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PubMed1998

Antimicrobial susceptibility testing of a clinical isolate of vancomycin-dependent enterococcus using D-alanine-D-alanine as a growth supplement.

Bacteremia due to a vancomycin-dependent enterococcus (VDE) occurred during long-term vancomycin therapy in a renal transplant recipient with underlying pancreatitis and a vancomycin-resistant enterococcal (VRE) wound infection and bacteremia. The VDE was isolated from blood during vancomycin therapy and grew only in the presence of vancomycin and D-alanine-D-alanine (DADA), a substance required for cell-wall synthesis. Colonies beyond the periphery of growth of the VDE around a vancomycin disk contained vancomycin-independent revertant mutants after 48 hours of incubation. Pulsed-field gel electrophoresis of the VDE, revertant mutant, the initial blood culture isolate of VRE, and an autopsy isolate showed that the four strains were identical. Antimicrobial susceptibility testing was performed using standard macrobroth and microbroth dilution methods. DADA was used as a growth supplement for macrobroth dilution susceptibility testing of the VDE isolate. Minimum inhibitory concentrations (MICs) were similar for the VRE isolate and the VDE revertant, which were both resistant to ampicillin, high-level gentamicin, ciprofloxacin, imipenem, vancomycin, and daptomycin, and were susceptible to fusidic acid, high-level streptomycin, rifampin, and a quinupristin-dalfopristin combination. The MICs of teicoplanin were 2 microg/mL or less and 16 microg/mL for the clinical VRE isolate and the VDE revertant, respectively. The autopsy isolate was resistant to all antimicrobials tested and showed a fourfold increase in MICs for quinupristin-dalfopristin compared with that of the original blood isolate. The VDE was susceptible to all drugs tested except vancomycin.

Alanine↗
PubMed2002

Post-termination complex disassembly by ribosome recycling factor, a functional tRNA mimic.

Ribosome recycling factor (RRF) together with elongation factor G (EF-G) disassembles the post- termination ribosomal complex. Inhibitors of translocation, thiostrepton, viomycin and aminoglycosides, inhibited the release of tRNA and mRNA from the post-termination complex. In contrast, fusidic acid and a GTP analog that fix EF-G to the ribosome, allowing one round of tRNA translocation, inhibited mRNA but not tRNA release from the complex. The release of tRNA is a prerequisite for mRNA release but partially takes place with EF-G alone. The data are consistent with the notion that RRF binds to the A-site and is translocated to the P-site, releasing deacylated tRNA from the P- and E-sites. The final step, the release of mRNA, is accompanied by the release of RRF and EF-G from the ribosome. With the model post-termination complex, 70S ribosomes were released from the post-termination complex by the RRF reaction and were then dissociated into subunits by IF3.

Escherichia coli↗
PubMed1984

The treatment of endocarditis by vancomycin.

The narrow spectrum of vancomycin includes the common causal bacteria of endocarditis. This agent has been used since the 1960s for therapy and prophylaxis of infections when first-line drugs are inappropriate because of antibiotic resistance or drug allergy. Some personal experiences of vancomycin usage and a literature survey are presented in this paper which is based on the subdivision of endocarditis into medical, surgical (early--less than 60 days after operation--or late), and addict-related. The commonest bacterial causes of medical or late surgical infections are streptococci, and of the early surgical and addict-related infections are staphylococci. Vancomycin is bactericidal for Gram-positive cocci, except enterococci, but for optimal action it is arguable that combinations with gentamicin, fusidic acid, rifampicin or erythromycin should be used for staphylococcal endocarditis. The attainment of bactericidal blood levels may still be accompanied by failure of monotherapy and the need for early surgery is stressed. The prophylaxis of endocarditis is primarily required for tooth extraction and for cardiac surgery. The streptococci and staphylococci involved are normally vancomycin-susceptible, and the rabbit model shows that it is a suitable alternative to a beta-lactam and aminoglycoside combination. The combination is therefore suitable for patients already in hospital, especially those with prosthetic valves or undergoing cardiac surgery.

Adult↗
PubMed1985

Laboratory studies on coagulase-negative staphylococci from CAPD-associated peritonitis.

This study compared the static and kinetic activities, in both broth and used-dialysate, of selected antibiotics against 23 strains of coagulase-negative staphylococci causing peritonitis in patients on continuous ambulatory peritoneal dialysis (CAPD). Vancomycin was shown to be effective against all isolates with similar rates of kill to flucloxacillin and cefuroxime, although a few strains were found to be resistant to cefuroxime. Gentamicin was rapidly bactericidal for sensitive strains which accounted for 60% of the strains tested. Fusidic acid was associated with significant resistance and lack of bactericidal activity in the kinetic studies. Emergence of resistance occurred with rifampicin. The combinations clavulanic acid/amoxycillin and sulbactam/ampicillin generally showed good static activity. In addition a broad range of biotypes and phage types were demonstrated among these organisms with biotype SII (Staphylococcus epidermidis) predominating. There was no correlation between biotype and antibiogram.

Anti-Bacterial Agents↗
PubMed1985

Comparative in-vitro activity of Sch 34343 and other antimicrobial agents against anaerobic bacteria.

The activity of Sch 34343 was determined against 575 strains of anaerobic bacteria by an agar-dilution method. Its activity was compared with that of benzylpenicillin, piperacillin, cefoxitin, imipenem, clindamycin, metronidazole, chloramphenicol, vancomycin, fusidic acid and bacitracin. Sch 34343 and imipenem were the most active agents tested. Based on these results, Sch 34343 appears to be a promising antimicrobial agent for anaerobic infections and warrants further clinical investigations.

Anti-Bacterial Agents↗
PubMed1985

Efficacy of topical mupirocin against an experimental Staphylococcus aureus surgical wound infection.

The efficacy of topically-applied mupirocin was evaluated against an experimental surgical staphylococcal wound infection in the guinea-pig. A suture impregnated with Staphylococcus aureus was inserted into a superficial wound, and topical therapy with mupirocin ointment was started 24 h after infection. In non-treated wounds, the bacterial counts increased to greater than 10(6) organisms/wound in the majority of animals at 24 h, remaining at this level for up to seven days. Therapy with placebo ointment (polyethylene glycol base) was ineffective, whereas twice daily application of mupirocin ointment resulted in elimination of the staphylococci. Mupirocin was as effective as topically-applied fusidic acid cream in reducing the bacterial counts of infected wounds.

Administration, Topical↗
PubMed1986

In-vitro activity of coumermycin against methicillin-resistant staphylococci: a comparison with six other agents.

The in-vitro activity of coumermycin was compared with that of vancomycin, rifampicin, fusidic acid, trimethoprim-sulphamethoxazole, norfloxacin and cefamandole against seven isolates of methicillin-resistant Staphylococcus aureus and 97 isolates of methicillin-resistant coagulase negative staphylococci. Apart from one strain of methicillin-resistant S. aureus all isolates were inhibited by less than or equal to 0.06 mg/l of coumermycin. Cefamandole was more active against strains of S. epidermidis than against other coagulase negative staphylococci.

Aminocoumarins↗
PubMed1988

Susceptibility of Hong Kong isolates of methicillin-resistant Staphylococcus aureus to antimicrobial agents.

Two hundred and sixty-six non-replicate Hong Kong isolates of methicillin-resistant Staphylococcus aureus were tested for their susceptibility to various anti-staphylococcal agents. Multiple resistance was common. More than 95% of patient isolates were resistant to both gentamicin and tetracycline, 68% to erythromycin, 37% to chloramphenicol, 10% to trimethoprim, 5% to rifampicin and 2% to fusidic acid. No isolate was resistant to all these agents, but nineteen different patterns of resistance were identified. Selected gentamicin-resistant isolates were tested against other aminoglycosides, and were sensitive to amikacin and netilmicin. The pattern of aminoglycoside resistance indicated that all isolates produced the aminoglycoside-modifying enzymes APH-(2") and AAC-(6')-I. All isolates were sensitive to vancomycin and teicoplanin. A single strain was resistant to three of the five quinolones tested, but resistance to all the quinolones could be induced easily in vitro by exposure to increasing subinhibitory concentrations of norfloxacin in broth.

Anti-Bacterial Agents↗
PubMed1988

Multiresistant Staphylococcus aureus: genetics and evolution of epidemic Australian strains.

Molecular and genetic analysis of multiresistant isolates of Staphylococcus aureus from widely separated hospitals in Australia has demonstrated that these are clearly related, and that the predominant strains possess up to three different plasmids, which fall into the following classes: (i) small 1.6 kb plasmids, such as pSK3, which are phenotypically cryptic, (ii) 4.5 kb chloramphenicol resistance plasmids, such as pSK2, and (iii) the pSK1 family of multiresistance plasmids, which range in size from 20 to 42 kb and variously encode resistance to antiseptics and disinfectants, trimethoprim (Tpr), penicillin (Pcr) and the aminoglycosides gentamicin, tobramycin and kanamycin (Gmr Tmr Kmr). Gmr Tmr Kmr is encoded on the pSK1 family plasmids by transposon Tn4001, which was also detected on the chromosomes of some clinical isolates. Tn4001 is composed of inverted repeats of the insertion sequence IS256; these repeats flank a Gmr Tmr Kmr sequence encoding for a 57,000 dalton bifunctional protein with aminoglycoside acetyltransferase [AAC(6')] and phosphotransferase [APH(2")] activities. A Tn4001-like structure, which is defective in transposition but encodes for a Gmr Tmr Kmr determinant homologous with that on Tn4001, occurs on conjugative plasmids from strains isolated in North America. Physical studies indicate that Pcr, via a beta-lactamase, and Tpr, via a trimethoprim-insensitive dihydrofolate reductase (DHFR), are also encoded on the pSK1 family by transposons; these transposons have been designated Tn4002 and Tn4003, respectively. Tn4003 is flanked by direct repeats of the insertion sequence IS257. The evolution of the pSK1 family of multiresistance plasmids is traced through the transposition and genetic rearrangement of resistance determinants. Transposition and genetic rearrangement have also contributed to the evolution of a multiresistant chromosome in Staph. aureus. In the majority of contemporary multiply resistant Staph. aureus strains the determinants for resistance to erythromycin (Emr), fusidic acid, methicillin (Mcr), minocycline, rifampicin, spectinomycin, streptomycin, sulphonamides, tetracycline (Tcr), cadmium (Cdr), and mercury (Hgr) are chromosomally encoded; these strains also possess chromosomally encoded Pcr, via a beta-lactamase. Evidence indicates that some of these determinants, Pcr, Cdr, Hgr, and Tcr, were plasmid encoded in isolates collected from Australian hospitals prior to 1970. Through transposition and site-specific integration, they have since been acquired by the chromosome in more recent Staph. aureus strains.(ABSTRACT TRUNCATED AT 400 WORDS)

Australia↗
PubMed1990

Skin carriage of antibiotic-resistant coagulase-negative staphylococci in untreated subjects.

A detailed microbiological analysis was made of the antibiotic resistant coagulase-negative staphylococcal flora of facial skin of 64 untreated individuals. The flora was quantified at primary isolation using both non-selective and selective media (each containing one of seven different antibiotics). The isolates obtained were tested against 18 antibiotics for multiple resistance and biotyped to species level. The incidence of the seven primary antibiotic resistance markers among the staphylococcal flora of 64 untreated subjects was: tetracycline 87.5%, erythromycin 68.8%, fusidic acid 56.3%, trimethoprim 42.4%, chloramphenicol 25%, clindamycin 9.4% and gentamicin 4.7%. In addition, penicillin resistant staphylococci were isolated from 98% of subjects. Multiply resistant strains were carried by 62.5% of individuals, with 27.9% carrying more than 100 multiply resistant staphylococci/cm2 skin. Analysis of the frequency distributions of the size of resistant staphylococcal populations revealed considerable individual variation, with many individuals carrying greater than 10(3) resistant staphylococci/cm2 skin. Multiply resistant staphylococci usually comprised less than 10% of the total staphylococcal flora, although this often represented a large number of multiply resistant organisms. Three people carried greater than 10(4) multiply resistant staphylococci/cm2 skin. Most of the singly and multiply resistant isolates were identified as strains of Staphylococcus epidermidis, which was found to carry up to eight resistances per isolate. In contrast, S. capitis, a common resident of human facial skin, was never found to carry more than two resistances per isolate. S. aureus was rarely detected on intact facial skin and the strains were not multiply resistant. Resistance to the major antistaphylococcal antibiotics was infrequent (gentamicin, methicillin) or absent (rifampicin, vancomycin, cephalothin). It was concluded that untreated individuals carry a significant pool of singly and multiply resistant staphylococci of sufficient size to be readily disseminated by direct contact and desquamation.

Adolescent↗
PubMed1996

In-vitro susceptibility of isolates of methicillin-resistant Staphylococcus aureus 1988-1993.

MICs for 423 strains of methicillin-resistant Staphylococcus aureus (MRSA) isolated in Hong Kong during 1988-1993 were performed for 15 antimicrobial agents: erythromycin, chloramphenicol, tetracycline, minocycline, gentamicin, netilmicin, trimethoprim, rifampicin, fusidic acid, ciprofloxacin, vancomycin, teicoplanin, sparfloxacin, clinafloxacin and RP 59500 (quinupristin/dalfopristin). Susceptibility to antibiotics generally remained stable throughout the study period, with the exception of the quinolones. Resistance to ciprofloxacin (breakpoint 4 mg/L) increased from a low of 9% in 1988 to a high of 82% in 1993. For sparfloxacin the corresponding figures were 9% and 78%, respectively. Six (1%) clinafloxacin-resistant strains were found. MIC50s and MIC90s of clinafloxacin increased from < or = 0.06 mg/L and 0.25 mg/L in 1988 to 1.0 mg/L and 2.0 mg/L, respectively, in 1993. All 423 strains were phage typed (typability 70%) and a diversity of phage types which changed during the observation period, with 13 dominating types, was observed. Ciprofloxacin resistance occurred in 12 of the dominating types, in 46 non-typable strains, and also in 23 strains of different, sporadically occurring types, indicating that the emergence of quinolone resistance was not due to dissemination of a single or few MRSA clones. The usefulness of quinolones in the treatment of MRSA infections is likely to be seriously constrained by the emergence of resistance. MICs for RP-59500 were < or = 2 mg/L for all isolates, suggesting that this agent merits further evaluation as an anti-MRSA agent. All MRSA remained susceptible to vancomycin and teicoplanin throughout the study period.

Anti-Infective Agents↗
PubMed1998

Resistance of staphylococci in The Netherlands: surveillance by an electronic network during 1989-1995.

An electronic surveillance network for monitoring antibiotic resistance in The Netherlands has been in operation since 1989. Seven public health laboratories participate and the system covers about 25% of all bacteriological determinations in The Netherlands. This paper reports the results of staphylococci isolated in the period 1989-1995. About 0.3% of the Staphylococcus aureus isolates in the study period were resistant to methicillin. This low percentage may be due to the restrictive use of antibiotics and to strict isolation measures aimed at eradicating methicillin-resistant S. aureus. Low frequencies of resistance among methicillin-resistant S. aureus were found for vancomycin (0%), chloramphenicol (11%), cotrimoxazole (11%), mupirocin (3% low-level resistance) and fusidic acid (7%). Twenty-one percent of the coagulase-negative staphylococci were resistant to methicillin. Low frequencies of resistance among these methicillin-resistant coagulase-negative staphylococci were those to vancomycin (0.4%), nitrofurantoin (2%), doxycycline (20%) and amikacin (20%). Coagulase-negative staphylococci from cerebrospinal fluid, blood and skin were less often resistant to quinolones than isolates from respiratory tract, faeces and urine. A significant increase in resistance of coagulase-negative staphylococci to methicillin, erythromycin, gentamicin and ciprofloxacin was observed in the investigated period but the resistance to doxycycline and co-trimoxazole decreased in the last few years. To confirm the determination of methicillin resistance and coagulase production, a PCR method was developed which detects both the mecA and the coagulase gene. The results of the PCR method correlated well with the methicillin MIC as determined by an agar-dilution method.

Anti-Bacterial Agents↗
PubMed2001

Natural antimicrobial susceptibilities of Plesiomonas shigelloides strains.

The natural susceptibility of 74 Plesiomonas shigelloides strains isolated from humans (n = 50), water (n = 22) and animals (n = 2) to 71 antibiotics was examined. MICs were performed using a microdilution procedure with Mueller-Hinton broth and an inoculum of 1 x 10(6) cfu/mL. Plesiomonas strains were naturally susceptible or naturally susceptible and intermediate to tetracyclines, several aminoglycosides, aminopenicillins in combination with beta-lactamase inhibitors, all cephalosporins except cefoperazone, ceftazidime and cefepime, carbapenems, aztreonam, quinolones, trimethoprim, sulfamethoxazole, azithromycin, chloramphenicol, nitrofurantoin and fosfomycin. Uniform natural resistance was found to all penicillins tested, roxithromycin, clarithromycin, lincosamides, streptogramins, glycopeptides and fusidic acid. Plesiomonas strains were naturally resistant and intermediate to streptomycin, erythromycin and rifampicin. There were two susceptibility patterns to piperacillin/tazobactam, several cephalosporins and aztreonam. In contrast to a previous study with beta-lactam antibiotics, susceptibility testing of non-beta-lactams revealed no alterations of the MICs of most antibiotics, using different inocula and media. A database is described of the natural susceptibility of P. shigelloides strains to a wide range of antibiotics. It can be used for the validation of susceptibility test results of these bacteria.

Animals↗
PubMed2003

Natural antimicrobial susceptibilities of strains of 'unusual' Serratia species: S. ficaria, S. fonticola, S. odorifera, S. plymuthica and S. rubidaea.

The natural susceptibility to 71 antibiotics of 104 Serratia strains of Serratia ficaria (n = 15), Serratia fonticola (n = 18), Serratia odorifera (n = 16), Serratia plymuthica (n = 32) and Serratia rubidaea (n = 23) was examined. MICs were determined using a microdilution procedure in IsoSensitest broth for all the strains and in cation-adjusted Mueller-Hinton broth for some strains. With few exceptions, all species tested were uniformly naturally resistant to penicillin G, oxacillin, cefazolin, cefuroxime, all tested macrolides, lincosamides, streptogramins, glycopeptides, fusidic acid and rifampicin, and naturally sensitive to several aminoglycosides, piperacillin, piperacillin/tazobactam, carbapenems, some cephalosporins, fluoroquinolones and folate-pathway inhibitors. Major species-related differences in natural susceptibility affecting clinical assessment criteria were seen with tetracyclines, some aminoglycosides, aminopenicillins, ticarcillin, cefaclor, loracarbef, cefoxitin, pipemidic acid, chloramphenicol, nitrofurantoin and fosfomycin. Differences in susceptibility dependent on the medium were seen with macrolides, tetracycline, fosfomycin and some beta-lactams. The natural antibiotic susceptibility patterns suggest novel species-specific mechanisms of antibiotic resistance. Uncharacterized species-specific aminoglycoside-modifying enzymes and multidrug efflux systems affecting tetracyclines, quinolones and chloramphenicol are probably responsible for some of the phenotypes observed. The natural amoxicillin sensitivity of several strains of some species combined with natural resistance to some narrow-spectrum cephalosporins indicate the expression of naturally occurring beta-lactamases with unique substrate profiles. beta-Lactamases of representative strains of each species were characterized phenotypically and genotypically. It was shown that all species expressed naturally occurring AmpC beta-lactamases and, with respect to S. fonticola, also a species-specific class A beta-lactamase. Inducibility of these enzymes was shown in all species with the exception of S. rubidaea and four of five strains of S. plymuthica.

Anti-Infective Agents↗
PubMed2003

Intra-hospital dissemination of quinupristin/dalfopristin- and vancomycin-resistant Enterococcus faecium in a paediatric ward of a German hospital.

OBJECTIVES: To demonstrate nosocomial transmission of Enterococcus faecium resistant to quinupristin/dalfopristin and vancomycin/teicoplanin among paediatric patients in a German hospital ward. MATERIALS AND METHODS: Multiply-resistant E. faecium were isolated from three female patients aged 9 months, 2 and 15 years during a 10 day time span. Antibiotic susceptibilities were determined by microbroth dilution. Clonal relatedness among the isolates was investigated via SmaI-macrorestriction analysis by PFGE, multilocus sequence typing (MLST), and plasmid profiling. Presence of virulence and resistance determinants was tested by polymerase chain reaction (PCR). Selected resistance genes were localized by Southern hybridizations. RESULTS: A single E. faecium isolate per patient was investigated. All exhibited resistances to quinupristin/dalfopristin, vancomycin/teicoplanin, streptomycin (high-level), penicillin/ampicillin, erythromycin, oxytetracycline, chloramphenicol, rifampicin and fusidic acid. The isolates were susceptible to linezolid only and intermediately resistant to fluoroquinolones including moxifloxacin. PFGE revealed identical patterns for all three isolates. PCRs for virulence determinants hyaluronidase and enterococcal surface protein, esp, were negative, whereas PCR for the enterocin A gene was positive. MLST identified clonal type [8-5-1-1-1-1-1] belonging to a clonal subgroup C1 of hospital- and outbreak-related E. faecium. Southern hybridizations located several resistance genes (erm(B), vat(D), vanA) on a large plasmid, which was transferable in mating experiments with an E. faecium recipient. CONCLUSIONS: These data show routes of dissemination of resistance to multiple antibiotics including streptogramins and glycopeptides in E. faecium via vertical and/or horizontal gene transfer. The isolates spread in the absence of a direct selective pressure, as none of the patients had received earlier streptogramin or glycopeptide therapy.

Anti-Bacterial Agents↗
PubMed2003

Antibacterial susceptibility of a vancomycin-resistant Staphylococcus aureus strain isolated at the Hershey Medical Center.

Staphylococcus aureus strain HMC3 isolated at the Hershey Medical Center, was resistant to vancomycin (VRSA) through the presence of the vanA resistance gene; it also contained mecA, erm(A), erm(B), tet(K) and aac(6')-aph(2"), conferring resistance to licensed beta-lactams, macrolides, tetracycline and aminoglycosides. HMC3 also had alterations in GyrA and GrlB and was resistant to available quinolones. Experimental drugs with low MICs (<2 mg/L) for VRSA HMC3 included cephalosporins BAL9141 and RWJ-54428; glycopeptides oritavancin and dalbavancin; the lipopeptide daptomycin; the glycolipodepsipeptide ramoplanin; new fluoroquinolones WCK 771 A, WCK 1153, DK-507k and sitafloxacin; and the DNA nanobinder GS02-02. These agents were all bactericidal as were trimethoprim/sulfamethoxazole and teicoplanin (MIC 4 mg/L). Oxazolidinones linezolid and ranbezolid; the injectable streptogramin quinupristin/dalfopristin; DNA nanobinders GS2-10547 and GS02-104; peptide deformylase inhibitors NVP-PDF713 and GS02-12; tetracycline derivative tigecycline; the antifolate iclaprim; mupirocin and fusidic acid were all active in vitro but bacteriostatic.

Aged↗
PubMed2004

Antibiotic treatment of gram-positive bone and joint infections.

Gram-positive organisms, particularly staphylococci and streptococci, are responsible for the majority of bone and joint infections. Treatment of these infections can be difficult, usually involving a prolonged course of antibiotics, often with surgical intervention. The selection of antibiotics depends on sensitivity profile, patient tolerance and long-term goals, e.g. cure or suppression, but there are few randomized controlled trials in patients comparing efficacy of different antibiotics. Different degrees of bone penetration and clinical outcome for specific antibiotics, e.g. the beta-lactams, clindamycin and quinolones, have been described, although the methodology in these studies is not standardized and findings cannot always be applied directly to patients. The effect of attaining minimum serum bactericidal concentrations in patients has also been studied but this is no longer routinely recommended in clinical practice. Comparative clinical trials are few but have demonstrated efficacy of oral fluoroquinolones in combination with either rifampicin or fusidic acid for selected Gram-positive infections. In the past decade, increasingly resistant organisms, e.g. methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci have been recognized as causes of orthopaedic infection. Individual case reports describe successful treatment using the newer antibiotics, e.g. linezolid and quinupristin/dalfopristin, but results of clinical trials are awaited.

Animals↗
PubMed2004

Antimicrobial susceptibility of bifidobacteria.

OBJECTIVES: The aim of our study was to analyse the antibiotic susceptibility of various strains of Bifidobacterium spp. to a wide range of antimicrobial agents. METHODS: Fifty strains belonging to eight species of bifidobacteria, isolated from humans, animals or probiotic products, were tested for susceptibility to 30 antibiotics by disc diffusion on Brucella agar supplemented with 5% laked sheep blood and vitamin K1 (1 mg/L). MICs of nine anti-anaerobe agents, including three new molecules (telithromycin, linezolid and gatifloxacin), were determined using the reference agar-dilution method. RESULTS: All strains of bifidobacteria, whatever the species, were sensitive to penicillins: penicillin G, amoxicillin (MIC(50) 0.06 mg/L), piperacillin, ticarcillin, imipenem and usually anti-Gram-positive antibiotics (macrolides, clindamycin, pristinamycin, vancomycin and teicoplanin). Susceptibility to cefalothin and cefotetan was variable. Most isolates (70%) were resistant to fusidic acid. As expected, high resistance rates were observed for aminoglycosides. Metronidazole, an agent known for its anti-anaerobe activity, was ineffective against 38% of the strains. The newly commercialized molecules, telithromycin, linezolid and gatifloxacin, were active with MIC(50)S of 1 mg/L. The only variation in susceptibility observed among the different species concerned Bifidobacterium breve, which appeared to be generally more resistant. Potentially acquired resistance was only observed against tetracycline and minocycline, in 14% of the strains. CONCLUSIONS: With regard to a general concern about the safety of probiotics, such as potential transferability of resistance determinants, bifidobacteria, with their low natural and acquired resistance to 30 antibiotics, appear risk-free.

Animals↗