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

Our investigation concerns 14 streptococcus D sepsis neonates, thirteen of which were collected over a six year period during which eighty-two neonate infections were recorded. This rate slightly higher than generally recorded and may be due to the initial prescription of third generation cephalosporin to the mothers. The clinical, hematological and biological data are not specifically those of group D streptococcus. The issue was unfavourable in 15% of our cases and in 8 to 33% of the recorded cases. The sensitivity to antibiotics varies depending on the species of group D streptococcus. The effectiveness of Amoxicillin, of Mezlocillin and of Ampicillin justifies the initial prescription in association with an aminoglycoside because of the possibility of synergy; cephalosporins are contraindicated as they are inactive on this germ.
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PMID:[Role of Streptococcus group D in infections in newborn infants]. 666 46

Aberrant filamentous forms of Escherichia coli were observed on direct Gram stain of blood cultures from a patient being treated with the beta-lactam antibiotic cephalexin. After the institution of an alternative antibiotic regimen which included a different cell wall-active agent, E. coli of normal morphology was detected in blood cultures for an additional 48 h. Filamentous forms of E. coli could be reproduced reliably in vitro by incubating the organism in Mueller-Hinton broth containing various concentrations of cephalexin. Both supra- and subinhibitory concentrations of cephalexin resulted in filament formation after 4 h of incubation, whereas 24 h of incubation yielded intact filaments at only a narrow range of subinhibitory concentrations of cephalexin. In vitro comparison of the ability of cephalexin, cephalothin, ampicillin, and gentamicin to cause filamentous forms of E. coli showed that cephalexin and cephalothin produced pure filament formation after 4 h of incubation at subinhibitory concentrations of as low as one-fourth the minimum inhibitory concentration of the antibiotic. Ampicillin was not associated with pure filament formation at concentrations below the minimum inhibitory concentration, and gentamicin produced no filaments at any concentration. The effect of preincubation of E. coli with subinhibitory concentrations of cephalexin on subsequent minimum inhibitory concentrations of ampicillin was examined in an effort to develop an explanation for the persistent sepsis exhibited by the patient. No diminution of the activity of ampicillin by preincubation with cephalexin could be demonstrated. Other possible clinical implications of filamentous forms of gram-negative bacilli are discussed.
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PMID:Aberrant forms of Escherichia coli in blood cultures: in vitro reproduction of an in vivo observation. 702

Pancreatic sepsis in acute pancreatitis is the most lethal complication of the disease. This study was done to create a rational basis for the choice of antibiotics used in the treatment of severe acute pancreatitis. We postulated that, unless the antibiotics were present in therapeutic concentrations in the pancreatic tissue during pancreatitis, their use was of no value. Six mongrel dogs were used to test each antibiotic, each dog acting as its own control. The doses were based on the weight of the dogs: 15.0 milligrams per kilogram of clindamycin; 50.0 milligrams per kilogram of chloramphenicol; 10.0 milligrams per kilogram of metronidazole; 5.0 milligrams per kilogram of gentamicin; 12.5 milligrams per kilogram of cefazolin, and 50.0 milligrams per kilogram of ampicillin. Baseline serum and pancreatic tissue levels were obtained after intravenous injection of the antibiotics. Bile-trypsin hemorrhagic pancreatitis was induced one week later, and the serum and pancreatic tissue level antibiotics were measured again. The results showed significant differences in bioactive levels of antibiotics between blood and the pancreas. Ampicillin, gentamicin and cefazolin reached therapeutic blood levels, but did not achieve a parallel therapeutic level in the normal pancreatic tissue or during pancreatitis. Only three of the antibiotics tested, clindamycin, metronidazole and chloramphenicol, achieved therapeutic tissue penetrance in the normal and inflamed pancreas. After 1982, based on these results, clindamycin became our prophylactic antibiotic of choice in instances of acute severe pancreatitis. This resulted in the eradication of Bacteroides as a cause of pancreatic sepsis between 1980 and 1985. In 1993, our recommendation is to use a broad-spectrum gram-negative and gram-positive antibiotic with good penetration of the pancreatic tissue, such as cefotaxime or imipenem.
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PMID:Antibiotics bioavailability in acute experimental pancreatitis. 816 85

Pulmonary edema and sepsis-like syndrome are grave complications of interleukin-2 (IL-2) therapy. Recent animal studies have suggested IL-2-induced microvascular injury as the underlying mechanism. Since complement factors have been shown to mediate increased vascular permeability in diverse conditions that lead to pulmonary injury and recombinant human IL-2 is known to activate the complement system in patients undergoing IL-2 therapy, we hypothesized that complement factors play a pivotal role in the development of increased vascular permeability after IL-2 treatment. To test this hypothesis, we evaluated the capacity of recombinant soluble human complement receptor type 1 (sCR1, BRL 55730), a new highly specific complement inhibitor, to attenuate IL-2-induced lung injury in the rat. Recombinant human IL-2 (intravenously for 60 minutes) at 10(6) U per rat (n = 4) elevated lung water content (37 +/- 6%, P < .05), myeloperoxidase activity (162 +/- 49%, P < .05), and serum thromboxane B2 (30 +/- 1 pg/100 microL, P < .01) and had no effect on serum tumor necrosis factor-alpha sCR-1 at 30 mg/kg (n = 5), but not at 10 mg/kg (n = 6), attenuated the elevation of lung water content (18 +/- 2%, P < .05) and myeloperoxidase activity (42 +/- 9%, P < .05) but failed to alter serum thromboxane B2 response to IL-2. These data suggest the involvement of complement in the pathogenesis of IL-2-induced pulmonary microvascular injury and point to the potential therapeutic capacity of complement inhibitors in combating this toxic effect of IL-2 therapy.
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PMID:Interleukin-2-induced lung injury. The role of complement. 829 71

Two broadly cross-reactive anti-lipopolysaccharide core monoclonal antibodies WN1 222.5 and SZ27/150.3 were used in an ELISA system to detect the accessibility of core epitopes in Escherichia coli (four clinical isolates and NCTC 10418) grown to early stationary phase in the absence and presence of a half, a quarter and an eighth the MIC of temocillin, ampicillin, chloramphenicol, gentamicin and ciprofloxacin. The bacteria were coated on to ELISA microtitre plates. By comparing ELISA-titre ratios, temocillin induced a significantly large increase in binding of WN1 222.5 to all strains except NCTC 10418. Ampicillin and chloramphenicol induced a small increase in the binding of WN1 222.5 in some instances. Ciprofloxacin and gentamicin caused no increase in binding. Lipopolysaccharide SZ27/150.3 was only tested against temocillin-grown bacteria, but binding was not increased significantly compared with WN1 222.5. The results obtained demonstrate the potential use of temocillin to improve the clinical efficacy of immunotherapeutic monoclonal antibodies in Gram-negative sepsis.
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PMID:The accessibility of cross-reactive anti-lipopolysaccharide-core monoclonal antibodies to Escherichia coli grown in sub-MICs of temocillin and other antibiotics. 833 96

We report a case of successful mitral valve replacement performed on the patient who is an infective endocarditis due to MRSA. She was 27-year-old female and treated by antibiotics medication because of remittent fever two years ago. On August 1995, cerebral infarction occurred and she was pointed out endocarditis. After high fever continued, blood cultures demonstrated MRSA. Furthermore, echocardiography showed vegetation on posterior mitral valve leaflet and moderate mitral regurgitation so, mitral valve replacement with a S.J.M. 25 mm performed to control MRSA sepsis condition. During operation, we used VCM 2 g into the extracorporeal circulation and after operation 0.5 g intravenously every 6 hours. Two weeks later we changed antibiotics to FOM, Viccillin and ABK according to the result of minimum inhibitory concentration (MIC) obtained through blood culture. The patient was discharged on the 44 th postoperative day because of her uneventful postoperative course.
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PMID:[A case report of an infective endocarditis caused by methicillin-resistant Staphylococcus aureus with successful mitral valve replacement]. 874 44

Group A streptococcal (GAS) septicemia is rare in occurrence but has a significant morbidity and mortality, whereas retropharyngeal abscess (RPA) is infrequent and it is most commonly found in children under the age of 6 years, with half of the cases occurring in children between 6 and 12 months old. This report concerns a case of GAS septicemia complicated with RPA. The patient, a five-year-old boy, was referred from a local medical department under the impression of meningitis. However, blood and throat cultures were both found to be positive for group A streptococci. Widening of the retropharyngeal space was noted in lateral neck roentgenography. RPA was confirmed by computed tomography (CT) of the neck. Ampicillin was prescribed for a period of four weeks. The patient was then discharged and oral form ampicillin was continued for four more weeks. No surgical incision and drainage was performed. Complete disappearance of the abscesses were noted via CT of the neck at an Outpatient Department follow-up.
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PMID:Group A streptococcal septicemia with retropharyngeal abscess: a case report. 931 31

We report the earliest case of urinary tract infection (UTI) so far described in term uncomplicated newborn infants. The unusual features of this case included early massive hematuria as the only presenting symptom and a host with no risk factors for either sepsis or localization of infection in the genitourinary tract. Reports of urinary analysis, urine cultures, renal ultrasound, and renal scan established the diagnosis of UTI. Massive hematuria in this case was probably precipitated by mild renal venous thrombosis. Ampicillin-resistant Escherichia coli was cultured from the urine, which responded promptly to appropriate treatment. A urine culture was done because of the predominantly urinary signs and symptoms. Although urine culture analysis is not routinely performed for the evaluation of possible sepsis before 72 hours of age, this investigation may be important in critically ill neonates who present with predominantly genitourinary signs and symptoms.
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PMID:Early neonatal urinary tract infection: a case report and review. 984 67

Urinary tract infections are very common during pregnancy. Escherichia coli is the most common pathogen isolated from pregnant women. Ampicillin should not be used because of its high resistance to Escherichia coli. Pyelonephritis can cause morbidity and can be life-threatening to both mother and fetus. Second and third-generation cephalosporins are recommended for treatment, administered initially intravenously during hospitalization. Cultures and the study of virulence factors of uropathogenic Escherichia coli are recommended for the adequate management of pyelonephritis. The lower genital tract infection associated with pyelonephritis is responsible for the failure of antibiotic treatment. Asymptomatic bacteriuria can evolve into cystitis or pyelonephritis. All pregnant women should be routinely screened for bacteriuria using urine culture, and should be treated with nitrofurantoin, sulfixosazole or first-generation cephalosporins. Recurrent urinary infection should be treated with prophylactic antibiotics. Pregnant women who develop urinary tract infections with group B streptococcal infection should be treated with prophylactic antibiotics during labour to prevent neonatal sepsis. Preterm delivery is frequent. Evidence suggests that infection plays a role in the pathogenesis of preterm labour. Experimental models in pregnant mice support the theory that Escherichia coli propagated by the transplacental route, involving bacterial adhesins, induces preterm delivery, but this has not been demonstrated in humans. Ascending lower genital tract infections are the most probable cause of preterm delivery, but this remains to be proved.
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PMID:Urinary tract infections in pregnancy. 1114 47

Desensitization of macrophages is important during the development of sepsis. It was our intention to identify mechanisms that promote macrophage deactivation upon contact with endotoxin (LPS) and interferon-gamma (IFN-gamma) in vitro. Macrophage activation was achieved with 12-O-tetradecanoylphorbol 13-acetate (TPA), and the oxidative burst (i.e., oxygen radical formation) was followed by oxidation of the redox-sensitive dyes hydroethidine and dichlorodihydrofluorescein diacetate. Prestimulation of macrophages for 15 h with a combination of LPS/IFN-gamma attenuated oxygen radical formation in response to TPA. Taking the anti-inflammatory properties of the peroxisome proliferator-activating receptorgamma (PPARgamma) into consideration, we established activation of PPARgamma in response to LPS/IFN-gamma by an electrophoretic mobility shift, supershift, and a reporter gene assay. The reporter contains a triple PPAR-responsive element (PPRE) in front of a thymidine kinase minimal promoter driving the luciferase gene. We demonstrated that PPRE decoy oligonucleotides, supplied in front of LPS/IFN-gamma, allowed a full oxidative burst to recover upon TPA addition. Furthermore, we suppressed the oxidative burst by using the PPARgamma agonists 15-deoxy-Delta12,14-prostaglandin J2, BRL 49653, or ciglitazone. No effect was observed with WY 14643, a PPARalpha agonist. We conclude that activation of PPARs, most likely PPARgamma, promotes macrophage desensitization, thus attenuating the oxidative burst. This process appears important during development of sepsis.
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PMID:Delayed activation of PPARgamma by LPS and IFN-gamma attenuates the oxidative burst in macrophages. 1115 69


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