Cases reported "Shock, Septic"

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1/28. Febrile lady with acute renal failure and desquamating erythema.

    A 63-year-old woman developed acute renal failure and streptococcal toxic shock syndrome caused by streptococcus group G. Initially, an erythema resembling vasculitis was misleading. The subsequent clinical course, however, was typical for streptococcal toxic shock syndrome and met the criteria put forward by The Working Group on Severe streptococcal infections. In patients infected with streptococcus group G, toxic shock syndrome is rare. The streptococcus group G strains isolated from this patient did not produce pyrogenic exotoxins. Instead they produced an M-like protein related to group C and G streptococci that do not act as superantigens.
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2/28. Toxic shock syndrome associated with newly diagnosed type I diabetes.

    Studies of two post-mortem pancreata of children at the onset of type I diabetes have suggested activation and expansion of islet infiltrating T cells by a superantigen. We present the first reported case of a superantigen mediated disease, toxic shock syndrome (TSS), occurring at the diagnosis of type I diabetes. A 12-year-old girl presented with TSS and newly diagnosed diabetes with ketoacidosis. At presentation she was unconscious, febrile and hypotensive, with a desquamating erythematous rash and Kussmaul breathing. During resuscitation, her renal impairment, diarrhoea, thrombocytopaenia and ketoacidosis resolved. vaginal discharge and blood cultures grew Staphylococcus aureus. T cell studies at 2 weeks after diagnosis detected a high level of spontaneous and islet antigen-specific proliferation with associated interleukin-10 production compared to human leucocyte antigen DR matched controls.
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3/28. Postpartum clostridium sordellii infection associated with fatal toxic shock syndrome.

    Clostridium bacteria are anaerobic Gram positive spore-form-ing bacilli, known to cause distinct clinical syndromes such as botulism, tetanus, pseudomembranous colitis and myonecrosis. The natural habitats of Clostridium species are soil, water and the gastrointestinal tract of animals and humans. In 5-10% of all women, Clostridium species are also found to be normal inhabitants in the microbial flora of the female genital tract. In case of a non-sexually transmitted genital tract infection, Clostridium species are isolated in 4-20%, and clostridium welchii seems to be the most common isolate. clostridium sordellii is rarely encountered in clinical specimens (1% of Clostridium species), but it has been described as a human pathogen with fatal potential. Two toxins, a lethal and a hemorrhagic (that antigenically and pathophysiologically appear similar to clostridium difficile toxins B and A, respectively) are responsible for this potential. Reviewing the obstetric literature, only six cases of postpartum endometritis caused by C. sordellii, are described - all being fatal. In addition, one lethal case of spontaneous endometritis resulting from C. sordellii is reported. The clinical aspects of these cases include: - sudden onset with influenza-like symptoms in previously healthy women - progressive refractory hypotension - local and spreading tissue edema - absence of fever Laboratory findings include: - marked leukocytosis - elevated hematocrit. This paper reports the seventh fatal postpartum C. sorlellii associated toxic shock syndrome - the first recognized in scandinavia.
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4/28. Primary staphylococcal infection and toxic shock syndrome diagnosed by polymerase chain reaction.

    Primary staphylococcal pneumonia complicated with toxic shock syndrome (TSS) is relatively uncommon in children. Staphylococcus aureus exotoxins are thought to function as superantigens, and seem to promote disease manifestations. The identification of staphylococcal toxin genes by polymerase chain reaction (PCR) offers a specific and rapid diagnostic method for TSS. We describe a 7-year-old child with TSS resulting from staphylococcal pneumonia. S. aureus enterotoxins A and B were detected in the sputum of this patient by PCR.
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5/28. Streptococcal toxic shock syndrome revealed by a peritonitis. Case report and review of the literature.

    Group A streptococcus (GAS) or streptococcus pyogenes cause a variety of life-threatening infectious complications including necrotizing fasciitis, purpura fulminans and streptococcal toxic shock syndrome (STSS). exotoxins that act as superantigens are felt to be responsible for STSS. These exotoxins are highly destructive to skin, muscle and soft tissue. This syndrome has a rapid and fulminant course with frequently fatal outcome. GAS remains sensitive to penicillin but in serious infection a combination of clindamycin and ceftriaxone or meropenemum is recommended. Several studies have shown that mortality was dramatically reduced in STSS patients treated with immunoglobulin g given intravenously (IVIG). Early recognition of this most rapidly progressive infection and prompt operative debridement are required for successful management. This report presents a female patient at two month post-partum with a peritonitis and multi-organ failure.
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6/28. Invasive Group C Streptococcus infection associated with rhabdomyolysis and disseminated intravascular coagulation in a previously healthy adult.

    Infections with Group C Streptococci can lead to severe disease, particularly in individuals with underlying illnesses such as cardiovascular disease, malignancy or immunosuppression. We report the first case of rhabdomyolysis and disseminated intravascular coagulation secondary to Group C Streptococcus in a previous healthy male. A toxic shock-like syndrome associated with Group C and Group G Streptococci has been reported. However, unlike with Group A Streptococci, production of endotoxins by these organisms is less well defined. We tested the patient's isolate for its ability to produce superantigenic toxins and to induce a mitogenic response. Although it is not known whether Group C Streptococci require special growth conditions for the production of superantigens, we could not demonstrate either the production of exotoxins or the induction of a mitogenic response.
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7/28. culture-negative severe septic shock: indications for streptococcal aetiology based on plasma antibodies and superantigenic activity.

    We present a severe septic shock syndrome patient with negative blood cultures. Acute and convalescent plasma samples from the patient were analysed for anti-streptolysin O titres, superantigen-neutralizing activity and presence of superantigenic activity. The plasma analyses implicated superantigen-producing streptococcus pyogenes as the causative agent.
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8/28. waterhouse-friderichsen syndrome after infection with group A streptococcus.

    We report a case of waterhouse-friderichsen syndrome associated with group A streptococcus (GAS) toxic shock syndrome in a previously healthy man. The patient presented with neck pain and fevers of 2 days' duration. Computed tomography of the neck revealed a mass in the retropharyngeal space, suggesting an abscess. Despite prompt treatment with appropriate antibiotics, the patient experienced a fulminant course and died within 8 hours of presentation. Antemortem blood cultures grew GAS positive for exotoxins A, B, and C. Postmortem examination revealed bilateral adrenal hemorrhage, consistent with waterhouse-friderichsen syndrome. Immunohistochemical analysis of the adrenal glands revealed the presence of GAS antigens. However, no disseminated intravascular coagulation was evident. This case demonstrates that adrenal hemorrhage can occur without associated coagulopathy and may result directly from the action of bacterial toxins.
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9/28. Lack of muco-cutaneous signs of toxic shock syndrome when T cells are absent: S. aureus shock in immunodeficient adults with multiple myeloma.

    Staphylococcal toxic shock syndrome (TSS) is an acute life threatening disease. The diagnosis can be made clinically based on diagnostic criteria. The clinical manifestations are caused in large part by there lease of high levels of T-cell-derived cytokines as a result of potent toxins, also called superantigens (SAg), produced by Staphylococcus aureus, but it is not clear which clinical symptoms/signs are strictly T-cell dependent. Here, we report on three adults with multiple myeloma (MM) presenting with S.aureus sepsis/shock, and two patients with typical TSS. The MM patients had compromised humoral immunity because of depression of normal immunoglobulin (Ig) levels at the expense of the M protein.In addition, their T cells were absent due to high dose chemotherapy initiated for bone marrow trans-plantation. The MM cases lacked mucosal hyperemia, erythroderma and desquamation, but were otherwise indistinguishable from the TSS cases. All patients grew S. aureus and in each case, SAg genes were detected by PCR. In several cases, the plasma contained biological SAg activity resulting in VP specific proliferation of indicator T cells in vitro. The same specific activity was observed with the supernatant fluids of S. aureus broth cultures from the respective bacterial isolates. This confirms the presence of bio-active toxins in the plasma but did not lead to full blown TSS when T cells were lacking.Thus, S. aureus sepsis/shock can be clinically distinguished from typical TSS, and we suggest that mucocutaneous manifestations of TSS are the most telling signs of massive T-cell-dependent cytokine release.
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10/28. Early and definitive diagnosis of toxic shock syndrome by detection of marked expansion of T-cell-receptor VBeta2-positive T cells.

    We describe two cases of early toxic shock syndrome, caused by the superantigen produced from methicillin-resistant staphylococcus aureus and diagnosed on the basis of an expansion of T-cell-receptor VBeta2-positive T cells. One case-patient showed atypical symptoms. Our results indicate that diagnostic systems incorporating laboratory techniques are essential for rapid, definitive diagnosis of toxic shock syndrome.
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