Phenotypic distinctiveness of Staphylococcus aureus strains associated with toxic shock syndrome

Abstract

Twenty Staphylococcus aureus strains from patients with toxic shock syndrome (TSS) and 20 from control patients (non-TSS) with infection but no clinical evidence of TSS were compared phenotypically in a collaborative, blinded, randomized study. TSS strains were significantly (P less than 0.05) more likely than non-TSS strains to produce various previously described but related toxic shock-associated proteins (pyrogenic exotoxin C, enterotoxin F, and TSS marker protein), as well as differing in other distinctive phenotypic characteristics, such as hemolysis, bacteriocin susceptibility, arsenate resistance, pigment production, and casein proteolysis. TSS strains were significantly less likely to carry plasmids than control strains. A combination of two variables--proteolysis and toxic shock-associated protein production--statistically accounted for all other phenotypic variations between TSS and non-TSS strains. Only proteolysis covaried with all other significant variables, suggesting a primary role in the phenotypic distinctiveness of TSS S. aureus strains and possibly in the pathogenesis of TSS.

Toxic shock syndrome.

“…Strain Characteristics S. aureus strains isolated from patients with TSS were originally reported to have a unique phenotype, reacting with group I bacteriophages and producing an apparently new epidermal toxin in the newborn mouse animal model (167). Several studies have compared the phenotype of TSS-associated strains with those of other S. aureus strains, supporting the general conclusion that most TSS organisms represent a unique subset of the overall S. aureus population (3,7,148,149,173). Besides reacting commonly with group I bacteriophages (2,3,167,173), TSS strains are less likely to contain plasmids (173) and more likely to produce the epidermal toxin (88) as well as other exoproteins, including enterotoxins and TSST-1 (173).…”

“…The majority of cases reported since 1978 have been associated with focal S. aureus wound infections or menstruation and tampon usage with S. aureus isolated from the patients' vaginal cultures. These S. aureus strains have characteristic phenotypes which differ from those of S. aureus strains in the general population (7,173). Further microbiologic evaluations of these strains have demonstrated at least one (and probably more) toxin (12,23,53,149) which in certain (but not all) animal models reproduces many of the symptoms of TSS (127,129,151,152,165).…”

“…or other S. aureus cutaneous infections do not usually show much inflammatory response. This probably is related to the phenotypic characteristics of these S. aureus strains, which differ significantly from characteristics of other S. aureus strains (173). When the clinical diagnosis of TSS is suspected, it is very important to surgically explore all wounds thoroughly to make sure any focus of infection has been thoroughly drained, successful therapy of TSS being often dependent on complete drainage.…”

“…In addition, many nonmenstrual cases of TSS were described in increasing numbers in males as well as females (8, 110, 132, 133, 177,185), and not all of the S. aureus strains isolated from these patients produced TSST-1 (45,84,132). Animal model studies suggested that under some circumstances TSST-1 was not particularly toxic (127); subsequently, other exoproteins have been described (including the previously described epidermal toxin) which may also play roles in the pathophysiology of TSS (41,65,145,151,170,173,192 Thus, after 10 years, TSS is still an important disease with many interesting clinical, epidemiologic, and microbiologic features. Concepts are evolving which may explain the apparent discrepancies between past assumptions and current observations.…”

Association of toxic shock toxin-1 determinant with a heterologous insertion at multiple loci in the Staphylococcus aureus chromosome

“…Typically, TSS strains of S. aureus are different from staphylococci isolated from asymptomatic carriers or from individuals with non-TSS staphylococcal infections. TSS strains are predominantly lysed by group I phage types 29/ 52/80, are generally plasmid free, are resistant to penicillin and heavy metals, are more proteolytic, are more susceptible to bacteriocins, are less hemolytic, and are less pigmented (1,2,18,20,36,37). Additionally, we have recently observed that most TSS strains are tryptophan dependent, whereas most non-TSS strains are not (12).…”