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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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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PMID:Lack of muco-cutaneous signs of toxic shock syndrome when T cells are absent: S. aureus shock in immunodeficient adults with multiple myeloma. 1203 93

We report a case of toxic shock-like syndrome due to a rare infection of group G Streptococcus bacteremia in a patient with idiopathic thrombocytopenic purpura and its successful treatment with continuous venovenous hemofiltration (CVVH). As the result of sepsis treatment with CVVH, in addition to administration of vasopressors and antibiotics, serum levels of interleukin-1beta, interleukin-10 and tumor necrosis factor-a fell and shock was controlled.
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PMID:Serum cytokine level during continuous venovenous hemofiltration in toxic shock-like syndrome due to group G beta Streptococcus bacteremia in a patient with idiopathic thrombocytopenic purpura. 1216 Jan 64

Since the mid-1980s, there has been a resurgence of severe forms of invasive group A streptococcal (GAS) disease in many Western countries. In Hong Kong, a similar increase has also been observed in recent years. One hundred seven GAS isolates collected from 1995 to 1998 from individuals with necrotizing fasciitis, toxic shock syndrome, meningitis, or other type of bacteremic sepsis (invasive group, n = 24) as well as from individuals with minor skin and throat infections (noninvasive group, n = 83) were characterized through serologic and/or emm sequence typing. Thirty-two M protein gene sequence types were identified. Types M1, M4, and M12 were the most prevalent in both the invasive group and the noninvasive group; together they accounted for 70.8 and 37.3% of the isolates, respectively. No clear pattern of skin and throat infection M types was observed. Type M1 was overrepresented in the invasive and pharyngeal isolates. The same pulsed-field gel electrophoresis pattern was shared by most invasive and all pharyngeal M1 isolates. Overall, resistance to erythromycin (32%) and tetracycline (53%) was high, but M1 isolates were significantly less likely to have resistance to either antimicrobial agent than non-M1 isolates. One novel emm sequence type, stHK, was identified in an isolate from a patient with necrotizing fasciitis. Minor emm gene sequence alterations were noted for 31 isolates, and for 13 of these isolates, deletion, insertion, or point mutations were seen in the hypervariable 50 N-terminal residues.
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PMID:Epidemiologic analysis of invasive and noninvasive group a streptococcal isolates in Hong Kong. 1262 12

In the research basing on data of literature we showed opinions on the subject of using IVIG in treatment of sepsis and of septic shock, especially in streptococcal toxic shock syndrome caused by Streptococcus pyogenes and Streptococcus pneumoniae.
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PMID:[The role of IVIG in treatment of generalized infections]. 1266 18

Sepsis understood as persistent bacteremia with considerable clinical symptomatology that can develop into septic shock, retains its clinical, diagnostic and therapcutic meaning. Its most recent definition as a systemic inflammatory secondary reaction to a verified infection may help us to understand the reactive events of the host against infections and prevent septic shock. We report clinical cases of sepsis with positive haemoculture observed in the Caltagirone (CT) Hospital in the last 15 years: 186 patients (117 males and 69 females), with particular focus on those over 61 years old and on patients admitted to the ICU. The clinical isolates and groups of the inpatients are listed. In particular, two cases of toxic shock syndrome and six cases of bacterial endocarditis are described. Mortality was about 30% for septic shock despite rational antibiotic therapy, support therapy and hospital admission to the intensive care unit
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PMID:[Sepsis: our series] 1274 44

Hypoglycemia is fatal if associated with sepsis in end-stage renal disease (ESRD) patients. We report a hemodialysis patient of streptococcal toxic shock syndrome presenting with hypoglycemia. She was found to be severely hypoglycemic with a plasma glucose level of 16 mg/dl. Immunoreactive insulin levels were undetectable throughout the clinical course. Several factors including reduced renal gluconeogenesis, reduced hepatic glucose output and excessive peripheral glucose utilization may account for the hypoglycemia in this patient. In conclusion, we would like to draw attention to the fact that septic ESRD patients without diabetes are prone to develop profound hypoglycemia with serious consequences.
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PMID:Streptococcal toxic shock syndrome presenting with spontaneous hypoglycemia in a chronic hemodialysis patient: pathophysiological mechanisms. 1279 13

The efficacy and safety of high-dose intravenous polyspecific immunoglobulin G (IVIG) as adjunctive therapy in streptococcal toxic shock syndrome (STSS) were evaluated in a multicenter, randomized, double-blind, placebo-controlled trial. The trial was prematurely terminated because of slow patient recruitment, and results were obtained from 21 enrolled patients (10 IVIG recipients and 11 placebo recipients). The primary end point was mortality at 28 days, and a 3.6-fold higher mortality rate was found in the placebo group. A significant decrease in the sepsis-related organ failure assessment score at days 2 (P=.02) and 3 (P=.04) was noted in the IVIG group. Furthermore, a significant increase in plasma neutralizing activity against superantigens expressed by autologous isolates was noted in the IVIG group after treatment (P=.03). Although statistical significance was not reached in the primary end point, the trial provides further support for IVIG as an efficacious adjunctive therapy in STSS.
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PMID:Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double-blind, placebo-controlled trial. 1288 57

Among innate immune cells, macrophages play an essential role in the sensing and elimination of invasive microorganisms. Binding of microbial products to pathogen-recognition receptors stimulates macrophages to release cytokines and other effector molecules that orchestrate the host innate and adaptive immune responses. Recently, the protein known as macrophage migration inhibitory factor (MIF) has emerged as a pivotal mediator of innate immunity. First identified as a T-cell cytokine, MIF was rediscovered as a protein released by pituitary cells after exposure to endotoxin [lipopolysaccharide (LPS)] or bacteria and in response to stress. Monocytes, macrophages and lymphocytes constitutively express MIF, which is rapidly released after stimulation with bacterial endotoxins and exotoxins, and cytokines. MIF induces powerful proinflammatory biological responses and has been shown to be an important effector molecule of septic shock. High levels of MIF have been detected in the circulation of patients with severe sepsis and septic shock. Inhibition of MIF activity with neutralizing anti-MIF antibodies or deletion of the Mif gene led to a marked reduction in cytokine production and protected mice from lethal bacterial sepsis and toxic shock induced by Gram-negative endotoxin or Gram-positive exotoxins. Investigations into the mechanisms whereby MIF modulates innate immune responses to endotoxin and Gram-negative bacteria have shown that MIF up-regulates the expression of Toll-like receptor 4 (TLR4), the signal-transducing molecule of the LPS receptor complex. Thus, MIF enables cells, such as the macrophage, that are at the forefront of the host antimicrobial defences, to sense promptly the presence of invading Gram-negative bacteria and mount an innate immune response. Given that it is a pivotal regulator of innate immune responses to bacterial infections, MIF appears to be a perfect target for novel therapeutic interventions in patients with severe sepsis.
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PMID:Macrophage migration inhibitory factor and host innate immune responses to microbes. 1462 Jan 37

Immunotherapy targeted against microbial toxins and host mediators has been studied in many preclinical investigations and clinical trials of sepsis during the past 20 y. Intravenous immunoglobulin, including both monoclonal and polyclonal antibodies, represents one such immunotherapeutic strategy. Mononclonal antibodies directed against endotoxin or tumour necrosis factor-alpha have been tested extensively in clinical trials, but have so far failed to reveal a significant effect on mortality rates. Several studies have assessed the efficacy of polyclonal intravenous immunoglobulin (IVIG) in sepsis, with varying results. Although there are no conclusive data available to date to support the use of IVIG therapy in all sepsis cases, there are strong indications that certain defined septic subgroups, such as streptococcal toxic shock syndrome caused by group A streptococcus, will benefit from its use. This review briefly summarizes the clinical trials on IVIG therapy in sepsis, and describes in more detail the mechanistic actions of IVIG and the clinical data that support the use of IVIG as adjunctive therapy in severe invasive group A streptococcal infections.
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PMID:Intravenous immunoglobulin adjunctive therapy in sepsis, with special emphasis on severe invasive group A streptococcal infections. 1462 Jan 55

Septic shock, toxic shock syndrome, acute respiratory distress syndrome, and catheter-related infections are conditions in which intensive care management of the patient may be necessary. Toxic shock syndrome is a toxin-mediated illness that is not limited to young menstruating women and should be considered in women and men who present with fever, hypotension, rash, and multiorgan dysfunction. Sepsis is the leading cause of death in critically ill patients in the United States and is the most common predisposing factor for acute lung injury or acute respiratory distress syndrome. Central venous catheters are often a necessity for optimal patient care in these critically ill patients.
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PMID:Critical care infectious disease. 1471 46


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