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M S Bergdoll

Publications and source records attributed to M S Bergdoll.

At least 73 records · Page 4Linked to original sources
PubMed1984

Identification, purification, and some physicochemical properties of staphylococcal enterotoxin C3.

A third staphylococcal enterotoxin C (C3) has been identified, purified, and characterized. Staphylococcal enterotoxin C3 was identified from a Staphylococcus aureus isolated received from England. The purified toxin was determined by gel permeation chromatography and sodium dodecyl sulfate-polyacrylamide gel electrophoresis to be a simple protein with a molecular weight of 26,900. The isoelectric point of the major band was determined by isoelectric focusing in polyacrylamide gels to be 8.15. The reaction of enterotoxin C3 with its specific antibody was not affected by tryptic digestion at pH 8.0 or peptic digestion at pH 4.5. The enterotoxin C3 consisted of 236 amino acid residues. Serine was shown to be the NH2-terminal amino acid residue by end group analysis. The protein was highly emetic in cynomolgus monkeys both per os and intravenously.

Amino Acids↗
PubMed1984

The disease spectrum, epidemiology, and etiology of toxic-shock syndrome.

From this composite picture of the history and recent developments related to TSS, several points are clear. TSS is not a new disease, and TST-producing strains of S. aureus are not new. What is new is the recent dramatic increase of this disease in young women who use tampons during menses and who lack antibody to TST. What is also new is the recognition that the disease commonly recurs but only in menstrually associated cases. What remains to be determined are the precise role of tampons, the factors leading to toxin induction, and the mechanism of action of this potent toxin. In order to better determine what these factors and mechanism of action are, and to determine if the TST marker protein is in fact the critical toxin, a reliable animal model is badly needed. Finally, a reliable laboratory test to confirm the clinical diagnosis is another high-priority need. The further unraveling of the secrets of this complex disease may greatly enhance our understanding of the disease associated with this toxin, of the intricacies of toxin production by other bacteria, and of the role that exogenous cofactors play in disease processes.

Adult↗
PubMed1984

Relation of enterotoxin production and lipolytic activity in Staphylococcus aureus strains isolated from acute diarrhoeal diseases to clinical course of illness.

Two sets of cases of acute diarrhoeal disease caused by plasma-coagulase-positive Staphylococcus aureus strains were studied. Testing the isolates for staphylococcal enterotoxin (SE) production and for lipolytic activity on egg-yolk agar in relation to the clinical course of the illness showed that only part of the cases could be attributed to the effect of SE and that lipolytic activity apparently also played some pathogenetic role. In one of the sets (205 cases) SE production was found in only 29% of the strains isolated; the clinical course in the corresponding patients was typical of staphylococcal enterotoxicosis. Pronounced lipolytic activity without SE production was demonstrated in 30% of strains; here the clinical course was much milder and protracted. Where both factors were produced (21% of cases), the clinical pattern of enterotoxicosis predominated but was somewhat modified. Two outbreaks in one of which SE production and in the other only clear-cut lipolytic activity were found also differed mutually in the clinical respect. The first displayed a picture of typical staphylococcal enterotoxicosis, the second comprised mild diarrhoeal cases with an incubation period of 6-9 hours, diffuse abdominal pain and no fever. Accordingly, the above observations showed a certain positive correlation between the presence of some staphylococcal exoproducts (SE, lipolytic-activity factor) and the clinical course of the disease. This was particularly striking in infants up to 2 years of age. Lipolytic activity seemed to be associated with mild diarrhoeal staphylococcal disease, although the co-participation of (an)other, so far undetermined factor(s), could not be precluded.

Adolescent↗
PubMed1983

Purification and some physicochemical properties of toxic-shock toxin.

A procedure for the purification of a protein marker for the staphylococci isolated from toxic-shock syndrome patients has been developed. The purification procedure involves the removal of the toxic protein from culture supernatant fluids of toxic-shock syndrome associated Staphylococcus aureus strains FRI-1169 and FRI-1183 by batch absorption with CG-50 resin, ion-exchange chromatography on CM-Sepharose CL-6B, and gel permeation chromatography on Sephacryl S-200. The purified toxin is a simple protein with a molecular weight of 24 000 +/- 500 as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The isoelectric point of the major band is 7.0 as determined by isoelectric focusing in polyacrylamide gels. The TS-toxin's reactivity with its specific antibody is not affected by tryptic digestion at pH 8.0 but is slowly reduced by treatment with pepsin at pH 4.5. The TS-toxin consists of 188 amino acid residues. Serine was shown to be the NH2-terminal amino acid residue by end-group analysis. Initial studies indicated the protein was emetic; thus tentatively it was called staphylococcal enterotoxin F. In this paper it is called TS-toxin because the emetic action in monkeys has not been confirmed.

Amino Acids↗
PubMed1983

Exfoliative dermatitis in an infant. Association with enterotoxin F-producing staphylococci.

A 2-month-old premature infant had an extensive exfoliative dermatitis with flaccid bullae, mucous membrane involvement, thrombocytopenia, and an elevated creatinine kinase level. A subepidermal cleavage plane with numerous necrotic epidermal cells and a polymorphonuclear cell infiltrate were present on a skin biopsy specimen. The isolates of Staphylococcus aureus obtained at the onset of her disease had a 29/52 bacteriophage lysis pattern and produced enterotoxins C and F and epidermal toxin, but no exfolliatins. In toxic shock syndrome (TSS), subepidermal blister formation has been described and a new toxin, epidermal toxin, which causes subepidermal cleavage in the newborn mouse model, has been identified. In some infants, exfoliative dermatitis may be a variant of the well-described TSS in older children and adults.

Bacterial Toxins↗
PubMed1983

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.

Adolescent↗
PubMed1983

Effect of Staphylococcus aureus enterotoxin F on human neutrophil oxidative metabolism.

Epidemiologic and animal challenge studies have suggested that SEF may play a critical role in toxic-shock syndrome [1]. However, the pathogenic mechanism of SEF activity is not known. One means by which this toxin could elicit the widespread organ dysfunction observed in toxic-shock syndrome would be by directly promoting PMN production of toxic oxygen species and the resultant secondary endothelial cell damage [2]. To evaluate this possibility, we assayed the effect of SEF on PMN oxidative metabolism. SEF at 0.01-100 ng/ml did not stimulate O2- release or O2 consumption by inactive PMNs. Similarly, incubation of PMNs with 10 ng of SEF/ml for 1 hr neither potentiated nor inhibited cellular O2 consumption stimulated by optimal (10 mg/ml) or suboptimal (0.1 mg/ml) concentrations of opsonized zymosan. Finally, SEF had no effect on O2- release by PMNs stimulated by PMA. PMN viability, as assessed by trypan blue exclusion, was unaffected by SEF. This study did not address the possibility that SEF might indirectly activate PMN oxidative metabolism by promoting leukocytic pyrogen production by monocytes and macrophages [3]. SEF neither directly activated PMN oxidative activity nor potentiated the cellular oxidative response to particulate or soluble stimuli. Consequently, direct stimulation of PMN-derived, O2- mediated damage to endothelial cells is not a tenable hypothesis to explain the mechanism of SEF toxicity.

Bacterial Toxins↗
PubMed1983

Enterotoxin production by atypical Staphylococcus aureus from poultry.

Phenotypically typical Staphylococcus aureus was isolated frequently from the necrotic bone and liver of poultry suffering from femoral head necrosis. Occasionally strains were isolated that differed from typical Staph. aureus in one or more of the major diagnostic tests, i.e. coagulase production, anaerobic fermentation of mannitol and production of a heat-stable deoxyribonuclease. Such atypical strains were also isolated from nasal swabs of healthy birds. Tests for enterotoxin production demonstrated that some atypical strains from both sick and healthy birds are capable of producing staphylococcal enterotoxins.

Animals↗
PubMed1982

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.

Adult↗
PubMed1982

Enzyme-linked immunosorbent assay for detection of staphylococcal enterotoxins in foods.

An enzyme-linked immunosorbent assay (ELISA) was developed for detection of staphylococcal enterotoxins in foods. The "double-antibody sandwich" protocol combines parts of several procedures reported previously. Horseradish peroxidase was conjugated to antibody specific for an enterotoxin, and the antibody-enzyme conjugate was assayed with a 2,2'-azino-di-(3-ethylbenzthiazoline sulfonic acid)-H2O2 substrate solution. Enterotoxins were added to a variety of foods that were representative of those implicated in staphylococcal food poisoning outbreaks. Extracts of the foods were assayed by the ELISA and radioimmunoassay. Enterotoxin levels below 1 ng/g of food were consistently detectable by the ELISA. These results compared favorably with those of the radioimmunoassay. Experiments confirmed the interference of protein A in double-antibody sandwich ELISAs. Although protein A interference has not been demonstrated to be a problem in food extracts, we suggest a screen for protein A interference in which immunoglobulin G from nonimmunized rabbits is used. All of the known staphylococcal enterotoxins could be detected by this method. Analysis of a food product for entertoxin by the ELISA can be completed in an 8-h working day.

Animals↗
PubMed1982

Emetic action of staphylococcal enterotoxin A on weanling pigs.

Peroral and intraduodenal administration of staphylococcal enterotoxin A (SEA) to weanling pigs elicited an emetic response. Peroral administration of an emetic dose of SEA resulted in a single emetic episode occurring 90 to 180 min after dosing. Intraduodenal administration via a surgically implanted catheter of 100 or 150 micrograms of SEA resulted in multiple emetic episodes occurring 150 to 210 min after dosing, suggesting an intestinal site of action for SEA. The 50% emetic dose for perorally administered SEA was between 40 and 50 micrograms for 4.1- to 9.1-kg weanling pigs and 20 micrograms in 0.9- to 2.3-kg weanling pigs. Neurobehavioral responses, including alternating periods of drowsiness and restlessness, staggering, temporary loss of the righting reflex, and refusal to feed were also observed in pigs given an oral dose of SEA. Based on the demonstrated responsiveness of pigs to SEA, pigs should be considered suitable animal models for studies on the sites and mode of action of the toxin.

Administration, Oral↗
PubMed1982

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.

Adolescent↗
PubMed1982

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.

Bacterial Toxins↗
PubMed1982

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.

Bacterial Toxins↗
PubMed1981

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.

Antibodies↗