Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ampicillin and tetracycline, in doses of 2 g a day, were compared in the treatment of acute exacerbations of chronic bronchitis. Seventy-nine patients were followed for 3 to 29 months and were treated for 118 exacerbations. Clinical improvement occurred after 10 days of treatment with either drug in over 80% of the cases. Haemophilus influenzae and Diplococcus pneumoniae were eradicated from the sputum more than 60% of the time, but in general there was a poor correlation between bacteriological clearing and clinical response. The effect of chemoprophylaxis with ampicillin and tetracycline in doses of 1 g a day on the frequency of acute exacerbations of bronchitis was compared with that of a placebo. Seven hundred eighty prophylactic regimens, consisting of one capsule every 12 hr for 5 days beginning with the first sign of a cold, were prescribed for 76 patients. Irrespective of the regimen, an acute exacerbation of bronchitis was encountered at approximately 13% of the follow-up visits to the clinic.
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PMID:Ampicillin and tetracycline in the treatment and prophylaxis of chronic bronchitis. 415 29

Ampicillin-cefotaxime was tested as initial therapy of presumptive bacterial meningitis in 55 children greater than or equal to 2 months of age at our hospital. During the first year of this ongoing trial, 11 patients, 10 whose CSF yielded ampicillin-resistant Haemophilus influenzae type b (MIC greater than 16 mg/l, beta-lactamase +) and one, indole-negative proteus (MIC 4 mg/l), were begun on ampicillin-cefotaxime and then continued on cefotaxime alone. All did well clinically except one who convulsed briefly but recovered without sequelae. The cefotaxime MICs/MBCs of the beta-lactamase-positive H. influenzae isolates (less than or equal to 0.007 to 0.03/less than or equal to 0.007 to 0.12) and the proteus isolate (0.03/0.12) were significantly lower than chloramphenicol MICs/MBCs (0.25 to 1.0/0.5 to 1.0 and 8/greater than 16). We followed 44 other children with meningitis due to ampicillin-sensitive organisms who were treated with ampicillin or penicillin after 1 or 2 days of ampicillin-cefotaxime. Aetiological agents included ampicillin-sensitive H. influenzae (25), pneumococci (9), meningococci (8), Strept. MG (1) and Listeria monocytogenes (1). 40/44 recovered uneventfully. There were 4 neurological complications: the streptococcal meningitis sustained a brain abscess and the three others were motor incoordination (sensitive haemophilus), hearing loss and subdural effusion (2 pneumococci). There were no deaths. 18/48 children managed initially with ampicillin-chloramphenicol during the same 12-month period one year earlier had significant neurological complications and/or sequelae and there was one death; aetiological agents included sensitive H. influenzae (30), pneumococci (9), ampicillin-resistant haemophilus (5), meningococci (3) and pneumococci plus strept. MG (1). The two groups were comparable except for the number of resistant haemophilus and meningococcal strains and underlying disease more frequent in the ampicillin-cefotaxime group. A significant reduction of neurological morbidity (5/55 or 9.1% vs. 18/48 or 37.5%:P less than 0.001) was therefore associated with the ampicillin-cefotaxime schedule in the initial treatment of proven bacterial meningitis. A prolonged hospitalization (greater than 15 days) was less frequent (P less than 0.01) in the ampicillin-cefotaxime group (3/55 or 5.5% vs. 13/48 or 27.1%). The results of the trial to date are considered to be very promising.
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PMID:A comparison of ampicillin-cefotaxime and ampicillin-chloramphenicol in childhood bacterial meningitis: an experience in 55 patients. 609 37

CP-45,899 is a new, semisynthetic beta-lactamase inhibitor. When tested alone, CP-45,899 displayed only weak antibacterial activity, with the notable exception of its potent action against penicillin-susceptible and -resistant Neisseria gonorrhoeae. A combination of 3.12 microgram of CP-45,899 per ml with 3.12 microgram of ampicillin per ml, tested in broth cultures, inhibited ca. 90% of resistant Staphylococcus and Haemophilus influenzae strains; similar data were obtained in a variety of media. The same combination of CP-45,899 with ampicillin or penicillin G inhibited 90% of Bacteroides fragilis as interpreted from agar dilution minimal inhibitory concentrations. Inhibitory concentrations of CP-45,899-ampicillin were bactericidal against H. influenzae strains and were as bactericidal as nafcillin or cephalothin against S. aureus. Ampicillin-resistant S. aureus, H. influenzae, and B. fragilis strains did not develop resistance to CP-45,899-ampicillin when transferred as many as six passages in the presence of a sublethal concentration of the combination.
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PMID:CP-45,899 in combination with penicillin or ampicillin against penicillin-resistant Staphylococcus, Haemophilus influenzae, and Bacteroides. 624 92

The emergence of beta-lactamase producing strains of Haemophilus influenzae and Neisseria gonorrhoeae has required fundamental changes in the antimicrobial therapy of disease caused by these organisms. Ampicillin resistance in both organisms is caused by plasmid mediated production of TEM beta-lactamase. This enzyme is specified by a sequence of mol. wt 3.2 X 10(6) which is capable of inserting itself at multiple sites in DNA replicons without the requirement for significant base sequence homology between donor and recipient replicon. Further, it does so without requirement for conventional recombination enzymes. Analysis of beta-lactamase specifying plasmids of H. influenzae show that they generally have a molecular mass in the order of 30 X 10(6) and contain the complete TnA sequence. They are conjugative but are incapable of mobilizing smaller beta-lactamase plasmids. Previous studies have presented evidence suggesting that these plasmids may have evolved by insertion of the TnA sequence (perhaps introduced from enteric bacteria) into a phenotypically cryptic plasmid of mol. wt 27 X 10(6) resident in rare strains of H. influenzae. In this study, we review data showing a high degree of homology between the small (3--7 X 10(6) mol. wt), nonconjugative beta-lactamase specifying plasmids of N. gonorrhoeae, H. parainfluenzae and H. ducreyl and present new evidence that cryptic plasmids highly homologous to the beta-lactamase plasmids are present in many strains of H. parainfluenzae. This suggests that the small beta-lactamase specifying plasmids of H. parainfluenzae, H. ducreyi and N. gonorrhoeae may have arisen by insertion of TnA into phenotypically cryptic plasmids present in H. parainfluenzae.
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PMID:Evolution of antibiotic resistance plasmids in Neisseria gonorrhoeae and Haemophilus species. 631 45

Mecillinam, an antibiotic of the beta-lactam group, is active against Gram negative bacilli, with the exception of a few species such as Haemophilus influenzae. The activities of ampicillin, mecillinam, and ampicillin-mecillinam combinations at ratios of 1/1, 2/1, 4/1, 1/2 and 1/4, on 21 Haemophilus influenzae strains, were studied by agar dilution and determination of minimal inhibitory concentrations (MIC). Ampicillin at concentrations of 0.12 to 0.25 mg/l was active on susceptible strains. Beta-lactamase-producing strains were inhibited by 4 and 8 mg/l ampicillin. MICs of mecillinam were above 128 mg/l for 19 strains; two strains were susceptible to 2 mg/l. In every case, antibacterial activity was greater with the ampicillin-mecillinam combination than with either one of the antibiotics alone. The maximum antibacterial effect was obtained at ratios of 1/1 and 1/2; in this case, susceptible strains were inhibited by 0.06 mg/l ampicillin. Kinetic evaluation (killing curves) showed that ampicillin has a bactericidal effect at concentrations under the MIC when it is combined with mecillinam at a 1/1 ratio.
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PMID:[Inhibitory activity of ampicillin and mecillinam on Haemophilus influenzae]. 633 Jun 48

Ampicillin resistance in Haemophilus influenzae is most often due to the plasmid-mediated production of TEM beta-lactamase. We studied four strains with high-level ampicillin resistance (MIC of 32 micrograms/ml with an inoculum of 10(5) CFU on solid media) which did not produce detectable beta-lactamase activity with two different detection methods. Two of the four strains contained extrachromosomal DNA by agarose gel electrophoresis. Conjugation failed to transfer ampicillin resistance; in contrast, transformation yielded ampicillin-resistant transformants in three of the four strains. These transformants did not contain detectable extrachromosomal DNA. In addition, mobilization of the resistance determinant by transformation to, or conjugation with, recombination-deficient strains was unsuccessful. DNA-DNA hybridization experiments revealed no homology of the DNA of these strains with two R plasmids (one coding for ampicillin resistance, the other for chloramphenicol and tetracycline resistance). We conclude that the genetic basis of the non-beta-lactamase ampicillin resistance in these strains appears to be chromosomally mediated. We investigated the mechanism of resistance in these strains. Enzymatic modification of penicillin was not detected by autoradiography of a thin-layer chromatogram of cell sonic extracts of three ampicillin-resistant transformant strains incubated with [14C]penicillin. To assess changes in permeability of the cell envelope, a plasmid coding for beta-lactamase was conjugated into these strains, and the hydrolysis of penicillin by intact cells and cell sonic extracts was compared. Only one of three transformant strains had significantly diminished permeability. Outer membrane proteins of these strains analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed apparent differences in comparison with the isogenic ampicillin-susceptible recipient strain. Autofluorography of a sodium dodecyl sulfate-polyacrylamide gel electrophoresis of Sarkosyl-solubilized crude membrane (the putative inner membranes) from these ampicillin-resistant transformant strains incubated with [3H]penicillin compared with the isogenic ampicillin-susceptible recipient strain revealed reduced binding to PBP 3 and 6, 3 and 4, or 4. In addition, affinity binding studies revealed decreased affinity of PBP 4 for ampicillin of all four transformants tested. We conclude that the major mechanism of resistance in these strains is altered penicillin-binding proteins; however, other mechanisms, including permeability, may also play a role.
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PMID:Characterization of non-beta-lactamase-mediated ampicillin resistance in Haemophilus influenzae. 633 8

Population studies from three counties indicate that meningitis occurs with a frequency of approximately 10 episodes per 100,000 population annually in the United States. Estimates based on this prevalence and a population of 2.3 X 10(8) suggest that approximately 23,000 episodes of meningitis occur annually in the United States. Available studies indicate that rapid and reasonably accurate identification of the etiologic agent can be made in greater than or equal to 75% of patients with meningitis by gram-staining of the cerebrospinal fluid, counterimmunoelectrophoresis, or other antigen detection techniques. These means of rapid diagnosis theoretically leave only approximately 7,000 episodes of meningitis annually in the United States in which empiric, as opposed to specific, therapy is necessary. Age-dependent variation in etiologic agents of meningitis markedly influences selection of therapeutic regimens. The preponderance of Enterobacteriaceae and group B streptococci as causes of meningitis in neonates has resulted in utilization of a penicillin (often ampicillin) combined with an aminoglycoside for empiric therapy. Continued high morbidity and mortality, especially in neonatal meningitis caused by Enterobacteriaceae, have been felt to reflect inadequate penetration of aminoglycosides into the cerebrospinal fluid, but careful prospective randomized studies of intrathecal and intraventricular administration of aminoglycosides failed to demonstrate any enhancement of therapeutic results. Ampicillin appeared to be an ideal agent for empiric therapy in older children, in whom meningitis is usually caused by Haemophilus influenzae, with Streptococcus pneumoniae and Neisseria meningitidis being less frequently implicated as etiologic agents. The occurrence of beta-lactamase-mediated resistance to ampicillin in as high as 15% of isolates of H. influenzae has resulted in combined use of ampicillin and chloramphenicol for meningitis in children. This approach is complicated by evidence of clinically important antagonism between ampicillin and chloramphenicol. Since almost all community-acquired meningitis in otherwise healthy adults is caused by meningococci and pneumococci, penicillin remains the agent of choice. In contrast, meningitis following trauma to and surgery involving the central nervous system and in the elderly is often caused by gram-negative bacilli and other "unusual" organisms; therapeutic problems in this group parallel those observed in neonatal meningitis.
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PMID:Empiric therapy for bacterial meningitis. 634 1

Annual ampicillin susceptibility rates for Haemophilus influenzae isolates at the St. Paul-Ramsey Medical Center gradually decreased from 100% in 1974 to 83.3% in 1980 and then remained stable at 88.90%. Penicillin susceptibility rates were similar to those for ampicillin. Ampicillin rates were source dependent: eye 95%, respiratory 90%, miscellaneous sources 82%, and blood and CSF 80%. Rates for Haemophilus parainfluenzae varied and showed no trend. H. parainfluenzae isolates were distinctly less susceptible to penicillin (70%) than to ampicillin (96%). H. influenzae isolates were highly susceptible to chloramphenicol (99.6%) and tetracycline (97.5%), with the latter also showing source dependency. Characterization of isolates for colony morphology and hemolysis showed no clinical relevancy. Ampicillin and penicillin MICs were determined for 128 clinical isolates saved in stock culture during 1978-1983. All 19 resistant isolates (MIC greater than or equal to 4 micrograms/mL) were resistant to both penicillin and ampicillin and produced beta-lactamase. Eight had penicillin MICs of 1 or 2 micrograms/mL and three had ampicillin MICs of 1 or 2 micrograms/mL. The significance of isolates with MICs of 1-2 micrograms/mL is discussed in relation to our findings and a review of the literature.
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PMID:Antimicrobial resistance in Haemophilus isolates: a Minnesota experience and literature review. 638 Feb 70

BRL 36650 is a new type of penicillin in which a formamido group has been introduced into the 6 alpha-position of the nucleus. The compound is highly active against aerobic gram-negative bacteria and is stable to a wide range of beta-lactamases produced by these organisms. Against members of the family Enterobacteriaceae, BRL 36650 was considerably more active than piperacillin, particularly against beta-lactamase-producing strains, and showed a similar level of activity to moxalactam, aztreonam, and the third-generation cephalosporins cefotaxime and ceftazidime. Against Pseudomonas aeruginosa and other Pseudomonas species, BRL 36650 was more active than piperacillin, cefoperazone, and aztreonam and compared favorably with ceftazidime. BRL 36650 was highly active against Haemophilus influenzae and Neisseria gonorrhoeae, including beta-lactamase-producing strains, and against Acinetobacter calcoaceticus. Clinical isolates of Enterobacter species and P. aeruginosa which showed markedly reduced susceptibility to cefotaxime, ceftazidime, and aztreonam were only slightly less susceptible to BRL 36650. Against Bacteroides fragilis and most gram-positive bacteria, BRL 36650 showed only a low level of activity. BRL 36650 was found to be only 35% bound to human serum protein, and the antibacterial activity was little affected by the presence of serum. In contrast, the composition of the test medium influenced the activity of BRL 36650 slightly, and an antagonistic effect could be demonstrated between the compound and a component of certain Mueller-Hinton media.
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PMID:In vitro antibacterial properties of BRL 36650, a novel 6 alpha-substituted penicillin. 644 Apr 79

Despite the availability of numerous beta-lactam antibiotics, benzylpenicillin remains the most important beta-lactam antibiotic in the treatment of bacterial endocarditis. Penicillin alone and in combination with an aminoglycoside is effective in the treatment of endocarditis due to all streptococci, Streptococcus pneumoniae, penicillin-susceptible Staphylococcus aureus, Haemophilus aprophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Listeria monocytogenes. Oral phenoxymethylpenicillin in combination with streptomycin is effective in treating endocarditis due to viridans streptococci. Ampicillin is effective in endocarditis due to Haemophilus influenzae, H. parainfluenzae, H. paraphrophilus, Listeria monocytogenes and Escherichia coli. Oral amoxicillin with gentamicin has been used to treat enterococcal endocarditis. The penicillinase-resistant penicillins are effective in treating S. aureus endocarditis. Carbenicillin or ticarcillin in combination with tobramycin or gentamicin are used to treat endocarditis due to Serratia marcescens and Pseudomonas aeruginosa. The use of piperacillin in combination with tobramycin against P. aeruginosa endocarditis has been associated with failure and increased resistance. The cephalosporins have been used to treat endocarditis caused by susceptible organisms. There have been few data on the efficacy of the newer cephalosporins in treating endocarditis. They have been used to treat septicaemia due to susceptible organisms with good results.
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PMID:The use of beta-lactam antibiotics in the treatment of septicaemia and endocarditis. 644 9


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