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PubMed2003

Toxic shock syndrome in a horse with Staphylococcus aureus pneumonia.

A 3-year-old Thoroughbred gelding was examined because of clinical signs of pneumonia and shock. Mucous membrane petechiation and ventral edema were observed and considered to be a result of vasculitis. Epidermal necrosis developed on the distal portions of the limbs. The horse had a persistent high fever that was unresponsive to nonsteroidal anti-inflammatory treatment, and Staphylococcus aureus was isolated from a nasal swab specimen and 2 transtracheal wash fluid samples. Antimicrobial, anti-inflammatory, and supportive treatment resulted in clinical improvement. However, resolution of the pulmonary infection required long-term (42 days) antimicrobial administration. Staphylococcus aureus strains isolated from this horse were positive for the toxic shock syndrome toxin-1 gene and were shown to produce toxic shock syndrome toxin-1, the causative factor in toxic shock syndrome in humans. The horse's clinical signs were attributed to toxic shock syndrome secondary to pulmonary S. aureus infection.

Animals↗

PubMed1998

Flush resuscitation for group A streptococcus toxic shock: a possible role for continuous renal replacement therapy and plasmapheresis.

Group A streptococcus has emerged as a major cause of aggressive life-threatening deep-seated infections. In addition, toxic shock syndrome caused by Group A streptococcus was recognized in 1983. Group A streptococcus produces several potent exotoxins which explain the pathophysiology of these invasive infections. Other virulence factors such as M protein, which can impede phagocytosis, are associated with some Group A streptococcus. M protein and streptococcal pyrogenic exotoxins may act as super antigens. Host factors may influence the severity of infection. Blood purification techniques such as continuous renal replacement therapy and plasmapheresis can remove streptococcal exotoxins as well as inflammatory mediators. Replacement with fresh-frozen plasma corrects coagulopathy and may provide some antibody protection. Four patients with Group A streptococcus-toxic shock syndrome treated with continuous renal replacement therapy, plasmapheresis, or both showed dramatic, rapid improvement in cardiovascular dynamics and respiratory parameters. Two patients died. The mainstay of treatment for Group A streptococcus-toxic shock syndrome remains early diagnosis, aggressive surgical control of the infection, and appropriate antibiotics (i.e., penicillin and clindamycin). Flush resuscitation may rescue some patients from profound toxic shock. The mechanisms of action need to be delineated.

Anti-Bacterial Agents↗

PubMed1984

Variant postpartum toxic shock syndrome with probable intrapartum transmission to the neonate.

We report a unique mother-infant pair with variant staphylococcal toxic shock syndrome and probable intrapartum transmission to the neonate. Diagnosis of probable toxic shock was supported by the finding of fever, desquamative skin rash, multi-organ system involvement, and pronounced mucocutaneous manifestations, including strawberry tongue, dermal swelling, pharyngitis, and vulvar edema, although hypotension was absent. Staphylococcus aureus was isolated from the vagina, placenta, chorioamnion, and surface swabs and gastric aspirates of the infant. The isolates produced enterotoxin C but not enterotoxin F, and illness developed in both mother and infant despite preexisting high antibody titers to enterotoxin F and enterotoxin C. This unique mother-infant pair highlights our present lack of knowledge of the precise etiology and pathogenesis of toxic shock syndrome and illustrates the consequent difficulty in clinical diagnosis and laboratory confirmation of this disease in certain patients with atypical presentations.

Adult↗

PubMed1991

Effects of staphylococcal toxic shock syndrome toxin 1 on aortic endothelial cells.

In staphylococcal toxic shock syndrome, hypotension and shock due to capillary leak may rapidly lead to death of the host. To investigate its pathogenesis, the cytotoxic effects of toxic shock syndrome toxin 1 (TSST-1) on porcine aortic endothelial cells (PAEC) were examined in vitro. TSST-1 killed PAEC (as measured by 51Cr release) in a dose- and time-dependent fashion and was blocked by anti-TSST-1 antibodies. Receptor-mediated endocytosis may be critical for the cytotoxic effects of TSST-1, as killing was inhibited by cold (4 degrees C) and by addition of chloroquine and methylamine. Furthermore, calcium and oxygen appeared necessary for TSST-1 effects on PAEC. Membrane receptor binding studies indicated PAEC bind TSST-1 with high affinity (Kd = 5.7 x 10(-7) M) and had 2.2 x 10(4) receptors/cell. Last, as measured by 125I-labeled albumin flux in a transendothelial permeability model, TSST-1 enhanced the permeability of PAEC monolayers in a dose- and time-dependent manner.

Animals↗

PubMed2004

[Recurrent catamenial encephalopathy secondary to toxic shock syndrome].

INTRODUCTION: Neurological clinical manifestations are often observed in toxic shock syndromes. However they unusually dominate the clinical picture. OBSERVATION: We present a case of recurrent catamenial encephalopathy, with epileptic seizures, revealing a menses toxic shock syndrome.

Adult↗

PubMed1988

Variable effect of toxic shock toxins from different sources on neutrophil function in vitro.

Toxic shock syndrome toxins (TSST) are 23-30 kD proteins that have been isolated from incubation media of strains of Staphylococcus aureus cultured from patients with toxic shock syndrome (TSS). Injection of TSST into animals produces many of the symptoms that characterize TSS including shock, fever, and multiple organ failure. We found that addition of increasing concentrations of TSST-1-VP1035-16A, but not TSST-PEC, TSST-SEC, staphylococcal enterotoxin A or B, progressively decreased human neutrophil bactericidal activity against S. aureus, 502A in vitro. TSST-1-VP1035-16A, but not the other toxins, also decreased superoxide anion and hydrogen peroxide concentrations in mixtures containing neutrophils and phorbol myristate acetate (PMA) in vitro. The results indicate that various preparations of TSST have different effects on neutrophil function in vitro and, accordingly, may have different effects in other in vitro and in vivo models of TSS.

Bacterial Toxins↗

PubMed1984

Comparative observations of fever and associated clinical hematological and blood biochemical changes after intravenous administration of staphylococcal enterotoxins B and F (toxic shock syndrome toxin-1) in goats.

The present investigation was undertaken to examine the characteristics of purified toxic shock syndrome toxin-1 (staphylococcal enterotoxin F) given intravenously to dwarf goats (dose, 0.02 to 20 micrograms kg-1). Rectal temperature, heart rate, rumen motility, plasma zinc and iron concentrations, and certain other blood biochemical and hematological values were studied and compared with the changes seen after intravenous administration of staphylococcal enterotoxin B (dose, 0.02 to 0.5 micrograms kg-1). Similar changes such as fever, tachycardia, inhibition of rumen contractions, drop in plasma zinc and iron concentrations, lymphopenia, and a decrease in serum alkaline phosphatase activity were observed. In contrast to the effects of toxic shock syndrome toxin-1, staphylococcal enterotoxin B induced colic, watery diarrhea with pseudomembranes, hemoconcentration, and a more pronounced increase in blood urea nitrogen. The results obtained demonstrate that (i) in the goat staphylococcal enterotoxin B is much more potent than toxic shock syndrome toxin-1 and (ii) the goat is a useful model to study the gastro-intestinal effects caused by staphylococcal enterotoxin B. The present finding that no clear relationship could be found between the temperature response and the alterations in zinc and iron levels in plasma support the theory that the febrile reactions and the changes in plasma trace metals are mediated by different polypeptides released by activated macrophages.

Animals↗

PubMed1992

Intravenous immunoglobulin therapy for toxic shock syndrome.

Staphylococcus aureus and group A Streptococcus pyogenes produce toxic shock syndrome characterized by hypotension and multisystem organ failure. While conventional therapy has consisted of antibiotics and intensive supportive care, some experimental evidence suggests that immunoglobulins directed against the toxins may be effective additional therapy. We report a case of "toxic strep syndrome" in which intravenous immunoglobulin was administered when signs and symptoms were worsening while the patient was receiving conventional therapy. Within hours of administration of the intravenous immunoglobulin, the patient experienced dramatic clinical improvement. This response suggests a possible therapeutic benefit of intravenous immunoglobulin in toxic shock syndrome.

Adult↗

PubMed1987

Binding of toxic-shock-syndrome toxin-1 to human peripheral blood mononuclear cells.

Toxic-shock-syndrome toxin-1 (TSST-1), produced by Staphylococcus aureus and associated with toxic shock syndrome, functions in vitro as both a lymphoproliferative and immunosuppressive protein for human peripheral blood mononuclear cells (PBMs). We analyzed TSST-1-target cell interactions by receptor-ligand binding analyses. In competitive binding experiments, 2 X 10(5) human PBMs or purified cell populations were incubated in the presence of small amounts of (5-50 ng) of 125I-labeled TSST-1 and increasing amounts of unlabeled TSST-1 (25-10,000 ng). Data were analyzed by the method of Scatchard. Toxin-specific receptors were shown to exist on T lymphocytes within the PBM population. T4+ cells had 27.5 X 10(6) receptors per cell, and T8+ cells had 9 X 10(6) receptors per cell. T4+ and T8+ receptors had dissociation constants of 2.58 X 10(-8) M and 1.8 X 10(-8) M, respectively. These studies confirm earlier work showing that TSST-1 causes the functional activation of a population of T lymphocytes involved in suppression of immunoglobulin responses.

Bacterial Toxins↗

PubMed2006

Drotrecogin alfa (activated) for nonmenstrual toxic shock syndrome associated with methicillin resistant Staphylococcus aureus infection.

Nonmenstrual toxic shock syndrome (TSS) due to Staphylococcus aureus can lead to significant morbidity and mortality. While drotrecogin alfa (DA) has been employed in patients with Methicillin-resistant Staphylococcus aureus (MRSA) severe sepsis and septic shock, its utility in TSS remains unclear. The authors report a case of severe sepsis in the setting of MRSA-associated TSS that responded to treatment with DA. This case illustrates a potential role for DA in the treatment of toxic shock syndromes and emphasizes the importance of aggressive diagnostic and therapeutic modalities in approaching these conditions.

Anti-Bacterial Agents↗

PubMed1983

Carpal tunnel syndrome. Complication of toxic shock syndrome.

Peripheral nerve complications occurred in four patients with toxic shock syndrome. Each patient had an acute carpal tunnel syndrome develop that was verified by nerve conduction studies. Recovery was rapid in two cases, but delayed in two others. Decompressive procedures were required in only one patient, with eventual recovery. Another condition, the toxic shock syndrome, must now be added to the long list of possible causes of compression of the median nerve in the wrist.

Adult↗

PubMed2000

Kallikrein-kinin system activation in streptococcal toxic shock syndrome.

A retrospective analysis of 7 patients with streptococcal toxic shock revealed isolated prolongation of the activated partial thromboplastin time, which returned to normal during recovery. Levels of factor XII were reduced in 2 patients who had single factor assays performed, consistent with activation of the kallikrein-kinin system. We speculate that bradykinin release following activation of the kallikrein-kinin system in streptococcal toxic shock may underlie the features of pain, capillary leaking, and severe hypotension characteristic of this syndrome.

Bradykinin↗

PubMedDate not supplied

Streptococcal toxic-shock syndrome: spectrum of disease, pathogenesis, and new concepts in treatment.

Since the 1980s there has been a marked increase in the recognition and reporting of highly invasive group A streptococcal infections with or without necrotizing fasciitis associated with shock and organ failure. Such dramatic cases have been defined as streptococcal toxic-shock syndrome. Strains of group A streptococci isolated from patients with invasive disease have been predominantly M types 1 and 3 that produce pyrogenic exotoxin A or B or both. In this paper, the clinical and demographic features of streptococcal bacteremia, myositis, and necrotizing fasciitis are presented and compared to those of streptococcal toxic-shock syndrome. Current concepts in the pathogenesis of invasive streptococcal infection are also presented, with emphasis on the interaction between group A Streptococcus virulence factors and host defense mechanisms. Finally, new concepts in the treatment of streptococcal toxic-shock syndrome are discussed.

Animals↗

PubMed1996

Toxic shock syndrome toxin-1-induced death is prevented by CTLA4Ig.

Lethal toxic shock syndrome (TSS) results from the MHC class II presentation of bacterial superantigens, most commonly toxic shock syndrome-1 (TSST-1), to specific TCR Vbeta-bearing T cells. This superantigen-induced stimulation of whole T cell subsets leads to the exuberant cytokine production that in turn causes the shock syndrome. Since T cell activation and cytokine production are known to be dependent upon costimulatory signals, we reasoned that interfering with costimulation could effect TSS outcome. To test that hypothesis, we evaluated the effect of CTLA4Ig, a fusion protein known to block costimulatory signaling, on TSST-1-induced responses. CTLA4Ig not only blocked TSST-1-stimulated T cell proliferation by 90% in vitro, it also strikingly ameliorated TSST-1 induced TSS in vivo. While all mice co-administered TSST-1 and control Ig died, 75% of the CTLA4Ig plus TSST-1-treated mice survived. This salutary CTLA4Ig effect correlated with markedly diminished TSST-1 induced serum levels of TNF-alpha and IFN-gamma, but TSST-1-triggered IL-2 release was not affected. Surprisingly, while CTLA4Ig treatment group survivors remained sensitive to TSS induced by an unrelated superantigen (staphylococcal enterotoxin B), they were completely resistant to a second TSST-1 challenge. Furthermore, this TSST-1 resistance could be transferred to naive C57BL/6 mice using CD8+ T cells from CTLA4Ig plus TSST-1-primed mice. These data suggest several novel interpretations: 1) that the release of TNF-alpha and IL-2 have a different costimulatory signal dependence in vivo, 2) that the TSS resistance conferred by CTLA4Ig was superantigen specific, and 3) that the delayed and transferable resistance to TSST-1 was due, at least in part, to CD8+ T cells with suppressor function.

Abatacept↗

PubMed2004

[Group A beta-hemolytic streptococcal toxic shock].

In the last years has been observed an increased incidence of invasive group A beta-hemolytic streptococcal infections, including the toxic shock syndrome. The most common portal of entry is the skin and mucous membranes. The toxic shock syndrome can occurred as a rare complication of pharyngitis. The association between varicella and the use of nonsteroidal antiinflammatory drugs with necrotizing fasciitis by Streptococcus pyogenes has been discussed without reach at consensus, but some authors disapproved the use of nonsteroidal antiinflammatory drugs in this viral infection. The authors reported the clinical case of a 12 year old adolescent, that 15 days after the diagnosis of mononucleosis infectious confirmed by serology and treated with ibuprofen, was internment by streptococcal toxic shock syndrome with rhabdomyolysis, hepatitis, cellulitis of the leg, arthritis of the knee and pleural effusion. Therapeutics was made with penicillin G and clindamycin. We present this case for the severity of the clinical situation and for the questions that rise.

Child↗

PubMed1993

Structure of toxic shock syndrome toxin 1.

The three-dimensional structure of toxic shock syndrome toxin 1 (TSST-1) from Staphylococcus aureus has been determined and refined to an R value of 0.226 for data between 8- and 2.5-A resolution. Overall, the structure of TSST-1 is similar to that of another superantigen, staphylococcal enterotoxin B (SEB). The key differences between these molecules are in the amino termini and in the degree to which a long central helix is covered by surface loops. The region around the carboxyl end of this central helix is proposed to govern the superantigenic properties of TSST-1. An adjacent region along this helix is proposed to be critical in the ability of TSST-1 to induce toxic shock syndrome.

Amino Acid Sequence↗

PubMed1988

Production of tumor necrosis factor by human monocytes in response to toxic-shock-syndrome toxin-1.

We studied the effect of toxic-shock-syndrome toxin-1 (TSST-1) on production of tumor necrosis factor (TNF) by human monocytes. Adherent mononuclear cells were stimulated with TSST-1 and their supernatants assayed for TNF by using L929 cells in a cytotoxicity assay. TSST-1 stimulated production of TNF over a wide range of concentrations. The cytotoxicity of monocyte supernatants was neutralized by antibody to TNF but not by antibody to interleukin-1 or by normal rabbit serum. TSST-1 and lipopolysaccharide (LPS) had a synergistic effect on monokine production. Monocytes "primed" with TSST-1 produced more interleukin-1 and TNF in response to LPS than did unprimed cells. Treating monocytes with LPS before TSST-1 and co-incubating the two agents with cells for 24 h also enhanced monokine production under some circumstances. These studies suggest a role for TNF in the pathogenesis of toxic shock syndrome, as a consequence of induction by TSST-1 alone or the synergistic effects of several bacterial products.

Bacterial Toxins↗

PubMed1982

Surveillance of toxic shock syndrome in Minnesota: comments on national surveillance.

In January 1980, the Minnesota Department of Health began the surveillance of toxic shock syndrome with epidemiologically defined active and passive components. The intensity of surveillance has been constant since its inception. As of 30 June 1981, 197 confirmed cases of toxic shock syndrome, 15% of all cases nationwide, have been identified in Minnesota. During the 18 months of active surveillance, the total cases reported per calendar quarter ranged from 20 to 24 cases, and the number of tampon-associated cases ranged from 15 to 21. There was no difference in the quarterly distribution of total (p greater than 0.2) or tampon-associated (p greater than 0.2) cases of toxic shock syndrome during the six quarters. Fifty-five tampon-associated cases had onset of illness during the 9 months of surveillance in which Rely tampons (Proctor & Gamble) were on the market; 59 tampon-associated cases had onset of illness during the 9 months after Rely tampons were removed from the market.

Adolescent↗