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PubMed1995

Detection of gyrA and gyrB mutations in quinolone-resistant clinical isolates of Escherichia coli by single-strand conformational polymorphism analysis and determination of levels of resistance conferred by two different single gyrA mutations.

Twelve quinolone-resistant clinical isolates of Escherichia coli (nalidixic acid MICs, 64 to 512 micrograms/ml; norfloxacin MICs, 0.25 to 8 micrograms/ml) were transformed with plasmid pJSW101 carrying the gyrA+ gene and with plasmid pJB11 carrying the gyrB+ gene to examine the proportion of gyrA and gyrB mutations. Transformation with pJSW101 resulted in complementation (nalidixic acid MICs, 4 to 32 micrograms/ml; norfloxacin MICs, 0.06 to 0.25 micrograms/ml). In contrast, no change in MICs were observed after transformation with pJB11. A 418-bp fragment of gyrA from the 12 strains was amplified by PCR. Direct DNA sequencing of that fragment identified the causes of quinolone resistance in eight strains as a single point mutation leading to a substitution of the serine at position 83 (Ser-83) to Leu and in four strains as a single point mutation leading to a substitution of Asp-87 to Gly. Exchange of the fragment from one of these strains with that of gyrA+ and transformation of resistance with the hybrid gyrA plasmid indicated the contribution of Gly-87 to resistance and the stabilities of mutants containing GyrA (Gly-87). Thus, gyrA gene mutations are probably encountered more often than gyrB gene mutations in clinical isolates of E. coli. In addition, the substitution of Asp-87 to Gly can be encountered in such strains. On the basis of the level of resistance found in the fragment exchange experiment, the quinolone resistance attributable to Gly-87 appears to be comparable to that attributable to Leu-83. The levels of resistance found in the clinical isolates shown to have a Gly-87 mutation (nalidixic acid MICs, 64 to 512 micrograms/ml; norfloxacin MICs, 0.5 to 4 micrograms/ml) suggest that the Gly-87 mutation causes resistance at the level of the nalidixic acid MIC (64 micrograms/ml) or the norfloxacin MIC (0.5 micrograms/ml or less) and that the additional increments in resistance seen in the other strains with higher levels of resistance may be attributable to additional mutations. The single-strand conformational polymorphism analysis with PCR products readily detected te Leu-83 and Gly-87 mutations.

Amino Acid Sequence↗

PubMed1980

Isopentenyladenine as a mediator of mevalonate-regulated DNA replication.

The mechanism by which the cholesterol precursor, mevalonate, regulates S-phase DNA replication was examined in synchronized BHK cells. As previously demonstrated by this laboratory, blocking 3-hydroxy-3-methylglutaryl-CoA reductase [mevalonate:NADP+ oxidoreductase (CoA-acylating), EC 1.1.1.34] with the competitive inhibitor compactin suppresses DNA synthesis specifically during the S phase of the cell cycle. In the present study, known mevalonate derivatives were examined as possible mediators by which mevalonate controls DNA replication. Of the compounds studied, only isopentenyladenine and its 4'-hydroxylated analogue, zeatin, could substitute for mevalonate in restoring DNA replication in compactin-blocked cells. Moreover, these two derivatives proved to be at least 100 times more active than mevalonate, and both restored DNA relication to normal within 15 min of their being added to the medium. In addition, isopentenyladenine, like mevalonate, stimulated DNA synthesis specifically during the S phase of the cell cycle. Isopentenyladenine also reversed the inhibition of DNA synthesis caused by nalidixic acid, an antibiotic that does not inhibit cholesterol synthesis. These findings indicate that isopentenyladenine or a closely related derivative may mediate the regulatory role of mevalonate in DNA replication and suggest that such isoprenes may act upon DNA replication at a site common to that inhibited by nalidixic acid.

Adenine↗

PubMed1984

A synthetic based medium for the isolation of Listeria monocytogenes.

We have compared two media (Tryptone Soya Nalidixic Acid Agar and Tryptone Soya Gum Base Nalidixic Acid Medium) for the isolation of L. monocytogenes from pathological and environmental specimens. These media were used in conjunction with Henry's Oblique Light System. We found that the gum based medium gave the better results. The medium is uniformly transparent, partially suppressive to unwanted organisms and allows colonies of Listeria to be readily identified.

Culture Media↗

PubMed1985

[Effect ofloxacin on Haemophilus influenza, Streptococcus pneumoniae and Neisseria meningitidis. Comparison with similar molecules].

The in vitro activities of the new quinolone derivatives ofloxacin, ciprofloxacin, norfloxacin, and pefloxacin against strains of Haemophilus influenzae, Streptococcus pneumoniae and Neisseria meningitidis were compared to that of nalidixic acid. Determination of minimal inhibitory concentrations (MICs) was done by agar dilution tests. The new drugs were more active than nalidixic acid. N. meningitidis and H. influenzae (regardless of beta-lactamase production) were highly susceptible. All H. influenzae strains were inhibited by less than or equal to 0.12 mg/l; mode MICs were 0.03 mg/l for norfloxacin and pefloxacin, and 0.50 mg/l for nalidixic acid. All N. meningitidis strains were inhibited by 0.06 mg/l and mode MICs of the new drugs were less than or equal to 0.03 mg/l. Mode MICs for S. pneumoniae were 4 mg/l for norfloxacin and pefloxacin (range 1-16 and 2-8 mg/l respectively) and 1 mg/l for ofloxacin (range 1-4 mg/l). Ofloxacin exhibited a bactericidal activity on H. influenzae (range MBC 0.06-0.50 mg/l; mode MBC: 0.06 mg/l).

Ciprofloxacin↗

PubMed1983

In vitro susceptibilities of canine urinary bacteria to selected antimicrobial agents.

Antimicrobial susceptibility tests were conducted on bacteria that were isolated from urine specimens collected by antepubic cystocentesis from dogs with urinary tract infections. Antimicrobics to which greater than or equal to 90% of these urinary bacteria were susceptible in vitro included trimethoprim-sulfamethoxazole (TMP-SMZ), nitrofurantoin, cephalexin, nalidixic acid, and gentamicin for isolates of Escherichia coli; ampicillin, TMP-SMZ, cephalexin, nalidixic acid, and gentamicin for isolates of Proteus mirabilis; ampicillin chloramphenicol, TMP-SMZ, nitrofurantoin, cephalexin, kanamycin, and gentamicin for isolates of coagulase-positive staphylococci; cephalexin, nalidixic acid, and gentamicin for isolates of Klebsiella pneumoniae; ampicillin, TMP-SMZ, and gentamicin for isolates of Streptococcus faecalis, Str faecium, and Str zymogenes; ampicillin, chloramphenicol, TMP-SMZ, and gentamicin for isolates of Str viridans; and ampicillin, chloramphenicol, TMP-SMZ, nitrofurantoin, cephalexin, kanamycin, and gentamicin for isolates of Str canis. No antimicrobial agent tested was effective in vitro at the 90% level for isolates of Pseudomonas aeruginosa, but gentamicin was closest, at 89%.

Animals↗

PubMed1991

Influence of growth media on Escherichia coli cell composition and ceftazidime susceptibility.

Cell composition and surface properties of Escherichia coli were modified by using various growth media to investigate the role of yet uncharacterized components in ceftazidime susceptibility. An eightfold dilution of Luria broth was used as the basic growth medium and was supplemented with up to 4% phosphate, 5% glucose, or 12% L-glutamate. Decreases in cephaloridine and ceftazidime susceptibility, of two- and eightfold, respectively, were observed only in the glucose-enriched medium. The outer membrane permeability to ceftazidime and cephaloridine was evaluated by crypticity indices. Indices were unchanged under all growth conditions. Fluorometry of whole cells with 1-N-phenylnaphthylamine showed that glucose does not affect the interaction of this hydrophobic probe with the membranes but showed that elevated concentrations of phosphate or glutamate cause a marked increase in cell hydrophobicity, which, in turn, correlates with an increase in the susceptibility of E. coli to nalidixic acid. Growth in phosphate- or glutamate-enriched media caused an augmentation in major phospholipid species and may explain the increased hydrophobicity and susceptibility of E. coli to nalidixic acid. These data showed that E. coli susceptibility to ceftazidime is not influenced by cell surface hydrophobicity and suggested that the contribution of a nonspecific lipophilic diffusion route for entry of ceftazidime into cells is not likely to occur or is distinct from that of more hydrophobic molecules such as nalidixic acid. Finally, the penicillin-binding proteins of the E. coli cells were also investigated. Penicillin-binding protein 8 was only markedly labeled with 125I-penicillin V in inner membranes extracted from cells grown with glucose. Results of this study suggest that the unexpected change in penicillin-binding protein 8 observed in the presence of glucose may be responsible for the increase in MICs of cephaloridine and ceftazidime.

Autoradiography↗

PubMed1989

Structure-epileptogenicity relationship of quinolones with special reference to their interaction with gamma-aminobutyric acid receptor sites.

The relationship between the chemical structure and epileptogenic activity of quinolones was investigated. When the quinolones were administered intravenously to mice concomitantly with oral biphenylacetic acid, a major metabolite of the nonsteroidal antiinflammatory drug fenbufen, enoxacin, norfloxacin, ciprofloxacin, and pipemidic acid, which have an unsubstituted piperazine moiety at the 7 position of their parent nuclei, provoked clonic convulsions and subsequent death at doses of 6.25 mg/kg or more in a dose-dependent manner. AM-1091 and T-3262, which have an unsubstituted aminopyrrolidine moiety at their 7 positions, were less epileptogenic than the compounds listed above were. In contrast, ofloxacin, AT-4140, and nalidixic acid, which have piperazine substituted with methyl group(s) or no piperazine moiety at their 7 positions, never induced convulsions, even at doses of 100 mg/kg. Lomefloxacin, which has a 3-methyl piperazine, however, provoked convulsions at doses of 6.25 mg/kg or more. In the presence of biphenylacetic acid, all the test quinolones except nalidixic acid competitively inhibited [3H]muscimol binding to receptor sites for gamma-aminobutyric acid (GABA) in vitro. Nalidixic acid did not inhibit the binding at all, even at the highest concentration tested, i.e., 10(-4) M. The 50% inhibition doses for [3H]muscimol binding varied within 4 orders of magnitude or more, between 10(-8) to more than 10(-4) M for various compounds, and there was a close correlation between the epileptogenic activities of quinolones and their inhibitory potencies for [3H]muscimol binding to GABA receptor sites. These results indicate that the epileptogenic activity of quinolones possibly relates to the GABA-like structures of substituents at their 7 positions, which act as antagonists of GABA receptors.

4-Quinolones↗

PubMed1981

Repair and plasmid R46 mediated mutation requires inducible functions in Proteus mirabilis.

In Proteus mirabilis nalidixic acid or a predose of UV induce Rec protein formation, a portion of post-UV replication repair and "post-UV replication enhancement." These inducible functions are not significantly affected by the plasmid R46, which renders P. mirabilis efficiently UV-mutable. The R46-mediated UV induction of rif mutations requires additional inducible functions, as existing after nalidixic acid treatment in rec+ strains. After a nalidixic acid pretreatment UV efficient induction of rif mutations occurs without an otherwise obligatory period of post-UV incubation prior to plating on rifampicin agar. THe inducible character of this "qualification" of plasmid R46-mediated UV mutagenesis in P. mirabilis is evident from the inhibitory effects of chloramphenicol and starvation. Constitutive high-level synthesis of Rec protein in cells harboring the recombinant (multi-copy) rec+ plasmid pPM1 reduced plasmid R46-mediated UV mutagenesis, probably by preventing (inducible?) functions required by the plasmid R46 repair-mutator.

DNA Repair↗

PubMed1977

Induction of protein X in Escherichia coli.

Certain treatments that damage DNA and/or inhibit replication in E. coli have been reported to induce synthesis of a new protein, termed protein X, in recA+ lexA+ strains. We have examined some of the treatments that might induce protein X and we have, in particular, tested the hypothesis of Gudas and Pardee (1975) that DNA degradation products play an essential role in the induction process. We confirmed that UV irradiation, nalidixic acid treatment, or thymine starvation result in protein X synthesis in wild type strains. However, we found that UV irradiation, unlike nalidixic acid, also induced protein X in recB strains, in which little DNA degradation occurs. Furthermore, we found that the presence of DNA fragments resulting from host-controlled restriction of phage lambda DNA did not affect protein X synthesis. We conclude that no causal relationship exists between the production of DNA fragments and induction of protein X. The presence of the plasmid R46, which confers enhanced mutagenesis and UV resistance on its host, did not affect protein X synthesis. Growth in the presence of 5-bromouracil, which does not result in production of degradation fragments, resulted eventually in a low rate of protein X synthesis. In dnaA mutants, deficient in the initiation of new rounds of replication, UV irradiation induced protein X, again unlike nalidixic acid. Thus, the inhibition of active replication forks is not an essential requirement for protein X induction.

Bacterial Proteins↗

PubMed1979

Laboratory and field evaluation of selective media for isolation of group B streptococci.

Problems encountered with currently recommended selective media for group B streptococci (GBS) (selective broth medium and CNA agar) prompted a searach for alternative culture methods in ongoing epidemiological studies. Previously recommended inhibitory agents were tested in vitro. Gentamicin, alone or in combination with nalidixic acid, proved inhibitory for many GBS strains. Among other agents tested, polymyxin was most complementary to the gram-negative spectrum of nalidixic acid, without compromising GBS growth. Crystal violet provided the simplest, most economical staphylococcal inhibitor. Broth and agar media, constituted with these three agents and designated NPC, were evaluated in vitro and in field studies. This investigation represents the first direct comparison of broth media containing inhibitory agents for the preferential isolation of GBS. In maternal colonization studies, NPC broth proved superior to Todd-Hewitt broth containing nalidixic acid and gentamicin at concentrations employed in the previously described selective broth medium (95% versus 59% recovery). Our comparisons were done without added sheep blood since GBS grow well in Todd-Hewitt broth. NPC broth proved more sensitive than NPC agar for detecting GBS colonization in newborns. The NPC agar medium was useful for further purification of broth cultures and quantitative culture techniques.

Bacteria↗

PubMed1991

Differing activities of quinolones against ciprofloxacin-susceptible and ciprofloxacin-resistant, methicillin-resistant Staphylococcus aureus.

The in vitro activities of nine quinolones (seven fluoroquinolones, nalidixic acid, and acrosoxacin) against methicillin-resistant Staphylococcus aureus (MRSA) were compared with those of the glycopeptides teicoplanin and vancomycin. MICs against 160 strains of ciprofloxacin-susceptible (MIC, less than 2.0 micrograms/ml) MRSA and 40 strains of ciprofloxacin-resistant (MIC, greater than or equal to 2.0 micrograms/ml) MRSA were determined. The following MICs for 50% of the strains tested (in micrograms per milliliter) were obtained for ciprofloxacin-susceptible and -resistant strains, respectively: tosufloxacin, 0.06 and 2.0; ofloxacin, 0.25 and 16; ciprofloxacin, 0.5 and 16; pefloxacin, 0.5 and 32; acrosoxacin, 1.0 and greater than 256; enoxacin, 1.0 and 64; fleroxacin, 1.0 and 32; norfloxacin, 2.0 and 64; nalidixic acid, 64 and 512; teicoplanin, 1.0 and 1.0; vancomycin, 2.0 and 2.0. In mutation rate studies using a range of antibiotic concentrations to reflect those achievable in vivo, resistant mutants grew only on plates containing nalidixic acid (rate of mutation to resistance, 10(-7) to 10(-8) and on plates containing low concentrations of ciprofloxacin, enoxacin, and norfloxacin (rate of mutation to resistance, 10(-8) to 10(-9). In time-kill studies, 99.9% killing was found within 8 h for all of the quinolones tested (norfloxacin and nalidixic acid were not tested). Teicoplanin and vancomycin were less rapidly bactericidal. For the clinical isolates of ciprofloxacin-resistant MRSA, different levels and patterns of quinolone resistance were found. Generally, cross-resistance among the fluoroquinolones was complete; however, incomplete cross-resistance did occur with the nonfluorinated quinolone acrosoxacin.

Anti-Bacterial Agents↗

PubMed1992

Contribution of the human kidney to the metabolic clearance of drugs.

OBJECTIVE: To demonstrate that the human kidney is capable not only of filtering and secreting drugs and their metabolites, but also of carrying out conjugation reactions such as acyl glucuronidation, N-glucuronidation, and glycination. DATA SOURCES: Plasma concentrations and renal excretion rates of drugs are measured and renal clearance is calculated in a series of selected pharmacokinetic studies in healthy human volunteers (some studies were conducted in the authors' laboratory and others were reported in the literature). BACKGROUND THEORY: It is generally agreed that the liver plays the dominant role in drug metabolism, and that the function of the kidneys is limited to excretion of parent drug and metabolites. This can be easily understood when a metabolite is present in both plasma and urine. When the metabolite is present in urine but is not measurable in plasma, then the possibility exists that the metabolite is formed by the kidneys. RESULTS: "Simple" excretion by the kidneys is demonstrated for sulfatroxazole/sulfamethoxazole. Ether glucuronides of codeine are formed in the liver, and the resulting glucuronide is excreted by the kidneys. Possible formation of N1- and N2-glucuronides by the kidneys is demonstrated for sulfadimethoxine, sulfametomidine, and sulfaphenazole. Acyl glucuronidation of probenecid and nalidixic acid is carried out by the kidneys. The acyl glucuronidation of probenecid shows a capacity-limited formation/excretion rate of 46 mg/h, which is subject dependent. During this process, the acyl glucuronidation of co-administered nalidixic acid is reduced from 53 to 16 percent compared with that of nalidixic acid alone. Probenecid and its acyl glucuronidation do not inhibit the ether glucuronidation of codeine in the liver, but only interfere with the active tubular secretion process. The acyl glucuronidation of the nonsteroidal antiinflammatory drug naproxen and its metabolite, O-desmethylnaproxen, may be carried out by the liver and kidneys. Glycination of benzoic acid and salicylic acid is carried out in both the liver and kidneys. CONCLUSIONS: It is difficult to recognize renal drug metabolism in the intact human body (in vivo); the glucuronides or conjugates must be measured via direct HPLC analysis. In cases where the metabolite is present in high concentrations in urine but not in blood, there may be an indication that the kidneys are responsible for the formation of the metabolite. Impaired kidney function not only affects renal excretion but may also affect renal metabolism.

Glucuronates↗

PubMed1993

[Effectiveness of the new quinolones, ciprofloxacin and pefloxacin in experimental plague].

Efficacy of ciprofloxacin and pefloxacin in plague infection was studies on albino mice by comparison with that of nalidixic acid. The mice were contaminated subcutaneously. The treatment with the drugs was started 6 or 24 hours after the contamination. The MICs of ciprofloxacin, pefloxacin and nalidixic acid were 0.01 to 0.02, 0.15 and 1.25 to 2.5 micrograms/ml respectively. By the ED50 ciprofloxacin proved to be the most efficient. Pefloxacin was 6 times less efficient and nalidixic acid was 100 times less efficient. The quinolones were shown to be highly efficient when administered at 48-hour intervals.

Animals↗

PubMed2005

Clonal expansion may account for high levels of quinolone resistance in Salmonella enterica serovar enteritidis.

We have observed a high incidence of isolated nalidixic acid resistance in Salmonella enterica serovar Enteritidis isolates in Ireland, particularly isolates of phage type 1 (PT1). A group of nalidixic acid-resistant (n = 22) and nalidixic acid-susceptible (n = 28) isolates of serovar Enteritidis from multiple sites in Ireland were selected. Isolates were typed by pulsed-field gel electrophoresis (PFGE) with XbaI, and the MICs for nalidixic acid and ciprofloxacin were determined. Mutations associated with nalidixic acid resistance in clinical isolates and laboratory mutants of serovar Enteritidis and 32 nalidixic acid-resistant isolates of 15 other salmonella serovars were identified. PFGE had limited discriminatory power. A specific point mutation (G246T) associated with amino acid substitution Asp87Tyr in the quinolone resistance determining region of the gyrA gene accounted for 95% of all mutations in serovar Enteritidis and for all mutations in PT1 isolates. Greater diversity of mutations was observed among all non-Enteritidis salmonella serovars studied. Rates of nalidixic acid resistance in serovar Enteritidis may predominantly reflect clonal expansion after infrequent mutation or selection events.

DNA Gyrase↗

PubMed1995

[Susceptibility to quinolones of Salmonella isolated from men and animals].

Fluoroquinolones are efficacious antibiotics for the treatment of Salmonella infections in humans. One of these quinolones, enrofloxacin, a precursor of ciprofloxacin, is used to treat respiratory infections in calves and poultry. There is a risk of developing resistant strains of Salmonella in animals, which may then contaminate humans. To evaluate current susceptibilities of Salmonella strains to quinolones, we collected 95 strains belonging to various serotypes in a district of intensive breeding (the Ille-et-Vilaine Département): 54 human strains, 24 bovine strains, and 17 poultry strains. The technique of dilutions in agar medium was used to determine Minimal Inhibitory Concentrations (MICs) for the following antibiotics: nalidixic acid, norfloxacin, pefloxacin, ofloxacin, ciprofloxacin, levofloxacin and clinafloxacin. Our results showed that human Salmonella strains remained very susceptible to quinolones. Only 3 animal strains had nalidixic-acid MICs > 128 mg/l. For these 3 strains, pefloxacin and ciprofloxacin MICs were respectively 1 or 2 mg/l and 0.25 mg/l. For all the other human and animal strains the nalidixic-acid MICs were < 4 mg/l, and their MICs 90 were: 0.12 mg/l for ofloxacin and norfloxacin, 0.06 mg/l for pefloxacin, 0.03 mg/l for ciprofloxacin, 0.016 mg/l for levofloxacin, and 0.004 mg/l for clinafloxacin.

Animals↗

PubMed2001

Inhibitory effect of quinolone antimicrobial and nonsteroidal anti-inflammatory drugs on a medium chain acyl-CoA synthetase.

The inhibitory effects of quinolone antimicrobial agents and nonsteroidal anti-inflammatory drugs on purified mouse liver mitochondrial medium chain acyl-CoA synthetase catalyzing the first reaction of glycine conjugation were examined, using hexanoic acid as a substrate. Enoxacin, ofloxacin, nalidixic acid, diflunisal, salicylic acid, 2-hydroxynaphthoic acid, and 2-hydroxydodecanoic acid, which do not act as substrates, were potent inhibitors. Diflunisal, nalidixic acid, salicylic acid, 2-hydroxynaphthoic acid, and 2-hydroxydodecanoic acid inhibited competitively this medium chain acyl-CoA synthetase with K(i) values of 0.6, 12.4, 19.6, 13.4, and 15.0 microM, respectively. Enoxacin and ofloxacin inhibited this medium chain acyl-CoA synthetase in a mixed-type manner with K(i) values of 23.7 and 38.2 microM, respectively. Felbinac, which is a substrate, inhibited the activity of this medium chain acyl-CoA synthetase for hexanoic acid (IC50 = 25 microM). The concomitant presence of enoxacin and felbinac strongly inhibited this medium chain acyl-CoA synthetase. These findings indicate that medium chain acyl-CoA synthetases may be influenced by quinolone antimicrobial and nonsteroidal anti-inflammatory drugs.

4-Quinolones↗

PubMed2002

Shifting serotypes, plasmid profile analysis and antimicrobial resistance pattern of shigellae strains isolated from Kolkata, India during 1995-2000.

One hundred and sixty-six shigellae strains, isolated from stool samples of paediatric patients (< 5 years old) at a Childrens' Hospital in Kolkata, India during the period of 1995-2000 were examined for serotyping, drug resistance pattern and plasmid profiles. Sh. flexneri (58 %) was found to be commonest isolate of total shigellae, followed by Sh. sonnei (28 %), Sh. boydii (9%) and Sh. dysenteriae (5%). This profile of species was in sharp contrast to the picture obtained before 1995, when Sh. dysenteriae 1 predominated over Sh. flexneri. In Sh. flexneri strains, Sh. flexneri 2a (35%) was the most prevalent serotype, following Sh. flexneri 3a (31%), Sh. flexneri 6 (14%), Sh. flexneri 2b (11%) and Sh. flexneri 4 (9%). Resistance patterns of the strains to 12 commonly used antimicrobial agents and minimum inhibitory concentrations (MICs) of the antibiotics were also tested. All strains were found uniformly susceptible to norfloxacin, but more than 90% strains were resistant to tetracycline, co-trimoxazole and 67% strains were resistant to ampicillin. Resistance to amoxicillin, chloramphenicol and nalidixic acid was found in 55% (range 45-74%), 46% (range 40-60%) and 29% (range 15-40%) strains respectively. Overall, shigellae strains showed statistically significant increase in resistance against tetracycline, nalidixic acid and furazolidone (P < 0.05) over the years of this study. This indicates decreased efficacy of furazolidone, cotrimoxazole and nalidixic acid for the empirical treatment of shigellosis in Kolkata. Although a few strains showed intermediate susceptibility to ciprofloxacin (4%) and cefotaxime (10%) by disk diffusion test, but the MICs of those antibiotics were within the normal limits. Almost 57% of the strains were resistant to four or more drugs with high MICs of the antibiotics. Plasmid profile analysis revealed presence of large plasmid of 220 kb in majority of the strains except in Sh. sonnei and a correlation between presence of smaller plasmids and shigellae serotypes. Hence this study reports epidemiological change of shigellae species in Kolkata, India with regard to serotypes and antibiotic resistance patterns.

Anti-Bacterial Agents↗

PubMed2002

The importance of pets as reservoirs of resistant Enterococcus strains, with special reference to vancomycin.

The purpose of the present study was to determine the prevalence of antibiotic resistance, with special attention to vancomycin, in 104 strains of Enterococcus, which is the sentinel bacterium isolated from dog and cat faeces samples. The phenotypic characterization of the isolates classified them as E. faecium (58%), E. avium (41%) and E. faecalis (1%). Sensitivity testing used the diffusion method according to the recommendations of CASFM (Comite de l'Antibiogramme de la Société Française de Microbiogie), to oxacillin, amoxycillin, amoxycilin + clavulanic acid, ampicillin, piperacillin, cefoperazone, imipenem, enrofloxacin, ciprofloxacin, ofloxacin, nalidixic acid, tetracycline, lincomycin, erythromicin and vancomycin. Minimum inhibitory concentration (MIC) determination by E test revealed a MIC to vancomycin of between 0.5 microg/ml and 3 microg/ml. All the strains were resistant to nalidixic acid, erythromycin, cefoperazone and oxacillin. We detected resistance to amoxycillin + clavulanic acid in 1.9% of isolates, to amoxycillin in 4.8%, to piperacillin in 13.5%, and to ampicillin in 21.2% of strains. A high prevalence of antibiotic resistance to lincomycin, tetracycline, enrofloxacin, ciprofloxacin and ofloxacin was found in 98.1%, 95.2%, 76.9%, 73.1% and 64.4% of strains, respectively. Resistance to vancomycin was not found, which indicates that there is no transmission risk of vancomycin-resistant enterococcal strains to man or transfer of their resistance genes to other bacteria belonging to the endogenous flora of humans.

Animals↗