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)

Resistance of Escherichia coli strain HB251 to the newer beta-lactam antibiotics, in particular ceftazidime and aztreonam, results from production of the extended-spectrum beta-lactamase TEM-6. The corresponding structural gene, bla(T)-6, and its promoter region were amplified by the polymerase chain reaction. Analysis of the sequence of the amplification product showed that bla(T)-6 differed by two nucleotide substitutions from bla(T)-1, the gene encoding TEM-1 penicillinase in plasmid pBR322. The mutations led to the substitution of a lysine for a glutamic acid at position 102 and of a histidine for an arginine at position 162 of the unprocessed TEM-1 protein. The presence of a 116 bp DNA insert upstream from bla(T)-6 resulted in the creation of hybrid promoter P6 in which the -10 region was that of TEM-1 promoter P3 whereas the -35 canonical sequence TTGACA was provided by the right end of the insert. P6 was found to be 10 times more active than P3 and to confer higher levels of antibiotic resistance upon the host. Analysis of the sequence of the insert indicated that the 116 bp fragment is related to insertion sequence IS1 but differs from it by three internal deletions that removed regions encoding the transposase. The distribution of the IS1-like element in clinical isolates of Enterobacteriaceae was studied by the polymerase chain reaction and by DNA-DNA hybridization. The element appeared to be widespread and was detected in strains producing TEM-6 or other TEM variants.
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PMID:An IS1-like element is responsible for high-level synthesis of extended-spectrum beta-lactamase TEM-6 in Enterobacteriaceae. 166 71

Production of TEM-1 beta-lactamase is the commonest cause of acquired resistance to amoxycillin and piperacillin in Escherichia coli, now occurring in c. 50% of isolates. Consecutive E. coli isolates producing TEM-1 beta-lactamase were collected at The London Hospital in 1982 (n = 50) and 1989 (n = 46). Enzyme quantities varied 150-fold amongst the isolates. Randomly-selected isolates from both years (n = 36; nine per quartile of the beta-lactamase activity distribution) were tested for susceptibility to combinations of amoxycillin or piperacillin with clavulanate or tazobactam or with BRL42715, a novel penem. The inhibitor concentrations needed to potentiate the penicillins related to the amount of beta-lactamase produced. BRL42715, at 1 mg/l, rendered all the isolates, including TEM-1 hyperproducers, susceptible to the recommended BSAC breakpoints of 8 mg amoxycillin/1 and 16 mg piperacillin/l. At 2 mg/l, BRL42715 almost always reduced amoxycillin and piperacillin MICs to the levels (1-2 mg/l) expected for E. coli isolates that lack TEM-1 enzyme. Tazobactam, at 1-2 mg/l, reduced piperacillin MICs to 1-2 mg/l for strains in the lower half of the beta-lactamase distribution, but greater than 8 mg tazobactam/l was required to reduce piperacillin MICs to 16 mg/l for one-third of the top quartile isolates. Clavulanate was a stronger potentiator of piperacillin than was tazobactam. On the other hand, amoxycillin was a more difficult substrate to potentiate than piperacillin, and isolates with enzyme levels in the top half of the distribution generally required greater than or equal to 8 mg clavulanate/l to reduce amoxycillin MICs to less than or equal to 8 mg/l.
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PMID:Susceptibility of Escherichia coli isolates with TEM-1 beta-lactamase to combinations of BRL42715, tazobactam or clavulanate with piperacillin or amoxycillin . 193 85

In July 1984 Klebsiella pneumoniae producing beta-lactamase CTX-1(TEM-3) (K. pneumoniae-CTX-1) spread from an Intensive Care Unit (ICU) throughout the hospitals of Clermont-Ferrand, France, and were isolated in four other hospitals of the region. A retrospective case control study was conducted in the ICU to characterize the risk factors for nosocomial infection with this organism. The cases were the 74 patients who had had K. pneumoniae-CTX-1 isolated from one or more clinical samples between July 1984 and December 1987. They were compared with 74 controls for host risk factors, underlying disease, procedures and antibiotic treatment. The monthly incidence of infection/colonization varied from 0% to 14.6%. The mortality rate attributable to this organism was 0.26% during the study period. The duration of stay of cases was longer than that of controls. More cases than controls had ventilatory assistance. However, the predominant risk factor was emergency abdominal surgery. Before K. pneumoniae-CTX-1 was isolated, cases received quinolones and trimethoprim sulphamethoxazole more often than controls. However, only 15% of cases had received third generation cephalosporins while at the onset of K. pneumoniae-CTX-1 infection colonization, 32 patients were no longer being given antibiotics. The use of antibiotic prophylaxis by, for example, selective digestive tract decontamination should be considered in patients at high risk of infection.
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PMID:A case-control study of an outbreak of infections caused by Klebsiella pneumoniae strains producing CTX-1 (TEM-3) beta-lactamase. 167 72

DNA fragments with promoter activity were isolated from the chromosome of Lactococcus lactis subsp. lactis. For the isolation, a promoter probe vector based on the cat gene was constructed, which allowed direct selection with chloramphenicol in Bacillus subtilis and L. lactis. Four of the putative promoters (P1, P2, P10, and P21) were analyzed further by sequencing, mapping of the 5' end of the mRNA, Northern (RNA blot) hybridization, and chloramphenicol acetyltransferase activity measurements. From these fragments, -10 and -35 regions resembling the consensus Escherichia coli sigma 70 and B. subtilis sigma 43 promoters were identified. Another set of promoters, together with a signal sequence, were also isolated from the same organism. These fragments promoted secretion of TEM beta-lactamase from L. lactis. When the two sets of promoters were compared, it was found that the ones isolated with the cat vector were more efficient (produced more mRNA). By changing the promoter part of the promoter-signal sequence fragment giving the best TEM beta-lactamase secretion into a more efficient one (P2), a 10-fold increase in enzyme production was obtained.
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PMID:Isolation and characterization of Lactococcus lactis subsp. lactis promoters. 170 5

Two crystal forms of Gram- bacteria TEM beta-lactamase have been obtained. The tetragonal form has a very large unit cell and diffracts to 3.0 A resolution. Orthorhombic crystals, grown using ammonium sulfate and a small amount of acetone as precipitating agents, belong to space group P2(1)2(1)2(1) with cell parameters a = 43.1 A, b = 64.4 A, c = 91.2 A and diffract to 1.7 A resolution. A seeding procedure has been designed that ensures reproducibility of the crystal properties. Molecular replacement, using a model reconstructed from the C alpha co-ordinates from Staphylococcus aureus PC1 beta-lactamase, gives a solution that satisfies crystal packing constraints.
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PMID:Crystallization and preliminary crystallographic data on Escherichia coli TEM1 beta-lactamase. 173 Oct 83

In a Tunisian hospital 27 babies, including 12 who were premature, in a single intensive care unit suffered acute gastroenteritis in the period from January to May 1988. The mean age at the onset of gastroenteritis was 8.4 days; nine babies died. Salmonella wien was isolated from stools (all babies) and blood (4 babies). It was also isolated from the stools of one nurse and from a mattress. Twelve of the babies had received cefotaxime, which was successfully replaced by oral colimycin. The outbreak was stopped by the implementation of infection control measures. All isolates of Salmonella wien were of the same biotype, and had the same antibiotic resistance pattern (third generation cephalosporins, monobactams, aminoglycosides, chloramphenicol, trimethoprim and sulphonamides) and plasmid DNA restriction pattern. The isolates were all susceptible to a combination of cefotaxime and clavulanic acid (a beta-lactamase inhibitor), which displayed synergy, suggesting the presence of a beta-lactamase (geometric mean MICs 11.24 micrograms/ml for cefotaxime alone and 0.24 micrograms/ml in combination with 0.1 micrograms/ml potassium clavulanate). All isolates produced TEM-1 and SHV-2 beta-lactamase which was not transferable to Escherichia coli by conjugation. The presence of the SHV-2 enzyme in Salmonella wien may allow it to adapt to newer beta-lactams which is a cause for concern in this hospital.
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PMID:Nosocomial outbreak of acute gastroenteritis in a neonatal intensive care unit in Tunisia caused by multiply drug resistant Salmonella wien producing SHV-2 beta-lactamase. 174 17

Cefcanel is a new orally absorbed cephalosporin. Its activity was compared with that of cefuroxime, cefaclor, cephalexin, and cefixime against gram-positive and negative aerobic and anaerobic bacteria. Cefcanel had excellent activity against methicillin-susceptible Staphylococcus aureus and Staphylococcus epidermidis, MIC90 1 micrograms/ml, superior to the other oral cephalosporins. However, methicillin-resistant staphylococci were resistant, MIC greater than or equal to 16 micrograms/ml. Streptococcus pyogenes and Streptococcus pneumoniae were inhibited by 0.015-1 micrograms/ml, concentrations comparable to other cephalosporins. Clostridium spp. were inhibited by 0.25 micrograms/ml, 8- to 128-fold lower concentrations than were found for other agents, but the MICs were greater than 64 micrograms/ml for Bacteroides spp. The MIC90 for Moraxella catarrhalis was 1 micrograms/ml, similar to cefuroxime but 16-fold greater than the MICs of cefixime. Escherichia coli and Klebsiella pneumonia which were high beta-lactamase producers were resistant, MICs greater than 64 micrograms/ml, and 50% of Enterobacter cloacae and Citrobacter freundii were resistant. Cefcanel was hydrolyzed by TEM-1, TEM-3 and Moraxella Bro-1 beta-lactamases. Escherichia coli containing TEM-1, 2, 3, 5, 7, and 9 had cefcanel MICs of greater than or equal to 16 micrograms/ml. Although cefcanel inhibited gram-positive species as well as or at lower concentrations than other cephalosporins, it lacked activity against gram-negative species that produced common plasmid beta-lactamase although it inhibited Haemophilus influenzae carrying TEM-1.
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PMID:In vitro activity of cefcanel versus other oral cephalosporins. 174 25

A series of C-terminal deletions of the dns-encoded extracellular deoxyribonuclease (DNS) of Vibrio cholerae, fused to the mature form TEM beta-lactamase (Bla) has been used to analyse the export of the DNase in both V. cholerae and Escherichia coli. All hybrid proteins were localized to the periplasmic space in E. coli and V. cholerae, with specific cleavage of the DNS-Bla fusion occurring in V. cholerae. Periplasmic accumulation of wt DNS was also seen in V. cholerae when present on a multicopy plasmid. DNS fusions retaining all six Cys residues of DNS displayed both DNase and Bla enzymatic activity. While hybrid proteins were unable to be secreted across the outer membrane in V. cholerae, the cleaved (active) DNS portion of these proteins was exported. Taken together, these data suggest that the periplasmic form seen in E. coli is a normal intermediate also seen in V. cholerae, and that the lack of secretion machinery in E. coli prevents further export across the outer membrane. Although the DNS portion of the protein fusions must be able to interact with secretion genes, the whole fusion proteins are not exported.
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PMID:Genetic analysis of the export of an extracellular DNase of Vibrio cholerae using DNase-beta-lactamase fusions. 176 Dec 28

Reference strains of Escherichia coli (ampicillin-susceptible and -resistant ATCC strains, and known TEM-1 and TEM-2 beta-lactamase producers) were tested in vitro and in the in-vivo mouse thigh infection model against four beta-lactamase inhibitor compounds (BICs: amoxycillin/clavulanic acid, ampicillin/sulbactam, ticarcillin/clavulanic acid, and piperacillin/tazobactam), selected cephalosporins, and imipenem. The ATCC strains (ampicillin-susceptible and -resistant) were susceptible to the BICs in disc and MIC tests. Three or more logs of killing were observed at the NCCLS breakpoint concentrations. However, the TEM-1 and TEM-2 producers were resistant in disc tests to ampicillin/sulbactam and amoxycillin/clavulanic acid, and showed intermediate susceptibility to ticarcillin/clavulanic acid. MICs were at or near the breakpoint, but bactericidal activity was only noted at the probable breakpoint concentration of piperacillin/tazobactam. Cefoxitin, cefotaxime, cefpirome and imipenem, but not cephalothin, showed greater bactericidal activity and lower MICs for the TEM-producing strains than the BICs. The viable count of the TEM-1 producer was not reduced in the mouse thigh model by ampicillin/sulbactam or amoxycillin/clavulanic acid, but cefpirome and cefotaxime reduced the viable count by approximately three logs. There was a 50% mortality rate in mice receiving the two BICs. The ampicillin-susceptible ATCC strain of E. coli was killed to a similar degree by all agents tested. Overall, the BICs appeared inferior, in both in-vivo and in-vitro tests to selected cephalosporins and imipenem when tested against reference strains of E. coli producing TEM-1 or TEM-2 beta-lactamase. The large inoculum effect and poor bactericidal activity observed with the BICs suggest they could be less effective in certain clinical situations.
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PMID:An in-vitro and in-vivo comparison of the activity of beta-lactamase inhibitor combinations with imipenem and cephalosporins against Escherichia coli producing TEM-1 or TEM-2 beta-lactamase. 142 30

High level tetracycline resistant strains of Neisseria gonorrhoeae (TRNG) have been shown to carry a 40.6 kb (25.2 MDa) conjugative plasmid with a Class M tetracycline resistance determinant. Restriction endonuclease analysis mapping showed that there were at least two different TRNG plasmid types which were found in geographically distinct locations. The physical maps of these two plasmids were compared to a gonococcal conjugative plasmid which did not encode tetracycline resistance. The plasmid type which is endemic in the Netherlands was found to be closely related to the gonococcal conjugative plasmid, which supports the established hypothesis that the 40.6 kb plasmid has evolved by transposition of the TetM determinant into the conjugative plasmid. The plasmid found in the United States has either evolved by substantial divergent evolution or it results from a different transposition event. In the UK there have been isolations of TRNGs carrying either of the two plasmid types reflecting a flow of people both across the Atlantic and in Europe. It is possible that further TetM-containing plasmids will be found in N. gonorrhoeae paralleling the family of TEM beta-lactamase encoding plasmids already described.
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PMID:Molecular evolution of tetracycline-resistance plasmids carrying TetM found in Neisseria gonorrhoeae from different countries. 177 50


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