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Toxic shock syndrome (TSS) secondary to mastitis or breast abscess is only seldom described. We report a case of definite TSS due to postpartum staphylococcal mastitis which evolved over a period of 3 weeks to a breast abscess, recurring after 2 months. Only the episode of acute mastitis was complicated with TSS, while Staph. aureus could be isolated during the period of mastitis from milk and during drainage of the second breast abscess.
Toxic shock syndrome (TSS) is a severe multi-system disorder resulting from a Staphylococcus aureus exotoxin. Primary presenting features consist of fever, hypotension, vomiting and diarrhea, and a diffuse macular erythroderma with later desquamation. Treatment is supportive accompanied by drainage and debridement of infection and antibiotics. TSS may occur following any infection with Staphylococcus aureus and is a well-documented complication of nasal surgery. Otolaryngologists should be aware of the manifestations of this disorder and its treatment. A case is presented, along with a review of the literature and management of TSS.
Toxic shock syndrome (TSS) is a recently recognized acute multisystem illness that may recur. Epidemiologic links with menstruation and use of tampons have been identified. We report the cases of seven patients (six women and one man), 12 to 31 years old, seen over nine months, who met the criteria for TSS. Four were menstruating at onset. All had hypotension, fever, erythematous rash and distal desquamation. A prodrome of myalgias and diarrhea occurred in all patients. Clinical features of the acute illness included pharyngitis, conjunctivitis, leukocytosis and renal dysfunction (7), hepatobiliary abnormalities (6), mental confusion (6) and coagulopathy (4). In three patients, examination of cerebrospinal fluid showed abnormalities. The illness progressed in three patients to adult respiratory distress syndrome and significant cardiac dysfunction. Staphylococcus aureus was isolated from mucosal sites in six. The disease recurred in two. There were no deaths. Possible transmissibility was illustrated by two patients, a married couple, with simultaneous illnesses. Pathophysiologic features of TSS suggest a toxicogenic cause. Management consists of early recognition, vigorous fluid resuscitation, inotropic support as needed, discontinuation of tampon use and treatment with antistaphylococcal antimicrobic drugs.
Toxic shock syndrome (TSS) is a rare, life-threatening, acute multisystem illness usually characterized by sudden onset of high fever, diffuse sunburn-like erythroderma and a variety of other signs and symptoms. It may progress rapidly to hypotension and shock with multiple organ failure. Its exact cause is unknown, but in almost all cases there has been an infection with exotoxin-producing strains of phage group I Staphylococcus aureus. Although initially described in association with the use of superabsorbent tampons in menstruation, TSS has complicated a variety of surgical procedures. Recently in head and neck surgery attention has focused on absorbent packing materials, such as those used in postoperative nasal care. TSS developed in a 12-year-old 28 hours after tonsillectomy, nasal septoplasty and inferior turbinectomy in which absorbent packing material was used. It is important to maintain a high index of suspicion for TSS in all postoperative patients with fever, hypotension and erythroderma.
Toxic shock syndrome toxin is already known to induce the production of interleukin-1 (IL-1) by preparations of monocytes and macrophages that are presumably contaminated with other types of cells. The response is enhanced by increasing the density of such monocytes, suggesting that the monocyte's response to toxic shock syndrome toxin may be augmented by its interaction with some other cell. Nevertheless, we now show that several human and murine macrophagelike cell lines (U937, J774, P388D1, and WEHI 3) produce IL-1 when exposed to toxic shock syndrome toxin, and therefore the basic response does not require the presence of cells of other lineages. The cultured cells generally produce less IL-1 than do monocytes, but considerably more IL-1 is induced from cells that have undergone a terminal differentiation as a result of exposure to 1 alpha,25-dihydroxyvitamin D3. High concentrations of cultured cels suppress the production of IL-1; this effect is apparently not due to long-lived inhibitors of IL-1 production or of IL-1 activity, but may be due to a short-lived inhibitor of production.
Twenty-six hybridoma cell lines that produced monoclonal antibodies to toxic shock syndrome toxin 1 (TSST-1) were generated by immunizing mice with a highly purified preparation of TSST-1 and fusing their splenic lymphocytes with SP2/0-Ag-14 cells. One monoclonal antibody of the immunoglobulin G1 isotype, designated as PEC-1 10-2SCH, was selected for extensive study. The specificity of this antibody was determined by testing spent culture fluid filtrates of TSST-1- and non-TSST-1-producing strains of Staphylococcus aureus by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and enzyme-linked immunoelectrotransfer blot techniques. Monoclonal antibody PEC-1-10-2SCH was specific for TSST-1-producing strains of S. aureus, reacting with TSST-1 and two other proteins which appear to be unique to S. aureus strains that produce TSST-1. Monoclonal antibody PEC-1-10-2SCH was used in conjunction with polyclonal rabbit antibodies to TSST-1 in a rapid, one-step, sensitive, specific, and quantitative enzyme-linked immunosorbent assay. This assay was shown to be more sensitive, faster, and simpler to perform than previously described isoelectric focusing, immunodiffusion, and solid-phase radioimmunoassays for TSST-1. Monoclonal antibody PEC-1-10-2SCH was not reactive with Staphylococcus protein A under the conditions of the test.
The toxic shock syndrome in a serious disease. It occurs predominantly in menstruating women using tampons. About 40 deaths are associated with toxic shock syndrome. In the majority of cases Staphylococcus aureus was isolated from cervix and vagina. Most of the cases were observed in United States.
Fatal toxic shock syndrome developed in a previously healthy 19-year-old man following arthroscopy. The fulminant presentation led to an initial diagnosis of pulmonary embolus. Toxic shock syndrome must now be considered in the differential diagnosis of cardiovascular catastrophes.
Toxic shock syndrome toxin 1 (TSST-1) and streptococcal pyrogenic exotoxin A (SPE A) belong to a family of pyrogenic toxins produced by Staphylococcus aureus and Streptococcus pyogenes, respectively. Both toxins are responsible for causing toxic shock syndrome (TSS) and related illnesses, clinically characterized by multiorgan involvement. The most severe TSS symptom is acute hypotension and shock after the initial febrile response. In this study, we examined possible mechanisms of shock development in TSS, particularly the role of T-cell proliferation, endotoxin enhancement by toxins, and capillary leakage. American Dutch belted rabbits, with subcutaneously implanted miniosmotic pumps filled with either TSST-1 or SPE A, served as the animal model. For both TSST-1 and SPE A-treated rabbits, administration of cyclosporin A prevented toxin-induced T-cell proliferation but failed to protect the rabbits. Polymyxin B treatment of rabbits, to neutralize endogenous endotoxin, partially protected rabbits from challenge with either exotoxin; two of six rabbits survived on day 2 when treated with only TSST-1, whereas six of six animals survived after challenge with TSST-1 and polymyxin B. Similarly, with SPE A-treated rabbits, only 1 of 10 animals without polymyxin B treatment survived on day 8, but 4 of 6 rabbits survived on day 8 when given polymyxin B. Fluid replacement was successful in preventing lethality. Twelve of 14 rabbits survived when given TSST-1 with fluid, and all rabbits treated with SPE A and fluid survived. Finally, by using miniosmotic pumps, staphylococcal exfoliative toxin A and concanavalin A were administered to rabbits in an attempt to induce lethality. These two T-cell mitogens caused T-cell proliferation but failed to induce lethality in rabbits. The data suggest that toxin interactions causing vascular leakage and to some extent endotoxin enhancement are of major importance in development of hypotension and shock in TSS. It appears that T-cell proliferation may not contribute significantly to the induction of shock and death.
The toxic-shock syndrome (TSS) is a recently recognized syndrome characterized by sudden onset of high fever, vomiting, and diarrhea with rapid progression to hypotension and shock. It is caused by one or more not yet clearly defined exotoxins from staphylococcus aureus. The disease primarily affects young women using tampons during their menstrual periods, although it occurs also in non-menstruating women and in men. In these cases extragenital staphylococcus aureus infections are found. Since 1981 the toxic-shock syndrome associated with menstruation has occurred less frequently, whereas the non-menses-related toxic-shock syndrome appears with similar frequency. The syndrome resembles Kawasaki disease (mucocutaneous lymph node syndrome) in several aspects, namely fever, rash with subsequent desquamation, and cardiovascular involvement. However, shock, which is prominent in toxic-shock syndrome, is not usually seen in Kawasaki disease.
Postinfluenza toxic shock syndrome is a recently described entity that results from a respiratory tract infection with toxin-producing Staphylococcus aureus following an episode of influenza or influenzalike illness. This report describes a 19-year-old man who developed an influenza B respiratory infection complicated by staphylococcal pneumonia and toxic shock syndrome. The patient improved rapidly with specific antibiotic therapy, emphasizing the importance of considering this otherwise highly lethal syndrome in any individual who becomes critically ill after an initial influenzalike illness.
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Although toxic shock syndrome toxin-1 (TSST-1) has been proposed as the toxin responsible for toxic shock syndrome, its role in this disease has not been proved. To study this question, we examined Staphylococcus aureus strains isolated from normally sterile sites in patients with nonmenstrual toxic shock syndrome for the presence of TSST-1 production. Only 20 (62.5%) of 32 produced TSST-1, compared with 41 (93%) of 44 vaginal isolates from patients with menstrual toxic shock syndrome. Of strains of S aureus from patients with nonmenstrual toxic shock syndrome, TSST-1-negative isolates were more likely to be associated with a fatal outcome and to not be phage group 1 than TSST-1-positive isolates. Seven of the TSST-1-negative strains were evaluated in a rabbit subcutaneous chamber model of toxic shock syndrome. Fifteen (60%) of 25 rabbits developed a toxic shock syndrome-like illness and nine died. Clinical signs and histopathologic findings in the rabbits were similar to those seen in rabbits inoculated with TSST-1-positive S aureus isolates. These results suggest that other, as yet unrecognized, toxins play a role in toxic shock syndrome, and that TSST-1 production may not be essential to the pathogenesis of toxic shock syndrome.
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BACKGROUND: Staphylococcus aureus toxic shock syndrome toxin-1 and enterotoxin B are the major causes of toxic shock syndrome. These toxins are produced in sufficient concentrations to produce illness in the presence of certain tampons. This necessitates evaluating tampons, as well as wound dressings for their effects on S. aureus growth and toxin production. STUDY DESIGN: In this study, the Merocel vaginal sponge was evaluated both in vitro and in vivo in a rabbit model for effect on S. aureus. The Merocel sponge was tested in Erlenmeyer shake flasks containing growth media and in dialysis tubing immersed in agar growth media for both effect on S. aureus plate counts compared to media alone and effect on production of toxic shock syndrome toxins. The in vivo test included placement of Merocel sponges subcutaneously along the flanks of rabbits with subsequent inoculation with toxic shock syndrome bacteria and evaluation for development of illness and death. RESULTS: In the two standard in vitro tests, the shake flask and tampon sac, the Merocel sponge inhibited both growth of toxic shock syndrome S. aureus and production of toxic shock syndrome toxin-1 and enterotoxin B. The Merocel sponge also prevented development of toxic shock syndrome in a rabbit model. CONCLUSIONS: The data suggest the Merocel sponge may reduce the risk of development of toxic shock syndrome in association with its use. These studies may serve as models for evaluation of other products that are intended to be used on mucosal and skin surfaces, for their effect on toxic shock syndrome toxins.
Toxic Shock Syndrome is an acute multisystemic disease, characterized by high fever, hypotension and involvement of the skin and mucous membrane, associated with multisystem dysfunction. It is a rare condition in the paediatric population. We describe a newborn child with asphyxia and meconium aspiration, who developed a temperature of > or =38.9 degrees C, severe hypotension and rash with desquamation, associated with evidence of coagulopathy and renal and muscular dysfunction. Strict CDC criteria of toxic shock syndrome were fulfilled in our patient, with all major criteria verified. These criteria have never been validated in neonates, but in this case some symptoms favour a diagnosis of toxic shock syndrome since they are not associated with birth asphyxia, viral intrauterine infection or other disease. We believe a probable intrapartum transmission occurred through ingestion or aspiration of contaminated amniotic fluid. The patient described in this report is, to our knowledge, one of the youngest described to fulfil all of the strict CDC criteria for Toxic Shock Syndrome.
BACKGROUND: Toxic shock syndrome is a rare but potentially fatal toxin-mediated febrile illness. Although classically associated with tampon use, it is now known that many nonmenstrual conditions are related to this syndrome. Serious morbidity and mortality can occur if this syndrome is not promptly recognized. METHODS: MEDLINE was searched from 1978 to the present using the phrase "toxic shock syndrome." Case reports and articles related to tampon-associated toxic shock syndrome were excluded from the literature review except when defining toxic shock syndrome or discussing the cause of the syndrome. A case of nonmenstrual toxic shock syndrome associated with an intrauterine device and a review of the definition, cause, diagnostic criteria, and management are reported. RESULTS AND CONCLUSIONS: Toxic shock syndrome can mimic many common diseases. Because it can be associated with a number of nonmenstrual-related conditions, patients with unexplained fever and rash and a toxic condition out of proportion to local findings should have the diagnosis of toxic shock syndrome in their differential diagnosis. Early recognition and aggressive management can decrease the overall morbidity and mortality.
The mortality from septic shock remains high despite the availability of modern critical care facilities. In recent years, new agents have been tested to reduce morbidity and mortality in patients with severe sepsis. Among them, recombinant human activated protein C (rhAPC) has been reported to significantly reduce mortality and morbidity in patients with severe sepsis and one or more acute organ failures. We describe our experience with this drug in the early reversal of septic shock from toxic shock syndrome.