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A Buu-Hoï

Publications and source records attributed to A Buu-Hoï.

17 recordsLinked to original sources
PubMed1997

Carbapenem resistance in a clinical isolate of Citrobacter freundii.

Carbapenem resistance was studied in two sets of Citrobacter freundii strains: (i) strain CFr950, resistant to imipenem (MIC, 16 microg/ml) and isolated in vivo during imipenem therapy, and strain CFr950-Rev, the spontaneous, imipenem-susceptible revertant of CFr950 selected in vitro, and (ii) strains CFr801 and CFr802, two imipenem-resistant mutants selected in vitro from the susceptible clinical isolate CFr800. In all strains, whether they were imipenem-susceptible or -resistant strains, production of the cephalosporinase was derepressed and their Km values for cephaloridine were in the range of 128 to 199 microM. No carbapenemase activity was detected in vitro. The role of cephalosporinase overproduction in the resistance was demonstrated after introduction of the ampD gene which decreased the level of production of cephalosporinase at least 250-fold and resulted in an 8- to 64-fold decrease in the MICs of the carbapenems. The role of reduced permeability in the resistance was suggested by the absence, in CFr950 and CFr802, of two outer membrane proteins (the 42- and 40-kDa putative porins whose levels were considerably decreased in CFr801) and the reappearance of the 42-kDa protein in imipenem-susceptible strain CFr950-Rev. This role was confirmed after introduction of the ompF gene of Escherichia coli into the CFr strains, which resulted in 8- to 16-fold decreases in the MICs of carbapenems for CFr802 and CFr950. We infer from these results that the association of reduced, porin-mediated permeability with high-level cephalosporinase production, observed previously in other gram-negative bacteria, may also confer carbapenem resistance on C. freundii.

Anti-Bacterial Agents↗
PubMed1990

High-level chromosomal gentamicin resistance in Streptococcus agalactiae (group B).

This is the first report of high-level gentamicin resistance in a group B streptococcus. Strain B128 of serotype II was isolated from an infected leg wound in 1987. B128 was resistant to high levels of gentamicin as well as of all other available aminoglycosides and was also resistant to tetracyclines. No bactericidal synergism was found between ampicillin or vancomycin and any of these aminoglycosides. Gentamicin, kanamycin, streptomycin, and tetracycline resistance determinants transferred by conjugation into a plasmid-free group B streptococcus recipient at a frequency of 10(-8) to 10(-9) transconjugants per donor cell. No transconjugants were detected when streptococci of groups A, C, and G, Streptococcus sanguis, or Enterococcus faecalis was used as a recipient. No plasmids were detected in B128 or in any of the four transconjugants tested. By DNA-DNA hybridization, homology was detected between gene aac6/aph2, of E. faecalis origin, and a 2.4-kilobase HindIII chromosomal fragment of B128; homology to the genes aph3 and aadE, of E. faecalis origin, was found with HindIII chromosomal fragments of the same size (3.0 kilobases). Strains like B128, which potentially can be responsible for severe neonatal infections, are of great clinical concern, since there are to date no antibiotic combinations exhibiting bactericidal synergism against them.

Blotting, Southern↗
PubMed1989

Genetic basis of antibiotic resistance in Aerococcus viridans.

Resistance to at least one of the following antibiotics was found in eight wild-type strains of Aerococcus viridans: erythromycin (six strains), tetracycline and minocycline (five strains), chloramphenicol (one strain), and high levels of streptomycin (one strain). None of the strains transferred any of their antibiotic resistance markers into streptococcal, enterococcal, or A. viridans recipients by conjugation. By DNA-DNA hybridization experiments, the ermB gene of transposon Tn917, of Enterococcus faecalis origin, was detected in five of the six strains resistant to erythromycin and was localized for one strain on the chromosome and for four strains on nonconjugative small (4.7- to 4.9-kilobase) plasmids. The tetM gene of the conjugative transposon Tn916, of E. faecalis origin, was localized on the chromosome of four of the five strains resistant to tetracycline and minocycline; in three of these strains a structure similar to that of Tn916 was found. Homology to the tetO gene of pUA466, of Campylobacter jejuni origin, was detected on the chromosome of the fifth strain. No sequence homology was detected in any strain with probes corresponding to the tetL gene of group B Streptococcus origin, to the ermA gene of the transposon Tn554 of Staphylococcus aureus origin, or to the cat genes of either pC194 or pC221 of S. aureus origin.

Anti-Bacterial Agents↗
PubMed1985

Vancomycin-resistant streptococci or Leuconostoc sp.

Two strains of gram-positive cocci highly resistant to vancomycin (MICs of 512 and 1,024 micrograms/ml) were isolated from blood cultures in two compromised patients. These organisms were identified as Leuconostoc spp. Leuconostoc spp. are gram-positive cocci found in vegetables and dairy products; they had not been isolated previously from clinical specimens. The susceptibility of eight Leuconostoc spp. strains, including the two clinical isolates, to 23 antimicrobial agents was determined.

Adult↗
PubMed1984

Bactericidal activity of five combinations of penicillin G with aminoglycosides against Streptococcus faecium.

Combinations of penicillin G and five aminoglycosides were tested against 7 strains of S. faecium. For all the strains that had a low-level of resistance to streptomycin, the combination of penicillin G with streptomycin was synergistic. Penicillin combined with either kanamycin or netilmicin was ineffective against all strains. The combination of penicillin and amikacin was synergistic against only one of the aminoglycoside-susceptible strains and ineffective against all the other strains. Penicillin G with gentamicin was the only combination synergistic against all strains. The clinical implications of these findings for the treatment of bacterial endocarditis caused by S. faecium are discussed.

Aminoglycosides↗
PubMed1984

Broad host range of streptococcal macrolide resistance plasmids.

Four macrolide-lincosamide-streptogramin B resistance plasmids transferred into 13 recipients belonging to Streptococcus, Staphylococcus, and Listeria genera. The plasmids were stably maintained in all new hosts except Streptococcus sanguis, Streptococcus pneumoniae, Staphylococcus aureus, and Listeria innocua and were identical to those found in the corresponding donor strains.

Anti-Bacterial Agents↗
PubMed1982

Antimicrobial susceptibility of Gemella haemolysans isolated from patients with subacute endocarditis.

Gemella haemolysans, a member of the family Streptococcacae, was isolated from patients with subacute endocarditis. The minimal inhibitory concentrations of 21 antimicrobial agents for five strains of the organism were determined. All strains were highly sensitive to penicillin G and ampicillin. Cefotaxime was the most active cephalosporin tested. All strains were sensitive to vancomycin, chloramphenicol and rifampin. Four strains were sensitive to tetracycline and erythromycin. All strains demonstrated a low level of resistance to aminoglycosides and were highly resistant to sulfonamides and trimethoprim. Killing curves and checker-board titration demonstrated synergism between penicillin G and streptomycin or gentamicin, and also between vancomycin and streptomycin or gentamicin. The results suggest that penicillin G combined with an aminoglycoside can be recommended for the treatment of subacute endocarditis caused by Gemella haemolysans.

Anti-Bacterial Agents↗
PubMed1982

High-level aminoglycoside resistance in group A, B, G, D (Streptococcus bovis), and viridans streptococci.

Of 20 clinical isolates of group A, B, G, D (Streptococcus bovis), and viridans streptococci, 5 transferred their antibiotic resistance markers into streptococcal recipients at a low frequency (10(-4) to 10(-8)) in the apparent absence of extrachromosomal elements. All strains carried genetic markers for high-level resistance to streptomycin, kanamycin, neomycin, lividomycin A, and ribostamycin, as well as resistance to macrolides and related drugs, tetracycline, and chloramphenicol.

Aminoglycosides↗
PubMed1982

[Antibiotic resistance genetic basis of human origin streptococci (author's transl)].

One hundred strains of group A, B, C, D (S faecalis, S. faecium, S. bovis) F, G, S. pneumoniae and viridans streptococci were studied. All these strains were clinical isolates from infective endocarditis and fron upper respiratory, skin, genital and urinary tract infections. These stains were resistant to one or several antibiotics : tetracycline, macrolide and related drugs, chloramphenicol, aminoglycosides (high-level resistance to streptomycin, kanamycin, gentamicin), and penicillin. Conjugative transfer of antibiotic resistance markers (except penicillin) into streptococcal recipients was obtained at a high frequency (10(-1) to 10(-4)) for 12 strains and at a low frequency (10(-5) to 10(-8)) for 29 strains. R plasmids carrying various groups of resistance markers were isolated with different molecular weights. Enzyme restriction analysis showed the existence of different molecular species of streptococcal plasmids. All attempts to detect extrachromosomal DNA in 17 wild-type strains and in the corresponding transconjugants were unsuccessful.

Anti-Bacterial Agents↗
PubMed1980

Conjugative transfer of multiple antibiotic resistance markers in Streptococcus pneumoniae.

Two antibiotic-resistant isolates of Streptococcus pneumoniae were investigated for conjugative transfer of their drug resistance markers into streptococcal (groups B and D) and pneumococcal (encapsulated and non-encapsulataed) recipients. Of these, 7 wild-type donor pneumococci transferred all their resistance markers (except Pc [penicillin], Su [sulfonamide], and Tp [trimethoprim]) into group D Streptococcus and non-encapsulated S. pneumoniae recipients at a low frequency (10(-5) to 10(-6)). The resistance markers transferred were Tc (tetracycline); Tc and Cm (chloramphenicol); Tc and MLS (macrolides, lincosamides, and streptogramin B); Tc, MLS, Km (kanamycin), and Cm. The transconjugants obtained retransferred their resistance markers into appropriate streptococcal or pneumococcal recipients or both. The resistance markers of streptococcal transconjugants could not be cured by chemical agents. All attempts to detect extra-chromosomal deoxyribonucleic acid from pneumococcal or streptococcal transconjugants were unsuccessful. The molecular weight of a streptococcal conjugative R plasmid (pIP501) was investigated after transfer into the non-encapsulated S. pneumoniae recipient and was found to be similar to that of the wild-type group B Streptococcus host (20 x 10(6)).

Acridine Orange↗