococcal infection.
*
Corresponding author. Mailing address: University of
Tennessee, Memphis, 956 Court Ave., Suite A-202, Memphis, TN 38163. Phone: (901) 448-7247. Fax: (901) 448-7208. E-mail:
mkotb{at}utmem1.utmem.edu.
Infection and Immunity, April 1999, p. 1871-1877, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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