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Group A beta-hemolytic Streptococcus (pyogenes) has been associated recently with toxic-shock-like syndrome similar to staphylococcal toxic shock as described originally in 1978. A group A beta-hemolytic streptococcal infection occurred in a recent postpartum patient and clinically resembled staphylococcal toxic shock.
A strain of Staphylococcus aureus producing toxic shock syndrome toxin-1 was repeatedly isolated from the nares of a neurosurgeon. This strain was identical to strains cultured from two of his patients who developed toxic shock syndrome after laminectomy. The relatedness of the isolates was shown by Southern blot hybridization analyses using chromosomal transposons as probes. This approach should be considered, in addition to standard bacteriologic techniques, as an effective method to analyze the relatedness of nosocomial isolates.
Toxic shock syndrome (TSS) is a multi system disorder resulting from superantigen-mediated cytokine production. Nearly 90% of the clinical cases of TSS arise due to an exotoxin, toxic shock syndrome toxin-1 (TSST-1), elaborated by toxigenic strains of Staphylococcus aureus. It is clearly established that besides antigen-specific signals a variety of costimulatory signals are required for full T cell activation. However, the nature and potential redundancy of costimulatory signals are incompletely understood, particularly with regards to superantigen-mediated T cell activation in vivo. Here we report that CD28-deficient mice (CD28-/-) are completely resistant to TSST-1-induced lethal TSS while CD28 (+/-) littermate mice were partially resistant to TSST-1. The mechanism for the resistance of the CD28 (-/-) mice was a complete abrogation of TNF-alpha accumulation in the serum and a nearly complete (90%) impairment of IFN-gamma secretion in response to TSST-1 injection. In contrast, the serum level of IL-2 was only moderately influenced by the variation of CD28 expression. CD28 (-/-) mice retained sensitivity to TNF-alpha as demonstrated by equivalent lethality after cytokine injection. These findings establish an essential requirement for CD28 costimulatory signals in TSST-1-induced TSS. The hierarchy of TSST-1 resistance among CD28 wild-type (CD28+/+), CD28 heterozygous (CD28+/-), and CD28-/- mice suggests a gene-dose effect, implying that the levels of T cell surface CD28 expression critically regulate superantigen-mediated costimulation. Finally, as these results demonstrate the primary and non-redundant role of CD28 receptors in the initiation of the in vivo cytokine cascade, they suggest therapeutic approaches for superantigen-mediated immunopathology.
Toxic shock syndrome (TSS) is a recently recognized condition associated with toxin-producing strains of Staphylococcus aureus. Patients affected with this syndrome are frequently young and have multisystemic complaints such as fever, headache, edema, myalgia, scarlatiniform rash, conjunctival injection, confusion, diarrhea, oliguria, hypotension and shock, This is followed by desquamation of the skin, especially the palms and soles. The majority of cases reported have been in menstruating women who used vaginal tampons regularly. Because similarities exist between toxic shock syndrome and Kawasaki's disease (mucocutaneous lymph node syndrome), as well as other conditions, proper diagnosis and management are of the utmost importance.
Recombinant toxic shock syndrome toxin-1 (rTSST-1) administered to MRL-lpr/lpr TCR V beta 8.2 transgenic mice at doses of 0.1 microgram/mouse resulted in 100% mortality. This was an unexpected finding since TSST-1 does not activate V beta 8.2 T cells. In contrast, control mice heterozygous at the lpr locus and also for the transgene (MRL-lpr/+; V beta 8.2/0) survived doses of superantigen 100 times higher. The transgenic mice which succumbed to rTSST-1 challenge exhibited histopathology of the liver consistent with toxic shock (generalized inflammation and hepatocellular necrosis) as well as substantially elevated serum TNF-alpha, IL-2, and IL-6 cytokine levels. Splenic T cells derived from transgenic mice stimulated with rTSST-1 in vitro did not undergo detectable proliferation as measured in a standard mitogen assay. However, PCR amplification of cDNA prepared from the V beta 8.2 splenocytes revealed the presence of minor populations of TSST-1-reactive V beta elements (i.e. V beta 3 and V beta 15). Furthermore, an expansion of the V beta 3 and V beta 15 T-cell families was detected by PCR assay of spleen cell cultures stimulated with rTSST-1. These results suggested that the exquisite sensitivity of the MRL-lpr/lpr V beta 8.2 transgenic animals to rTSST-1 was not dependent exclusively on T-cell proliferation but was augmented by the influence of a defective fas antigen receptor expressed in homozygous lpr mice. To test this hypothesis more directly, we compared the sensitivity of MRL-lpr/lpr mice (not carrying the V beta 8.2 transgene) to MRL-+/+ mice. The MRL-lpr/lpr fas antigen-defective mice were substantially more susceptible to rTSST-1 challenge. Mice carrying the lpr mutation on another genetic background (C57BL/6.C3H-lpr/lpr) were also more sensitive to rTSST-1 challenge than were C57BL/6.C3H-+/+ mice. Although induction of toxic shock is clearly associated with T-cell proliferation, defects in fas antigen receptor or ligand may also contribute substantively to superantigen-mediated lethal shock by still undefined mechanisms.
BACKGROUND: Puerperal sepsis due to group A beta-hemolytic streptococcal (GAS) toxic shock syndrome is associated with very high morbidity and mortality. Luckily it is now rare, but diagnosis is not always easy. This report demonstrates the problem of recognizing this disease, and summarizes the current knowledge on the pathomechanism and management of streptococcal toxic shock syndrome. CASE: Two cases of postpartum streptococcal toxic shock syndrome due to GAS are described. In both cases the correct diagnosis was delayed for several days. The first patient was sent home with the diagnosis of German measles; the second patient was transferred to our neurological intensive care unit with the diagnosis of meningitis. Both patients were admitted to the intensive care unit in profound shock, both developed multiple organ failure, and one patient died. CONCLUSIONS: GAS may produce virulence factors that cause host tissue pathology. Besides aggressive modern intensive care treatment, early diagnosis and correct choice of anti-streptococcal antibiotics are crucial. A possible adverse effect of non-steroidal anti-inflammatory agents requires confirmation in a multicenter study.
A case of toxic shock syndrome (TSS) with meningismus as main symptom is presented. The case illustrates that, in cases of rigidity of the neck and back, not directly explainable, TSS should be considered as a possible diagnosis. Toxic syndrome (TSS) is a severe, acute infectious disease with great variations in symptomatology (1,2). Its lethality is approximately 5% (3). The prognosis depends on early diagnosis and treatment.
Toxic shock syndrome, a potentially lethal multisystem illness that usually affects menstruating women, is characterized by the acute onset of fever, hypotension, skin and mucous membrane changes, nausea, vomiting, diarrhea, myalgias, capillary leak, vascular collapse and multiorgan dysfunction. The disease is mediated by toxin produced by distinct strains of Staphylococcus aureus. We describe a case in which a toxin producing strain growing in a continent urinary diversion produced toxic shock syndrome.
In response to case reports of toxic shock syndrome, six case-comparison studies were done in 1980. Early cases were predominantly in menstruating women, and the use of tampons was strongly associated with the onset of illness. Because of the widespread publication of this finding, the case-comparison studies had problems due to differential ascertainment and recall bias. However, the number of cases among women was so great and the relation with tampon use so marked that unreasonable assumptions are necessary if the results are to be attributed to these biases. The studies show the power of epidemiologic methods, even given the unfavorable circumstance of an uncommon condition, associated with a common practice. Although the absolute risk of toxic shock syndrome is small, tampon users have more than a tenfold excess risk of the condition over women not using tampons, and the use of tampons is an adequate explanation for the excess risk of women over men.
Fifteen patients with toxic shock syndrome were seen in a 2-yr period at a university medical center. Five (33%) patients had severe cardiorespiratory failure and underwent hemodynamic monitoring before and during infusion of dobutamine hydrochloride (dobutamine). Three distinct hemodynamic stages were identified. Initially there was a hyperdynamic cardiovascular state with a high cardiac index (5.5 +/- 0.9 L/min X m2, mean +/- SEM), normal pulmonary artery wedge pressure (11.5 +/- 1.5 mm Hg), and low mean blood pressure (66 +/- 5 mm Hg). The second stage (decompensated) revealed myocardial dysfunction with decreased left ventricular fractional shortening. Serial two-dimensional and M-mode echocardiograms performed on two patients showed left atrial and left ventricular end-diastolic diameters at the upper limits of normal. The mean blood pressure recorded for all five patients was essentially unchanged; however, cardiac index decreased to 3.1 +/- 0.4 L/min X m2 and wedge pressure increased to 17.5 +/- 2.1 mm Hg. This decompensated stage responded to iv infusion of dobutamine by an increase in cardiac index to 5.4 +/- 0.5 L/min X m2, a decrease in wedge pressure to 11.0 +/- 2.0 mm Hg, and an increase in mean blood pressure to 100 +/- 10 mm Hg. During recovery, echocardiograms returned to normal. All five patients developed severe adult respiratory distress syndrome. All had reversible ECG findings of sinus tachycardia, diffuse loss of voltage, flattened T waves and diffuse nonspecific ST-T wave changes. Our findings suggest a reversible toxic cardiomyopathy as the cause of cardiorespiratory failure in toxic shock syndrome. Our experience suggests inotropic support with dobutamine is beneficial in selected cases.
A noncompetitive enzyme-linked immunosorbent assay that enables the quantitation of toxic shock syndrome toxin 1 (TSST-1) to as little as 30 pg/ml and the detection of TSST-1 to 10 pg/ml in phosphate-buffered saline including 33% human serum or plasma was developed. It takes only 3 h to complete this assay after plate preparation. In this study, 64 human serum samples obtained from 30 patients with toxic shock syndrome or toxic shock syndrome-like symptoms were subjected to testing for the detection of TSST-1. With a cutoff level for TSST-1 of less than 100 pg/ml, 28 samples obtained from 12 patients were positive for TSST-1. The mean and maximum concentrations for these TSST-1-positive samples were 440 and 5,450 pg/ml, respectively. Of these 12 patients, 8 were Staphylococcus aureus culture positive, 3 were negative upon bacterial culturing, and 1 had no cultures done.
The primary cause of toxic shock syndrome is toxic shock syndrome toxin 1 (TSST-1), a 22,049-dalton exotoxin. Approximately 20% of Staphylococcus aureus isolates produce TSST-1; the production of this toxin is therefore a variable genetic trait. The TSST-1 gene and its flanking sequences are found on a genetic element that is present in TSST-1-positive isolates and absent in TSST-1-negative isolates. Preliminary sequence data and Southern hybridization experiments with the cloned flanking sequences have provided evidence that the TSST-1 element is 4-7 kilobases in size. Hybridization analysis of whole-cell DNA from two genetically mapped TSST-1-positive strains has demonstrated that the TSST-1 element has at least two chromosomal locations. This finding suggests that the element is mobile. Biotyping of 75 TSST-1-positive isolates showed that the large majority were tryptophan-negative, and Southern hybridization analysis of whole-cell DNA from these isolates revealed a common blotting pattern--an observation suggesting that these strains are clonal.
IgM antibodies against toxic shock syndrome toxin-1 (TSST-1) in 1990 human sera and in 14 human immunoglobulin preparations were determined using an enzyme linked immunosorbent assay. High levels of IgM antibody titres could be found beginning with the third month of life within the first 5 years of age. They were also very common in the age group of 21 up to 25 years. In no case of IgM antibodies with titres higher than 1:251 symptoms could be observed as described for toxic shock syndrome. Of the human immunoglobulin preparations, Pentaglobin contained IgM antibodies against TSST-1 only. The results show that most of the infections with TSST-1 producing Staphylococcus aureus are of subclinical nature or are of less dramatic course than the commonly known toxic shock syndrome.
Two previously healthy men who presented with hypotension, constitutional symptoms, and targetoid and discrete spotty erythematous plaques were diagnosed with toxic shock syndrome based on histopathological findings. Specifically, their biopsies revealed necrotic keratinocytes, neutrophils in the epidermis, and neutrophils surrounding dilated superficial vessels. In one case, the diagnosis of toxic shock syndrome was confirmed with rising titers to toxic shock syndrome toxin-1. Both patients recovered with supportive care and clindamycin administration. We suggest that patients with fever, hypotension, constitutional symptoms and rash should be started on clindamycin and have a skin biopsy as part of their initial evaluation. An understanding that toxic shock syndrome can strike anyone has manifold dermatological manifestations and defined histopathological findings is important for its early diagnosis and effective treatment.
Spontaneous mutants that have pigmentation different than that of their parents were isolated from three Staphylococcus aureus strains associated with toxic shock syndrome. These mutants produced toxic shock syndrome toxin 1 in amounts varying from less than 0.05 to greater than 25 times that produced by the parents. The occurrence of nonpigmented variants may be overlooked if only one isolate from a patient with toxic shock syndrome is selected for analysis.
Native toxic shock syndrome toxin 1 (TSST-1) purified from Staphylococcus aureus has been crystallized in four different forms. The highest resolution data (2.05 A) was collected from orthorhombic crystals belonging to the space group C222(1). The unit cell dimensions are a = 108.7 A, b = 177.5 A, c = 97.6 A. Rotation function analysis of this form indicates that there is trimer of toxin molecules in the asymmetric unit with a local 3-fold axis parallel to the crystallographic c axis. Crystals of a double mutant of TSST-1 have been grown which has a single molecule in the asymmetric unit and diffract to 1.9 A. The space group is P2(1) with unit cell parameters of a = 44.4 A, b = 34.0 A, c = 55.2 A, beta = 93.0 degrees.
The etiology of toxic shock syndrome (TSS) has been extensively investigated in recent years. It is generally accepted that the causative organism is Staphylococcus aureus. Certain strains of this bacterium produce one or more toxins which are thought to be responsible for the symptoms associated with TSS. There is no general agreement, however, as to why menstruating women who use tampons are of particular risk for developing this disease. More recently, TSS has also been associated with the use of absorbent contraceptive sponges. In this paper I will present evidence that the introduction of oxygen into the vaginal cavity during tampon insertion is responsible in part for the development of TSS. Furthermore, I will discuss several methods for the safe removal of this exogenous oxygen.
Three cases of toxic shock syndrome are presented. All exhibited hypotension and involvement of three or more organ systems. Staphylococcus aureus was isolated in all cases. All patients recovered without sequelae. The etiology, clinical features, differential diagnosis, therapy, and preventive measures are discussed.