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PubMed1976

In vitro sensitivity of enteric bacteria to epicillin, chloramphenicol, ampicillin and furazolidone.

Strains of Salmonella typhi (148) and Salmonella paratyphi A (27) isolated from the blood of patients with clinical features of enteric fever were tested in vitro for their sensitivity to epicillin, ampicillin, chloramphenicol and furazolidone. Results from both the disc and tube dilution methods showed that greater percentages of the two strains were sensitive to epicillin than to the other antibiotics.

Adolescent↗
PubMed1994

Effects of furazolidone on duration of righting reflex loss induced with hexobarbital and zoxazolamine in the rat.

Effects of furazolidone (FZ) on the sleeping time induced with hexobarbital (HEX) and paralysis time induced by zoxazolamine (ZOX) were investigated by measuring the length of time required to recover from righting reflex loss in rats after oral administration of FZ at doses of 50, 100, 200 and 400 mg/kg/day for 4 successive days. Administration of 50 mg/kg to rats of both sexes induced no effect on the HEX sleeping time, but of 100 mg/kg FZ or more induced prolongation of sleeping time dose-dependently. In female rats, HEX sleeping time of the control group was twice that of the male rats, but HEX sleeping time after receiving FZ above 200 mg/kg was approximately the same as in the male rats. ZOX paralysis time exhibited no sex differences in the control rats, and it was significantly prolonged by FZ at a dose of 100 mg/kg or more. No significant differences in blood levels of HEX and ZOX at the time of recovery were found between the control and FZ treated rats, suggesting that FZ produced prolongation of the drug effects was due to the maintenance of the blood levels rather than the change in the sensitivities of rats at the receptor sites. Body weight gains were inhibited in the rats treated with FZ at doses over 100 mg/kg. Cytochrome P-450 content in hepatic microsomes in the rats which received 100 mg/kg FZ were slightly increased. It is suggested that successive oral administration of FZ to rats at high doses impaired drug clearance and this resulted in the prolongation of HEX sleeping and ZOX paralysis times.

Administration, Oral↗
PubMed1998

Evidence of 14C-furazolidone metabolite binding to the hepatic DNA of trout.

Furazolidone (FZ) is a nitrofuran drug commonly used in aquaculture. In the present study, [methylidene-14C]-FZ or [oxazolone-4,5-14C]-FZ was offered to rainbow trout (Oncorhyncus mykiss) in medicated feed at a daily dose of 135 mg/kg b. wt. for 10 days. The trout were sacrificed at specific time points post-dosing and the liver removed for DNA-bound 14C characterization. Both forms of the 14C-labelled FZ were converted by trout to reactive metabolite(s) which bound irreversibly to the hepatic DNA. The amount of 14C bound to the hepatic DNA increased with post-dosing time and was higher in trout pretreated with [methylidene-14C]-FZ than in trout pretreated with [oxazolone-4,5-14C]-FZ. The identity of the FZ reactive metabolite(s) remained to be elucidated. However, a part of the FZ reactive metabolite(s) could be released as 3-amino-2-oxazolidone by acid hydrolysis. An appreciable amount of 14C was also found to bind irreversibly with the hepatic DNA of trout following an i.v. injection of [oxazolone-4,5-14C]-FZ. Results of these studies indicate that FZ is metabolized by trout to a reactive metabolite(s) which binds irreversibly to the DNA of trout liver.

Animal Feed↗
PubMed1978

Activity of alpha-1, 4-glucosidase in furazolidone-induced glycogenosis.

Furazolidone (FZ) at 700 and 800 p.p.m. was added to feed mixtures fed turkey poults two and three weeks posthatching, respectively, to induce acute experimental cardiomyopathy. Poults in the control pen received the same ration but without FZ. From EKG data obtained at 2, 4, and 5 weeks of age, control unaffected and experimental affected poults were selected for sacrifice. Poults were sacrificed by cervical dislocation and appropriate samples of hepatic tissue were removed for assays of activity of alpha-1, 4-glucosidase. Results indicate that enzyme activity in affected FZ-treated poults is similar to that in unaffected control poults. Lack of significant differences in activity of this lysosomal enzyme suggests that FZ-induced glycogenosis may be related to the adult form of idiopathic generalized glucogenosis, the etiology of which remains unidentified.

Animals↗
PubMed1980

Distribution of myocardial glycogen in turkey poults during development of furazolidone-induced cardiomyopathy.

Furazolidone (FZ) at 700 ppm was added to feed mixtures fed turkey poults two weeks posthatching to induce experimental cardiomyopathy. Poults in the control pen received the same ration but without FZ. From ECG data obtained at weekly intervals, poults were selected for sacrifice at 3, 4, and 5 weeks of age. Myocardial samples from the right and left ventricular free walls were analyzed for glycogen by biochemical assay technics. Levels of glycogen were significantly (p less than .01) elevated in the FZ-treated poults at 3, 4, and 5 weeks of age. At all ages, the increase occurred in both the acid-soluble (TCA) and acid-insoluble (KOH) fractions with a proportionately greater increase in the TCA fraction. Results suggest that the effect of FZ on myocardial glycogen metabolism occurs very early and is more pronounced in the right ventricle than in the left ventricle even though both chambers may exhibit similar gross changes.

Animals↗
PubMed1981

Effect of furazolidone on plasma enzyme and protein levels in turkey poults.

Furazolidone (FZ) at a dose of 700 ppm was fed to turkey poults beginning at 2 weeks of age. In trial 1, plasma collected by venipuncture was assayed for glutamic oxalacetic transaminase (GOT), lactate dehydrogenase (LDH), and total protein at 19, 23, 26, and 30 days of age. Significant (P less than or equal to .05) differences were noted only in levels of plasma LDH, which were elevated in FZ-fed poults at all stages studied. In Trial 2, plasma collected by venipuncture was assayed for creatine phosphokinase (CPK), GOT, glutamic pyruvic transaminase (GPT), and LDH daily from 15 through 19 days of age and for protein at 19 days of age. Significant elevations (P less than or equal to .05) were noted in levels of plasma a) CPK at 15 days, b) GOT at 18 days, and c) LDH at 17 and 19 days. A significant (P less than or equal to .01) depression in plasma protein was observed at 19 days. Plasma GPT was either absent or present in very low concentrations. These data suggest that FZ exerts its primary effect on the myocardium. THe initial myocardial changes occur prior to their detection by known electrocardiographic (ECG) technics.

Animals↗
PubMed1983

Monoamine oxidase inhibition and furazolidone-induced cardiomyopathy in turkey poults.

Furazolidone (FZ), a potent inhibitor of monoamine oxidase (MAO), fed at concentrations of 700 ppm to turkey poults 2 through 5 weeks of age, produces cardiomyopathy and cardiomegaly. To determine the role of MAO inhibition in FZ-induced cardiomyopathy, the effects of FZ were compared with those of a chemically different MAO inhibitor, tranylcypromine (TCP), and a chemically similar non-MAO inhibitor, nitrofurazone (NFZ). At 14 days of age, poults were divided randomly into four groups. Control poults were fed a standard turkey starter ration, and poults in the experimental groups were fed the standard ration that included one of the following drugs at the given concentrations: 700 ppm FZ, 350 ppm NFZ, or 50 ppm TCP. Activity of MAO was assayed in liver and kidney homogenates from poults chosen at random at 14, 17, 21, 28, and 35 days of age in one trial and on heart homogenates at 14, 15, 17, 19, and 28 days of age in another trial. Development of cardiomyopathy was assessed using an electrocardiographic (ECG) technique and substantiated with necropsy examination. Inhibition of MAO was observed only in the heart in FZ-fed poults, only in the kidney in NFZ-fed poults, and in all three tissues studied in TCP-fed poults. Under the conditions of this study, an increase in the incidence of cardiomyopathy, based on ECG data and necropsy results, occurred only in the FZ-fed group. The inability of the potent MAO inhibitor, TCP, to produce cardiomyopathy in this study supports the conclusion that the primary mechanism of FZ-induced cardiomyopathy in turkey poults is probably not due to MAO inhibition.

Animals↗
PubMed2001

High-performance liquid chromatographic determination of carbadox, olaquindox, furazolidone, nitrofurazone, and nitrovin in feed.

A high-performance liquid chromatography with gradient programming method was developed to determine the amount of carbadox (CBX), olaquindox (OLQ), furazolidone (FZ), nitrofurazone (NF), and nitrovin (NTV) in feed simultaneously. Complete separation of the drugs was obtained using a C8 silica gel column with gradients of acetonitrile as mobile phase. The mobile phase used an acetonitrile gradient with an initial hold time of 1 min at 0% acetonitrile, followed by an increase to 50% acetonitrile over 10 min. The correlation coefficients (r) for calibration curves of the five feed additives were greater than 0.999. The relative standard deviations (RSDs) of peak areas from four injections for these drugs at three concentrations were less than 3.0%, although the RSD for NTV at 5 ppm was somewhat large (6.7%). The medicated feeds were extracted by pretreating with water, extracted with 95% dimethylformamide overnight at room temperature, and cleaned up on a column of alumina oxide. Recoveries of CBX, OLQ, FZ, NF, and NTV from low level spiked feed were 102.0, 94.6, 97.4, 110.6, and 66.0%, respectively, and from high level spiked feed, they were 114.09, 99.1, 97.3, 109.9, and 62.7%, respectively.

Animal Feed↗
PubMedDate not supplied

Blood glucose and tissue glycogen levels in turkey poults with spontaneous round heart disease and furazolidone-induced cardiomyopathy.

Furazolidone (FZ) at 700 ppm was added to feed mixtures fed turkey poults two weeks posthatching to induce acute experimental cardiomyopathy. Poults in the control pen received the same ration but without FZ. Four of the control poults developed spontaneous round heart disease. From EKG data and blood samples obtained at weekly intervals, poults were selected for sacrifice at 5 weeks of age. Tissue samples from the left myocardial wall, liver, and pectoralis major and tibialis anterior muscles were analyzed for glycogen by biochemical assay. Blood glucose was determined with the Technicon autoanalyzer. Deposition of glycogen increased significantly (p less than 0.05) in the myocardium of all affected poults and in the liver of all FZ-treated poults. Glycogen levels of the pectoralis major and tibialis anterior muscles were not affected by FZ, but a significant increase (p less than 0.05) was apparent in the pectoralis major muscle of spontaneous round heart poults. It was concluded that FZ influences glycogen metabolism, probably by enzyme inhibition, and that it tends to magnify effects seen in the spontaneous round heart syndrome. Glycogen infiltration of tissues such as the heart and white skeletal muscle suggests that the round heart syndrome may be a manifestation of the glycogen storage disease, idiopathic generalized glycogenosis. Lack of significant differences in the blood serum glucose levels of all poults indicates that these levels are not a reliable clinical parameter for monitoring development of the round heart syndrome.

Animals↗
PubMedDate not supplied

Effect of furazolidone on heart weights and myocardial moisture content in turkey poults.

Furazolidone (FZ) at 700 ppm in feed mixtures fed turkey poults from 2 to 5 weeks posthatching significantly increased the ratio of heart weight to body weight (p less than 0.001) and myocardial moisture content (p less than 0.05). The increase in myocardial moisture content is believed to be related to increased glycogen deposition under the influence of FZ since FZ removal from the diet decreased myocardial glycogen levels and moisture content to normal levels.

Animals↗
PubMedDate not supplied

[Long term observation of children with Giardia intestinalis invasion treated with metronidazole and furazolidone].

The results of a long-term (3-year) follow-up of children infected with G. intestinalis treated with metronidazole and furazolidone are presented. Therapy was effective in 84-95% of cases, depending of the duration or the follow-up. Repetition of therapy with tinidazole was indicated in 5% of children after 6 months and in 15% of children after 1 and 2 years of observation because of persisting symptoms of the infection or recurrence. More frequent the treatment was necessary in children under 3 years of age. Some (14%) children required milk free diet and in a few cases (underlying disease--coeliac) gluten-free diet or a diet free of main allergens.

Adolescent↗
PubMed1990

Toxicological and biological studies on Japanese quails fed graded levels of furazolidone.

Furazolidone (FZ) was administered to 42-day-old female Japanese quails as a feed additive at doses of 0, 200, 400, 600 and 800 ppm for a period of 28 days. Dose-dependent effects were observed. High levels of FZ (600 and 800 ppm) significantly altered growth, decreased feed consumption, caused marked atrophy of the ovaries and oviducts leading to cessation of egg laying, and resulted in higher mortality. Hepatotoxicity was evidenced by an increase in serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase and a decrease in serum total protein, in addition to degenerative changes of the hepatocytes in FZ-treated birds. A rise in serum urea was also observed. Symptoms leading to death included a loss of appetite causing emaciation followed by nervous disturbances (compulsive movements and circling). No signs of cardiomyopathy were observed. Japanese quails did not tolerate FZ at a concentration (400 ppm) recommended for the prevention of salmonellosis in poultry.

Animals↗
PubMedDate not supplied

[Sensitivity of enteropathogenic bacteria to furazolidone].

The sensitivity in vitro of 348 strains of 18 enteropathogen agents to furazolidone was investigated during the period of 1987-1989. All strains of Shigella sonnei (17), S. flexneri (17), S. boydii (16), Escherichia coli enteropathogen (40), E. coli enteroinvasive (20), Campylobacter jejuni (50), Vibrio cholerae 01 (5), Vibrio cholerae non 01 (5), V. parahaemolyticus (5), V. alginolyticus (2), Aeromonas hydrophila (5), A. caviae (5), A. sobria (5), and Plesiomonas shigelloides (12) were sensitive (MIC < or = 8 mg/l), except a strains of E. coli enteropathogen (MIC 16 mg/l). The 15.5% of the 51 strains of Salmonella enterica belonging to the type I isolated between 1987 and 1989 were resistant (MIC > or = 16 mg/l). A similar degree of resistance was observed in 20 strains of this agent isolated between 1978 and 1980. The 30 strains of Yersinia (including 15 strains of Y. enterocolitica 03) presented extreme values of MICs of 8 and 16 mg/l.

Dose-Response Relationship, Drug↗
PubMedDate not supplied

Cystic testicular degeneration in furazolidone toxicosis of sexually immature ducks.

Cystic testicular tubular dilatation was seen in ducklings fed a ration containing furazolidone at 250, 400, 550, or 700 ppm for 28 days. Gross evidence of cystic testicular dilatation was observed at necropsy in 16% (32/203) of the ducklings that survived to the end of the study. Gross testicular lesions consisted of various degrees of enlargement with increased translucency in moderately to severely enlarged testicles. Histological evidence of cystic testicular dilatation was present in 45% (41/91) of the testicles examined. Histologically, the tubules were in various states of dilatation with attenuation of the seminiferous epithelium proportional to the severity of dilatation. In the most severely affected testicles, tubules were greatly dilated, distorted, and fluid-filled, with extensively flattened epithelium visible on the inner margin of the tubule as a thin rim of cytoplasm with a protuberant nucleus. Interstitial tissues were compressed to thin septa between the dilated tubules.

Animals↗
PubMedDate not supplied

Furazolidone toxicity in neomycin-treated turkey poults.

Furazolidone (FZ) toxicity was evaluated in turkey poults treated with neomycin at a dose of 20 mg/kg body weight for 5, 10, or 26 days. Neomycin treatment had no effect on FZ-induced anorexia, delayed the onset of altered electrocardiographic patterns by approximately 1 week, and did not significantly affect the development of FZ-induced cardiomyopathy. Data indicated that FZ toxicity is not significantly altered by the gut microflora.

Animals↗
PubMed1988

Topically applied furazolidone or parenterally administered oxytetracycline for the treatment of infectious bovine keratoconjunctivitis.

The effectiveness of topically applied furazolidone (FZ) or parenterally administered oxytetracycline (OTC) for treatment of infectious bovine keratoconjunctivitis was determined in a field study. Between June 13 and Aug 6, 1985, a study was conducted on a ranch in northern California. Eyes of Hereford calves (n = 103) were examined 3 times each week for 7 weeks. After daily examinations on June 13 and 14, calves were allotted randomly to 3 groups. On June 17, calves (that had corneal ulcers) of groups 1 (n = 35) and 2 (n = 35) were treated with OTC and FZ, respectively. Treatments were administered again only if new ulcers were observed, if an existing ulcer worsened, or if a healed ulcer recurred. Calves of group 3 remained untreated (controls). Corneal ulcers developed in 35 of the FZ-treated calves, in 33 of the OTC-treated calves, and in 33 of the untreated calves. Corneal perforations were observed in 3 untreated and 2 FZ-treated calves but were not observed in any OTC-treated calves. Panophthalmitis developed in one eye of an untreated calf. Corneal ulcers in the OTC-treated calves were smaller and healed more rapidly than did corneal ulcers in calves of the other groups. By the 22nd day of the study (July 3), the number of OTC-treated calves with corneal ulcers was less than that of the other 2 groups. Calves of the OTC treatment group had the fewest multiple corneal ulcer recurrences, but calves of all 3 groups had a similar number of single corneal ulcer recurrences.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗
PubMedDate not supplied

Furazolidone-associated cardiomyopathy in two Indiana flocks of ducklings.

Furazolidone (FZ)-induced congestive cardiomyopathy was diagnosed as the cause of high mortality and unthriftiness in two flocks of white pekin ducklings. Cumulative mortality at 7 weeks of age was 10.0-14.4%. Samples of FZ-supplemented feeds fed to flocks 1 and 2 from day 1 to day 14 had 140 and 150 mg FZ/kg, respectively. Both flocks had various degrees of water restriction. Clinically, the ducklings had dyspnea, incoordination, and abdominal distention. Necropsy findings included pulmonary edema and congestion, ascites, atrophic congested livers covered with sheets of fibrin, and cardiac enlargement with biventricular dilatation. Cardiac alterations were minimal by light microscopy. Ultrastructurally, scattered myocytes had myofibrillar lysis. These outbreaks occurred following intake of FZ at therapeutic dosages and emphasize the high susceptibility of young ducklings to FZ cardiotoxicity.

Animals↗
PubMed1979

High pressure liquid chromatographic detection and estimation of furazolidone and nitrofurazone in animal feeds.

The feed sample is extracted with acetone or dimethylformamide-acetone (1 + 1) and the filtered extracts are evaporated to dryness. The residue is dissolved in chloroform and transferred to a silica gel column. The nitrofurans are eluted with methanol-chloroform (50 + 50). A portion of the eluate is evaporated to dryness and the residue is redissolved in a small volume of methanol. Aliquots of the methanolic solution are injected into a liquid chromatograph with a muBondapak C18 column, using 30% acetonitrile as the eluting solvent and ultraviolet detection at 365 nm. Several samples spiked with 0.5--50 ppm furazolidone or nitrofurazone and 2 commercial samples were analyzed by the proposed method.

Animal Feed↗