[Toxic shock syndrome in the puerperium].
A toxic shock syndrome on 6th postpartal day is described. Symptoms, etiology, course and therapy are discussed.
Adult↗
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The toxic shock syndrome revisited.
The association between toxic shock syndrome and the staphylococcal toxin TSST-1 is not entirely consistent. In vitro, the elaboration of the toxin occurs only under aerobic conditions, whereas the environment of the vagina is largely anaerobic. So far, moreover, the materials of which tampons are composed seem not especially to favour the growth of the causative micro-organisms. Further, the relationship between the disease and tampon absorbability is not entirely established. Nevertheless, the effect of particular fibres cannot be discounted.
Bacterial Toxins↗
[Pulmonary manifestations in a case of toxic shock syndrome].
The evolution of a toxic shock syndrome in a young adult has yielded particular pleural and lung lesions concomittantly with phenomena of insufficiency of other organs and systems (kidney, digestive, CNS a.o.). X-ray aspect of bilateral bronchopneumonia with small diffuse infiltrates are noted, together with an aspect of bilateral spontaneous pneumothorax, which appeared successively with a tendency to relapse. Hemodynamic alterings during the acute phase of the syndrome initiated by staphylococcal exotoxin are similar to those during the initial phase of the septic shock, requiring a careful monitoring during the treatment.
Acute Disease↗
Purulent osteomyelitis associated with empyema and toxic shock syndrome.
This is a report on purulent osteomyelitis associated with empyema and toxic shock syndrome. In China, this syndrome is still very rare. A review of recent research on toxic shock syndrome is included.
Adult↗
Toxic shock syndrome: modification and comparison of methods for detecting marker proteins in Staphylococcus aureus.
Development of a new medium and modification of incubation conditions increased production of toxic shock syndrome marker proteins and enabled detection of small volumes of pyrogenic exotoxin C (PEC) by isoelectric focusing and staphylococcal enterotoxin F (SEF) by a newly developed solid-phase radioimmunoassay. The results were compared with those obtained with previously described methods. The results were identical, and all PEC-positive isolates were SEF positive. In a second study of 262 randomly selected Staphylococcus aureus isolates examined by isoelectric focusing and solid-phase radioimmunoassay but grown in fresh beef heart medium, 47 (17.9%) isolates were PEC and SEF positive; however, 9 (3.4%) were PEC positive and SEF negative, and 3 (1.1%) were SEF positive and PEC negative. When grown in buffered beef heart yeast extract medium, six of the previously PEC-positive and SEF-negative isolates were PEC negative. Autoradiographic analysis of selected isolates demonstrated that PEC- and SEF-positive strains bound SEF antitoxin to the protein at isoelectric point 7.2, suggesting that in staphylococci from patients with toxic shock syndrome, PEC and SEF are the same protein. In screening staphylococci for toxic shock syndrome marker proteins, isoelectric focusing to identify PEC may detect false-positive proteins and may be more susceptible to technical variation than immunological methods to detect SEF.
Bacterial Proteins↗
Toxic shock syndrome following carbon dioxide laser treatment of genital tract condyloma acuminatum.
Toxic shock syndrome was observed in the postoperative period in a patient who underwent carbon dioxide laser treatment of genital condyloma acuminatum. Laser vaporization of the vagina produces areas of denuded mucosa. These areas may act as the portal of entry for staphylococcal toxins producing toxic shock syndrome.
Adult↗
Serum antibodies to enterotoxins produced by Staphylococcus aureus with special reference to enterotoxin F and toxic shock syndrome.
The presence of antibodies to staphylococcal enterotoxins (enterotoxins A through F) in sera of healthy subjects (n = 567) and in sera of patients with toxic shock syndrome (n = 20) was determined. Furthermore, production of enterotoxins by Staphylococcus aureus isolated from humans was investigated. In 46, 86, 78, 41, 20, and 91% of the sera of healthy subjects, antibodies were found against enterotoxins A, B, C, D, E, and F, respectively. The high percentage of sera with antibodies against enterotoxin F correlated with the relatively high frequency of enterotoxin F-producing S. aureus isolated from humans (one-third of the isolates produced enterotoxin F). In patients with toxic shock syndrome, antibodies against enterotoxin F were not present or were present only at very low levels. An increase of antibodies after onset of the disease was observed in two of eight patients investigated. From the results, it can be concluded that only those humans who show low levels of antibodies are susceptible to toxic shock syndrome.
Adolescent↗
Alteration of proteins reacting with antibody to toxic shock syndrome toxin 1 by endogenous proteases of Staphylococcus aureus.
Many cases of toxic shock syndrome (TSS) have been associated with Staphylococcus aureus strains that produce in vitro a 22,000-dalton protein called toxic shock syndrome toxin 1 (TSST-1). TSST-1 has been shown to be linked phenotypically to the production of the type II (thiol) staphylococcal protease; however, some strains clearly associated with TSS do not produce TSST-1. With the use of a variety of antibodies to TSST-1, representatives of both TSST-1-positive and TSST-1-negative TSS-associated strains were shown to produce proteins of 32,000, 53,000, and 76,000 daltons that cross-reacted with TSST-1 but that did not appear to be TSST-1 aggregates or to be protein A. TSST-1-negative strains were significantly (P less than .05) more likely than TSST-1-producing strains to produce the type I protease and less likely to produce the type II protease. In vitro the type I (serine) protease digests purified TSST-1. When combinations of type II and type III protease chemical inhibitors were used, the production of the high-molecular-weight cross-reacting proteins during in vitro growth could be selectively enhanced. Since the infected foci (e.g., abscess, vagina) associated with TSS may contain natural protease inhibitors, it is possible that such TSST-1 cross-reacting proteins may be expressed in vivo or that levels of TSST-1 may be increased by an inhibitor of the serine protease.
Animals↗
[Gram-positive septic-toxic shock with bullae. Intraepidermal splitting as an indication of toxin effect].
A fourteen-year-old girl with acute otitis media died from gram positive sepsis and toxic shock despite intensive treatment. The definitive bacteriological results showed positive cultures for both S. aureus and S. pyogenes serotype A. In vitro the bacteria produced the bacterial superantigens TSST-1, enterotoxin A, enterotoxin C (S. aureus) and erythrogenic toxin C (S. pyogenes). The patient presented with large flaccid sterile bullae on her chest and arms as well as necrotizing fasciitis. Tzanck test showed keratinozytes without necrosis and no inflammatory cells. Frozen-section and conventional skin biopsy specimens revealed subcorneal intraepidermal cleavage. These cytological and histological findings are those of staphylococcal scalded skin syndrome (SSSS) and differ from bullous erysipelas or toxic epidermal necrolysis (TEN). Therefore bacterial exotoxins are most likely responsible for the intraepidermal blistering in our case just as in SSSS. Bullae are an unfavorable prognostic sign in gram positive toxic shock syndrome. Both Tzanck test and frozen-section biopsy are easy to perform and useful in the early and rapid recognition of gram positive bullous toxic shock syndrome.
Adolescent↗
Postoperative toxic shock syndrome.
We conducted a retrospective review of all cases of postoperative toxic shock syndrome (PTSS) occurring in two community hospitals from 1981-1993, during which time 390,000 surgical procedures were performed. The incidence was 0.003% (12 cases). All wounds in these 12 cases, from those with scant superficial exudates to those with gross purulence, yielded Staphylococcus aureus. All tested isolates were susceptible to methicillin or cephalothin. Patients had a mean maximal temperature of 40 degrees C. All patients had a rash, most in a truncal, "sunburn" pattern. Eleven patients had desquamation. Mean time from surgery to onset of symptoms was 4 days. All patients required vigorous fluid resuscitation. No correlation could be demonstrated between the development of toxic shock syndrome and a patient's age, sex, preoperative skin preparation or administration of antibiotics, members of the surgical team, or duration of procedure. All patients with PTSS survived. PTSS should be considered in the differential diagnosis for the acutely febrile, systemically ill postoperative patient, even when surgical wounds are deceptively benign in appearance. Early recognition and treatment of PTSS is essential for successful outcome.
Adolescent↗
[Streptococcus pyogenes toxic shock. A clinical case].
Toxic shock-like syndrome (TSLS) due to Streptococcus pyogenes has been recently reported in both children and adults. This syndrome is characterized by hypotension or shock, fever, multiorgan system involvement and death in 30 to 60% of patients. This syndrome closely resembles the more frequent staphylococcal TSLS. Only one case of TSLS caused by streptococcus has been reported, up to now, in our Country. We describe a second case of fatal streptococcus pyogenes TSLS in a 64-year-old man, in which the site of infection was in the soft tissues. The illness was characterized by rapid progression of shock, erythematous rash, multisystem organ involvement and finally death. Clinicians must be aware of the presentation of this disease as its incidence appears to be increasing.
Humans↗
[A case of toxic shock syndrome secondary to mastitis caused by methicillin-resistant Staphylococcus aureus].
Toxic Shock Syndrome (TSS) secondary to mastitis is seldom described. We present a case of TSS due to postpartum mastitis caused by Methicillin-resistant Staphylococcus aureus (MRSA). Five weeks after giving birth to a healthy boy, a 23-year-old secundipara was readmitted to the hospital with a fever, systemic erythema, nausea, vomiting, diarrhea, diffuse myalgia, generalized itching, orthostatic syncopes, photophobia, oligurea and pain in the left breast. Laboratory data on admission revealed deteriorated renal and coagulation function. Administration of Vancomycin, Imipenem, dopamin and nafamostat mesilate was started immediately after admission, that was effective. The patient recuperated steadily over the next week with apparent desquamation of the skin on her face, breast and extremities especially palms and soles. MRSA isolated from her milk was coagulase type II producing toxic shock syndrome toxin-1 (TSST-1) and enterotoxin C. Also immunoglobulin G against TSST-1 was not detected from her sera both on admission and on discharge, which suggested that the patient belongs to the high risk group of TSS recurrence.
Adult↗
Effects of toxic shock syndrome Staphylococcus aureus, endotoxin and tampons in a mouse model.
Synthetic tampons and toxic shock syndrome toxin-one (TSST-1)-producing strains of Staphylococcus aureus have been linked to an increased incidence of toxic shock syndrome (TSS). While recent reports attempt to define the tampon connection as the creation of an optimal environment for the production of TSST-1, the role of other factors in disease expression in an animal model remain under investigation. To understand the role of tampons and bacteria, pools of Swiss mice were inoculated with permutations of effluents from TSS strains of S. aureus and Escherichia coli grown inside tampons. Depending on tampon brand, when all 3 factors were combined mortality ranged from 20-100%. In controls inoculated with single effluents, or effluents from growth in the presence of cotton, no deaths were observed. Likewise, when hairless mice were inoculated with exotoxin, endotoxin, and tampon leachables, mortality was 100%. In the absence of any 1 component, mortality ranged from 0-40%. Lethal toxicity can be the result of enhancement, since animal death in apparent shock was observed in all pools containing the 3 components, and in all pools containing effluents of TSS S. aureus and E. coli grown in the presence of synthetic tampons, but not in their absence. A retrospective analysis of fatal vs non-fatal TSS in humans supports the hypothesis of enhancement.
Adolescent↗
[Toxic shock syndrome in 2 girls with pharyngeal infection and wound infection].
In 1981, a 13 year old girl died of her shock lung. She had been admitted with the classical toxic shock syndrome then still unknown to us. Staphylococcus aureus had been cultured from a pharyngeal swab. But even in 1987, it took us 48 hours to correctly diagnose the toxic shock syndrome in a 17 year old girl. The diagnosis became evident when she was found to have a staphylococcus aureus wound infection after a surgical procedure. For pediatricians, it is crucial to know this syndrome well. Not only menstruating girls using tampons, but also quite young children can acquire this disease. Quick diagnosis and prompt institution of the correct therapy can be life saving.
Abscess↗
[Infectious-toxic shock in patients with acute pneumonia].
An analysis of case records, medical documentation of the emergency service and out-patient departments of 629 patients with acute pneumonia (AP) showed that infectious-toxic shock was an early grave complication of acute pneumonia. It was observed in 9.4% of patients with acute pneumonia and resulted in a fatal outcome in 5.1%. Infectious-toxic shock developed prevalently in males of young or middle age suffering of concomitant diseases in acute pneumonia due to viral-bacterial associations. At the pre-hospital period shock was detected only in 5.1% of patients due to inadequate examination, underestimation of symptoms and their erroneous interpretation. Clinical manifestations of infectious-toxic shock, their polymorphism may masquerade acute pneumonia symptoms and lead to diagnostic errors.
Acute Disease↗
Toxic shock syndrome as a complication of dermatologic surgery.
We report a case of toxic shock syndrome occurring after an excisional skin biopsy in an otherwise healthy woman. Her clean-appearing wound grew Staphylococcus aureus and was implicated as the source of toxin. Dermatologists should be aware that toxic shock syndrome may occur as a complication of simple dermatologic surgery.
Adult↗
Effect of trace metals on the synthesis of toxic shock syndrome toxin 1.
The effect of 10 trace metals on the production of toxic shock syndrome toxin 1 (TSST-1) was studied in a metal-deficient chemically defined medium (CDM) with toxic shock syndrome (TSS) and non-TSS strains of Staphylococcus aureus. When individual metals were tested, only Mg++ stimulated cell growth and TSST-1 production. TSST-1 yield was responsive to the concentration of Mg++ in the medium, with a maximal yield occurring at 0.1 mM. When other metals were studied in the presence of Mg++ with and without 1 mM ethylenediamine tetraacetic acid, it was found that Ca++, Co++, Cu++, Fe++, Mn++, molybdate-, Ni++, vanadate-, and Zn++ produced some stimulation of either cell growth or TSST-1 synthesis or both. The stimulating effect of Mg++ on TSST-1 synthesis was significantly enhanced by adding 0.3 mM Zn++ and 0.003 mM Fe++. TSST-1 production by 11 strains of S. aureus in CDM with optimal concentrations of trace metals was two to seven times greater than that produced in brain-heart infusion broth.
Bacterial Toxins↗
Co-production of staphylococcal enterotoxin A with toxic shock syndrome toxin-1 (TSST-1) enhances TSST-1 mediated mortality in a D-galactosamine sensitized mouse model of lethal shock.
It has previously been reported that staphylococcal enterotoxin A (SEA) is frequently co-expressed with toxic shock syndrome toxin-1 (TSST-1) in menstrual Toxic Shock Syndrome (MTSS)-associated Staphylococcus aureus. It was hypothesized that co-production of SEA and TSST-1 might yield a more virulent strain than one that produced TSST-1 but not SEA. To test this hypothesis, a TSST-1+/SEA- derivative of S. aureus RN3984 (TSST-1+/SEA+) was constructed by plasmid integration, and the isogenic pair were introduced into a D-galactosamine sensitized mouse model of lethal shock. At 72 h, 27 out of 30 (90%) mice inoculated with the parental strain died, as compared to 21 out of 30 (70%) mice inoculated with the isogenic derivative (P=0.05, Fisher's exact test; 1-tailed; 95% confidence limits, 0.80-20.80). Our results suggest that co-production of SEA with TSST-1 does enhance the ability of this strain of S. aureus to induce lethal shock in vivo. This enhanced virulence could be due to an additive or synergistic activity of the toxin combination on T cell proliferation and cytokine production in the animal model.
Animals↗