Showing papers by "Donald E. Low published in 1996"

Plasma from patients with severe invasive group A streptococcal infections treated with normal polyspecific IgG inhibits streptococcal superantigen-induced T cell proliferation and cytokine production.

Abstract: Previous studies have suggested a central role for superantigen-induced immune responses in the pathogenesis of streptococcal toxic shock syndrome. The production of streptococcal superantigens by clinical group A streptococcal (GAS) isolates was studied, and the ability of plasma collected from patients with severe invasive GAS infections to neutralize the proliferative- and cytokine-inducing activities of these superantigens was investigated. Overnight culture supernatants from all GAS isolates obtained from patients with invasive disease were found to contain superantigenic activity, as evident from their ability to drive potent T cell proliferation, induce high production of cytokines, and stimulate T cells in a V beta-specific manner. Twelve patients with severe invasive GAS infections, including 11 streptococcal toxic shock syndrome cases and one necrotizing fasciitis without shock, were treated with i.v. infusions of normal polyspecific Ig (IVIG). Plasma samples collected from each patient before and after IVIG administration were analyzed for their ability to neutralize the activity of streptococcal superantigens produced by the GAS isolate that caused their disease. In all IVIG-treated patients, the capacity to neutralize the superantigenic activity, produced by their respective GAS isolate or by purified streptococcal pyrogenic exotoxins, increased in plasma following IVIG administration. Of particular clinical relevance, post-IVIG plasma from each patient completely blocked cytokine production elicited by their respective GAS culture supernatants or by purified streptococcal pyrogenic exotoxins. This study shows that IVIG treatment confers in vivo inhibitory activity against a large array of streptococcal superantigens and suggests that IVIG may be useful in the treatment of severe invasive streptococcal infections.

Streptococcal toxic shock syndrome in dogs.

Abstract: Objective To determine the clinical, pathologic, and bacteriologic findings in dogs that developed severe invasive infections with group G streptococci (GGS) over a 6-month period in southern Ontario. Design Prospective case series. Animals 7 dogs n southern Ontario with severe streptococcal infection during a 6-month period. Procedure Using pulsed-field gel electrophoresis, molecular typing of streptococcal isolates was performed. Isolates were examined for the M protein gene emm1.0, pyrogenic exotoxin genes speA, speB, speF, hyaluronic acid synthase genes hasA, hasB, and for C5a peptidase gene scpA by use of DNA probes or polymerase chain reaction. Results 3 dogs with streptococcal shock without necrotizing fasciitis died or were euthanatized within 48 hours of admission, whereas 4 dogs with streptococcal shock and necrotizing fasciitis survived following surgical debridement, supportive medical treatment, and treatment with antibiotics. Of the 6 Lancefield group G streptococcal isolates available for characterization, 5 were Streptococcus canis and 1 had characteristics of group G streptococcal strains of human origin. Results of molecular typing indicated that isolates were unrelated to each other. Examination of the canine isolates for putative virulence genes found in human group A streptococci resulted in identification of the emm1.0 gene only in 1 of the isolates. The canine isolates otherwise lacked virulence genes associated with human group A streptococcal toxic shock infections. CLINICAL-IMPLICATIONS: The development of severe invasive infection in dogs resulting from GGS indicates that a virulent form of GGS has developed in southern Ontario.