Gene/Protein Disease Symptom Drug Enzyme Compound
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 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reported cases of toxic shock syndrome (TSS) following nasal surgery or functional endonasal sinus surgery (FESS) are uncommon. Classic TSS is a serious multisystem disorder resulting from Staphylococcus aureus phage I toxic shock syndrome toxin 1 (TSST-1), and it is characterized by fever, rash, hypotension, mucosal hyperemia, vomiting, diarrhea, and laboratory evidence of multisystem organ dysfunction. TSS cases following nasal surgery have been associated with nasal packing, mucosal barrier violation, prior S aureus phage I colonization, as well as low antitoxin antibody levels. Of the 1700 FESS procedures performed at our institution, 3 cases were complicated by classic TSS, with 2 additional patients having a postsurgical course compromised by a milder degree of TSS. Diagnostic criteria, clinical presentation, management, and etiology are discussed, and the possibility of a continuum from mild-to-classic TSS is addressed.
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PMID:Toxic shock syndrome after functional endonasal sinus surgery: an all or none phenomenon? 805 75

A thirty-three year old female presented to our emergency department complaining of severe abdominal pain, nausea, and vomiting. On physical examination she was hypotensive with a firm, tender abdomen, cervical motion tenderness and a diffuse erythematous rash. A surgical diagnosis of Acute Pelvic Inflammatory Disease was made during laparoscopy. Coagulant studies, liver function tests, culture results, and the desquamation of the patient's palms led to the additional diagnosis of Toxic Shock Syndrome. A literature search failed to reveal any similar cases of Pelvic Inflammatory Disease (PID) and Toxic Shock Syndrome (TSS) occurring concomitantly. Patients may present severely ill with either of these disease entities but potential for serious illness is greater when both of these syndromes occur in the same patient. We conclude that in patients with a similar presentation, the symptoms should not be attributed completely to PID without further investigation and consideration of a concomitant disease process including TSS.
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PMID:A 33-year-old white female with abdominal pain, nausea, vomiting and hypotension. 834 May 81

Four days after being bitten by an insect a 35-year-old woman without any serious underlying disease developed an extensive phlegmonous inflammation of the left eyelid which soon spread to the entire left half of her face. Streptococcus pyogenes serotype M1, which produced the erythrogenic toxin A in vitro, was isolated from two blood cultures. The course of the illness was characterized by high fever, diarrhoea, vomiting, circulatory failure, consumption coagulopathy, abnormal renal functions and a generalized exanthem with desquamation of the skin, exhibiting the full-blown picture of a toxic shock syndrome caused by S. pyogenes. She eventually recovered completely under intensive care involving administration of catecholamines, fresh frozen plasma and antithrombin III substitution, as well as antibiotic treatment with clindamycin (600 mg three times daily), ampicillin/sulbactam (4 g three times daily)--after 3 days replaced by imipenem (0.5 g four times daily)--and gentamycin (80 mg three times daily) for two weeks. Extensive necroses later required plastic surgery to the left eyelid, cheek and temporal region.
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PMID:[Toxic shock syndrome caused by Streptococcus pyogenes]. 840 89

The features of toxic shock syndrome in burned children have been described in a review of seven patients (J. D. Frame et al., Burns 1985; 11, 234). These include a 'prodromal' 24-48 h period with diarrhoea, vomiting, general malaise, pyrexia, tachycardia and tachypnoea. The white cell count and haemoglobin concentration fall prior to the 'shock' phase, which occurs 3-4 days postburn. Once 'shock' has occurred the mortality of the condition is approximately 50 per cent; in the absence of 'shock' it is much reduced. We have undertaken a retrospective review of six burned children who were admitted in a 2-year period to the Mount Vernon NHS Trust Burns Unit with a clinical diagnosis of toxic shock syndrome. The evidence from our patients suggests that reliable early diagnostic signs are a rapidly developing severe pyrexia of 39.5 degrees C or above, and a simultaneously increasing tachycardia and tachypnoea to high levels. There is a sudden profound fall in the white cell count and haemoglobin concentration over a period of hours between 1 and 3 days from injury. Specific treatment should be instituted before the onset of 'shock'. The name staphylococcal toxaemia might promote earlier diagnosis and treatment of this condition and so reduce its mortality.
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PMID:Early diagnosis of staphylococcal toxaemia in burned children. 835 73

We report a rare case of non-menstrual toxic shock syndrome (TSS) in the course of Staphylococcus aureus sepsis in a 31-year-old primigravida who developed high fever and severe pulmonary and cardiovascular failure within a few hours at the end of the 29th week of a twin pregnancy. Mechanical ventilation was necessary due to signs of adult respiratory distress syndrome (ARDS) and catecholamines were needed to maintain a somewhat adequate blood pressure. A forceps delivery was performed immediately. Postoperatively, the patient was brought to the intensive care unit (ICU) due to the suspicion of severe septic shock. In addition to the extreme cardiovascular instability and massive disturbance of pulmonary gas exchange, the clinical picture was characterised by a disseminated intravascular coagulopathy (DIC) with marked petechial bleeding and ecchymoses on all extremities. Moreover, a confluent, spotty exanthem of the trunk and extremities could be seen. Despite all therapeutic efforts, the patient died within a few hours after admission to the ICU with signs of multiorgan failure. Post-mortem, multiple staphylococcal abscesses were found in the kidneys, liver, and uterus. Moreover, acute ulcerous endocarditis of the mitral valve and septic myocardial foci with myocarditis were seen. The Staph. aureus strain isolated from the blood cultures was shown to produce TSS toxin 1 (TSST-1) and enterotoxin B. In summary, the clinical picture can be interpreted as severe staphylococcal sepsis complicated by TSS. TSS is a specific type of infectious disease, occurring mainly in young women during the menstrual period (80%-90%), but it has also been reported in non-menstrual cases (10%-20%). It is characterised by sudden-onset high fever, hypotension, rash, mucosal hyperaemia, and various additional symptoms such as myalgia, vomiting, and diarrhoea. The clinical course depends on the extent of the organ failure due to decreased tissue perfusion during hypotension. Severe cases are accompanied by multiple organ-system failure including impaired renal function, which is reversible in nearly all cases. Respiratory failure ranges from interstitial and alveolar aedema to ARDS in 10% of cases; severe DIC is seen in 10%-15%. Another severe clinical complication is cardiac insufficiency. The etiology of TSS is based on a localized or, rarely, systemic infection with certain Staph. aureus strains that are capable of producing toxins, the most important one being TSST-1. Staph. aureus strains can also produce various other enterotoxins that may be involved in the pathogenesis of TSS. The pathogenetic importance of the toxins is supported by the antibody titers in TSS patients: more than 80% of healthy adults show high levels of antibody titers, whereas 90% of TSS patients exhibit low levels in the acute phase followed by a significant increase during convalescence. It is not clear whether the toxins cause TSS by a direct effect or by release of mediators due to their function as superantigens. The clinical characteristics of non-menstrual TSS are identical to those of menstrual TSS, but it can occur in many clinical settings in both sexes at any age. Severe clinical courses are more frequent in non-menstrual TSS: the mortality is about 8%-11% in non-menstrual TSS compared to 2%-5% in menstrual TSS. The diagnosis is based mainly on clinical signs and the isolation of toxin-producing Staph. aureus strains. Besides antibiotic therapy, treatment is primarily directed to the correction of hypotension and additional organ-system failure. Other therapeutic measures such as the elimination of toxins by plasma separation or the administration of antibodies or gamma-globulins are subjects of investigation with no general recommendations at this time.
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PMID:[Lethal, non-menstrual toxic shock syndrome associated with Staphylococcus aureus sepsis]. 859 62

Toxic shock syndrome is a life-threatening exotoxin mediated disease caused by Staphylococcus aureus, which was originally described as affecting menstruating women, but has lately been reported after surgical procedures and burns. The high mortality emphasises the importance of early diagnosis. In most cases there is a prodromal period with fever (> 38.9 degrees C), myalgia, headache, and vomiting before the onset of hypotension and multiorgan failure. We present two cases in children with minor burns, and review current recommendations for treatment.
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PMID:Toxic shock syndrome after burn injuries in children. 907 92

The most common complication in children with varicella is cutaneous superimposed infection with pyogenic bacteria. Group A beta-hemolytic streptococci, which are known to cause life-threatening infections in both previously healthy children and those with underlying diseases, are the most frequently associated pathogens. A newly recognized disease, called streptococcal toxic shock syndrome, is associated with severe morbidity and mortality. We report a 3-year-old boy with a diagnosis of this syndrome who presented with increasing fever, vomiting, and lethargy 7 days after the development of a classic varicella skin lesion. In spite of aggressive fluid supply, administration of inotropic agents, and cardiopulmonary resuscitation, a rapidly deteriorating clinical course led to death 4 hours after hospitalization. This is the first report of this association in Taiwan. Pediatricians evaluating children with varicella must be mindful of the potential for Group A beta-hemolytic streptococcal infection.
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PMID:Streptococcal toxic shock syndrome complicating varicella in children. 930 31

Two previously healthy women, aged 30 and 35 years, suffered pain in the lower abdomen, one before and the other after spontaneous delivery at 40 and 33 4/7 weeks of amenorrhoea, respectively, while a third woman, aged 33, at 36 weeks of amenorrhoea developed pain in the lower abdomen, fever, vomiting, and diarrhoea. All three women were found to have a uterine infection caused by streptococci of Lancefield group A (group A Streptococcus, GAS). In one woman, the diagnosis was made rapidly so that antibiotic treatment could be instituted in time; the other two developed sepsis and multiorgan failure, with a fatal issue in one of them. The three children also were septic, two recovered after treatment and one died. Since the eighties, serious GAS infection has been on the increase. The worst manifestation is the toxic shock syndrome caused by streptococci. Abdominal pains after delivery may be a first sign of this, and should not too readily be interpreted as just after pains. The condition may also develop before delivery. In view of the high mortality rate, early diagnosis and antibiotic treatment are of vital importance for mother and child.
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PMID:[Puerperal fever: an old enemy in aggressive form]. 954 40

We report the case of a 21-year-old man who had been developing acute renal failure with Methicillin-resistant Staphylococcus aureus (MRSA) colitis and sepsis. He was admitted for consciousness disturbance, nausea, vomiting, and diarrhea. Oliguria was also observed and his serum creatinine level was elevated to 10 mg/dl. Urinary protein was positive and an abundance of hyaline cast were seen in urinary sedimentation. Diarrhea and pyrexia were prolonged and serum C-reactive proteins were elevated, but lymphocyte and leukocyte counts temporarily decreased from the 3rd to the 6th hospital day and remained low until normalizing after the 14th day. His clinical symptoms improved with hemodialysis (HD) and effective antibiotic therapies. An MRSA strain producing toxic shock syndrome toxin-1 (TSST-1), a super antigen which specifically stimulates human V beta 2-positive T cells, was separated from his feces and blood. To ascertain the cause of his renal dysfunction, a renal biopsy was performed on the 8th day. His renal histology revealed acute interstitial nephritis with severe inflammatory cell infiltration around the medullary areas without glomerular changes. Most of the infiltrated cells were small monocytes, and lymphoid cells were rich in the interstitium. With immunohistochemical staining, over 70% of T-cells were V beta 2-positive. TSST-1-producing MRSA was detected in his blood specimen. Furthermore, V beta 2-positive T cells were accumulated in the renal intersititium, and transient lymphocytopenia was observed. These data suggested the following possible pathogenesis for interstitial nephritis: TSST-1 acts as a super antigen in the renal interstitium where major histocompatibility complex (MHC) is class-2-positive, thereby resulting in interstitial nephritis with T cell migration.
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PMID:[A case of interstitial nephritis induced by a super antigen produced by methicillin-resistant Staphylococcus aureus (MRSA) presenting as acute renal failure]. 1036 25

Staphylococcus aureus and Streptococcus pyogenes express pyrogenic toxin superantigens (PTSAgs) that are associated with toxic shock syndrome (TSS) and staphylococcal food poisoning (SFP). Most PTSAgs cause TSS in deep-tissue infections, whereas only TSS toxin 1 (TSST-1) is associated with menstrual, vaginal TSS. In contrast, SFP has been linked only with staphylococcal enterotoxins (SEs). Because of the differential abilities of PTSAgs to cause systemic or localized symptoms in a site-dependent manner, the present study was undertaken to assess the toxins' abilities to cross mucosal barriers. The activity of three PTSAgs when delivered orally, vaginally, or intravenously to rabbits and orally to monkeys was investigated. TSST-1 induced shock via all three routes in rabbits. Although active when administered intravenously, SEC1 and streptococcal pyrogenic exotoxin A (SPEA) did not cause symptoms when administered orally or vaginally. Only SEC1 induced emesis in the monkey feeding assay. TSST-1, albeit less stable than SEC1 and SPEA to pepsin, induced diarrhea in monkeys. Our results may explain the unique association of TSST-1 with menstrual TSS and why SPEA is only rarely associated with TSS after pharyngitis, despite being highly associated with TSS after subcutaneous infections. Finally, our studies indicate that enterotoxicity in SFP is not the result of superantigenicity.
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PMID:Pyrogenic toxin superantigen site specificity in toxic shock syndrome and food poisoning in animals. 1081 21


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