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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mouse model of intraperitoneal meningococcal sepsis was used to evaluate the antiendotoxic activity of polymyxin B sulfate independent of its antibiotic effects. Administered either before or after the infective challenge therapeutic doses of polymyxin B sulfate produced small but significant increases in survival over unprotected animals. These results also suggest that endotoxin contributes to the outcome in this variety of Gram-negative infection.
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PMID:Protective effect of polymyxin B sulfate in experimental meningococcal infection in mice. 20 Mar 29

Transrectal biopsy of the prostate resulted in anaerobic septicemia in two patients, despite parenteral gentamicin sulfate prophylaxis. Bacteroides fragilis sepsis developed subacutely in one patient having a postbiopsy pelvic abscess. Clostridium perfringens sepsis occurred fulminantly in another patient 24 hours after biopsy of a gland extensively involved with adenocarcinoma. These cases indicate a potential hazard of sepsis due to anaerobic contamination with rectal microflora at the time of transrectal prostatic biopsy and the futility of prophylaxis directed only at aerobic bacteria.
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PMID:Anaerobic septicemia after transrectal prostatic biopsy. 20 64

The mouse model of intraperitoneal enterobacterial sepsis was used to evaluate the anti-endotoxic effect of polymyxin B sulfate. Single or multiple therapeutic doses of polymyxin, administered either before or after lethal challenge with Serratia marcescens, produced statistically and clinically significant protective effects.
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PMID:Protective effect of polymyxin B sulfate in experimental enterobacterial infection in mice. 23 6

Twenty-five patients were treated with ticarcillin disodium, 18 of whom had anaerobic infections that included pleuropulmonary infections (seven), mandibular osteomyelitis (four), perirectal abscess (two), sepsis, primary site unknown (one), liver abscess (one), pelvic abscess (one), decubitus ulcer (one), and synergistic gangrene (one). Seven had no anaerobic infections. Three had anaerobic septicemia. Culture results included anaerobes: peptococci (ten), peptostreptococci (ten), Bacteroides fragilis (six), Bacteroides not fragilis (ten), eubacteria (three), fusobacteria (two), Clostridium (one), Veillonella (one), and acidaminococcus (one); aerobes: Proteus (three), Klebsiella (two), Escherichia coli (two), and streptococci (two). Six patients with mixed aerobic infections initially received gentamicin sulfate in addition. The serum levels were 110 +/- 20 microgram/ml one hour after intravenous infusion of 5 g of ticarcillin disodium. All anaerobic isolates were susceptible at less than or equal to 100 microgram/ml and 85% by less than or equal to 25 microgram/ml of ticarcillin. Sixteen patients responded well to ticarcillin and two failed to respond. Our study suggests that ticarcillin is useful in the treatment of anaerobic infections.
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PMID:Ticarcillin disodium in anaerobic infections. 71 11

Antibacterial activity of gentamycin sulfate was studied in vitro and in treatment of albino mice with experimental infections. Gentamycin was superior to kanamycin with respect to its antibacterial effect against clinical strains of Staphylococcus, Coli bacteria, Proteus and Ps. aeruginosa. High efficiency of gentamycin was found with respect to acute and chronic staphylococcal infection, acute Proteus and Coli sepsis. The antibiotic was characterized by low LD50, high chemotherapeutic index, rapid decrease in isolation of the causative agent from the animal organs. The activity of gentamycin against infections caused by Ps. aeruginosa was the main advantage of gentamycin in comparison to kanamycin.
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PMID:[Experimental study of the chemotherapeutic activity of gentamicin sulfate]. 79 17

Hospital nursery A has used chloramphenicol and nursery B has used the combination of penicillin G sodium and kanamycin sulfate routinely in the treatment of neonatal sepsis and other bacterial infections. A hypothesis was formulated that these different antibiotic pressures would select out a substantial number of populations of resistant bacteria in each of the two nurseries. This was tested by periodic sampling of the skin, mouth, and rectal flora of babies and the permanent personnel in these nurseries. These bacteria were studied for susceptibility to a number of antibiotics. The population of resistant strains selected out was correlated with the antibiotics used in each nursery. There is a need for continuing surveillance of hospital nursery strains of bacteria for in vitro susceptibilities to commonly prescribed antimicrobials.
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PMID:Susceptibilities of bacteria to different antibiotic regimens. Study in two nursery populations. 109 52

The covalent modification of receptor proteins via phosphorylation and dephosphorylation is one of the principal mechanisms controlling carbohydrate metabolism and is known to be regulated by various protein kinases. Recent studies indicated that many hormones may exert their effects on cellular metabolism by regulating intracellular c-AMP levels and by activating a c-AMP dependent protein kinase, i.e., protein kinase A. The metabolic disturbances during sepsis are characterized by an initial hyperglycemia followed by a progressive hypoglycemia and a depletion of hepatic glycogen content. The latter is coupled with a slowdown in glycogenesis, an accelerated glycogenolysis, and a depression in gluconeogenesis in the liver. Since the liver is the major organ that regulates the homeostatic level of blood glucose, it is conceivable that the sepsis-induced glucose dyshomeostasis might be mediated by changes in protein kinase activity and the kinetic characteristics of enzymes. The present experiment was designed to study the correlation between protein kinase A and the pathophysiology of hepatic glucose dyshomeostasis during sepsis. Sepsis was induced in rats by cecal ligation and puncture (CLP). Late sepsis occurred 18 hours after CLP. Protein kinase A was extracted from the rat livers by acid precipitation and ammonium sulfate fractionation, and then partially purified by DEAE-cellulose. The results show that in the late sepsis, type-I protein kinase A (eluted at low ionic strength) activity was significantly decreased by 34-52% (P < 0.01). The kinetic parameters such as Vmax's for ATP, histone, and c-AMP were also significantly decreased from the control values of 6.1 +/- 0.9, 5.4 +/- 0.8, and 5.1 +/- 1.9 nmoles/mg.min. to 3.6 +/- 0.5, 2.8 +/- 0.3, and 2.5 +/- 0.5 nmoles/mg.min., respectively. Analysis using Hill's equation indicates that the S0.5 and n (Hill coefficient) values of the various substrates and activators for type-I protein kinase A remained unchanged. In the case of type-II protein kinase A (eluted at high ionic strength), the Vmax, S0.5, and n values for ATP, histone, and c-AMP were unchanged during late sepsis. The results of the present study indicate that the activities and kinetic characteristics of type I protein kinase A in rat liver are modified during late sepsis. Since protein kinase A is known to regulate glucose metabolism through adrenergic receptor mediation, these findings may have a pathophysiological significance in the understanding of hepatic glucose dyshomeostasis during sepsis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Kinetic studies of protein kinase A in rat liver during late sepsis]. 129 61

Acute respiratory failure in pregnancy is an important cause of maternal and fetal morbidity and mortality. Causes include: ARDS, venous air embolism, beta-adrenergic tocolytic therapy, asthma, thromboembolic disease, pneumothorax, and pneumomediastinum. The most common predisposing diseases for ARDS complicating pregnancy are sepsis, pneumonia, aspiration of gastric contents, and amniotic fluid embolism. Knowledge of normal maternal-fetal physiology and determinants of fetal oxygen delivery (uterine blood flow, placental transfer, fetal circulation) can help sustain normal fetal development, usually without compromising maternal care. The increased microvascular permeability seen in ARDS is likely mediated by neutrophils, proinflammatory mediators (e.g., tumor necrosis factor, interleukin-1, arachidonic acid metabolites) and activation of the complement cascade. Treatment of respiratory failure in pregnancy is largely supportive, including mechanical ventilation, hemodynamic support, nutrition, and prophylaxis against thromboembolism. No specific therapy has as yet been proven effective for ARDS, other than treating the underlying cause. Respiratory failure from status asthmaticus is treated with vigorous bronchodilator therapy, high-dose glucocorticosteroids, magnesium sulfate, and careful ventilator management. Occasionally, more experimental therapies (e.g., isoproterenol infusion, halothane anesthesia) are indicated. Certain strategies can help prevent respiratory failure from aspiration of gastric contents, beta-adrenergic tocolytic therapy, and thromboembolic disease.
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PMID:Acute respiratory failure in pregnancy. 136 44

Group B streptococci (GBS) cause the majority of cases of neonatal sepsis and meningitis in the United States. Immunization of women of childbearing age is one strategy under consideration for the prevention of neonatal disease. The beta C protein, a 130-kDa antigen present in many clinical isolates of GBS, was purified from GBS by extraction into sodium dodecyl sulfate (SDS)-containing buffer, preparative SDS-polyacrylamide gel electrophoresis, and electroelution. Purified beta C protein antigen (25 micrograms) with Freund's adjuvant was used to immunize rabbits. Rabbits developed enzyme-linked immunosorbent assay titers of > 1:1.6 x 10(6), and sera from immunized rabbits were administered to pregnant mice. Their neonatal pups were then challenged with a strain of GBS expressing beta C protein; 68% of these pups were protected by immune antiserum, whereas no controls were protected (P < 0.001). The immune serum (diluted 1:100) facilitated opsonophagocytic killing of GBS strains expressing the beta C protein but not those that do not express the antigen (mean log kill +/- standard deviation = 0.71 +/- 0.8 log10 CFU for beta+ strains and 0.09 +/- 0.2 for beta- strains; P = 0.02). In subsequent experiments, adult female mice were actively immunized with two doses of 2, 5, or 10 micrograms of beta C protein 2 months prior to mating. One- to two-day-old offspring of these dams were challenged with GBS and were protected in a dose-dependent manner, with 96% survival in the high-dose (10-micrograms) group and 20% survival in a sham-immunized control group (P < 0.001). Thus, active immunization of mice with the GBS beta C protein confers protection against lethal infection with beta+ GBS to their offspring.
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PMID:Protection of neonatal mice from group B streptococcal infection by maternal immunization with beta C protein. 145 29

Pharmacokinetic values after IV administration of amikacin sulfate were determined for clinically normal and hospitalized foals during the first week of life. The relations between drug disposition and sepsis score and serum creatinine concentration also were studied. In clinically normal foals, differences in sepsis score, serum creatinine concentration, and pharmacokinetic variables of amikacin were not found between foals 1 to 3 and 4 to 7 days old. In hospitalized foals, sepsis score, serum creatinine concentration, area under the curve, area under the moment curve, and mean residence time were greater, and total clearance was decreased, compared with values in clinically normal foals. Sepsis score and serum creatinine concentration were inversely correlated to amikacin clearance and appeared to be useful indicators of altered drug disposition.
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PMID:Relation between pharmacokinetics of amikacin sulfate and sepsis score in clinically normal and hospitalized neonatal foals. 160 17


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