The absence of evidence of staphylococcal toxin involvement in the pathogenesis of kawasaki disease

Masaru Terai; Keishi Miwa; Tommy Williams; William Kabat; Mayumi Fukuyama; Yoshitomo Okajima; Hideo Igarashi; Stanford T. Shulman

doi:10.1093/infdis/172.2.558

The absence of evidence of staphylococcal toxin involvement in the pathogenesis of kawasaki disease

Masaru Terai, Keishi Miwa, Tommy Williams, William Kabat, Mayumi Fukuyama, Yoshitomo Okajima, Hideo Igarashi, Stanford T. Shulman^*

^*Corresponding author for this work

Pediatrics

Research output: Contribution to journal › Article › peer-review

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Abstract

To detect a causative superantigen and to clarify a possible role for staphylococci in Kawasaki disease (KD), culture supernatants of individual bacterial isolates from 11 acute-stage patients were studied. Toxic shock syndrome toxin-1 (TSST-1) and antibody to TSST-1 and enterotoxins A (SEA), B (SEB), and C (SEC) in acute (mean, day 7) and late convalescent (mean, month 15) sera from 26 patients (12 with coronary artery aneurysms) and 22 age-matched controls were measured. Only 1 of 60 supernatants was mitogenic for human lymphocytes; it was 1 of the 4 Staphylococcus aureus isolates. Mitogenicity was neutralized by sera obtained after administration of intravenous gamma globulin (mean, week 4) but not by late convalescent sera. TSST-1 was detectable in 2 of 26 acute sera and 1 of 22 control sera. No KD but 1 control serum had IgM to TSST-1. IgG seroconversion rates to TSST-1, SEA, SEB, and SEC were 10%, 15%, 21%, and 16%, respectively. These data do not support the involvement of toxin-producing staphylococci in KD.

Original language	English (US)
Pages (from-to)	558-561
Number of pages	4
Journal	Journal of Infectious Diseases
Volume	172
Issue number	2
DOIs	https://doi.org/10.1093/infdis/172.2.558
State	Published - Aug 1995

Funding

Received 5 December 1994; revised 9 March 1995. Informed consent was obtained from parents of patients. Financial support: Kawasaki Research Fund and Rogers Fellowship, Children's Memorial Hospital. Reprints or correspondence: Dr. Stanford T. Shulman, Division ofInfectious Diseases, Children's Memorial Hospital, 2300 Children's Plaza, Chicago, IL 60614.

ASJC Scopus subject areas

General Medicine

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title = "The absence of evidence of staphylococcal toxin involvement in the pathogenesis of kawasaki disease",

abstract = "To detect a causative superantigen and to clarify a possible role for staphylococci in Kawasaki disease (KD), culture supernatants of individual bacterial isolates from 11 acute-stage patients were studied. Toxic shock syndrome toxin-1 (TSST-1) and antibody to TSST-1 and enterotoxins A (SEA), B (SEB), and C (SEC) in acute (mean, day 7) and late convalescent (mean, month 15) sera from 26 patients (12 with coronary artery aneurysms) and 22 age-matched controls were measured. Only 1 of 60 supernatants was mitogenic for human lymphocytes; it was 1 of the 4 Staphylococcus aureus isolates. Mitogenicity was neutralized by sera obtained after administration of intravenous gamma globulin (mean, week 4) but not by late convalescent sera. TSST-1 was detectable in 2 of 26 acute sera and 1 of 22 control sera. No KD but 1 control serum had IgM to TSST-1. IgG seroconversion rates to TSST-1, SEA, SEB, and SEC were 10%, 15%, 21%, and 16%, respectively. These data do not support the involvement of toxin-producing staphylococci in KD.",

author = "Masaru Terai and Keishi Miwa and Tommy Williams and William Kabat and Mayumi Fukuyama and Yoshitomo Okajima and Hideo Igarashi and Shulman, {Stanford T.}",

note = "Funding Information: Received 5 December 1994; revised 9 March 1995. Informed consent was obtained from parents of patients. Financial support: Kawasaki Research Fund and Rogers Fellowship, Children's Memorial Hospital. Reprints or correspondence: Dr. Stanford T. Shulman, Division ofInfectious Diseases, Children's Memorial Hospital, 2300 Children's Plaza, Chicago, IL 60614.",

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AU - Okajima, Yoshitomo

AU - Igarashi, Hideo

AU - Shulman, Stanford T.

N1 - Funding Information: Received 5 December 1994; revised 9 March 1995. Informed consent was obtained from parents of patients. Financial support: Kawasaki Research Fund and Rogers Fellowship, Children's Memorial Hospital. Reprints or correspondence: Dr. Stanford T. Shulman, Division ofInfectious Diseases, Children's Memorial Hospital, 2300 Children's Plaza, Chicago, IL 60614.

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N2 - To detect a causative superantigen and to clarify a possible role for staphylococci in Kawasaki disease (KD), culture supernatants of individual bacterial isolates from 11 acute-stage patients were studied. Toxic shock syndrome toxin-1 (TSST-1) and antibody to TSST-1 and enterotoxins A (SEA), B (SEB), and C (SEC) in acute (mean, day 7) and late convalescent (mean, month 15) sera from 26 patients (12 with coronary artery aneurysms) and 22 age-matched controls were measured. Only 1 of 60 supernatants was mitogenic for human lymphocytes; it was 1 of the 4 Staphylococcus aureus isolates. Mitogenicity was neutralized by sera obtained after administration of intravenous gamma globulin (mean, week 4) but not by late convalescent sera. TSST-1 was detectable in 2 of 26 acute sera and 1 of 22 control sera. No KD but 1 control serum had IgM to TSST-1. IgG seroconversion rates to TSST-1, SEA, SEB, and SEC were 10%, 15%, 21%, and 16%, respectively. These data do not support the involvement of toxin-producing staphylococci in KD.

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The absence of evidence of staphylococcal toxin involvement in the pathogenesis of kawasaki disease

Abstract

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