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PubMed1984

Furazolidone versus ampicillin in the treatment of traveler's diarrhea.

Ninety-four U.S. students who acquired diarrhea in Mexico were treated with furazolidone (47 subjects) or ampicillin (47 subjects) on a double-blind random basis. Of 47 students, 26 (55%) who received furazolidone (100 mg four times daily for 5 days) recovered from illness within 48 h after initiation of therapy, in contrast to 15 of 47 (32%) who received ampicillin (500 mg four times daily for 5 days) (P less than 0.05). Altogether, 74% of students treated with furazolidone and 49% of those receiving ampicillin were well within 72 h (P less than 0.05). When furazolidone was compared with ampicillin, clinical illness was shortened on the average from 65 to 61 h for enterotoxigenic Escherichia coli diarrhea, from 83 to 58 h for shigellosis, from 82 to 51 h for diarrhea unassociated with a detectable agent, and from 72 to 57 h for all cases irrespective of etiology. Although not dramatically effective in the current trial, the broad spectrum of activity of furazolidone is of interest. Because of in vitro activity against Campylobacter strains and known effectiveness in treating giardiasis, furazolidone should be considered in therapy for diarrhea of unknown etiology in certain settings when laboratory processing of stools for etiological agent is not feasible.

Ampicillin↗

PubMed2001

Second-line Helicobacter pylori eradication with a furazolidone-based regimen in patients who have failed a metronidazole-based regimen.

BACKGROUND/AIM: In developing countries the standard quadruple therapy containing metronidazole results in suboptimal eradication rates of Helicobacter pylori (<75%). In a retrospective study, we undertook to evaluate efficacy and tolerability of a furazolidone-based regimen (omeprazole, furazolidone, bismuth, and tetracycline) in patients who had previously failed the standard metronidazole-based regimen (omeprazole, metronidazole, bismuth, and amoxicillin). METHODS: The records of H. pylori infected patients who were referred to outpatient clinic (from March 1999 to August 1999) and who underwent previous eradication regimens were studied. A total of 320 cases were noted to have received a metronidazole-based quadruple regimen. From these 320 patients, 80 were noted to have failed this regimen based on a urea breath test. These 80 patients were enrolled in the study and given the furazolidone-based regimen. Side effects were assessed at follow-up visits. At least 2 months after the end of each therapy regimen, a (14)C-urea test was performed in each subject to document the cure of the patients. RESULTS: A total of 80 patients (39 males and 41 females) with a mean age of 43.8 +/- (SD) 13.3 years were studied. The H. pylori eradication rate was 90% with the furazolidone-based regimen. The side effects of this regimen were minor. CONCLUSIONS: A furazolidone-based regimen is effective in patients who do not achieve cure of H. pylori infection with the metronidazole-based quadruple therapy. In areas where the metronidazole resistance is high, initial therapy with a furazolidone-based regimen is recommended.

Adult↗

PubMed1987

The elimination of furazolidone and its open-chain cyano-derivative from adult swine.

1. A sensitive method for the determination of 3-(4-cyano-2-oxobutylidene amino)-2-oxazolidone, the open-chain cyano-derivative of the veterinary drug furazolidone, in swine plasma and tissues is described. 2. After dosing adult swine orally with furazolidone (690 mg/animal per day) for 10 days no furazolidone was detected in liver, kidney and muscle (less than 2 ng/g). The half life of furazolidone as measured from the terminal phase of the plasma curves was 45 minutes. In urine, small amounts (less than 0.3% of total dose) of furazolidone were detected. 3. In contrast to other animals, 3-(4-cyano-2-oxobutylidene amino)-2-oxazolidone is a minor metabolite in swine with a plasma half life of 4 h. No cyano-derivative was detected in liver and kidney (less than 5 ng/g) 2 h after the last administration of furazolidone; 24 h after the last administration, the concentration in plasma was less than 2 ng/ml and in muscle less than 5/g. 4. The cyano-derivative was not mutagenic in the Salmonella/microsome test, with or without metabolic activation.

Animals↗

PubMed1991

Reversibility of furazolidone-induced cardiotoxicosis in ducklings.

Furazolidone cardiotoxicosis was induced in 2 groups (FZ and FZ-CR groups) of newly hatched male Pekin ducklings (100/group) by feeding a ration containing 650 mg of furazolidone/kg of feed (ppm) for 28 days. A third group (control ration, CR group; n = 100) was fed the same ration without furazolidone. On day 28, the control ration was initiated for the FZ-CR group initially given the furazolidone-containing ration, to allow recovery from the effects of the drug, whereas ducklings of the FZ group continued to consume the furazolidone-containing ration. Biweekly, beginning with week 4, ducklings were euthanatized to assess severity of gross lesions and to obtain sections of myocardium for histologic and ultrastructural examination. Clinical evidence (increased weight gain, increased feed consumption, decreased mortality, reduced prevalence of palpable ascites) of regression of cardiotoxicosis of ducklings of the FZ-CR group was nearly complete by day 56 (28 days after cessation of furazolidone intake). Likewise, regression of gross lesions, as measured by overall prevalence of gross lesions, left ventricular volume, and ascites prevalence and severity, were also essentially complete by day 56. Myofibrillar lysis was not seen in sections from the heart (examined ultrastructurally) obtained from ducklings of the CR group that were euthanatized on day 28, 56, or 98. Myofibrillar lysis was detected in all ducklings (4/4) fed furazolidone (FZ and FZ-CR groups) and euthanatized on day 28. Myofibrillar lysis was not seen in the heart of ducklings of the FZ-CR group that were euthanatized on day 56 or 98. Myofibrillar lysis was detected in the heart from all ducklings of the FZ group that were euthanatized on day 56.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

The efficacy of furazolidone and metronidazole in the treatment of chronic gastritis associated with Helicobacter (Campylobacter) pylori--a randomized double-blind placebo-controlled clinical trial.

Seventy-two patients with Helicobacter pylori-associated chronic gastritis were randomized to a 3-week oral treatment with furazolidone 0.1g t.i.d. or metronidazole 0.2g t.i.d. or placebo. Endoscopy was performed before and after treatment, and biopsy specimens were taken from the antrum of the stomach for histological examination and culture of Helicobacter pylori. Disappearance rates of Helicobacter pylori in furazolidone, metronidazole and the control groups were 74% (20/27) if considering completion of therapy, the 20/25 or 80%, 33.3% (8/24) and 14.3% (3/21) respectively. There was a significant difference in the disappearance rate of Helicobacter pylori between furazolidone and metronidazole, and between furazolidone and the placebo group (p less than 0.01), but there was no such difference between metronidazole and the placebo group (p greater than 0.05). In the patients receiving furazolidone, the eradication of Helicobacter pylori was accompanied by marked improvement in both inflammatory infiltration in the gastric mucosa and symptoms. These results reasonably suggest that Helicobacter pylori may play an etiological role in the pathogenesis of chronic gastritis, and that furazolidone is effective in the treatment of Helicobacter pylori-associated chronic gastritis.

Adolescent↗

PubMed1995

Furazolidone in typhoid fever--correlation of clinical efficacy with serum bactericidal activity.

Treatment of typhoid fever with furazolidone produces a high cure rate. This is a clinical curiosity, as furazolidone is described to be poorly absorbed. The present study examined whether furazolidone could produce unequivocal clinical response and, if so whether this was due to the drug producing bactericidal levels in the serum. Twenty one patients selected by defined criteria were treated with furazolidone and evaluated for definite clinical response in 5-7 days. Bactericidal activity of pre dose and post dose sera were estimated in seven patients showing definite clinical response. All the seven patients had a clinical cure without the drug producing significant bactericidal levels in the blood. Hence we concluded that the major site of action of furazolidone was in the intestine. It is our postulate that the organisms reaching the intestine in large numbers from bile are prevented from gaining re-entry into the circulation by the action of furazolidone in the intestine. After repeated cycles of entry of organisms into the intestine from bile and the simultaneous prevention of its re-entry into the circulation, the number of organisms remaining in circulation comes down considerably, thus helping the immune system to bring about a cure.

Anti-Infective Agents↗

PubMed1995

Comparative efficacy of furazolidone and nalidixic acid in the empirical treatment of acute invasive diarrhea: randomized clinical trial.

Efficacy of furazolidone and nalidixic acid was compared in a randomized trial involving 72 children with acute invasive diarrhea. Thirty six children received furazolidone (7.5 mg/kg/day) and 36 children received nalidixic acid (55 mg/kg/day). Clinical characteristics of the two treatment groups were comparable on admission. Of these, 34 children in furazolidone treated group and 29 children in nalidixic acid treated group completed the full course of treatment and were analyzed finally for clinical efficacy. Clinical cure was observed in 29(85.3%) children treated with furazolidone and 29(100.0%) children treated with nalidixic acid. Nalidixic acid treated group had statistically significantly higher cure rate (p = 0.039) as compared to furazolidone treated group. However, 85% cure rate in furazolidone treated group may be potentially useful for the treatment of acute invasive diarrhea because of decreasing efficacy of nalidixic acid against shigellosis in many countries.

Anti-Infective Agents↗

PubMed1983

Five v ten days' therapy with furazolidone for giardiasis.

In previous uncontrolled studies it has been reported that five days' treatment with furazolidone is effective for giardiasis. Efficacy of five v ten days of treatment was evaluated in a prospective, randomized study of 22 children with giardiasis. Eleven of 12 patients (92%) treated for ten days were cured based on clinical and parasitological response; one patient did not tolerate furazolidone and was treated with quinacrine hydrochloride. Only two of ten patients (20%) treated with a five-day regimen were cured. Of the other eight patients, five had prompt relapse of diarrhea after furazolidone treatment was stopped, diarrhea persisted in two, and diarrhea diminished but Giardia persisted in one. Six of eight patients in whom the five-day regimen failed were re-treated with furazolidone for ten days, and five patients were cured. Therapy with furazolidone for less than seven to ten days cannot be recommended for children with giardiasis.

Child, Preschool↗

PubMed1987

Investigation on the metabolic degradation of the side chain of furazolidone.

The investigation was aimed at providing insight into the side chain metabolism of furazolidone in mice. The agents used in the experiments were furazolidone, 3-amino-2-oxazolidinone, oxazolidinone, nitrofurantoin, 3-aminohydantoin and hydantoin, administered intraperitoneally at five equimolar doses ranging from 0.178 to 0.888 mmol/kg. The parameters investigated included ethane and ethylene expiration, formation of malondialdehyde and total glutathione content in the liver. Ethylene expiration was found to be strongly enhanced by aminooxazolidinone and slightly increased by furazolidone. Ethane expiration was increased after aminooxazolidinone administration. Malondialdehyde formation was not affected by any of the agents used. Total glutathione was decreased by furazolidone and nitrofurantoin. The above findings indicate that, in vivo, the azomethine linkage of the side chain of furazolidone hydrolyses to form 3-amino-2-oxazolidinone, subsequently cleaved to ethylene.

Animals↗

PubMed1983

Some pharmacological and toxicological properties of furazolidone.

The pharmacological and toxicological properties of furazolidone have been briefly reviewed. Among the most important pharmacological actions of furazolidone is the inhibition of mono- and diamine oxidase activities, which seem to depend, at least in some species, on the presence of the gut flora. The drug also seems to interfere with the utilization of thiamin, which is probably instrumental in the production of anorexia and loss of body weight of the treated animals. Furazolidone is known to induce a condition of cardiomyopathy in turkeys, which could be used as a model to study alpha 1-antitrypsin deficiency in man. The drug is most toxic to ruminants. The toxic signs observed were of nervous nature. Experiments are in progress in this laboratory to try to explain the mechanism(s) by which this toxicity is brought about. It is uncertain whether the use of furazolidone at the recommended therapeutic dose would result in drug residues in tissues of treated animals. This is a matter of public health importance as the drug has been shown to possess a carcinogenic activity. It is important that a simple and reliable method of identification and estimation of furazolidone residues be devised. More work is needed to elucidate the mode of action and biochemical effects caused by the drug in both the host and the infective organisms.

Adrenal Glands↗

PubMed2002

The effects of the antiprotozoal drugs metronidazole and furazolidone on trophozoites of Giardia lamblia (P1 strain).

The effects of metronidazole and furazolidone on Giardia lamblia trophozoites were analyzed by video-light and transmission electron microscopy. In addition, growth curves were drawn based on four concentrations of the drugs. The IC50 was 4.6 microM for metronidazole and 2.9 microM for furazolidone. By light microscopy we observed that metronidazole-treated cells maintained the characteristic body shape, but many showed bubbles in the dorsal and ventral surfaces. The effects of furazolidone include changes in the morphology (the cells were roundish) and also cytoplasmic extrusions. When observed by transmission microscopy, cells treated with metronidazole appeared rounder than usual and membranous structures were observed in the cytoplasm. Cells treated with furazolidone showed the cytoplasm depleted of its contents and great changes in volume. Our results show that furazolidone was more effective than metronidazole and its effects were observed in cells treated with 1 microg/ml (the lowest concentration) as early as 6 h after the start of exposure.

Animals↗

PubMed1981

Radiomimetic property of furazolidone and the caffeine enhancement of its lethal action on the vibrios.

Sensitivities of the strains belonging to four vibrio biotypes to the action of furazolidone were investigated. Vibrio cholerae (classical) was most and Vibrio parahaemolyticus least sensitive to this drug. Statistical analyses revealed significant differences between any two of the four types of vibrio in respect of their sensitivity to furazolidone. The drug was radiomimetic in action, the doses of UV light (DUV) and furazolidone (Df) required for 10% survival of the vibrios being correlated by the equation, Df = 0.28 exp. (0.008 DUV). Caffeine exhibited lethal synergism with furazolidone and the synergistic effect depended on the mode of caffeine treatment, the effect being maximum when caffeine was present along with and also after furazolidone treatment. UV spectrophotometric study revealed that caffeine did not bind with native DNA but did so with denatured DNA resulting in a bathochromic shift and a quenching of the caffeine absorption maximum at 209.4 nm. The binding isotherm (Scatchard plot) indicated the presence of a heterogeneity in the binding sites and that the parameters for the strongest mode of bonding were n = 0.254 and k = 7.5 X 10(5) M-1.

Caffeine↗

PubMed1991

Fate and microbiological effects of furazolidone in a marine aquaculture sediment.

Furazolidone is used in the treatment of bacterial diseases in farmed fish. During application a large proportion of the administered drug reaches the environment directly or via feces. The persistence and metabolism of furazolidone in sediment from a Norwegian salmon farm is described. Furazolidone, in contrast to oxytetracycline and oxolinic acid, is actively metabolized by microorganisms in the sediment. The main metabolite is 3-(4-cyano-2-oxobutylidene-amino)-2-oxazolidone. This is a well known metabolite of the degradation of furazolidone in mammals, fish and Escherichia coli. 3-(4-Cyano-2-oxobutylideneamino)-2- oxazolidone had no detectable antibacterial activity. The half-life of furazolidone in the sediment at 4 degrees C was calculated to be 18 h.

Animals↗

PubMed1991

Use of pig hepatocytes to study the inhibition of monoamine oxidase by furazolidone.

Primary cultures of pig hepatocytes were used to examine the irreversible inhibition of monoamine oxidase (MAO), which has been observed in tissues of a number of different animal species after oral treatment with furazolidone. The rapid biotransformation of the MAO substrate p-tyramine by intact cells could effectively and irreversibly be inhibited with the known MAO inhibitors iproniazid and clorgyline. Incubation of cells with beta-hydroxyethylhydrazine and also 3-amino-2-oxazolidinone, which were previously proposed as the metabolites of furazolidone responsible for the in vivo effect, resulted in an irreversible inhibition of the MAO activity. Incubation of cells with furazolidone also resulted in a dose-related inhibition, but this effect was completely reversible on withdrawal of the drug. A similar MAO inhibition was observed after treatment of cells with nitrofurazone and furaltadone but not with nitrofurantoin. The results obtained with intact cells were confirmed by studies with 13,000 g pellets of homogenates made from cells preincubated for 24 hr with the compounds, which showed an irreversible inhibition in the case of iproniazid and 3-amino-2-oxazolidinone, but not in the case of furazolidone. The present study shows that hepatocytes are capable of transforming 3-amino-2-oxazolidinone, but not furazolidone itself, into a potent irreversible type of MAO inhibitor.

Animals↗

PubMed2002

Effects of furazolidone, PCB77, PCB126, Aroclor 1248, paraquat and p,p'-DDE on transketolase activity in embryonal chicken brain.

The effect of in ovo exposure to PCBs, DDE and paraquat on transketolase activity was measured in 19-day-old chicken embryos. Furazolidone was used as a positive control for decreased activity of the enzyme. The potency of contaminants to interact with transketolase was also tested in an in vitro system, using control brain 7000xg supernatants containing the enzyme. No effects were found on transketolase activity after in ovo or in vitro exposure to PCB126, Aroclor, DDE or paraquat. PCB77 decreased transketolase activity in vitro, but only at concentrations that, extrapolated to in ovo exposure, would be lethal to the embryo. Furazolidone decreased transketolase activity both in ovo and in vitro. For this contaminant, thiamine residues were analysed in the yolk sacs, but no differences were found between exposed and non-exposed eggs. Transketolase is dependent on thiamine pyrophosphate as a cofactor, and therefore, the decreased enzyme activity could be the result of an interaction between furazolidone and thiamine metabolism. Since thiamine residues were not affected by furazolidone and transketolase inhibition in vitro was similar to the inhibition after in ovo exposure, it was concluded that furazolidone interacted with transketolase on the enzymatic level rather than by a depletion of thiamine.

Animals↗

PubMed1974

Hazards involved in the use of furazolidone for the prevention of salmonellosis in broiler chickens.

The purpose of this work was to study the effects of interrupted, continuous and post-salmonella inoculation treatment with furazolidone in the feed on the colonization of Salmonella infantis in the intestines of chickens, as well as the influence of furazolidone in vitro on the effect of a mixed culture used for the prevention of salmonellosis in chickens.It was shown that chickens given interrupted treatment with 0.01% furazolidone had significantly more salmonellas in the caeca than either chickens fed continuously with this drug or chickens without any treatment. The use of 0.01% furazolidone after inoculation with Salmonella infantis had no effect on Salmonella infantis in the caeca of chickens.The mixed bacterial culture from the normal intestinal flora lost its preventive effect on salmonellosis when cultured with 0.01% furazolidone.

Administration, Oral↗

PubMed1984

Antibiotic resistance in Escherichia coli causing generalized infections in chickens in the UK in 1982: the relationship between the results of in vitro and in vivo furazolidone sensitivity tests.

Compared with a similar survey conducted ten years previously, a survey conducted in 1982, eleven years after the implementation of legislation forbidding the routine use of feeds containing 'therapeutic' antibiotics, revealed a decreased incidence of resistance to tetracyclines, furazolidone and sulphonamides in Escherichia coli strains causing generalized infections in chickens in the UK; the decrease was particularly marked in the case of tetracycline resistance, 17.9% of strains in 1982 being resistant to this antibiotic compared with 31.2% in 1972. Giving furazolidone to groups of chickens inoculated intramuscularly with O2:K1 strains of E. coli of differing degrees of furazolidone sensitivity indicated that great care is required in the performance and interpretation of laboratory tests for sensitivity to this antibiotic. Infections caused by strains that required as little as 1.25 micrograms/ml of furazolidone to inhibit their multiplication in laboratory tests responded poorly to furazolidone treatment; those that were inhibited by less responded well, better than to treatment with tetracycline, chloramphenicol, ampicillin or trimethoprim.

Animals↗

PubMed1999

Furazolidone-containing short-term triple therapies are effective in the treatment of Helicobacter pylori infection.

BACKGROUND: A furazolidone-containing therapeutic regimen for Helicobacter pylori infection has attracted special interest in the face of a rising world-wide metronidazole resistant H. pylori, and the expense of currently used antimicrobial regimens. AIM: To evaluate the efficacy of furazolidone-containing regimens in eradicating H. pylori. METHODS: One-hundred and forty H. pylori positive patients with endoscopically confirmed duodenal ulcer or functional dyspepsia received one of four different regimens to eradicate H. pylori. In the first trial, the patients were randomly assigned to receive a 1-week course of furazolidone 100 mg b.d. and clarithromycin 250 mg b.d., with either tripotassium dicitrato bismuthate (TDB) 240 mg b.d. (FCB group) or lansoprazole 30 mg daily (FCL group). In the second trial, the patients were randomly assigned to receive a 1-week course of clarithromycin 250 mg b.d. and omeprazole 20 mg daily, with either furazolidone 100 mg b.d. (FCO group) or metronidazole 400 mg b.d. (MCO group). Endoscopy was repeated 4 weeks following completion of therapy with re-assessment of H. pylori status on gastric biopsies by histology and culture. RESULTS: Four patients (1 in FCB, 1 in FCO and 2 in MCO groups) dropped out because they refused a follow-up endoscopy. Eradication rates of H. pylori on an intention-to-treat basis in the FCB, FCL, FCO and MCO groups were 91% (32/35, 95% CI: 82-99%), 91% (32/35, CI: 82-99%), 86% (30/35, CI: 74-97%) and 74% (26/35, CI: 60-89%) (all P > 0.05), respectively. Mild side-effects occurred in 15% of the 140 patients. In MCO group, the eradication rate in the patients infected with metronidazole-sensitive isolates of H. pylori was 86%, but dropped to 67% in those with metronidazole-resistance strains (P = 0.198). CONCLUSION: One-week regimens containing furazolidone and clarithromycin in combination with TDB or a proton pump inhibitor fulfil the criteria for successful H. pylori therapy.

2-Pyridinylmethylsulfinylbenzimidazoles↗