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PubMed1978

In vitro susceptibility of Mycoplasma hyopneumoniae and Mycoplasma hyorhinis to fifty-one antimicrobial agents.

By a tube dilution assay technique, 51 antimicrobial agents were singly tested against 9 strains of Mycoplasma hyopneumoniae and 1 strain of M. hyorhinis for the purpose of obtaining information useful for selecting an agent for testing in vivo against porcine mycoplasmal pneumonia. Based on determining minimal inhibitory concentrations and chemically grouping the agents into nine classes, all M. hyopneumoniae strains were found resistant to penicillins and peptides and susceptible to sulfonamides and tetracyclines, and, in other classes, were either susceptible or resistant depending on the particular agent being tested. Strains were susceptible to the same 33 of the 51 agents. Minimal inhibitory concentrations ranged from 0.06 to 9.20 mug/ml. M. hyorhinis was susceptible to 19 of the 33 agents that M. hyopneumoniae was susceptible to. Minimal inhibitory concentrations ranged from 0.03 to 8.10 mug/ml. All strains of M. hyopneumoniae differed from M. hyorhinis in that they were susceptible to cephaloglycin and nitrofurazone.

Anti-Bacterial Agents↗
PubMed1984

Antibacterial activities of nitrothiazole against Campylobacter jejuni and Campylobacter coli.

Niridazole (Ambilhar) and three other newly synthesized nitrothiazole derivatives were highly active against 19 microaerophilic campylobacters (minimum concentration required to inhibit 50% of strains [MIC50], 0.0075 to 0.015 mg/liter). There were, however, considerable differences in the susceptibility among strains tested, and one nitrothiazole derivative was rather inactive (MIC50, 2 mg/liter). Nitroimidazole derivatives, such as metronidazole and tinidazole, were less active (MIC50, 2 and 4 mg/liter, respectively). The nitrofuran derivatives, such as nitrofurazone and nitrofurantoin, were also less active (MIC50, 1 mg/liter). Niridazole and another potent nitrothiazole derivative killed the campylobacters rapidly at low concentrations. In contrast, much higher concentrations of metronidazole were required to achieve bactericidal values.

Anti-Bacterial Agents↗
PubMed2002

Enzymes associated with reductive activation and action of nitazoxanide, nitrofurans, and metronidazole in Helicobacter pylori.

Nitazoxanide (NTZ) is a redox-active nitrothiazolyl-salicylamide prodrug that kills Helicobacter pylori and also many anaerobic bacterial, protozoan, and helminthic species. Here we describe development and use of a spectrophotometric assay, based on nitroreduction of NTZ at 412 nm, to identify H. pylori enzymes responsible for its activation and mode of action. Three enzymes that reduce NTZ were identified: two related NADPH nitroreductases, which also mediate susceptibility to metronidazole (MTZ) (RdxA and FrxA), and pyruvate oxidoreductase (POR). Recombinant His-tagged RdxA, FrxA, and POR, overexpressed in nitroreductase-deficient Escherichia coli, each rapidly reduced NTZ, whereas only FrxA and to a lesser extent POR reduced nitrofuran substrates (furazolidone, nitrofurantoin, and nitrofurazone). POR exhibited no MTZ reductase activity either in extracts of H. pylori or following overexpression in E. coli; RdxA exhibited no nitrofuran reductase activity, and FrxA exhibited no MTZ reductase activity. Analysis of mutation to rifampin resistance (Rif(r)) indicated that NTZ was not mutagenic and that nitrofurans were only weakly mutagenic. Alkaline gel DNA electrophoresis indicated that none of these prodrugs caused DNA breakage. In contrast, MTZ caused DNA damage and was strongly mutagenic. We conclude that POR, an essential enzyme, is responsible for most or all of the bactericidal effects of NTZ against H. pylori. While loss-of-function mutations in rdxA and frxA produce a Mtz(r) phenotype, they do not contribute much to the innate susceptibility of H. pylori to NTZ or nitrofurans.

Biotransformation↗
PubMed1978

Antibiotic resistance patterns of gram-negative bacteria isolated from environmental sources.

A total of 2,445 gram-negative bacteria belonging to fecal coliform, Pseudomonas, Moraxella, Acinetobacter, and Flavobacterium-Cytophaga groups were isolated from the rivers and bay of Tillamook, Oregon, and their resistances to chloramphenicol (25 microgram/ml), streptomycin (10 microgram/ml), ampicillin (10 microgram/ml), tetracycline (25 microgram/ml), chlortetracycline (25 microgram/ml), oxytetracycline (25 microgram/ml), neomycin (50 microgram/ml), nitrofurazone (12.5 microgram/ml), nalidixic acid (25 microgram/ml), kanamycin (25 microgram/ml), and penicillin G (10 IU/ml) were determined. Among fecal coliforms the bay isolates showed greater resistance to antibiotics than those from tributaries or surface runoff. No such well-defined difference was found among other bacterial groups. The antibiotic resistance patterns of gram-negative bacteria from different sources correlated well, perhaps indicating their common origin. The antibiotic resistance patterns of gram-negative bacteria of different general also correlated well, perhaps indicating that bacteria which share a common environment also share a common mode for developing antibiotic resistance.

Anti-Bacterial Agents↗
PubMed2003

Vibrio harveyi nitroreductase is also a chromate reductase.

The chromate reductase purified from Pseudomonas ambigua was found to be homologous with several nitroreductases. Escherichia coli DH5alpha and Vibrio harveyi KCTC 2720 nitroreductases were chosen for the present study, and their chromate-reducing activities were determined. A fusion between glutathione S-transferase (GST) and E. coli DH5alpha NfsA (GST-EcNfsA), a fusion between GST and E. coli DH5alpha NfsB (GST-EcNfsB), and a fusion between GST and V. harveyi KCTC 2720 NfsA (GST-VhNfsA) were prepared for their overproduction and easy purification. GST-EcNfsA, GST-EcNFsB, and GST-VhNFsA efficiently reduced nitrofurazone and 2,4,6-trinitrotoluene (TNT) as their nitro substrates. The K(m) values for GST-EcNfsA, GST-EcNfsB, and GST-VhNfsA for chromate reduction were 11.8, 23.5, and 5.4 micro M, respectively. The V(max) values for GST-EcNfsA, GST-EcNfsB, and GST-VhNfsA were 3.8, 3.9, and 10.7 nmol/min/mg of protein, respectively. GST-VhNfsA was the most effective of the three chromate reductases, as determined by each V(max)/K(m) value. The optimal temperatures of GST-EcNfsA, GST-EcNfsB, and GST-VhNfsA for chromate reduction were 55, 30, and 30 degrees C, respectively. Thus, it is confirmed that nitroreductase can also act as a chromate reductase. Nitroreductases may be used in chromate remediation. GST-EcNfsA, GST-EcNfsB, and GST-VhNfsA have a molecular mass of 50 kDa and exist as a monomer in solution. Thin-layer chromatography showed that GST-EcNfsA, GST-EcNfsB, and GST-VhNfsA contain FMN as a cofactor. GST-VhNfsA reduced Cr(VI) to Cr(III). Cr(III) was much less toxic to E. coli than Cr(VI).

Cloning, Molecular↗
PubMed1967

Survey of chemical compounds tested in vitro against rumen protozoa for possible control of bloat.

Over 170 chemical agents were screened for antiprotozoal action in bovine ruminal fluid. Compounds were tested at 0.1 and 0.05% concentrations. Tested compounds included inorganic compounds, antibiotics, biocides, neuromuscular agents, arsenicals, plant and animal hormones, antimalarials, surface-active agents, anthelmintics, and many others. The most active compounds were cupric sulfate, nickel sulfate, nitrofurazone, hydrogen peroxide, dodecyl sodium sulfate, pelargonic acid, iodoacetic acid, 1-diethylaminoethylamino-4-methylthiaxanthrone, sodium arsanilate, sodium arsenate, bismuth glycolyl arsanilate, 1-beta-hydroxyethyl-2-methyl-5-nitroimidazole, and p-nitroaniline. Copper ion was not particularly effective against entodinia; nickel ion had no effect on holotrichs. Hydrogen peroxide and iodoacetic acid were effective at a concentration of 0.005%. Anionic surface-active agents were very effective, especially long-chain sulfates and phosphates. These antiprotozoal agents warrant further in vivo studies for possible use in treating or curing bloat in ruminants.

Animals↗
PubMed2006

Role of Pseudomonas aeruginosa dinB-encoded DNA polymerase IV in mutagenesis.

Pseudomonas aeruginosa is a human opportunistic pathogen that chronically infects the lungs of cystic fibrosis patients and is the leading cause of morbidity and mortality of people afflicted with this disease. A striking correlation between mutagenesis and the persistence of P. aeruginosa has been reported. In other well-studied organisms, error-prone replication by Y family DNA polymerases contributes significantly to mutagenesis. Based on an analysis of the PAO1 genome sequence, P. aeruginosa contains a single Y family DNA polymerase encoded by the dinB gene. As part of an effort to understand the mechanisms of mutagenesis in P. aeruginosa, we have cloned the dinB gene of P. aeruginosa and utilized a combination of genetic and biochemical approaches to characterize the activity and regulation of the P. aeruginosa DinB protein (DinB(Pa)). Our results indicate that DinB(Pa) is a distributive DNA polymerase that lacks intrinsic proofreading activity in vitro. Modest overexpression of DinB(Pa) from a plasmid conferred a mutator phenotype in both Escherichia coli and P. aeruginosa. An examination of this mutator phenotype indicated that DinB(Pa) has a propensity to promote C-->A transversions and -1 frameshift mutations within poly(dGMP) and poly(dAMP) runs. The characterization of lexA+ and DeltalexA::aacC1 P. aeruginosa strains, together with in vitro DNA binding assays utilizing cell extracts or purified P. aeruginosa LexA protein (LexA(Pa)), indicated that the transcription of the dinB gene is regulated as part of an SOS-like response. The deletion of the dinB(Pa) gene sensitized P. aeruginosa to nitrofurazone and 4-nitroquinoline-1-oxide, consistent with a role for DinB(Pa) in translesion DNA synthesis over N2-dG adducts. Finally, P. aeruginosa exhibited a UV-inducible mutator phenotype that was independent of dinB(Pa) function and instead required polA and polC, which encode DNA polymerase I and the second DNA polymerase III enzyme, respectively. Possible roles of the P. aeruginosa dinB, polA, and polC gene products in mutagenesis are discussed.

Bacterial Proteins↗
PubMed1998

Oxygen-insensitive nitroreductases: analysis of the roles of nfsA and nfsB in development of resistance to 5-nitrofuran derivatives in Escherichia coli.

Nitroheterocyclic and nitroaromatic compounds constitute an enormous range of chemicals whose potent biological activity has significant human health and environmental implications. The biological activity of nitro-substituted compounds is derived from reductive metabolism of the nitro moiety, a process catalyzed by a variety of nitroreductase activities. Resistance of bacteria to nitro-substituted compounds is believed to result primarily from mutations in genes encoding oxygen-insensitive nitroreductases. We have characterized the nfsA and nfsB genes of a large number of nitrofuran-resistant mutants of Escherichia coli and have correlated mutation with cell extract nitroreductase activity. Our studies demonstrate that first-step resistance to furazolidone or nitrofurazone results from an nfsA mutation, while the increased resistance associated with second-step mutants is a consequence of an nfsB mutation. Inferences made from mutation about the structure-function relationships of NfsA and NfsB are discussed, especially with regard to the identification of flavin mononucleotide binding sites. We show that expression of plasmid-carried nfsA and nfsB genes in resistant mutants restores sensitivity to nitrofurans. Among the 20 first-step and 53 second-step mutants isolated in this study, 65 and 49%, respectively, contained insertion sequence elements in nfsA and nfsB. IS1 integrated in both genes, while IS30 and IS186 were found only in nfsA and IS2 and IS5 were observed only in nfsB. Insertion hot spots for IS30 and IS186 are indicated in nfsA, and a hot spot for IS5 insertion is evident in nfsB. We discuss potential regional and sequence-specific determinants for insertion sequence element integration in nfsA and nfsB.

Amino Acid Sequence↗
PubMed1979

The mutagenic activity of 61 agents as determined by the micronucleus, Salmonella, and sperm abnormality assays.

A comparison of two rapid and inexpensive in vivo mammalian assays and the Ames Salmonella assay is presented for 61 agents; Acetylsalicylic acid; Acriflavine; Actinomycin D; 2(2-furyl)-3-(5-nitro-2-furyl)acrylamide (AF-2); Aflatoxin B1; 2-aminofluorene; Aminopterin; Aroclor 1254; Ascorbic acid; Azathioprine; Benzo(a)pyrene; 5-Bromo-2'-deoxyuridine; Busulphan, Butylated hydroxytoluene; Cadmium chloride; Caffeine; Calcium cyclamate; Chloral hydrate; Chloromycetin succinate; Codeine phosphate, Colchicine; Cycloheximide; Cyclophosphamide; DDT; 2,4-Diaminoanisole; Dibutylnitrosamine; 9, 10 Dimethyl-1,2-benzanthracene; 1,1-Dimethylhydrazine; Dimethylnitrosamine; Epinephrine; Ethyl methane sulphonate (EMS); 2-formylamino-4-(5-nitro-2-furyl)thiazole (FANFT); 2-(2-formylhydrazino)-4-(5-nitro-2-furyl)thiazole (FNT); Glucose, Griseofulvin; Hycanthone methane sulphonate; Hydroxyurea; 5-Iodo-2'-deoxyuridine; Lead acetate; Mechlorethamine; 3-Methylcholanthrene; Methyl mercury acetate; Methyl methane sulfonate (MMS); N-methyl-N-nitro-N'-nitrosoguanidine; Mitomycin C; Monosodium glutamate; 1-Naphthalamine; 2-Naphthalamine; Nitrofurazone; 4-Nitro-O-phenylene diamine; 4-Nitro-quinoline-1-oxide (4-NQO); Phenobarbitone; Procarbazine; Quinacrine dihydrochloride; Radiation (gamma-rays); Sodium chloride; Triethylene thiophosphoramide; Trimethyl phosphate; Tris(2-methyl-1-arizidinyl) phosphine oxide; Urethan; Vinblastine. The results support the concept of multiple assays for mutagenicity and show that some combinations of assays are superior to others.

Animals↗
PubMed2000

Type I nitroreductases in soil enterobacteria reduce TNT (2,4,6,-trinitrotoluene) and RDX (hexahydro-1,3,5-trinitro-1,3,5-triazine).

Many enteric bacteria express a type I oxygen-insensitive nitroreductase, which reduces nitro groups on many different nitroaromatic compounds under aerobic conditions. Enzymatic reduction of nitramines was also documented in enteric bacteria under anaerobic conditions. This study indicates that nitramine reduction in enteric bacteria is carried out by the type I, or oxygen-insensitive nitroreductase, rather than a type II enzyme. The enteric bacterium Morganella morganii strain B2 with documented hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) nitroreductase activity, and Enterobacter cloacae strain 96-3 with documented 2,4,6-trinitrotoluene (TNT) nitroreductase activity, were used here to show that the explosives TNT and RDX were both reduced by a type I nitroreductase. Morganella morganii and E. cloacae exhibited RDX and TNT nitroreductase activities in whole cell assays. Type I nitroreductase, purified from E. cloacae, oxidized NADPH with TNT or RDX as substrate. When expression of the E. cloacae type I nitroreductase gene was induced in an Escherichia coli strain carrying a plasmid, a simultaneous increase in TNT and RDX nitroreductase activities was observed. In addition, neither TNT nor RDX nitroreductase activity was detected in nitrofurazone-resistant mutants of M. morganii. We conclude that a type I nitroreductase present in these two enteric bacteria was responsible for the nitroreduction of both types of explosive.

Enterobacter cloacae↗
PubMed2004

Severe facial dermatitis as a late complication of aesthetic rhinoplasty; a case report.

BACKGROUND: Contact dermatitis, as a cutaneous complication after rhinoplasty, is of early onset, limited and transient. The cause of this dermatitis is irritant or allergic. Late onset skin complications are rare and non-inflammatory. CASE PRESENTATION: We are reporting an unexpected, severe allergic contact dermatitis of the face, in a young female, appearing one month following aesthetic rhinoplasty. She failed to respond to ordinary treatments for dermatitis. We did standard battery--including nitrofurazone, tincture of benzoin and hydrocortisone--patch test for the patient that showed sensitivity to benzoin and corticosteroid. CONCLUSIONS: In summary we report a case of a severe allergic contact dermatitis of the face, in a 21-year-old girl who underwent corrective aesthetic rhinoplasty, appearing one month following surgical operation. We were unable to find a similar report in the medical literature.

Adult↗
PubMed1987

Ovarian toxicity and carcinogenicity in eight recent National Toxicology Program studies.

Ovarian toxicity and/or carcinogenicity has been documented for at least eight chemicals recently tested in National Toxicity Program prechronic and chronic rodent studies. The chemicals that yielded treatment-related ovarian lesions were 1,3-butadiene, 4-vinylcyclohexene, vinylcyclohexene deipoxide, nitrofurantoin, nitrofurazone, benzene, delta-9-tetrahydrocannabinol, and tricresylphosphate. Typical nonneoplastic ovarian changes included hypoplasia, atrophy, follicular necrosis, and tubular hyperplasia. The most commonly observed treatment-related neoplasms were granulosa cell tumors and benign mixed tumors. A relationship between antecedent ovarian hypoplasia, atrophy, and hyperplasia and subsequent ovarian neoplasia is supported by some of these National Toxicology Program studies. Pathologic changes in other tissues such as the adrenal glands and uterus were associated with the treatment-related ovarian changes.

Animals↗
PubMed1999

The use of a modified Dakin's solution (sodium hypochlorite) in the treatment of Vibrio vulnificus infection.

We report the first clinical use of a modified Dakin's solution (0.025% sodium hypochlorite [NaOCl]) to halt the progress of severe cutaneous Vibrio vulnificus infection in a critically ill patient. The regimen used arose from an initial in vitro study designed to examine the sensitivity of Vibrio species to topical antimicrobial agents. Twenty-eight wound isolates were tested against the following eight topical preparations: silver sulfadiazine (Silvadene), nitrofurazone, mupirocin ointment (Bactroban), polymyxin B/bacitracin, mafenide acetate (Sulfamylon), nystatin/Silvadene, nystatin/polymyxin B/bacitracin, and 0.025% NaOCl solution. The results showed that V vulnificus, along with the other 18 Vibrio species tested, was most sensitive to the modified NaOCl solution.

Administration, Cutaneous↗
PubMed2002

A critical review on Chagas disease chemotherapy.

In this "Critical Review" we made a historical introduction of drugs assayed against Chagas disease beginning in 1912 with the works of Mayer and Rocha Lima up to the experimental use of nitrofurazone. In the beginning of the 70s, nifurtimox and benznidazole were introduced for clinical treatment, but results showed a great variability and there is still a controversy about their use for chronic cases. After the introduction of these nitroheterocycles only a few compounds were assayed in chagasic patients. The great advances in vector control in the South Cone countries, and the demonstration of parasite in chronic patients indicated the urgency to discuss the etiologic treatment during this phase, reinforcing the need to find drugs with more efficacy and less toxicity. We also review potential targets in the parasite and present a survey about new classes of synthetic and natural compounds studied after 1992/1993, with which we intend to give to the reader a general view about experimental studies in the area of the chemotherapy of Chagas disease, complementing the previous papers of Brener (1979) and De Castro (1993).

Chagas Disease↗
PubMed1990

Current treatment recommendations for topical burn therapy.

Infections in burn patients continue to be the primary source of morbidity and mortality. Topical antimicrobial therapy remains the single most important component of wound care in hospitalised burn patients. The goal of prophylactic topical antimicrobial therapy is to control microbial colonisation and prevent burn wound infection. In selected clinical circumstances topical agents may be used to treat incipient or early burn wound infections. At the present time silver sulfadiazine is the most frequently used topical prophylactic agent; it is relatively inexpensive, easy to apply, well tolerated by patients, and has good activity against most burn pathogens. In patients with large burns the addition of cerium nitrate to silver sulfadiazine may improve bacterial control. Mafenide acetate has superior eschar-penetrating characteristics, making it the agent of choice for early treatment of burn wound sepsis. However, the duration and area of mafenide application must be limited because of systemic toxicity associated with prolonged or extensive use. Other agents, such as nitrofurazone or chlorhexidine preparations, may be useful in isolated clinical situations. The undesirable side effects of silver nitrate solution limit its use by most clinicians at the present time.

Administration, Topical↗
PubMed1991

Inhibition of microsomal lipid peroxidation and cytochrome P-450-catalyzed reactions by nitrofuran compounds.

(5-Nitro-2-furfurylidene)amino compounds bearing triazol-4-yl, benzimidazol-1-yl, pyrazol-1-yl, triazin-4-yl or related groups (a) stimulated superoxide anion radical generated by rat liver microsomes in the presence of NADPH and oxygen; (b) inhibited the NADPH-dependent, iron-catalyzed microsomal lipid peroxidation; (c) prevented the NADPH-dependent destruction of cytochrome P-450; (d) inhibited the NADPH-dependent microsomal aniline 4-hydroxylase activity; (e) failed to inhibit either the cumenyl hydroperoxide-dependent lipid peroxidation or the aniline-4-hydroxylase activity, except for the benzimidazol-1-yl and the substituted triazol-4-yl derivatives, which produced minor inhibitions. Reducing equivalents enhanced the benzimidazol-1-yl derivative inhibition of the cumenyl hydroperoxide-induced lipid peroxidation. The ESR spectrum of the benzimidazol-1-yl derivative, reduced anaerobically by NADPH-supplemented microsomes, showed characteristic spin couplings. Compounds bearing unsaturated nitrogen heterocycles were always more active than those bearing other groups, such as nifurtimox or nitrofurazone. The energy level of the lowest unoccupied molecular orbital was in fair agreement with the capability of nitrofurans for redox-cycling and related actions. It is concluded that nitrofuran inhibition of microsomal lipid peroxidation and cytochrome P-450-catalyzed reactions was mostly due to diversion of reducing equivalents from NADPH to dioxygen. Trapping of free radicals involved in propagating lipid peroxidation might contribute to the overall effect of the benzimidazol-1-yl and substituted triazol-4-yl derivatives.

Aniline Hydroxylase↗
PubMedDate not supplied

Engineering out the risk for infection with urinary catheters.

Catheter-associated urinary tract infection (CAUTI) is the most common nosocomial infection. Each year, more than 1 million patients in U.S. acute-care hospitals and extended-care facilities acquire such an infection; the risk with short-term catheterization is 5% per day. CAUTI is the second most common cause of nosocomial bloodstream infection, and studies suggest that patients with CAUTI have an increased institutional death rate, unrelated to the development of urosepsis. Novel urinary catheters impregnated with nitrofurazone or minocycline and rifampin or coated with a silver alloy-hydrogel exhibit antiinfective surface activity that significantly reduces the risk of CAUTI for short-term catheterizations not exceeding 2-3 weeks.

Cross Infection↗
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↗