Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0276640 (TEM)
 20,729 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection with herpes simplex virus type 1 (HSV-1) induces different morphological changes in different cell lines. This is demonstrated by comparative scanning (SEM and transmission (TEM) electron microscopic investigations of cell cultures prepared under identical conditions. SEM of HSV-1 infected HEp-2 cells reveals a slightly altered cell surface: only the number of the microvilli is reduced. Large amounts of released virions are detectable adhering to the outer plasma membrane. Ultra-thin sections show typical virus maturation steps in the nuclei (formation of nucleocapsids and virus budding from the inner lamella of the nuclear membrane) and in the cytoplasm (egress of enveloped nucleocapsids through membranous structures). HSV-infected primary chick embryo fibroblast (CEF) cells are characterized by crumpled and rough surfaces without virus particles adhering to the membrane. Ultra-thin sections exhibit atypical virus maturation with many unenveloped nucleocapsids within the cytoplasm. The distribution of HSV-induced antigen(s) on the surface of the infected cells is identical in the two cell systems as determined by the peroxidase labelling technique. The c.p.e. (as seen by phase contrast light microscopy) is similar in both HEp-2 and CEF cells: both fusion and rounding up is induced in the infected cells.
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PMID:Differences in the morphology of herpes simplex virus infected cells: I. Comparative scanning and transmission electron microscopic studies on HSV-1 infected HEp-2 and chick embryo fibroblast cells. 23 Feb 92

Strains of Escherichia coli (N = 124) and Proteus mirabilis (N = 29) harboring known beta-lactamases were analyzed as to their susceptibility to ampicillin, amoxicillin, and piperacillin alone and in combination with sulbactam, clavulanate, and tazobactam. With TEM 1-producing E. coli, a correlation between specific beta-lactamase activity and the MIC of piperacillin and ampicillin-sulbactam was observed. These strains also showed significant differences in susceptibilities to the various combinations, suggesting that, at least in strains resistant to one combination, several beta-lactam/beta-lactamase inhibitor combinations should be tested in the laboratory. All combinations tested enhanced the activity of the beta-lactam towards TEM 1-producing E. coli, piperacillin-tazobactam being the most active. The drugs were less active to OXA 1 enzymes; solely with piperacillin-tazobactam 90% of strains were within the therapeutic range of the drug. Sulbactam acted synergistically to chromosomally encoded beta-lactamases, whereas amoxicillin-clavulanate was inactive. Piperacillin and piperacillin-tazobactam inhibited all strains producing chromosomally encoded beta-lactamases at concentrations within the therapeutic range of the drugs. In contrast, TEM 2 of P. mirabilis was not sensitive to ampicillin-sulbactam, but to the other combinations; here again piperacillin-tazobactam was the most active.
Infection
PMID:Comparative in vitro activities of amoxicillin-clavulanate, ampicillin-sulbactam and piperacillin-tazobactam against strains of Escherichia coli and proteus mirabilis harbouring known beta-lactamases. 164 71

From the microbiological point of view a variety of highly active compounds has contributed to improved efficacy of antibacterial chemotherapy during the last few decades. In some cases, however, resistance has increased due to different molecular mechanisms. Resistance to the new generation of broad-spectrum beta-lactams is in the cases of TEM and SHV enzymes based upon the stepwise acquisition of point mutations within the structural gene. Multiresistance to aminoglycosides is caused by a combination of different genes coding for aminoglycoside modifying enzymes on transferable plasmids. Resistance to glycopeptides has recently been detected in enterococci and is due to a new mechanism of resistance. These substances have so far had unlimited activity against methicillin-resistant Staphylococcus aureus and have been widely used for treatment of pseudomembranous colitis. While all the three mechanisms of resistance mentioned above are transferable among different strains, no evidence exists so far for transferable resistance to 4-quinolones. However, for S. aureus and Pseudomonas aeruginosa an increase of resistance has been reported. The underlying mechanisms seem to be unchanged. The detection of global changes in the development of resistance and the discrimination of these changes from local events requires recording of statistically significant data obtained with approved methods and evaluation of the data with standardized international breakpoints. Consequently, the use of new agents should be controlled efficiently.
Infection 1991
PMID:[Evaluation of the development of resistance as a factor for the limitation of therapeutic possibilities]. 190 Oct 50

Oral cephalosporins (cefixime, cefdinir, cefetamet, ceftibuten, cefpodoxime, loracarbef, cefprozil, cefuroxime, cefaclor, cefadroxil and BAY 3522) were compared by their antibacterial profile including stability against new beta-lactamases. Both activity and antibacterial spectrum of compounds structurally related to third generation parenteral cephalosporins (of the oximino class) were superior to established compounds. Activity against staphylococci was found to be highest for cefdinir, cefprozil and BAY 3522. Cefetamet, ceftibuten and cefixime demonstrate no clinically meaningful antistaphylococcal activity while the other compounds investigated demonstrate intermediate activity. The antibacterial spectrum was broadest for cefdinir and cefpodoxime. New oral cephalosporins are equally inactive as established compounds against Enterobacter spp., Morganella, Listeria, Pseudomonas and Acinetobacter spp., methicillin-resistant staphylococci, Enterococcus spp., penicillin-resistant pneumococci and anaerobes. New extended broad-spectrum betalactamases (TEM-3, TEM-5, TEM-6, TEM-7, SHV-2, SHV-3, SHV-4, SHV-5, CMY-1, CMY-2, and CTX-M) are active against the majority of oral cephalosporins. Ceftibuten, cefetamet, cefixime and cefdinir were stable against some of these enzymes even to a higher extent than parenteral cephalosporins. New oral cephalosporins should improve the therapeutic perspectives of oral cephalosporins due to their higher activity against pathogens marginally susceptible to established compounds (higher multiplicity of maximum plasma concentrations over MICs of the pathogens) and furthermore by including in their spectrum organisms resistant to established absorbable cephalosporins (e.g. Proteus spp., Providencia spp., Citrobacter spp., and Serratia spp.).
Infection 1990
PMID:[Antibacterial activity and beta-lactamase stability of eleven oral cephalosporins]. 207 78

New plasmidic beta-lactamases inactivating so far stable cephalosporins, aztreonam and cephamycins restrict the use of these antibiotics in therapy of infections, e.g., by Escherichia coli and Klebsiella. Thus, combinations of beta-lactamase inhibitors and beta-lactam antibiotics were investigated in vitro with regard to their therapeutic perspectives. Minimal inhibitory concentrations and the kinetics of killing in a pharmacodynamic model were determined. Extended broad spectrum beta-lactamases (EBS-beta-lactamases) representative both for the TEM- and SHV-type were included. None of the available fixed combinations of penicillins and beta-lactamase inhibitors appears useful for therapy of infections caused by producers of EBS-beta-lactamases. In contrast, combinations of piperacillin and tazobactam or sulbactam plus cephalosporins (cefoperazone, cefotaxime, ceftazidime) or aztreonam are highly active (both by their MICs and bactericidal activity) against TEM-type EBS-beta-lactamases, but less promising for the SHV-type EBS-beta-lactamases, and plasmidic cephamycinase. Of the beta-lactams available, the monobactam carumonam and the carbapenems (imipenem, meropenem) remain safe in infections caused by E. coli and Klebsiella EBSBase producers.
Infection
PMID:Perspectives of beta-lactamases inhibitors in therapy of infections caused by Escherichia coli or Klebsiella with plasmidic resistance to third generation cephalosporins. 217 38

Escherichia coli GRI was isolated from an ear exudate of a newborn. The strain was highly resistant to cefotaxime (MIC 128 mg/l). Resistance to cefotaxime and the majority of beta-lactam antibiotics was readily transferred to an Escherichia coli recipient strain. Both the wild type and the transconjugant strains are different in their resistance phenotype from TEM-3 beta-cefotaximase producers by higher MICs to the majority of beta-lactams and lower MICs to ceftazidime. The isoelectric point of the cefotaximase of E. coli GRI was 8.9 in comparison with 6.3 for TEM-3. Thus, the enzyme produced by E. coli GRI represents a new plasmidic (plasmid pMVP-3) broad spectrum beta-lactamase (CTX-M) which may not be closely related to either the TEM- oder SHV-family of extended broad spectrum beta-lactamases.
Infection
PMID:A new plasmidic cefotaximase in a clinical isolate of Escherichia coli. 227 23

Extended broad spectrum beta-lactamases such as TEM-3 (CTX-1), TEM-5 (CAZ-1), TEM-10 and RHH-1 were purified and found to have lower specific activities than the TEM-1 or TEM-2 beta-lactamases. Total hydrolytic activity in crude extracts was also lower for the extended broad spectrum enzymes. These beta-lactamases hydrolyzed not only penicillins such as carbenicillin, cloxacillin and piperacillin, but also cephalosporins and monobactams. The most notable differences in substrate profiles between the extended broad spectrum enzymes and TEM-2 enzymes occurred with oxime-containing antibiotics. Although all the extended broad spectrum enzymes described above hydrolyzed cefotaxime, ceftazidime and aztreonam, the four enzymes could be easily differentiated: TEM-3 hydrolyzed cefotaxime preferentially, TEM-5 and RHH-1 hydrolyzed ceftazidime approximately three times faster than cefotaxime, whereas TEM-10 hydrolyzed ceftazidime 42 times faster than cefotaxime. All the enzymes were inhibited well by clavulanic acid, with I50 values ranging from 4.3 to 12 nM, compared to 130 nM for TEM-2. Inhibition by sulbactam was also better for the extended broad spectrum than for the TEM-2 beta-lactamases, with I50 values of 12-940 nM for the extended broad spectrum enzymes, compared to 1600 nM for the TEM-2 beta-lactamase.
Infection
PMID:Biochemical characteristics of extended broad spectrum beta-lactamases. 261 37

The incidence of strains producing transferable beta-lactamases capable of hydrolyzing third generation cephalosporins or aminothiazole-oximino substituted monobactams in five Buenos Aires hospitals during a four month period was studied. These enzymes were categorized by 1) MIC greater than or equal to 1 mg/l for third generation cephalosporins; 2) MIC less than 0.06 mg/l for third generation cephalosporins combined with clavulanic acid or sulbactam; 3) sensitivity to imipenem or cephamycins (excluding permeability mutants); and 4) transferable resistance by conjugation. Beta-lactamases hydrolyzing aminothiazole-oximino substituted monobactams were produced by 17.2% of Enterobacteriaceae from intensive care unit patients; 3.6% from inpatients of other units and 1.2% from outpatients. Producers were mainly Klebsiella spp. (45/46) resistant to aminoglycosides (most of them AAC 3'-AAC 6' producers). Three strains had a an isoelectric point of 6.0, two of 6.5 and three of 7.7. TEM-1 beta-lactamase (isoelectric point 5.4) was detected in 6/8 strains. An inocolum effect was observed in 40/46 strains. A Klebsiella pneumoniae strain preserved since 1982 also produced a transferable beta-lactamase hydrolyzing aminothiazole-oximino substituted monobactams.
Infection
PMID:Incidence of strains producing extended spectrum beta-lactamases in Argentina. 261 38

A plasmid-encoded beta-lactamase conferring extended broad spectrum resistance including cephamycins was identified in a Klebsiella pneumoniae strain isolated from a patient's wound. Strains harbouring the plasmid pMVP-1 were resistant to penicillins, cephalosporins of all generations (parenteral and new oral compounds) cephamycins, aztreonam, tetracycline, chloramphenicol, sulfonamides and to all aminoglycosides modified by AAC-(6)-I-transferase. beta-lactams still active against these strains were temocillin, ceftazidime, cefpirome, carumonam and the carbapenems imipenem and meropenem. The new cephamycinase (CMY-1) was more strongly inhibited by sulbactam in the majority of combinations than by clavulanic acid or tazobactam. MICs of ceftazidime and carumonam were not reduced by inhibitors in the wild type and the transconjugant. A transferable plasmid (pMVP-1) of about 9.6 x 10(7) dalton was demonstrated by gel-electrophoresis. In the wild type and the transconjugant a beta-lactamase with an isoelectric point of 8.0 was identified. This enzyme CMY-1 is different from the other extended broad spectrum beta-lactamases (TEM-3 to TEM-10, SHV-2 to SHV-5). The incidence of this enzyme may be underestimated, since resistance to cephamycins in Klebsiella and Escherichia coli has so far been regarded as almost exclusively chromosomally encoded and sensitivity of CMY-1 to clavulanic acid is low. Therefore, screening for CMY-1 beta-lactamases by the usual double disk test including clavulanic acid is not sensitive enough to detect CMY-1 producers. Sulbactam (e.g. in combination with ampicillin) disks and a cephamycin should therefore be used as well when screening for super extended broad spectrum (SEBS-) beta-lactamases.
Infection
PMID:Extended broad spectrum beta-lactamase in Klebsiella pneumoniae including resistance to cephamycins. 268 49

Beta-lactamases play a major part in resistance, as recently redemonstrated by the emergence of extended spectrum beta-lactamases. Since its discovery in FR Germany, SHV-2 has been reported from four continents and CTX-1 (TEM-3) was established in at least 26 French hospitals. More than 12 other enzymes have been individualized. The newest aspect of resistance was probably underestimated because most strains of enterobacteria (mainly Klebsiella pneumoniae) appeared susceptible to oxyimino-beta-lactams as suggested by MICs or diameters of inhibition zone sizes. The double-disk synergy test between amoxicillin/clavulanic acid and oxyimino-beta-lactams was useful to easily detect two susceptibility patterns (CTX, CAZ). Extended spectrum beta-lactamases isolated among nosocomial isolates of enterobacteria (urines, blood, wound, sputum cultures) mostly from intensive care units have spread through hospitals. If outbreaks were described, numerous serotypes were identified in Klebsiella pneumoniae. In France the distribution of extended spectrum beta-lactamases showed that CTX-1 (TEM-3) was well distributed among ten species unlike SHV-type enzymes (SHV-2, SHV-3, SHV-4) preferentially detected in Klebsiella pneumoniae. A majority of strains produced CAZ-type enzymes in Escherichia coli. Some isolates produced two extended spectrum beta-lactamases. In Tunisia extended spectrum beta-lactamase producing strains were mainly identified among pediatric isolates of Klebsiella pneumoniae, Salmonella and Escherichia coli; SHV-2 was predominant but recently CTX-1 and two other types with an isoelectric point of 6.35 and 5.4 (phenotype CTX) were individualized. Because plasmid-encoded, this mechanism was spreading in France among enterobacteria with other resistance markers (e.g. netilmicin, amikacin) for CTX-1 unlike SHV-2.(ABSTRACT TRUNCATED AT 250 WORDS)
Infection
PMID:Epidemiology of extended spectrum beta-lactamases. 268 54


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