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Query: UMLS:C0243026 (sepsis)
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Since 1992, there has been an increase in the incidence of Enterobacter sepsis in the neonatal intensive care unit (NICU) of the authors' hospital. From 1995 to 1997, a prospective molecular epidemiological survey of the colonizing and infecting strains isolated from neonates was conducted. Enterobacter cloacae was the most frequent cause of neonatal sepsis, accounting for 19.2% of all neonatal infections, reaching a peak incidence of 2.2/1000 during 1996. Fifty isolates from the NICU and four epidemiologically unrelated strains were characterized by pulse-field gel electrophoresis (PFGE), ribotyping, enterobacterial repetitive intergenic consensus (ERIC)-PCR and plasmid profiling. PFGE was the most discriminatory technique and identified 13 types (two of them classified into two and three subtypes) compared with ERIC-PCR, plasmid profiling and ribotyping that identified 11, 11 and seven types, respectively. A good correlation was found between all techniques. Five different clones caused 15 cases of sepsis. Clones A and B were prevalent in 1995 and 1996, but they were not isolated in 1997. An outbreak caused by clone G in 1997 was controlled by cohort nursing and hygienic measures, without changing the antibiotic policy. Strains were characterized by their antibiotic resistance pattern and divided into three groups. Group I correlated with PFGE types A, B1 and B2, which hyperproduced Bush type 1 chromosomal beta-lactamase and expressed extended-spectrum ?-lactamases (ESBLs). Group II only hyperproduced Bush type 1 chromosomal beta-lactamase and correlated with PFGE-types D1, D2, D3 and I. Finally, Group III, with inducible beta-lactamases, correlated with the rest of PFGE types. The sudden disappearance of E. cloacae after reinforcement of hygienic measures confirms the importance of patient-to-patient transmission.
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PMID:Molecular epidemiological typing of Enterobacter cloacae isolates from a neonatal intensive care unit: three-year prospective study. 1171 34

TEM- or SHV-type extended-spectrum beta-lactamases (ESBLs) are of clinical concern in Europe and the United States, whereas bacterial strains producing such types of ESBLs have not been reported in Japan. We report here two cases of infection due to Klebsiella pneumoniae resistant to extended-spectrum cephalosporins in Japan. A ceftadizime-resistant K. pneumoniae strain (minimum inhibitory concentration; 32 &mgr;g/ml) was isolated transiently from the sputum of an 87-year-old woman with acute myocardial infarction and pneumonia (patient 1). Ceftadizime-susceptible and -resistant (minimum inhibitory concentration; >/=8 &mgr;g/ml) K. pneumoniae strains were isolated over a month from the blood, ascites, and feces of a 44-year-old man after bone marrow transplantation for acute lymphoblastic leukemia (patient 2); this patient died of K. pneumoniae sepsis and peritonitis followed by multiple organ failure. These isolates produced penicillinase, which was inhibited by clavulanic acid. A polymerase chain reaction (PCR) study showed that both isolates carried the SHV or LEN genes, but not the TEM, Toho-1, and IMP-1 genes. The pulsed-field gel electrophoresis profile of the strain isolated from patient 1 was genetically distinguishable from the profiles of the strains isolated from patient 2. It appeared that mutation of the beta-lactamase gene may have occurred in the body of patient 2, since the genotypes of the ceftadizime-susceptible and -resistant isolates from this patient were identical. Another 12 strains of K. pneumoniae, isolated from other patients in the same wards during the period in which the K. pneumoniae strains were isolated from patients 1 and 2, did not produce ESBLs and showed different genotypes. The results suggest that these isolates of resistant K. pneumoniae did not spread by cross transmission in the hospital and that the two cases were sporadic. Surveillance of these types of resistant bacteria is necessary, since they may well be present in other hospitals in Japan. Although the organisms are suspected to produce SHV-type ESBLs or LEN-1 variant beta-lactamases, further studies are necessary to specify the resistance genes.
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PMID:Two sporadic cases of infections due to Klebsiella pneumoniae resistant to expanded-spectrum cephalosporins in Japan. 1181 Apr 97

In spite of advances in critical care, nosocomial infections still have a considerable impact on Intensive Care Unit (ICU) and hospital length of stay, mortality and costs. Several authors suggest that antibiotic therapy should be instituted as soon as sepsis is suspected in critically patients. Over the last two decades the rates of occurrence for pathogens have significantly changed under selective pressure from broad-spectrum antimicrobial therapy. Shifts from predominance of gram-negative to gram-positive organisms and outbreaks of resistant pathogens address the need for appropriate empirical regimens. Agents such as ceftazidime, imipenem and, more recently, meropenem and tazobactam have been used successfully as monotherapy. Two different clinical trials have reported that meropenem monotherapy is significantly more effective than ceftazidime-based therapy. Because of the outbreak of methicillin-resistant Staphylococcus aureus and Staphylococcus epidermidis, some investigators suggest adding a glycopeptide to beta-lactamase inhibitor and carbapenem as initial empirical therapy. Such a regimen should be administered before definitive proof of infections and until the results of microbial investigation are available (de-escalation antimicrobial chemotherapy). On the other hand, several authors do not recommend glycopeptide administration in an attempt to limit nosocomial outbreaks of vancomycin-resistant enterococci (VRE) and staphylococci (VRS) and to avoid secondary drawbacks, such as nephrotoxicity and ototoxicity. De-escalation antimicrobial chemotherapy should be tailored to critically ill patients according to their clinical status, severity of illness and suspicion of sepsis or nosocomial pneumonia.
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PMID:De-escalation antimicrobial chemotherapy in critically III patients: pros and cons. 1193 69

Lemierre's syndrome is characterized by thrombosis of the internal jugular vein that develops following an oropharyngeal infection. Sepsis and septic metastases frequently ensue and affect the lungs, the musculoskeletal system, and occasionally the liver. Most cases are caused by infection with Fusobacterium necrophorum. This infection responds to antibiotic therapy with beta-lactamase-resistant compounds that exert good anaerobic coverage. Anticoagulation and surgical intervention can be helpful in advanced cases. Fewer than 160 cases of classic Lemierre's syndrome have been described; approximately one-third of these reported cases have occurred since 1988. We describe a new case of Lemierre's syndrome that occurred in an otherwise healthy 27-year-old man. Thrombosis of both internal jugular veins extended through the subclavian system and into both upper extremities. The patient was treated with intravenous antibiotics and heparin during 14 days of hospitalization. He was discharged on oral clindamycin and warfarin sodium, and after 6 months he was able to return to full activity. To our knowledge, this is the first reported case of Lemierre's syndrome in which internal jugular vein thrombosis occurred bilaterally. By reporting this previously undescribed manifestation of Lemierre's syndrome, we hope to increase practitioner awareness of this disease entity.
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PMID:Bilateral Lemierre's syndrome: a case report and literature review. 1198 41

Effective management of intra-abdominal infections requires a combination of preoperative preparation, antibiotic prophylaxis and appropriate surgical technique. Antibacterial prophylaxis should provide coverage of all likely pathogens, including aerobic and anaerobic organisms. Whereas antibacterial combination therapy is appropriate in certain situations, single-agent prophylaxis is appropriate for the majority of patients and ampicillin/sulbactam, with its broad-spectrum anti-aerobic/anti-anaerobic activity, is an attractive prophylactic option. Surgery involving the gastrointestinal tract provides a special challenge by virtue of its high, predominantly anaerobic, bacterial load. However, the requirement for prophylaxis varies depending upon the precise site of intervention. Biliary tract surgery requires prophylaxis in high-risk patients only, whereas hepatobiliary or pancreatic surgery requires prophylaxis in all patients. Gastroduodenal operations require prophylaxis in the presence of risk factors, such as abnormal gastric acidity or bleeding. Colorectal procedures present a high risk of anaerobic infection and sepsis, and require adequate prophylaxis combined with a thorough preoperative preparation designed to reduce considerably the bacterial load of the bowel. Where peritonitis does follow intra-abdominal surgery, patients should receive antibacterial therapy commensurate with the risk of serious infection. A small proportion of patients will be at risk of severe infection and will require triple-agent therapy. However, most patients are likely to develop mild-to-moderate infections only and can be treated with a single, broad-spectrum antibiotic agent, such as ampicillin/sulbactam, a beta-lactam/beta-lactamase inhibitor.
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PMID:New perspectives in antibiotic prophylaxis for intra-abdominal surgery. 1199 40

AM-112 [(1'R,5R,6R)-3-(4-amino-1,1-dimethyl-butyl)-6-(1'-hydroxyethyl)oxapenem-3-carboxylate] is a novel oxapenem compound which possesses potent beta-lactamase-inhibitory properties. Fifty-percent inhibitory concentrations (IC(50)s) of AM-112 for class A enzymes were between 0.16 and 2.24 micro M for three enzymes, compared to IC(50)s of 0.008 to 0.12 micro M for clavulanic acid. Against class C and class D enzymes, however, the activity of AM-112 was between 1,000- and 100,000-fold greater than that of clavulanic acid. AM-112 had affinity for the penicillin-binding proteins (PBPs) of Escherichia coli DC0, with PBP2 being inhibited by the lowest concentration of AM-112 tested, 0.1 micro g/ml. Ceftazidime was combined with AM-112 at 1:1 and 2:1 ratios in MIC determination studies against a panel of beta-lactamase-producing organisms. These studies demonstrated that AM-112 was effective at protecting ceftazidime against extended-spectrum beta-lactamase-producing strains and derepressed class C enzyme producers, reducing ceftazidime MICs by 16- and 2,048-fold. Similar results were obtained when AM-112 was combined with ceftriaxone, cefoperazone, or cefepime in a 1:2 ratio. Protection of ceftazidime with AM-112 was maintained against Enterobacter cloacae P99 and Klebsiella pneumoniae SHV-5 in a murine intraperitoneal sepsis model. The 50% effective dose of ceftazidime against E. cloacae P99 and K. pneumoniae SHV-5 was reduced from >100 and 160 mg/kg of body weight to 2 and 33.6 mg/kg, respectively, when it was combined with AM-112 at a 1:1 ratio. AM-112 demonstrates potential as a new beta-lactamase inhibitor.
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PMID:In vitro and in vivo activities of AM-112, a novel oxapenem. 1270 36

Over a 6-year period (1997 to 2002), 56 strains of Proteus mirabilis (12% of the total number of P. mirabilis isolates obtained) resistant to ampicillin, piperacillin, cefazolin and cefoperazone by routine antimicrobial testing method, were isolated in Saitama Medical School Hospital. Of the 56 strains resistant to 4 beta-lactams, 12 strains were studied and were found to produce extended-spectrum beta-lactamases, identified as CTX-M-10 group and Toho-1 group in 8 and 2 strains, respectively. Susceptibility testing showed that 12 strains were resistant to cefotaxime, and cepodoxime, and ceftriaxon but susceptible to ceftazidime. Moreover, all of the beta-lactamases were inhibited by clavulanic acid. Of the 12 strains, one strain showed resistance to cephamycins such as cefoxitin, cefmetazole and cefotetan. Four of the twelve patients had infections caused by ESBL producing P. mirabilis, and eight patients were colonized, as confirmed by clinical and laboratory findings. The infections were urinary tract infections (two episodes), pneumonia (one episode), and sepsis (one episode). These patients had a favorable response to antibiotic therapy including cephalosporin. From these findings, CTX-M-type beta-lactamase producing P. mirabilis strains were confirmed from clinical specimens in our hospital.
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PMID:[Study of resistance mechanism on cefotaxime resistant Proteus mirabilis isolated from clinical specimens and its clinical background]. 1510 87

Serious urinary tract infections (UTIs) in adults--defined as acute complicated UTIs or pyelonephritis requiring initial intravenous antimicrobials and/or hospitalisation and nosocomial infections--cause significant morbidity and economic burden. In the US, UTIs are responsible for nearly 7 million outpatient physician office visits, 1 million emergency room visits and over 100 000 hospital admissions annually. Complicated UTIs often affect patients with underlying functional, metabolic or anatomical defects of the urinary tract, whereas most nosocomial UTIs (~80%) are related to short- or long-term catheterisation. Serious UTIs are often difficult to treat because infection involves a diverse array of Gram-negative and Gram-positive bacteria, coupled with increasing antimicrobial resistance in some uropathogens, and a higher rate of recurrent infections. Although Escherichia coli remains a common aetiology (< or =60%), other Enterobacteriaceae, Gram-negative bacilli (e.g. Pseudomonas aeruginosa), and Gram-positive bacteria (e.g. Staphylococcus aureus) are frequently isolated. Patients with long-term catheterisation have UTIs typically caused by organisms that produce biofilms making eradication even more difficult. Overall, aetiology and resistance patterns are not predictable for those with serious UTIs, necessitating confirmation by culture and susceptibility testing.Numerous intravenous and oral antimicrobial treatment options are available and the majority of patients with serious UTIs will need initial intravenous therapy because of the possibility of bacteraemia/sepsis or impaired gastrointestinal absorption. Many experts concur that empirical therapy for the institutionalised or hospitalised patient with a serious UTI should include an intravenous antipseudomonal agent because of an increased risk of urosepsis. While state-of-the-art treatment guidelines are lacking for these infections, targeted therapy should be initiated once susceptibility data are known. The use of targeted therapy--emphasising the "correct antibacterial spectrum" and pharmacodynamic superiority--is likely to provide important benefits (e.g. reduced morbidity and associated costs, reduced emergence of resistance). Agents commonly prescribed include aminoglycosides, beta-lactam/beta-lactamase inhibitor combinations, imipenem, advanced-generation cephalosporins and fluoroquinolones. Fluoroquinolones are often recommended when conventional agents have failed or are less desirable (e.g. toxicity/hypersensitivity concerns), or when resistance is high. Several pivotal clinical trials support the use of fluoroquinolones for serious UTIs with most experience garnered with ciprofloxacin, including a new once-daily extended-release tablet formulation.Treatment of patients with serious UTIs remains challenging. Physicians should choose empirical therapy based on patient demographics/medical history, presumed aetiology and local resistance patterns until more definitive guidelines become available.
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PMID:Role of fluoroquinolones in the treatment of serious bacterial urinary tract infections. 1520 Mar 49

A strain of an Enterobacter sp. with reduced susceptibility to imipenem, which produced a plasmid-mediated class A carbapenem-hydrolyzing enzyme, KPC-2 beta-lactamase, was isolated from a patient with sepsis at a Boston hospital. This is the first report of the production of a plasmid-encoded KPC-2 beta-lactamase by an Enterobacter sp.
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PMID:Plasmid-mediated carbapenem-hydrolyzing enzyme KPC-2 in an Enterobacter sp. 1550 76

Nine premature infants developed early onset sepsis and/or pneumonia with Haemophilus influenzae during a period of 53 months (January 2000 -May 2004). Their respiratory problems were pneumonia-like rather than classic respiratory distress syndrome. In 8 of the cases, the pathogen was a beta-lactamase-negative, nontypable H. influenzae. In the remaining case, the Haemophilus identified was type d. Before January 2000, no case of beta-lactamase-negative, nontypable H. influenzae sepsis or pneumonia had been recorded.
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PMID:A cluster of early neonatal sepsis and pneumonia caused by nontypable Haemophilus influenzae. 1554 67


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