The infection connection. Help wanted.
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Biomedical subjects
Publications and source records attributed to K West.
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The article describes a study conducted on general surgical and thoracic surgical floors of a 1000-bed hospital to assess the impact of a new network for portable patient care devices. This network was developed to address the needs of hospital patients who need constant, multi-parameter, vital signs surveillance, but do not require intensive nursing care. Bedside wall jacks were linked to UNIX-based workstations using standard digital network hardware, creating a flexible system (for general care floors of the hospital) that allowed the number of monitored locations to increase and decrease as patient census and acuity levels varied. It also allowed the general care floors to provide immediate, centralized vital signs monitoring for patients who unexpectedly became unstable, and permitted portable monitors to travel with patients as they were transferred between hospital departments. A disk-based log within the workstation automatically collected performance data, including patient demographics, monitor alarms, and network status for analysis. The log has allowed the developers to evaluate the use and performance of the system.
The incidence and severity of pneumonia, sepsis, and other infections was evaluated in a group of 30 premature infants with moderate to severe bronchopulmonary dysplasia (BPD), half of whom were randomly treated with intravenous immunoglobulins (group A). The patients were treated until the age of 6 months. They were compared with an untreated control group (group B). The number of pneumonic episodes (5 in group A and 15 in group B) and other infections, excluding sepsis (1 in group A and 7 in group B), were significantly reduced in the treated group (P less than .05). The number of episodes of sepsis, suspected sepsis, and necrotizing enterocolitis were similar in the two groups. The decrease in the number of respiratory and other infections in BPD infants treated with IVIG requires verification by a larger trial.
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Administration of rimantadine to mice via drinking water, following a prophylactic dose, reduced lung virus titers by greater than 3 log10 plague-forming units (pfu)/ml but caused only marginal reductions in lung virus titers when therapy was started 8 h after exposure to virus. Mice given rimantadine prophylactically plus therapeutically were resistant to rechallenge with virus at a dose equivalent to that used for the primary infection (50 pfu/mouse) but not to a high dose (1 x 10(5) pfu/mouse). Virus-neutralizing-antibody titers were reduced only by rimantadine treatment, which included prophylaxis, whereas the cytotoxic T lymphocyte (CTL) response was depressed by treatment given with or without prophylaxis. Mice infected with rimantadine-resistant virus had no decrease in CTL or antibody responses when treated with rimantadine. Therefore, the depression in CTL and antibody responses associated with rimantadine treatment appears to be due to a decrease in the amount of viral antigen available or interference with viral antigen processing and not to nonspecific immunosuppressive effects.
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Rimantadine HCl was assessed for its effect on influenza A virus titer in lungs of infected BALB/c mice. Rimantadine administered orally via drinking water, with and without an intraperitoneal prophylactic loading dose, was compared to intraperitoneal administration. Mice were infected with a non-lethal dose of influenza A/Port Chalmers/H3N2 virus and the pulmonary virus titers were determined at intervals over a 21 day period. Prophylactic treatment with rimantadine followed by oral administration resulted in up to a 4 log10 reduction in pulmonary virus titer. The oral doses given to the mice were comparable on a mg/kg/day basis to those recommended for treatment of human infections. Reductions in pulmonary virus titers also occurred after intraperitoneal rimantadine treatment which included a prophylactic dose, but the reductions in pulmonary virus titers were less striking and not consistent over the course of infection. There were no significant reductions in pulmonary virus titers by either route if treatment was started 8 h after exposure to virus.
Citrobacter diversus has been increasingly recognized as a cause of life-threatening neonatal meningitis with frequent abscess formation. This condition is associated with high mortality and extremely poor prognosis. We report our experience with C. diversus septicemia without meningitis in critically ill newborns. Thirteen patients with mean birthweight 1530 +/- 925 gm and mean gestational age 31.3 +/- 3.5 weeks were affected. They were compared with a group of infants affected by Escherichia coli sepsis, matched for weight, gestational age, and age at diagnosis. The groups did not differ in the incidence of perinatal complications, peripheral white blood cells, platelet count, and death rate. Hypotension was more frequently found in E. coli sepsis (p less than 0.05). All C. diversus isolates were resistant to gentamicin but sensitive to cephalosporins. C. diversus has become the most common nosocomial pathogen in our unit. Plasma profile analysis suggests that two different strains of C. diversus were involved in the outbreak reported here. Therapy for suspected C. diversus septicemia should include cephalosporins whenever resistance to aminoglycosides is demonstrated.
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Using the L5178Y mouse lymphoma cell thymidine kinase locus and the Salmonella his locus assays, the mutagenic potentials of several catecholamines and related compounds were examined. No supplementary metabolic activation systems were used. In the mouse lymphoma assay, the dihydroxybenzenes catechol and hydroquinone had similar and appreciable mutagenic potentials, whereas resorcinol was less active. Derivatives of catechol, such as dopamine and epinephrine, were mutagenic, whereas the related monohydroxylated compounds tyramine and synephrine were inactive. The primary amine, arterenol, and the corresponding secondary amine, epinephrine, induced similar mutagenic responses. Carboxylation of the side chain of dopamine, giving L-dopa, reduced the maximum mutagenic response. The introduction of charged groups directly on to the aromatic ring also reduced mutagenic activity, while an intervening methylene reversed this effect. Thus, 3,4-dihydroxyhydrocinnamic acid was more active than 3,4-dihydroxybenzoic acid. The compound active at the lowest doses was 4-tert-butyl catechol. The activities of these compounds are highly dependent upon substituent groups. Experiments with superoxide dismutase gave circumstantial evidence for some of the mutagenic activity being due to superoxide anion. Active oxygen species might be responsible for some of the observed effects, but this cannot be concluded from the superoxide dismutase experiments. Mutagenic responses in Salmonella were very low but were significant for L-dopa in three strains and for epinephrine and arterenol in one strain. Limited DNA association studies of 14C-dopamine suggest interactions in L5178Y and Salmonella cells and in mouse liver. The mutagenicity of dopamine in L5178Y is reduced by high serum concentrations during the exposure period, while the apparent association with DNA is unaffected.
Twenty one children with achalasia of the esophagus were treated from 1970 to 1986. There were 11 girls and ten boys (average age, 10.9 years; range, 6 months to 16 years). Diagnosis was established by barium swallow in 21 cases and confirmed by manometrics and motility studies in 14. Four children had unsuccessful dilatation (range, 1 to 16 dilatations/pt). All 21 children underwent modified anterior Heller esophagomyotomy (transabdominal in 15 and transthoracic in six). Concomitant Nissen fundoplication was performed in three. Follow-up from 1 to 14 years (mean, 6.3 years) showed complete relief of obstruction in 18 patients (86%), while three required additional procedures for persistent dysphagia. One child improved after a single dilatation, but two others eventually required a second esophagomyotomy. Three additional patients subsequently developed gastroesophageal reflux (GER), and two were managed with Nissen fundoplication; the third responded to medical management. The mortality for this series was zero. Postoperative complications occurred in nine children (42%) and was due to atelectasis and postoperative fever. Modified Heller esophagomyotomy is safe and effective in children with achalasia (mortality, 0%; relief of obstruction, 86%). Results were similar after a transabdominal or transthoracic approach. Esophageal dilatation was not an effective method of treatment. Although postsurgical barium swallow showed relief of obstruction, abnormal esophageal motility persisted, suggesting that long-term follow-up is important.
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In this study, a new glucose reflective meter was compared with a conventional laboratory measure of glucose concentration. The excellent correlation found (r = 0.988) simplicity and economic cost make the new method suitable for use in the neonatal intensive care (NICU) environment. The authors believe that the physician dealing with premature or small-for-dates infants, or infants of diabetic mothers, can base emergency therapy on the results obtained by this bedside method of blood glucose measurement pending confirmation by the clinical laboratory.
A full-thickness burn wound in adult sheep releases prostanoids when they are injected locally with E. coli endotoxin, 2 micrograms/kg, resulting in an increase in pulmonary artery pressure (Ppa) from 20 +/- 3 to 34 +/- 5 mm Hg, and a decrease in mean arterial oxygen tension (PaO2) from 88 +/- 6 to 70 +/- 5 torr; this corresponds to an increase in venous plasma TxB2 content from a baseline of 220 +/- 79 pg/ml to 440 +/- 90 pg/ml. Burn prostanoid production, measured in lymph, increased ten- to fifteen-fold for both thromboxane A2, measured as TxB2, and prostacyclin, 6-keto-PGF1 alpha. The intravenous administration of ibuprofen, 12.5 mg/kg, eliminated both the increase in Ppa and decrease in PaO2 as well as the increase in burn lymph prostanoids. However, plasma prostanoids were also decreased below baseline, a potentially deleterious effect. A topical ibuprofen cream, 5% ibuprofen in a water-soluble ester, was applied to the burn hide every 6 hrs x 4 after which endotoxin was again injected below the hide. The pulmonary dysfunction was prevented as was the increase in plasma TxB2 with the value remaining at baseline. Burn lymph levels were only increased three- to five fold. Ibuprofen levels in burn lymph were maintained at 1-2 mcg/ml. The addition of the cream to the burn, however, did increase the wound bacterial content to 10(5)-10(7) bacteria/gram of tissue compared to 10(2)-10(3) for the dry, untreated burn, probably due to softening of the burn. Topically applied ibuprofen, therefore, can decrease burn wound prostanoid production from local endotoxin, preventing lung dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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We injected Escherichia coli endotoxin, 2 micrograms/kg, beneath the eschar of sheep with 25% total body surface full-thickness burns to determine whether burn tissue in the presence of endotoxin releases prostanoids, particularly thromboxane A2, (TxA2), and if increased local TxA2 production can lead to distant lung dysfunction. We compared this response to the lung injury produced by the same dose given intravenously. We noted a marked increase in burn tissue TxA2 production after subeschar endotoxin as reflected in significant increases in burn lymph and pulmonary artery TxB2 levels. Pulmonary artery pressure increased from 22 to 38 mm Hg and PaO2 decreased from 89 to 71 torr while lung lymph flow (QL) increased only modestly with no evidence of increased lung permeability. The TxA2 production and the lung response were prevented by the subeschar injection of ibuprofen, 12.5 mg/kg. Circulating endotoxin was noted in only one of five sheep. After intravenous (endotoxin), a significant increase in lung TxA2 production was noted and a characteristic two-phase lung injury was seen with an initial phase basically identical to that seen with the subeschar injection followed by an increase in lung protein permeability. Burn tissue endotoxin can stimulate local TxA2 production leading to distant lung dysfunction without the need for circulating endotoxin. The source of the TxA2 is the burn, while with endotoxemia the source is the lung.