Investigation by syringe method of effect of tampons on production in vitro of toxic shock syndrome toxin 1 by Staphylococcus aureus.

A syringe method was designed to test the effect of tampons on the growth of three toxic shock syndrome-associated strains of Staphylococcus aureus and their in vitro production of toxic shock syndrome toxin 1 (TSST-1) under different conditions. Various amounts of TSST-1 were recovered from different tampons inoculated with these strains. Generally, the addition of 10% porcine blood to the growth medium, incubation in the presence of 5% CO2, or the combination of these two factors resulted in the stimulation of TSST-1 production.

Involvement of staphylococcal enterotoxins in nonmenstrual toxic shock syndrome.

Adequate evidence is available to show that the major toxin responsible for toxic shock syndrome (TSS) is TSS toxin 1 (TSST-1). More than 90% of the staphylococcal strains isolated from TSS patients produce this toxin. However, approximately 60% of these strains produce one or more of the staphylococcal enterotoxins, with a number of them producing only enterotoxin, primarily enterotoxin B. Of 55 staphylococcal strains isolated from nonmenstrual cases, 46 produced TSST-1; 42 produced one of the enterotoxins, including 8 that produced only enterotoxin B. The fact that the enterotoxins can produce in monkeys many signs and symptoms similar to those observed in TSS in humans implicates them as the cause of some cases of TSS.

Toxin involvement in toxic shock syndrome.

Cultures for Staphylococcus and sera from 434 individuals with confirmed or probable toxic shock syndrome (TSS) were studied. Three hundred forty-eight (91.6%) of the staphylococcal isolated produced TSS toxin-1 (TSST-1) alone or in combination with one or more staphylococcal enterotoxins. Isolates producing both staphylococcal enterotoxin C and TSST-1 had a higher association with nonmenstrual and fatal cases than did any other toxin combination. The sera of 284 patients with TSS were tested for antibodies to TSST-1, and 234 (82.4%) had no detectable level of antibody compared with 80 (77.7%) of 103 healthy controls having antibody levels of greater than or equal to 1:800. The sera from patients with TSS also had lower levels of antibody to staphylococcal enterotoxins A, B, and C than did the controls, a result indicating that these subjects may have an immunodeficiency that inhibits the production and/or maintenance of antibodies to the staphylococcal enterotoxins and TSST-1.

Involvement of coagulase-negative staphylococci in toxic shock syndrome.

Coagulase-negative staphylococci that produce toxic shock syndrome toxin 1 (TSST-1) or a staphylococcal enterotoxin or both were isolated from various sources. Coagulase-negative strains that produce TSST-1 alone or with enterotoxin A were the only staphylococci isolated from seven patients with toxic shock syndrome. Two other toxic shock syndrome patients had coagulase-positive staphylococci also, but only the coagulase-negative strains produced TSST-1. Coagulase-positive and coagulase-negative strains that produced TSST-1 were isolated from two other toxic shock syndrome patients. In addition, coagulase-negative staphylococci that produced toxins were isolated from patients with other staphylococcal infections and from food implicated in a case of food poisoning.

Staphylococcus aureus--toxic shock syndrome toxin-1 antibody titers in serum of German women.

In a prospective study the distribution of Toxic-1 (TSST-1) antibody titers was proved by 236 menstruating, tampon using volunteers. They are divided in 7 different age groups. Up to 11% of the volunteers under 25 years had no TSST-1 antibody-titers at all. Over 25 years of age this could be detected. In the group over 40 years of age 98% were found with antibody-titers up than 1:100. So it may be suggested that there is no general causal relationship between any type of tampon on TSS.

Development of serum antibody to toxic shock toxin among individuals with toxic shock syndrome in Wisconsin.

The presence of Staphylococcus aureus producing toxic shock toxin (TST) and the absence of antibody to TST (anti-TST) in acute-phase sera are markers for toxic shock syndrome (TSS). We used radioimmunoassay methods to examine 133 acute-phase and 277 convalescent-phase serum specimens from 181 patients with TSS for anti-TST. Among confirmed menstrual cases, nine (9.5%) of 95 patients had demonstrable anti-TST in acute-phase sera obtained during the first seven days of illness; patients with probable or non-menstrual TSS had a higher prevalence of anti-TST in acute-phase sera. Five (33.3%) of 15 individuals with confirmed menstrual TSS developed anti-TST as early as seven to nine days after TSS onset; 32 (62.7%) of 51 patients had demonstrable anti-TST in sera obtained more than one year after their episode of TSS. This study demonstrates a gradual rate and low magnitude of development of anti-TST after TSS and supports the diagnostic usefulness of measuring anti-TST levels in sera from patients suspected of having TSS.

Toxic shock syndrome--the role of the toxin.

From isolates of Staphylococcus aureus derived from patients suffering from toxic shock syndrome a toxin was identified by tests in monkeys and was found to be distinct from the enterotoxin responsible for staphylococcal food poisoning. When purified, this TSS toxin (TSST-1) was characterised and used to generate antibodies in rabbits. Only a small proportion of routine staphylococcal isolates produce TSST-1, though it is clear that this toxin has existed for some years. At the same time, TSST-1 producing staphylococci have been isolated in every continent, yet very few cases of toxic shock syndrome have been recognised in developing countries. Using the purified TSST-1, human sera have been examined for the presence of antibodies. Patients with the disease had either no antibodies, or low titres.

Spread of a toxic-shock syndrome-associated strain of Staphylococcus aureus and measurement of antibodies to staphylococcal enterotoxin F.

A gentamicin-resistant isolate of Staphylococcus aureus producing staphylococcal enterotoxin F (SEF) was isolated from a burn unit nurse during three episodes of toxic-shock syndrome (TSS). The nurse's reciprocal titer of antibodies to SEF was less than or equal to 5 during the three episodes, and when the titer rose to 1,000 no further relapses occurred despite continued colonization. The unusual antibiotic susceptibility pattern of the organism enabled demonstration of its spread. During four months, 12 (41%) of 29 burn unit patients, three other burn unit nurses, and a household contact of the nurse with TSS became colonized. None, including two patients whose initial reciprocal titers were less than or equal to 5, developed TSS. This experience illustrates significant cross-transmission of a TSS-associated strain and a temporal association of antibodies to SEF with cessation of recurrences of TSS. Additional factors must explain why other individuals lacking antibodies to SEF did not develop TSS.

Prevalence of serum antibody to staphylococcal enterotoxin F among Wisconsin residents: implications for toxic-shock syndrome.

Staphylococcal enterotoxin F (SEF) has previously been shown to be a marker for toxic-shock syndrome (TSS)-associated strains of Staphylococcus aureus, whereas the serologic absence of antibody to SEF (anti-SEF) has been shown to be a marker for susceptibility of persons to TSS. In this study, anti-SEF was measured by radioimmunoassay in 689 banked sera obtained from Wisconsin residents during 1960, 1970, and 1980. The prevalence of anti-SEF as estimated by logistic regression analysis was 47%, 58%, 70%, 88%, 96%, and 99% at ages one, five, 10, 20, 30, and 50 years, respectively. Evidence for the transplacental transfer of anti-SEF is also presented. Despite the reported increased incidence of TSS occurring during the past five years, with a preponderance of cases occurring among women, no significant differences in the prevalence of anti-SEF were noted between sexes or longitudinally between the years 1960, 1970, and 1980. These data enhance our understanding of the epidemiology of TSS and further identify the population that may be susceptible to TSS.

Recovery of staphylococcal enterotoxin F from the breast milk of a woman with toxic-shock syndrome.

At 22 hr after an uncomplicated delivery of a healthy full-term infant, a 26-year-old woman developed toxic-shock syndrome (TSS). A vaginal culture yielded a coagulase-positive Staphylococcus that produced staphylococcal enterotoxin F (SEF) but no other enterotoxins. Breast milk specimens obtained on postpartum days 5, 8, and 11 contained 3.0, 2.5, and 2.0 ng of SEF/ml, respectively. Sera obtained from the mother on postpartum days 4 and 38 had titers (by radioimmunoassay) of antibody to SEF of 1:5 and less than 1:5, a result demonstrating a persisting lack of antibody to SEF after the first episode of TSS; the infant's serum titer of antibody to SEF on day 38 was also less than 1:5. Further longitudinal monitoring of SEF and antibody to SEF in breast milk from this patient is presented. This case is the first isolation of SEF from a body fluid obtained from a patient with TSS further strengthens the association between SEF and TSS.

Toxic shock syndrome: management and long-term sequelae.

Little information is available on the optimal management of toxic shock syndrome and on its sequelae. The most appropriate antibiotic treatment, the efficacy of colloid infusions, and the potential role of gamma globulin preparations have not yet been completely ascertained. Coagulase-positive staphylococci associated with toxic shock syndrome had minimal inhibitory concentrations of 0.06 microgram/mL or less to rifampin, 0.25 microgram/mL or less to gentamicin, and 0.50 microgram/mL or less to both nafcillin and clindamycin. In the 36 patients studied abnormal chest roentgenograms were commoner in those who had received albumin than in those who had not. Radioimmunoassay showed antibody titers to staphylococcal enterotoxin F, a marker protein in toxic shock syndrome, of 1:4000 or more for intravenous gamma globulin (12/15 lots) and 1:40 000 or more for intramuscular gamma globulin. Major sequelae of toxic shock syndrome include late-onset rash, compromised renal function, cyanotic extremities, and prolonged neuromuscular abnormalities.

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.

Staphylococcus aureus associated with toxic shock syndrome: phage typing and toxin capability testing.

Phage type 29 Staphylococcus aureus was identified singly or with type 52 in 64.1% of 248 coded isolates from patients with toxic shock syndrome. These phage types also have a high capability of producing pyrogenic exotoxin C and enterotoxin F. The origin and development of these toxigenic strains were explored by studying 25,220 isolates of S. aureus stored in a staphylococcal bank between 1960 and 1979. A small percentage of phage types 29, 52 were found in 1960, but their prevalence increased between 1961 and 1970, and continued at elevated levels through 1979. The toxigenic capabilities of these phage types were apparently acquired about 1971 and increased up to 1975. High levels of prevalence persisted during the following 4 years, and receded in 1980 and 1981. Other evidence during 1980 and 1981 indicates that these strains of S. aureus have become an important pathogen in surgical wounds, burns, and other infections.

A new staphylococcal enterotoxin, enterotoxin F, associated with toxic-shock-syndrome Staphylococcus aureus isolates.

612 (93.8%) of 65 Staphylococcus aureus strains isolated from 65 patients with toxic-shock syndrome (TSS) produced an enterotoxin-like protein, tentatively identified as staphylococcal enterotoxin F (SEF). One of the other strains produced staphylococcal enterotoxin B and another exterotoxin C. In two blind studies all 34 TSS-associated S. aureau strains examined and 3 (11.5%) of 26 control S. aureau strains produced SEF. 2 of the latter strains were isolated from the vaginas of women who had no history of TSS. SEF was purified, and specific antibodies to it were prepared. Only 4 (4.6%) of 87 S. aureau strains from other sources were found to produce SEF. 5 (17.2%) of 29 TSS patients whose acute sera were available had anti-SEF antibody present in titres of greater than or equal to 1:100 as determined by radioimmunoassay, compared with 44 (78.6%) of 56 controls--demonstrating a greater serosusceptibility of TSS patients to SEF. It is suggested that staphylococcal enterotoxin, particularly SEF, may be a cause of the signs and symptoms of TSS.