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

Infected, neutropenic animals are used as experimental models to evaluate the relative efficacies of antimicrobial agents and host-pathogen-antibiotic interactions. In the past, these models used death as the study end point. Because of the concern about use of death as an end point, we evaluated the accuracy with which various signs of infection predicted mortality in a neutropenic guinea pig model of treated and untreated Pseudomonas aeruginosa sepsis. The potential surrogate markers studied included ruffled fur, respiratory distress, diarrhea, hunched posture, lethargy, abnormal neurologic movements (twitching, paralysis of a limb), inappetence for > 48 h, the inability to ambulate, and the inability of a supine animal to stand. In addition, we evaluated whether percentage of weight loss or change in daily food and water consumption were predictive of mortality. Animals were inspected for these signs at least every 4 h during the day and every 8 h in the evening. In treated and untreated animals, 100% of subjects that were unable to ambulate or to rise from the supine position died (positive predictive value for death was 100% for either sign). Guinea pigs that could not rise from a supine position expired between 1 and 8 h after this sign was observed. Those that could not ambulate died between 4 and 40 h after that sign was observed. In treated and untreated animals, none of the survivors manifested either sign of disease (100% specificity for each sign). However, 59% of untreated and 69% of treated animals that were ambulatory were found dead at the next observation period, underscoring the rapidity with which this infection progresses to death when it enters its final stage. No other signs of infection distinguished animals that survived or died. Thus, the inability of neutropenic, infected guinea pigs to rise from a supine position and the inability to ambulate were the only signs that accurately predicted death and, therefore, are the only signs that can be used as surrogates for death in this experimental model of P. aeruginosa sepsis.
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PMID:Predictive value of several signs of infection as surrogate markers for mortality in a neutropenic guinea pig model of Pseudomonas aeruginosa sepsis. 943 98

In this study, 207 patients with neonatal tetanus admitted to Erciyes University, Faculty of Medicine, Unit of Neonatology between 1976 and 1994 were investigated retrospectively. One hundred and sixty-seven (80.6%) patients had non-hygienic home deliveries and none of the mothers of the children had been immunised with tetanus toxoid. Of the 207 patients, 161 (77.8%) were males, 46 (22.2%) were females. Failure to suck and twitching were the most frequent symptoms. The mean age of patients who died or survived was 6.9 and 8.8 days respectively (p > 0.05). Mean birth weight was 3092 g for the fatal cases and 3317 g for the survivors (p < 0.05). Mean age of onset of symptoms was 5.5 days for the fatal cases and 6.5 days for the survivors (p < 0.05). Mean period between onset of symptoms and hospital admission was 1.5 days for the fatal cases and 2.1 days for the survivors (p > 0.05). Ninety-seven (46.8%) of the 207 patients died. Mean age of death was 9.3 days and most of the patients died at the fifth day of admission to hospital. Sex, age on admission and duration of symptoms did not affect the prognosis. In addition, the efficacy of the diazepam, phenobarbital sodium and chlorpromazine used for sedation in neonatal tetanus was investigated. Of 207 patients, 43 patients were treated with diazepam, 33 patients with phenobarbital sodium, another 33 patients with phenobarbital sodium + chlorpromazine and 94 patients were treated with diazepam + phenobarbital sodium +/- chlorpromazine called as "combined therapy". The least mortality rate was found in the group treated with "combined therapy" and the highest mortality rate in the group treated with phenobarbital sodium + chlorpromazine (p < 0.001). The most frequent cause of death was apnea in the first week and sepsis in the later period.
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PMID:A review of 207 newborn with tetanus. 978 42

Critical illness polyneuromyopathy (CIP) leads to major muscle weakness correlated with peripheral nerve and/or muscle alterations. Because sepsis seems to be the main factor, we used an experimental model of chronic sepsis in rats to study the localization of the first alterations on isolated motor units of soleus muscle. Seven days of chronic sepsis leads to a decrease in muscle force and an increase in muscle fatigability. Muscle twitch contraction time is also slower and all the motor units exhibit a slow profile in septic rats. Motor axon conduction velocity remains normal. We observed a significant increase in the latency between nerve and muscle action potentials but no modifications in the electromechanical delay. The first action of sepsis on motor units seems to be a delayed trigger of muscle action potential along with a muscle weakness but without nerve conduction impairment.
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PMID:Effects of chronic sepsis on rat motor units: experimental study of critical illness polyneuromyopathy. 1731 11

Neisseria meningitidis is a major cause of sepsis and bacterial meningitis worldwide. This bacterium expresses type IV pili (Tfp), which mediate important virulence traits such as the formation of bacterial aggregates, host cell adhesion, twitching motility, and DNA uptake. The meningococcal PilT protein is a hexameric ATPase that mediates pilus retraction. The PilU protein is produced from the pilT-pilU operon and shares a high degree of homology with PilT. The function of PilT in Tfp biology has been studied extensively, whereas the role of PilU remains poorly understood. Here we show that pilU mutants have delayed microcolony formation on host epithelial cells compared to the wild type, indicating that bacterium-bacterium interactions are affected. In normal human serum, the pilU mutant survived at a higher rate than that for wild-type bacteria. However, in a murine model of disease, mice infected with the pilT mutant demonstrated significantly reduced bacterial blood counts and survived at a higher rate than that for mice infected with the wild type. Infection of mice with the pilU mutant resulted in a trend of lower bacteremia, and still a significant increase in survival, than that of the wild type. In conclusion, these data suggest that PilU promotes timely microcolony formation and that both PilU and PilT are required for full bacterial virulence.
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PMID:Loss of meningococcal PilU delays microcolony formation and attenuates virulence in vivo. 2250 57

Phage therapy against bacterial pathogens has been resurrected as an alternative and supplementary anti-infective modality. Here, we observed that bacterial group motilities were impaired in Pseudomonas aeruginosa strain PA14 lysogens for some temperate siphophages; the PA14 lysogens for DMS3 and MP22 were impaired in swarming motility, whereas the PA14 lysogen for D3112 was impaired in twitching motility. The swarming and twitching motilities of PA14 were also affected in the presence of MP22 and D3112, respectively. The in vitro killing activities of D3112 and MP22 toward PA14 did not differ, and neither did their in vivo persistence in the absence of bacterial infections in mice as well as in flies. Nevertheless, administration of D3112, not MP22, significantly reduced the mortality and the bacterial burdens in murine peritonitis-sepsis and Drosophila systemic infection caused by PA14. Taken together, we suggest that a temperate phage-mediated twitching motility inhibition might be comparably effective to control the acute infections caused by P. aeruginosa.
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PMID:Antibacterial efficacy of temperate phage-mediated inhibition of bacterial group motilities. 2290 58