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PubMed1984

Comparison of various methods for differentiation of staphylococci and micrococci.

A modified oxidase test (Remel, Lenexa, Kans.) and susceptibility to furazolidone and lysostaphin (Remel) were evaluated in conjunction with the Staph-Ident strip (Analytab Products, Plainview, N.Y.) to accurately differentiate between staphylococci and micrococci. A total of 414 clinical isolates of catalase-positive, gram-positive cocci were each tested with the Staph-Ident strip and by glucose fermentation, acid production from glycerol, susceptibility to furazolidone and lysostaphin, and the oxidase test. Based on the reference methods of glucose fermentation and acid production from glycerol, 396 (95.6%) of the organisms were classified as Staphylococcus species and 18 (4.4%) were classified as Micrococcus species. Of the staphylococci, 99% were oxidase negative and susceptible to furazolidone; 82% were susceptible to lysostaphin. All of the micrococci were oxidase-positive and resistant to furazolidone and lysostaphin. Of the staphylococci, 99% were identified to species by the Staph-Ident strip. However, six (33%) of the micrococci were incorrectly identified as Staphylococcus species (three each of Staphylococcus hominis and Staphylococcus saprophyticus). Because of the demonstrated sensitivity and specificity of the oxidase and furazolidone susceptibility tests, it is suggested that either of these methods be used in the clinical laboratory to accurately differentiate between staphylococci and micrococci. It is also suggested that when working with the Staph-Ident strip, additional testing such as furazolidone susceptibility or oxidase activity should be performed to provide increased accuracy in the differentiation and characterization of members of the family Micrococcaceae.

Bacteriological Techniques↗
PubMed1975

The effect of antibiotic therapy on the faecal excretion of Salmonella typhimurium by experimentally infected chickens.

Chickens in groups of 40 were infected orally with a nalidixic acid-resistant mutant of Salmonella typhimurium and then fed continuously on diets containing ampicillin, chloramphenicol, furazolidone, neomycin, oxytetracycline, polymixin, spectinomycin, streptomycin or a mixture of trimethoprim and sulphadiazine. The amount of S. typhimurium excreted in their faeces was estimated at intervals by culture on brilliant green agar containing sodium nalidixate, both direct and after enrichment in selenite broth; the amount of Escherichia coli excreted was estimated by culture on MacConkey agar. The feeding of diets containing 500 mg./kg. of ampicillin, furazolidone, neomycin, polymixin, spectinomycin or streptomycin or 100 mg./kg. of trimethoprim and 500 mg./kg. of sulphadiazine for 46 days reduced to a varying degree the amount of S. typhimurium and E. coli excreted, the greatest reduction in S. typhimurium being brought about by the last treatment. The effect was less obvious when the concentration of the antibiotics in the food was decreased fivefold. An important reason for the very limited effect of some of the antibiotics was the emergence of antibiotic-resistant populations of S. typhimurium and E. coli. High concentrations of antibiotic-resistant organisms also arose in the faeces of the chickens fed diets containing tetracyclines and chloramphenicol, treatments which had no apparent effect on the amount of S. typhimurium and E. coli excreted. Much of the antibiotic resistance encountered was determined by R factors, a particular R factor usually being found in the E. coli populations of individual chickens before it was found in their S. typhimurium populations. No S. typhimurium or E. coli were isolated that possessed R factors determining resistance to polymixin, furazolidone or trimethoprim. No S. typhimurium or E. coli were isolated that were polymixin-resistant and no S. typhimurium that were furazolidone-resistant. The few trimethoprim-resistant S. typhimurium isolated were thymine-dependent. The feeding of diets containing the higher concentrations of trimethoprim/sulphadiazine, neomycin, furazolidone or ampicillin for 9 days reduced the amount of S. typhimurium excreted. After the withdrawal of these diets, the amount of S. typhimurium excreted increased to the numbers found in chickens given ordinary diets throughout; the chickens that had been given trimethoprim/sulphadiazine or furazolidone did not remain faecal excreters of S. typhimurium longer than the chickens that had been given ordinary diets. Similar results were obtained with trimethoprim/sulphadiazine when the start of the 9-day treatment period was delayed for an extra 9 days or when it was extended to 18 days.

Animal Feed↗
PubMedDate not supplied

Evaluation of different antibiotics in inhibiting colonization of Vibrio cholerae O1 and O139 in the rabbit intestine.

The effects of furazolidone, erythromycin and azithromycin in inhibiting colonisation of Vibrio cholerae O1 and O139 in the rabbit intestine were tested. Both V. cholerae O1 and O139 highly colonised the gut in control rabbits. The colonisation of furazolidone-resistant strains in the rabbit intestine was prevented effectively by both erythromycin and azithromycin. In furazolidone-sensitive strains, the efficacies of erythromycin and azithromycin were very much comparable to furazolidone. These results suggested that azithromycin may be subjected to clinical trial in comparison to furazolidone and erythromycin for the treatment of cholera due to O1 and O139 infection in children.

Animals↗
PubMed2004

In vitro susceptibility of Blastocystis hominis isolated from patients with irritable bowel syndrome.

This study aims to determine the growth pattern and in vitro susceptibility of clinical isolates of Blastocystis hominis to different concentrations of metronidazole, furazolidone and ciprofloxacin. Stool specimens from 25 consecutive patients with irritable bowel syndrome presenting to the gastroenterology department of Aga Khan University Hospital between January and May 2003 are examined by microscopy and cultured for B. hominis. Drug susceptibility assays are performed for metronidazole, furazolidone, and ciprofloxacin using final concentrations of 0.01 mg/mL and 0.1 mg/mL. The effect of the drugs is assessed after B. hominis culture for 48 h. With furazolidone and metronidazole, 68% (17/25) and 60% (15/25) of B. hominis isolates, respectively, failed to grow at drug concentrations of both 0.01 mg/mL and 0.1 mg/mL. However, ciprofloxacin failed to suppress growth completely at both concentrations. B. hominis resistance to furazolidone, metronidazole and ciprofloxacin at 0.01 mg/mL was 32% (8/25), 40% (10/25) and 100% (25/25), respectively. B. hominis isolates varied in their degree of susceptibility to the three drugs studied, being greater with furazolidone than with metronidazole, and complete resistance with ciprofloxacin.

Animals↗
PubMed1994

Biotransformation of furaltadone by pig hepatocytes and Salmonella typhimurium TA 100 bacteria, and the formation of protein-bound metabolites.

1. The major metabolite resulting from the biotransformation of furaltadone (5-morpholinomethyl-3-[5-nitrofurfurylidene-amino]-2-oxazoli dinone) by pig hepatocytes was shown to result from the N-oxidation of the tertiary nitrogen in the morpholino-ring, leaving the nitrofuran ring unchanged. 2. No evidence could be obtained for the formation of an open-chain cyano-metabolite, a minor metabolite in the case of the related nitrofuran drug furazolidone (N-(5-nitro-2-furfurylidene)-3-amino-2-oxazolidinone). This metabolite was the major metabolite, following incubation of furaltadone and furazolidone with Salmonella typhimurium bacteria. 3. The N-oxide was not further metabolized by pig hepatocytes or bacteria, and gave negative test results in the Ames-test (TA 100, no S9-mix) at the highest tested dose of 1 microgram/plate. Furaltadone gave a positive result at 10 ng/plate. 4. The biotransformation of both drugs by pig hepatocytes and bacteria resulted in the formation of protein-bound metabolites, with no clear quantitative differences between the two drugs. The intact 3-amino-2-oxazolidinone (AOZ) and 5-morpholinomethyl-3-amino-2-oxazolidinone (AMOZ) side-chains of furazolidone and furaltadone, respectively, could be released from these metabolites by mild acid treatment. 5. Hepatocytes incubated with the AMOZ side-chain of furaltadone showed a decreased monoamine oxidase activity at high dose levels (IC50 3.7 mM), whereas exposure to the AOZ side-chain of furazolidone resulted in a clear inhibition at 10,000-fold lower concentrations (IC50 0.5 microM). In the presence of 1% dimethylsulphoxide (DMSO), the MAO-inhibition by AMOZ and especially AOZ was remarkably reduced. 6. It is concluded that protein-bound metabolites containing an intact and releasable side-chain might be present in tissues of animals treated with furaltadone. However, these residues might be of less toxicological concern than those of furazolidone.

Animals↗