Raoul F. Reiser

An enterotoxin-like protein in Staphylococcus aureus strains from patients with toxic shock syndrome.

An enterotoxin-like protein, tentatively labeled enterotoxin F, was isolated from Staphylococcus aureus strains taken from patients with toxic shock syndrome. Antibodies specific for enterotoxin F were prepared in rabbits. Use of these antibodies showed that 130 (91.5%) of 142 S. aureus strains from patients with toxic shock syndrome produced enterotoxin F. Strains from toxic shock patients in eight other countries were identified as enterotoxin F producers. Only a small number of S. aureus strains from sources other than patients with toxic shock syndrome were found to produce enterotoxin F. Twenty-one of 111 controls had low antibody titers (less than 1:100) to enterotoxin F whereas 86 of 92 toxic shock patients had low acute phase antibody titers (less than 1:100) to enterotoxin F. Eight of 52 patients had serum conversion as shown by an increase in antibody titer to enterotoxin F in sera taken 21 to 60 days after onset of the illness. It may be possible to identify persons susceptible to toxic shock syndrome by measuring their antibody titer to enterotoxin F.

Application of Radioimmunoassay for Detection of Staphylococcal Enterotoxins in Foods

The staphylococcal enterotoxins can be iodinated with chloramine-T, lactoperoxidase or gaseous iodine. Low concentrations of enterotoxin, chloramine-T and 125I are recommended to avoid possible damage to the enterotoxin. The antigen-antibody complex can be separated from the unreacted enterotoxin by antibodies adsorbed onto tubes or bromoacetyl-cellulose or by precipitation of the complex with a second antibody or protein A cells. As little as 1 ng of enterotoxin per gram of food can be detected in food extracts with the solid-phase tube method or by precipitation of the antigen-antibody complex with protein A cells.

Low Incidence of Toxic Shock Syndrome in Children with Staphylococcal Infection

Children have frequent staphylococcal infections, and many lack antibody to TSST-1, a toxin associated with the toxic shock syndrome (TSS). To determine why there have been no nonmenstrual cases of TSS reported in children in Utah, the authors tested S. aureus isolated from children for TSST-1 by radial immunodiffusion and sera from other hospitalized children by radioimmunoassay for antibody to TSST-1. TSST-1 was produced by 25% of S. aureus. Fifty-two children had infections with toxin producing strains. None had TSS. The prevalence of presumably protective levels of antibody (⩾1: 100) was high in newborns (80%), declined until age 2 years and then gradually increased with age. Therefore, there may have been about 20 children with toxigenic infection who lacked protective antibody but did not show the usual features of TSS. We conclude that the rarity of TSS in children is not caused by misdiagnosis, underreporting, or the absence of toxigenic strains or susceptible patients. Additional factors, such as local conditions or duration of carriage, may influence the clinical presentation of infection with TSST-1 producing staphylococci.