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

Thirteen cases of group D streptococcal neonatal sepsis and/or meningitis were identified at the Cincinnati Children's Hospital from 1970 to 1976. Ages at onset of disease ranged from 1 to 25 days. The most frequent symptoms were fever (five cases), lethargy (five cases), and respiratory difficulty (four cases). Blood cultures for seven infants were positive; CSF cultures for five infants were positive; and CSF and blood cultures for one infant were both positive. In 12 patients, parenteral antibiotic therapy consisted of a penicillin and an aminoglycoside. One infant with a severe meningomyelocele died. The other 12 infants showed a rapid clinical response with seven patients improving within 48 hours of the start of therapy. Infection with group D streptococcus results in a low-grade systemic disease in both full-term and premature infants that responds favorably to appropriate therapy.
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PMID:Systemic group D streptococcal infection in newborn infants. 10 22

An important adaptation of the gastrointestinal tract to the extrauterine environment is its development of a mucosal barrier against the penetration of harmful substances (bacteria, toxins and antigens) present within the intestinal lumen. At birth, the newborn infant must be prepared to deal with bacterial colonization of the gut, with formation of toxic byproducts of bacteria and viruses (enterotoxins and endotoxins) and with the ingestion of antigens (milk proteins). These potentially noxious substances if allowed to penetrate the mucosal epithelial barrier under pathological conditions can cause inflammatory and allergic reactions which may result in gastrointestinal and systemic disease states. To combat the potential danger of invasion across the mucosal barrier the infant must develop an elaborate system of defence mechanisms within the lumen and on the luminal mucosal surface which act to control and maintain the epithelium as an impermeable barrier to uptake of macromolecular antigens. These defences include a unique immunological system adapted to function in the complicated milieu of the intestine as well as other non-immunological processes such as a gastric barrier, intestinal surface secretions, peristaltic movement and natural antibacterial substances (lysozyme, bile salts) which also help to provide maximum protection for the intestinal surface. Unfortunately, during the immediate postpartum period, particularly for premature and small-for-dates infants, this elaborate local defence system is incompletely developed. As a result of the delay in the maturation of the mucosal barrier newborn infants are particularly vulnerable to pathological penetration by harmful intraluminal substances. The consequences of altered defence are susceptibility to infection and the potential for hypersensitivity reactions and for formation of immune complexes. With these reactions comes the potential for developing life-threatening diseases such as necrotizing enterocolitis, sepsis and hepatitis. Fortunately, 'nature' has provided a means for passively protecting the 'vulnerable' newborn against dangers of a deficient intestinal defence system, namely human milk. It is now increasingly apparent that human milk contains not only antibodies and viable leucocytes but many other substances which can interfere with bacterial colonization and prevent antigen penetration.
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PMID:Gastrointestinal host defence: importance of gut closure in control of macromolecular transport. 26 21

In the modern hospital gram negative bacteremia and the associated condition of septic shock are common occurrences. In the United States the estimated incidence of gram negative bacteremia ranges from 71,000 to 330,000 cases annually. Fatalities attributed to this disease are between 18,000 and 132,000 each year. Sepsis is defined as a systemic disease caused by microorganisms or their products in the blood. Bacteremia is the presence of viable organisms in the circulation. Gram negative bacteremia in the critically ill patient is synonymous with gram negative sepsis. Septic shock is a clinical syndrome characterized by circulatory insufficiency and inadequate tissue perfusion. Septic shock is associated primarily although not exclusively with gram negative bacilli. Focus is on predisposing factors, microbiology, pathophysiology, and the 4 components of therapy -- antibiotics, volume replacement, steroids, and surgical drainage. The underlying illness of the patient is the primary factor determining the outcome of an episode of gram negative bacteremia. Patients with a life threatening disorder have a very poor prognosis, while sepsis in a previously healthy person carries a good prognosis. The overall mortality in gram negative bacteremia is 25%. When septic shock develops, the mortality increases to 50-60%. Appropriate antibiotics that are synergistic against the infecting organism can decrease the mortality, but the overwhelming infleunce of host factors in predicting the outcome suggests that prevention and early treatment are the best means of decreasing mortality.
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PMID:Gram negative sepsis and shock. 35 39

1. Endotoxins are very potent and widely spread inflammation-inducing substances. 2. In the course of local infections endotoxins represent one of the main principles of the pathogenicity of gram-negative bacteria by inducing acute nonspecific inflammation. 3. The pharmacological activities of endotoxins consist primarily in generating and liberating the classic mediators of acute nonspecific inflammation. 4. Endotoxins are able to enter into the circulation through their capicity to activate pharmacological mediators. 5. The endotoxic mediators which increase the permeability of the microcirculation of the intestinum enable endotoxins as components of the physiological intestinal flora to enter into the circulation; these induce systemic disease or shock depending on their concentration in the circulation. 6. In the course of chronic inflammation recidivism or recrudescence as trasient acute inflammatory outburst can be caused by local effects of endotoxins. 7. According to some recent observations the inflammation inducing capacity of endotoxins may promote the entry of aerobic bacteria into the blood stream which can result in mixed septicemia.
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PMID:The inflammatory response to endotoxins. 38 May 59

Splenomegaly is usually the result of systemic disease. The differential diagnosis can logically be subdivided into infectious, hematologic, metabolic, vascular, and neoplastic diseases which result in abnormalities of the lymphoid, reticuloendothelial, or vascular components of the spleen. Splenic enlargement increases the risk of traumatic rupture of the spleen. Splenectomy, although indicated in some conditions, does not always relieve the hypersplenic state, and its benefit must be weighed against the hazard of life-threatening episodes of sepsis.
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PMID:Splenomegaly in children. Identifying the cause. 42 50

Patients requiring a major amputation for ischemia are frequently gravely ill. Physiologic amputation obtained by freezing the leg, usually with a tourniquet, will permit delay and intensive preoperative therapy. In an efficient, safe, and convenient method which we have developed and used in 46 patients, a pump circulates antifreeze solution through a specially constructed boot. The last 32 patients so treated have been analyzed as to indications and results. Advantages obtained control of sepsis, correction of diabetic coma, dialysis for chronic renal failure, improvement in congestive heart failure, and improvement in pulmonary function. Four patients had successful below-knee amputations after control of infection that had previously seemed to dictate above-knee amputation. The control of pain and odor, the resultant appreciation of the family, and the lessened demand on nursing staff offer worthwhile benefits in many of the patients, even in some in whom advanced systemic disease prevented survival.
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PMID:Freezing an extremity in preparation for amputation. 68 74

Angiofollicular lymph node hyperplasia (Castleman's disease) is a relatively rare disease of differential diagnostic interest in patients with lymphadenopathy. The etiology and pathogenesis are still not elucidated. The disease is classified into localized and systemic types. The localized form is divided histologically into hyaline-vascular type and plasma cell types. The former is usually demonstrated incidentally as a widening of the mediastinum in otherwise asymptomatic patients. The plasma cell type usually presents in the abdominal lymph nodes and is accompanied by fever, loss of weight, anemia and hypergammaglobulinemia. Surgical treatment is curative in the localized disease. The systemic disease involves multiple lymph nodes, and multiple organs are affected. The prognosis is dubious, and frequently the patients rapidly die from septicemia or other infectious complications. Some patients develop malignancies. Treatment with glucocorticosteroids and chemotherapy has only demonstrated a limited effect. The diagnosis requires both a characteristic histopathology and typical clinical symptoms. A current illustrative case report is presented.
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PMID:[Angiofollicular lymph node hyperplasia (Castleman disease)]. 154 67

There have been only a few investigations that have considered renal disease or any disturbance of renal function in the calculation of risk in cardiac surgery. Risks of cardiac surgery have to be considered for renal disease without direct connection to heart disease (e.g., infections of the kidney and of the urinary tract, primary and secondary glomerulonephritis, parenchymal renal disease, and impaired renal function of unknown origin), as well as in renal disease with concomitant influence on heart and kidney (e.g., infective endocarditis, arterial hypertension, systemic disease of heart and kidney such as with diabetes mellitus, disturbance of kidney function or electrolyte balance due to heart failure). In most cases, the problem is solved by therapeutic intervention and postponement of cardiac surgery. A limited or negative operative indication is found with untreatable infection of the kidney or urinary tract, with untreatable nephrotic syndrome, in advanced renal disease with heart transplantation, as well as in case of severe arterial hypertension with possible organ complications, and in advanced diabetes mellitus with ESRD and multiorgan involvement. After cardiac surgery, acute renal failure represents a critically important complication. Primary therapeutic procedures must include prophylaxis of hemodynamic unstable situations, as well as prophylaxis of infectious complications. Cardiac surgery in dialysis patients and post-transplant patients is basically possible and only has a slightly increased risk compared to patients with normal renal function. Seventy-seven dialysis patients were operated (49 aorto-coronary bypass operations, 19 single-valve and multiple-valve replacements, five patients with valve replacement and aorto-coronary bypass, and four other cardiac surgical operations). Only in valve replacement, was mortality significantly higher than in renal healthy persons, the main causes of death being cerebrovascular complications and septicemia.
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PMID:[Extracardiac risk factors in heart surgery--the kidney]. 208 10

Aspiration or ingestion of contaminated amniotic fluid or vaginal secretions has been suggested as a cause of systemic group B streptococcal (GBS) infection in the neonate. Suckling rat studies disagree on whether systemic disease will develop after an oral challenge of GBS. Our goal was to determine if systemic GBS disease would occur following oral colonization in the suckling rat and the effect of bacterial, host and environmental factors. Suckling rat littermates received oral inoculation on one of the first four days of life with varying doses and strains of GBS. Studies confirmed gastric inoculation without aspiration. Mortality and bacteremia decreased with age, increased with dose, varied with strain, and increased with asphyxia. Autopsy confirmed sepsis, intestinal colonization, meningitis, and pneumonia. Bacteremia was associated with an abnormal immature: total neutrophil ratio at 24 hr, thrombocytopenia at 48 hr, and neutropenia at 72 hr after inoculation. GBS can cause systemic infection in the host after oral colonization which appears age-, dose, strain-, and environment-dependent. Evaluation of GBS entry in the susceptible host may facilitate therapies directed toward preventing mucosal invasion.
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PMID:Systemic group B streptococcal disease in the neonate: characterization of an oral colonization model using the suckling rat. 214 5

Molecular biology has provided new technology for evaluating the traits of bacterial pathogens that are important in the pathogenesis of infections. The ability to derive isogenic strains that differ by a single trait provides a powerful tool for investigating the interaction of a putative virulence factor with the host at any of the various steps in pathogenesis. Recombinant DNA techniques afford the opportunity to clone the genes involved in the biosynthesis of a particular virulence factor. Once the gene(s) are cloned, a vast amount of information can be learned about their composition, structure, and regulation, and similarity with genes in other organisms. Understanding the molecular biology of a virulence factor also provides information about potential targets for future therapies and preventive modalities. The molecular analysis of two virulence factors from the type III group B streptococcus has been reviewed to provide specific examples of how these techniques can be used. The data has shown that the capsular polysaccharide is an essential factor in GBS virulence. The structural influence of sialic acid on the capsule plays a major role in its virulence properties. The importance of the capsule has been tested in several assays to identify its role in pathogenesis. Its primary role appears to be evading host phagocytic mechanisms, but it does not appear to be essential in the vascular response observed during GBS sepsis. Using the isogenic strains, we have also learned that the capsule does not mask a fibronectin receptor on GBS. In contrast to the capsule, the beta-hemolysin of GBS does not appear to be essential for systemic disease once the organism has invaded. Its role in the initial invasive steps in GBS pathogenesis has not been tested, but the availability of isogenic mutants in beta-hemolysin production will allow this question to be answered once the model systems are available.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular analysis of two group B streptococcal virulence factors. 217 47


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