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

A case of toxic-shock syndrome due to Streptococcus pyogenes is reported. A 76-year-old female was admitted with complaints of fevers and chills. She had been suffering from cellulitis on her right dorsum pedis for 7 months. Laboratory data on admission showed elevated values of WBC, CRP, and dysfunction of the liver and kidney. She was diagnosed as sepsis due to the cellulitis, and was treated with PIPC and FMOX. However, several hours after admission, her blood pressure decreased and oliguria appeared. Bacteriological examinations from the blood and the cellulitis revealed group A beta-hemolytic Streptococcus which gave streptococcal pyrogenic exotoxin (T-28, SPE.B + C). She died 23 hours after her admission in spite of changing antibiotics to a high-dose of PC-G therapy. This is one of the rare cases of toxic shock-like syndrome due to Streptococcus pyogenes from the cellulitis of the dorsum pedis.
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PMID:[A case of toxic shock-like syndrome due to Streptococcus pyogenes]. 759 93

The multiorgan failure syndrome caused by group A streptococci (GAS) designated streptococcal toxic shock syndrome (STSS) is believed to be mediated by cytokines induced by superantigens. In order to study the relationship between superantigen production, cytokine levels in patient sera, and clinical GAS manifestation we examined acute-phase sera and strains from 25 patients with GAS bacteremia. The patients had various disease manifestations, including STSS (44%), erysipelas (28%), septicemia (24%), wound infections (16%), and pneumonia (12%). Serotype T1M1 dominated, representing 56% of the isolates, but also strains of other serotypes were identified. The strains were found to produce the streptococcal pyrogenic exotoxins (Spe) A, B, and F, as determined by immuno-blot analyses. There was no difference in amounts of toxin produced between strains isolated from patients with different manifestations of disease. Levels of TNF alpha, IL1 alpha, IL6, IL8, and IFN gamma in acute-phase sera were determined by use of ELISA and RIA assays. The analyses showed higher levels of IL6 in sera from patients with STSS than in sera from patients with bacteremia without shock. TNF alpha was elevated in sera from patients with STSS, as compared to sera from patients with uncomplicated pharyngotonsillitis. No increase in the levels of IL1 alpha, IL8, and IFN gamma could be found in the patient sera and there was no difference in the level of those cytokines between the various patient categories.
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PMID:Correlation between serum TNF alpha and IL6 levels and severity of group A streptococcal infections. 766 74

Serious staphylococcal infections remain a significant clinical problem despite advances in antibacterial therapy. Resistance to penicillin is common and methicillin-resistant staphylococci have become troublesome nosocomial pathogens in many institutions. Penicillinase-resistant penicillins (e.g. flucloxacillin, cloxacillin and oxacillin) are the preferred drugs for all methicillin-susceptible staphylococcal infections, although first generation cephalosporins, beta-lactam/beta-lactamase inhibitor combinations, clindamycin, and occasionally erythromycin and cotrimoxazole (trimethoprim/sulfamethoxazole) are alternatives. Serious infections due to methicillin-resistant staphylococci should be treated with parenteral vancomycin. Teicoplanin, where available, is a suitable alternative. Rifampicin, fusidic acid and some fluoroquinolones may be useful oral alternatives, although resistance develops rapidly if they are used as single agents. Cotrimoxazole and minocycline have also proven useful when strains are susceptible. Staphylococcal toxic shock syndrome often requires aggressive resuscitation and anti-staphylococcal therapy for generally 10 to 14 days. Staphylococcus aureus bacteraemia remains a life-threatening condition which, in all but one-third of cases, is associated with an underlying septic focus such as endocarditis, osteomyelitis or occult abscess. Differentiating between complicated and uncomplicated bacteraemia is critical to define the appropriate treatment regimen. Serious staphylococcal sepsis such as endocarditis and acute osteomyelitis generally requires prolonged (4 to 6 weeks) antibiotic treatment. Coagulase-negative staphylococci are the commonest cause of prosthetic device infection, and generally require prolonged therapy with an agent to which they have proven to be sensitive, e.g. a penicillinase-resistant penicillin or vancomycin. Removal of infected foreign or prosthetic material, and drainage of deep collections remain a critical aspect of all therapy.
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PMID:Optimum treatment of staphylococcal infections. 768 6

Before the introduction of antibiotics, serious infections caused by Streptococcus pyogenes (Lancefield Group A streptococci) were common. Before World War II, this bacterium was responsible for as many as 50% of postpartum deaths and was the major cause of death in patients with burns. Also common were the sequelae of streptococcal infections-rheumatic fever and post-streptococcal glomerulonephritis. With the use of penicillin, however, Streptococcus pyogenes was believed to be virtually eliminated as a pathogen. The organism was consigned to the history books, but not for long. In the mid-1980s, focal resurgences of rheumatic fever began to be reported from different areas in the USA, such as Salt Lake City, Utah. In such communities, where increases in cases of rheumatic fever had been reported, the serotypes M-1, 3, 5, 6 and 18 were isolated which, on culture, produced characteristic mucoid colonies. At the same time, reports of increases in invasive streptococcal disease began to surface in both the USA and Europe. Two syndromes were described; invasive streptococcal infection, occurring in previously healthy children and adults, commonly associated with septicaemia resulting from a deep focus of infection such as bone or lung; and streptococcal toxic shock syndrome, involving a cutaneous focus, accompanied by necrotizing or bullous soft tissue changes. Septicaemia is rare in streptococcal toxic shock syndrome, but the most characteristic feature is one of rapidly progressing multi-organ failure. A high proportion of the strains of Streptococcus pyogenes associated with this condition are serotype M-1, and fatality rates approaching 50% have been reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Invasive streptococci. 772 68

Monophosphoryl lipid A (MPL) is a less toxic derivative of lipid A that enhances survival from endotoxemia. This study examined whether MPL induced resistance to Gram-positive sepsis and cytokines. Mice were administered MPL or saline (phosphate-buffered saline) and challenged 24 h later with live Staphylococcus aureus (SA), staphylococcus enterotoxin B (SEB), toxic shock syndrome toxin (TSST-1), and tumor necrosis factor (TNF). Survival was determined at 72 h. A separate set of animals was phlebotomized for determination of cytokines. MPL increased survival from S. aureus bacteremia from 20 to 87% (p < .05). Interleukin-6 (IL-6) and interleukin-1 (IL-1) and TNF were also significantly decreased. SEB and TSST survival were enhanced from 10 to 90% (p < .05). In SEB-treated animals, TNF and IL-6 levels were significantly decreased. Survival from TNF infusion was increased from 20 to 100% with MPL, however, no significant differences in cytokines were observed. These data suggest that MPL induces resistance to Gram-positive sepsis and cytokine-mediated activity.
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PMID:Monophosphoryl lipid A protects against gram-positive sepsis and tumor necrosis factor. 775 20

During the last years the cases of severe group A streptococcus infection have increased. The clinical manifestation of this streptococcal toxic shock syndrome is similar to the better known toxic shock syndrome (TSS) provocated by staphylococcus. Shock, bacteremia and acute respiratory distress syndrome are common features, and death has been associated with this infection in 30% of patients. We present the case of a 46-year-old man who fell gravely ill with sepsis, diarrhoe, scarlatina rash, desquamation of hands and feet and acute abdomen caused by group A streptococcus infection. Finally we discussed the possible port of entry of this infection, the different clinical manifestation and the concepts of treatment.
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PMID:[Diarrhea and peritonitis in infection caused by type A beta hemolytic streptococcus]. 787 13

At toxic doses, cardiotropic drugs may compromise cardiac output leading to circulatory shock. Specific treatment varies depending on the nature and the dose of the drugs ingested as well as causal mechanism including vasopegia, hypovolaemia, cardiogenic effects and sepsis. Progress in our understanding of the pharmacodynamic aspects of intoxication and the development of specific antidotes has led to reduced morbidity and mortality. In addition to the classical inotropes, mainly catecholamines and phosphodiesterase inhibitors, other therapeutic agents may have specific inotrope effects in such ad hoc situations. These include hypertonic alkaline saline solution, calcium, glucagon, hydroxocobalamine and other cobalt salts, oxygen and immunotoxicotherapy. Together with volum replacement, dobutamine at the dose of 7 to 20 micrograms/kg/min can usually restore cardiac performance in cases of carbamate-induced circulatory shock. In case of tricyclic antidepressant overdose, treatment should include respiratory assistance and infusion of alkaline sodium solutions to both reverse the extracellular acidosis and correct sodium balance. Catecholamines may be necessary in cases with severe hypotension. Major vasoplegia and impaired intraventricular conduction may be induced by overdoses of chloroquine and class I antiarrhythmic drugs. Signs of gravity are: ingested dose above 4 g, QRS > or = 0.12 s or systolic arterial pressure < or = 80 mmHg. Treatment with epinephrine, respiratory assistance and diazepam has been proven effective during the acute phase, but right catheterism is often required due to major haemodynamic instability during the first 72 first hours. Beta-blockers have both a bronchoconstrictor and respiratory depressor effects favouring cardiovascular failure by hypoemia. Symptoms occur in 30-40% of the cases of overdose. Shock results from the reduction in blood pressure and cardiac inotropism. Glucagon, isoprenaline and epinephrine, prescribed in that order, can considerably reduce mortality to less than 4%. Despite the development of specific molecules, the risk of mortality due to toxic shock caused by antiarrhythmics, chloroquine, colchicine, calcium inhibitors and paraquat remains high.
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PMID:[Shock caused by poisoning. Use of cardiotropic agents]. 797 61

In Pennsylvania, a 29-year-old woman was admitted to Temple University Health Sciences Center in Philadelphia with hypotension (100/80 mmHg), fever (105.3 degrees Fahrenheit), and a diffuse, nondesquamating erythroderma. Five weeks earlier, she had delivered her last child vaginally. Three days before admission, she had undergone endotracheal intubation so surgeons could perform a laparoscopic tubal ligation with Falope Rings. Two days before the tubal ligation, she had had a sore throat. She experienced no surgical complications and was discharged the same day as the operation. The day before her latest admission, she experienced nausea, vomiting, diarrhea, fever, chills, and diffuse abdominal pain. Upon admission, her surgical incisions were clean and dry and had no erythema. Her pulse rate was 140 beats/minute. Her respiration rate was 20/minute. The white blood cell count was 15,200 cells/cu. m (71% neutrophils, 23% band forms, 2% lymphocytes, and 4% monocytes). Her potassium level was 3.2 mmol/l. The anion gap was 22. All blood and urine cultures were negative. She experienced mild uterine tenderness. Upon admission, physicians administered ticarcillin-clavulanate and vancomycin for suspected postoperative pelvic infection. After learning that cervical and pharyngeal cultures were positive for Streptococcus pyogenes, physicians changed to ampicillin, 1 g intravenously every 6 hours. On the 6th day, she was discharged and prescribed 500 mg oral amoxicillin every 8 hours for 2 weeks. Within 2 weeks, she felt fine, had a normal physical examination, no fever, and no rash. The major signs and symptoms indicated a toxin-mediated illness. Both mucosal surfaces colonized by S. pyogenes were manipulated during laparoscopy and manipulation may have caused minor tissue injury and hyperemia with subsequent dissemination of streptococcal toxin. In conclusion, the patient had a S. pyogenes toxin-induced toxic shock-like syndrome that mimicked a pelvic wound infection with gram-negative septicemia.
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PMID:Streptococcal toxic shock-like syndrome as an unusual complication of laparoscopic tubal ligation. A case report. 799 32

Renal failure occurs commonly in children with shock, coagulopathy and multi-organ failure. Successful management of these patients requires not only management of the renal failure, but recognition and treatment of the underlying process. In addition to common and well-recognised causes of renal failure and shock, such as Gram-negative sepsis, there are a number of syndromes which are either less well recognised or confined to specific geographic locations. This article reviews the clinical and epidemiological features of the syndromes with shock and renal failure, focusing on the more recently recognised syndromes such as staphylococcal and streptococcal toxic shock syndrome, haemorrhagic shock and encephalopathy syndrome and viral haemorrhagic fevers.
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PMID:Syndromes with renal failure and shock. 801 5

Early-onset neonatal group B beta-hemolytic streptococcus (GBS) infection exhibits pathophysiologic characteristics of a toxic shock syndrome, in which a cascade of inflammatory mediators are involved. Thromboxane A2 (TXA2) is thought to play an important role as a mediator of the pulmonary response to GBS toxin, because high lung lymph concentrations of a TXA2 metabolite have been observed after GBS toxin injections in sheep. The aim of this study was to evaluate the effects of a selective antagonist of the TXA2-prostaglandin endoperoxide receptor (SQ 29,548). Six unanesthetized young lambs, each serving as its own control, were given SQ 29,548 or vehicle control followed by GBS toxin challenge. Hemodynamic and lung function (lung mechanics, lung volume, ventilation) responses were followed for 5 h. When compared with the control studies, treatment with SQ 29,548 significantly altered the response to GBS toxin. SQ 29,548 reduced the increase in pulmonary and systemic vascular resistance, improved cardiac output and stroke volume, improved dynamic lung compliance but not airway resistance, and improved oxygenation. The attenuating effect of SQ 29,548 was most pronounced during the first phase of toxin response (15-90 min after toxin infusion), but significant treatment effects were also seen during the second phase (120-300 min after toxin infusion). This study demonstrates that TXA2 is an important mediator of the response to GBS toxin and is responsible for hemodynamic and lung function changes. Thromboxane receptor blockade may offer a potential therapeutic approach to infants with severe early-onset GBS sepsis.
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PMID:Thromboxane receptor blockade (SQ 29,548) in group B streptococcal toxin challenge in young lambs. 806 40


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