Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1275122 (TEM)
 21,810 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ampicillin-resistant Haemophilus influenzae strain Ve445 which caused purulent meningitis and septicaemia in a newborn child in Germany contained a 4.4 megadalton (Mdal) plasmid (pVe445) and produced a TEM type beta-lactamase. The transformation to ampicillin resistance of a sensitive Escherichia coli strain with isolated pVe445 DNA proved that the structural gene for the beta-lactamase resided on this plasmid genome. Molecular DNA-DNA hybridization studies and electron microscope DNA heteroduplex analysis indicated that pVe445 probably contained 38 to 41% of the ampicillin translocation DNA segment (TnA) found on R factors of enteric origin. The TnA fragment present in pVe445 most likely does not contain both of the inverted repeat sequences of TnA. DNA-DNA polynucleotide sequence studies indicated that the 4.4 Mdal plasmid pVe445 was unrelated to the 30 to 38 Mdal H. influenzae R plasmids but was closely related to the 4.1 Mdal ampicillin resistance specifying H. influenzae plasmid RSF0885 isolated in the U.S.A. The H. influenzae plasmid pVe445 shared 91% of its base sequences with the beta-lactamase specifying Neisseria gonorrhoeae plasmid pMR0360 (4.4 Mdal) and had 85% of its base sequences in common with the beta-lactamase specifying N. gonorrhoeae plasmid pMR0200 (3.2 Mdal). All of the four 3.2 to 4.4 Mdal beta-lactamase specifying R plasmids of H. influenzae and N. gonorrhoeae investigated probably have a common evolutionary origin.
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PMID:Molecular characterization of a small Haemophilus influenzae plasmid specifying beta-lactamase and its relationship to R factors from Neisseria gonorrhoeae. 11 Sep 7

Ampicillin-resistant Haemophilus influenzae does occur now in the FRG. In one isolate a plasmid with resistance genes (R-factor) could be demonstrated as cause of the ampicillin resistance. This R-factor influences production of a beta-lactamase of the TEM type which destroys ampicillin. The infectious nature of the ampicillin resistance was proven by the fact that it was transferable to other bacterial species through cocultivation. Parallel to ampicillin resistance tetracycline resistant Haemophilus influenzae has occurred in the FRG. Here the resistance was equally bound to plasmids. These R-factors are infectious as well. Molecular analysis of the 3 isolated resistance factors in Haemophilus influenzae showed that they carry the same resistance genes which are known from R-factors of Enterobacteriaceae. In the therapy of purulent infections due to Haemophilus influenzae such as childhood meningitis one can no longer rely on general ampicillin sensitivity of the offender. Apart from ampicillin and tetracycline resistant Haemophilus influenzae chloramphenicol resistance has been observed in a few cases.
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PMID:[Infectious resistance to antibiotics in Haemophilus influenzae (author's transl)]. 30 40

A multiple trauma patient failed treatment with ceftazidime and amikacin for bacteremia and meningitis due to a Klebsiella pneumoniae strain that produced a novel, plasmid-mediated beta-lactamase. Both pre- and posttreatment isolates were resistant to ceftazidime (MIC, greater than or equal to 64 micrograms/ml) and various penicillins but not to other expanded-spectrum cephalosporins. The beta-lactamase had a pI of 5.25 and was encoded on a conjugal plasmid of approximately 150 kilobases. DNA hybridization studies indicated that the enzyme was a TEM derivative.
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PMID:Failure of ceftazidime-amikacin therapy for bacteremia and meningitis due to Klebsiella pneumoniae producing an extended-spectrum beta-lactamase. 220 6

Documented ampicillin treatment failures of systemic Haemophilus influenzae type b infections have been associated with synthesis of a TEM-1 beta-lactamase. A patient with H. influenzae type b meningitis in whom ampicillin treatment failed is described; the isolate was beta-lactamase-negative according to the cell suspension chromogenic cephalosporin assay. The false-negative result occurred in a strain which elaborated a novel, plasmid-mediated beta-lactamase with characteristics which distinguish it from TEM-1 beta-lactamase. Clinically important ampicillin resistance in H. influenzae type b occurs by mechanisms other than by synthesis of TEM-1 beta-lactamase. Diagnostic microbiology laboratories should perform antibiotic susceptibility tests in addition to tests for beta-lactamase production.
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PMID:Ampicillin treatment failure of apparently beta-lactamase-negative Haemophilus influenzae type b meningitis due to novel beta-lactamase. 611 76

Piperacillin is one of the new generation of semisynthetic penicillins which can be administered intravenously or intramuscularly. It has a broad spectrum of activity against Gram-positive and Gram-negative aerobic and anaerobic bacteria. Although piperacillin has shown greater activity against beta-lactamase-producing organisms than the other penicillins, it is hydrolysed by the plasmid-mediated beta-lactamases (TEM-1). Activity against Pseudomonas aeruginosa is better than that of ticarcillin, carbenicillin and mezlocillin. Although only limited controlled studies have been reported, in those which have been conducted and in a larger number of open studies piperacillin was effective in the treatment of complicated urinary tract infections and lower respiratory tract infections, particularly pneumonia, caused by Gram-negative bacilli. Favourable clinical results have been obtained in patients with infections caused by mixed aerobic/anaerobic organisms (such as intra-abdominal infections) but the relatively average in vitro activity of piperacillin against Bacteroides fragilis may not indicate its usage in situations where this organism is the suspected or proven pathogen. Piperacillin in combination with an aminoglycoside or a 'third generation' cephalosporin gave encouraging results in the treatment of infections in immunocompromised patients, whilst its penetration into the diseased central nervous system and lack of toxicity indicate a potential value in the treatment of neonatal Gram-negative bacillary meningitis, particularly where the causative organism is Pseudomonas aeruginosa. Whether piperacillin alone is appropriate therapy for conditions usually treated with aminoglycosides (other than pseudomonal infections) needs additional clarification, but if established as equally effective in such conditions it has the advantages of its apparent lack of serious adverse effects and freedom from the need to undertake plasma concentration monitoring. These advantages would not, however, apply when considering one of the new (third generation) cephalosporins as alternative therapy in non-pseudomonal infections. Generally, however, it is still considered necessary to treat serious and complicated infections with combination therapy, either a cephalosporin, or in cases of resistance to P. aeruginosa an aminoglycoside.
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PMID:Piperacillin. A review of its antibacterial activity, pharmacokinetic properties and therapeutic use. 639 88

In a review of 13 documented cases of fetal alcohol syndrome (FAS), an increased incidence of life-threatening bacterial infections as well as a propensity to minor infections was observed. Five of 13 patients had had at least one episode of pneumonia, two had meningitis, and one had sepsis. A comprehensive immunologic evaluation of FAS was completed, and results were compared to an age-matched control group of children with intrauterine growth retardation without FAS. Children with FAS were shown to have decreased E rosette-forming lymphocytes (35 +/- 5% versus 55 +/- 5% or 1328 +/- 274 versus 2333 +/- 112 per mm3), low EAC rosette-forming lymphocytes (15 +/- 2% versus 18 +/- 1% or 524 +/- 109 versus 740 +/- 75 per mm3), and diminished mitogen-induced stimulation responses to mitogens: 31616 +/- 5337 versus 58076 +/- 4455 cpm for phytohemagglutinin, 17582 +/- 5436 versus 35018 +/- 5346 for pokeweed mitogen, and 32460 +/- 7044 versus 54996 +/- 5531 for concanavalin A, P less than 0.05. Nine patients had dysgammaglobulinemia, FAS subjects also had a marked eosinophilia (624 +/- 154 versus 72 +/- 27 mm3). Other parameters of immune function including absolute lymphocyte and neutrophil counts, total hemolytic complement, delayed cutaneous hypersensitivity, and nitroblue tetrazolium dye reduction assays, were not different from control children. Impairment of immunity may explain an increased susceptibility to infection in FAS.
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PMID:Immune deficiency in fetal alcohol syndrome. 719 40

Sensorineural hearing loss was studied in a rabbit model of experimental bacterial meningitis using electrophysiological and ultrastructural techniques. Hearing impairment was monitored by auditory brain-stem evoked responses (ABERs) and concomitant structural lesions were identified by both transmission (TEM) and scanning (SEM) electron microscopy. Meningitis was induced by intra-cerebrospinal fluid injection of either Escherichia coli (strain 2073 and type K-12) or Haemophilus influenzae type b. Auditory loss of approximately equal to 10 dB occurred in all rabbits by about 10 hours post infection and progressed in severity until by 20 h following infection, hearing losses up to and > 60 dB were obtained. At levels of hearing loss < 20 dB ultrastructural damage to the organ of Corti was barely detectable. With greater levels of hearing loss, patchy structural damage to hair cells, synaptic nerve terminals, supporting cells and inner spiral sulcus cells and cells of the stria vascularis was clearly evident. Bacteria were found in scala tympani, the basilar membrane, the organ of Corti, scala media, the spiral ligament and at the margin of the stria vascularis. Evidence of bleeding was found in some cochleas; erythrocytes were found in scala tympani, scala media, amongst hair cells and beneath the tectorial membrane. The results show that hearing loss is associated with bacterial invasion and damage to the organ of Corti and that the cause of hearing loss is likely to result from multiple lesions within the cochlea. Lesions to sensory cells almost certainly will produce permanent hearing loss. Lesions to supporting cells, nerve terminals and to stria vascularis may well produce only temporary hearing loss.
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PMID:The cochlear lesion in experimental bacterial meningitis of the rabbit. 748 46

Two Salmonella typhimurium isolates were studied, one as a representative from a series of neonatal meningitis cases treated at an Istanbul teaching hospital, the other from a gastro-enteritis case seen at a different Istanbul hospital. Both isolates were resistant to extended-spectrum cephalosporins, as well as penicillins, aminoglycosides and chloramphenicol. Cephalosporin resistance depended on production of PER-1 beta-lactamase, which is an extended-spectrum class A enzyme that is only distantly related to TEM and SHV enzymes, and which was previously known only from Pseudomonas aeruginosa isolates. The PER-1 gene was carried by an 81-MDa plasmid, which also determined resistance to aminoglycosides and chloramphenicol. Although it was not self-transmissible to Escherichia coli, this element did transfer if mobilised with plasmid pUZ8. The two S. typhimurium isolates gave indistinguishable DNA restriction patterns and, in addition to their 81-MDa plasmid, also contained 52- and 2.8-MDa plasmids, the last of these encoded TEM-1 enzyme. The two isolates were identical in serotype, antibiogram and plasmid-profile but nevertheless differed in phage type, and, therefore, represented distinct strains. The emergence of cefotaxime and ceftriaxone resistance in salmonellae is disturbing, since these agents are preferred therapy for neonatal meningitis caused by members of the genus.
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PMID:Resistance to extended-spectrum cephalosporins, caused by PER-1 beta-lactamase, in Salmonella typhimurium from Istanbul, Turkey. 756 92

Thirty children in the age group 0-4 years with tuberculous meningitis (TBM) were investigated for their immune status (cell-mediated and humoral). Twenty age, sex and nutritional status matched children were investigated on the same lines, who served as controls. Absolute T cell counts were significantly increased (3126 +/- 1623) (p < 0.01) in TBM, though T cell percentages were comparable (59.8% in TBM versus 54.44% in controls). Leucocyte migration inhibition (LMI) test positivity was high (93%) in TBM patients. Mean LMI index showed a highly statistically significant difference (p < 0.001) between the 'Before-therapy' (0.62 +/- 0.16) and 'During-therapy' (0.77 +/- 0.23) groups in TBM patients. Mantoux test positivity with 1 TU of PPD was low (53.0%) in TBM in comparison to LMIT positivity. In humoral immune response, quantitative function measured by EAC rosettes was not altered. However, there was a significant decrease in the levels of IgA (79.48 +/- 33.78 IU) (p < 0.01), IgG (115.01 +/- 32.56 IU) (p < 0.01) and IgM (148.50 +/- 51.88 IU) (p < 0.05) in TBM patients. There was no significant difference in the complement levels in the TBM and control groups. The results show a well developed CMI response but a poor humoral response in TBM and represent an inverse relationship between the CMI and humoral responses.
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PMID:Tuberculous meningitis in children: manifestation of an immune compromised state. 807 8

We evaluated the pharmacokinetics and therapeutic efficacies of piperacillin and tazobactam, a beta-lactamase inhibitor, given either alone or in different combinations (80:10, 200:10, and 80:25 mg/kg/h), in experimental meningitis due to a strain of Klebsiella pneumoniae producing the TEM-3 extended-spectrum beta-lactamase. Treatment was administered intravenously as a 7-h constant infusion preceded by a bolus of 20% of the total dose. The mean (+/- standard deviation) rates of penetration into the cerebrospinal fluid (CSF) of infected animals were 6.7 +/- 3.9% for piperacillin given alone and 36.3 +/- 21.9% for tazobactam given alone. Combination treatment significantly magnified the concentration of either drug in CSF. Concentrations of bacteria in CSF increased throughout therapy in animals given either drug alone, even at high dosages. In animals given the combination at dosages of 80:10 and 200/10 mg/kg/h, only a suboptimal reduction of CSF bacterial titers was obtained in vivo, i.e. -0.49 +/- 0.34 and -0.73 +/- 0.49 log CFU/ml/h, respectively. An increase in the tazobactam dosage within the combination (80:25 mg/kg/h) was required in order to obtain a significantly faster elimination of viable organisms from the CSF (-0.97 +/- 0.35 log CFU/ml/h). The study shows that tazobactam is able to provide effective protection against piperacillin hydrolysis by the TEM-3 enzyme within the CSF. Appropriate dosage regimens of various beta-lactam-tazobactam combinations may deserve comparative studies in experimental meningitis caused by organisms producing extended-spectrum beta-lactamases.
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PMID:Different ratios of the piperacillin-tazobactam combination for treatment of experimental meningitis due to Klebsiella pneumoniae producing the TEM-3 extended-spectrum beta-lactamase. 819 42


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