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PubMed1977

[Immunosuppressive activity of several drugs and their effect on antibody formation in pullorum disease].

Furazolidon given alone or in combination with chloramphenicol, with spectinomycin, with gentamycin or with sodium arsenilate as well as chlorpyrazine, applied alone, suppress the clinical manifestation of pullorum disease in birds both in the experimental and in the spontaneous outbreak of the disease. These medicinal drugs lower the production of agglutinins in birds--mostly the combination furazolidon+chloramphenicol, followed by furazolidon+sodium arsenilate. The same combinations do not prove essentially effective in influencing the development of the morphologic lesions and do not fully exempt the body from the causative agent of pullorum disease.

Agglutinins↗
PubMed2004

[Five-day rabeprazole-based triple therapy for helicobacter pylori infection].

OBJECTIVE: To evaluate the efficacy of a 5-day rabeprazole-based triple therapy regimen for helicobacter pylori infection, and to improve the eradication rates of antibiotic-resistant Helicobacter pylori with rabeprazole plus clarithromycin and furazolidone. METHODS: We selected 95 H. pylori-positive patients with gastric or duodenal ulcers or erosive gastritis and randomized them into 2 groups. The patients were given a 7-day triple standard therapy and 5-day triple standard therapy, consisting of rabeprazole 10 mg twice daily, clarithromycin 500 mg twice daily and furazolidone 100 mg twice daily. H. pylori status was checked by rapid urease test or 14C urea breath test and histology before and 4 weeks after the therapy. RESULTS: The eradication rate of H. pylori for patients under the 5-day treatment vs. 7-day treatment were 77.8% vs. 82% by per protocol and 94.4% vs. 97.6% by intention to treat analysis (no significant comparisons). The ulcer and erosion healing rate was 97.6% vs. 97.8% (no significant comparisons). No major side-effects were reported. CONCLUSION: The 5-day rabeprazole-based triple therapy( combined with clarithromycin and furazolidone) for helicobacter pylori infection is an effective regimen with excellent patient acceptability and compliance.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2006

Antimicrobial resistance of Helicobacter pylori isolates from Iranian adults and children.

BACKGROUND: Helicobacter pylori isolates from 84 adults and 51 children were assessed during the period of 2001 through 2004 to find out whether their susceptibilities to metronidazole, clarithromycin, amoxicillin, tetracycline, and furazolidone differ between the two groups or have changed compared with the results from our previous study done between 1997 - 2000. METHODS: Biopsies from 135 dyspeptic patients were cultured on Brucella blood agar. Pure cultures of H. pylori isolates were used for antibiotic susceptibility tests. Disk diffusion method was recruited to assess the susceptibility of H. pylori isolates to different dilutions of the above mentioned antimicrobials. Results obtained from the two groups were compared and minimum inhibitory concentrations determined. RESULTS: Thirty-five percent of H. pylori isolates from adults and 37% from children were resistant to metronidazole. Clarithromycin resistance rate was 2.4% and 5.9% in H. pylori isolates from adults and children, respectively. Amoxicillin resistance was 2.4% in isolates from adults and 5.9% in isolates from children. Tetracycline resistance rate was 0% in H. pylori isolates from adults and 2.0% in isolates from children. Resistance to furazolidone was not observed. CONCLUSION: Resistance rates of H. pylori isolates from adults and children to metronidazole, clarithromycin, amoxicillin, tetracycline, and furazolidone are similar and not significantly affected by age and time.

Adolescent↗
PubMed1986

The use of furoxone: a perspective.

Acute infectious diarrhoea is a widespread cause of morbidity and mortality. Some of the major diarrhoeal diseases are cholera, typhoid fever, shigellosis (bacillary dysentery), salmonellosis, "travellers' diarrhoea", and giardiasis These diseases can be avoided with proper education, sanitation, and hygiene. However, the majority of these diseases occur most frequently in areas of the world where political and social upheaval, poverty, overcrowding, and a lack of education prevail. Although vaccines are available for some of the diseases, they are not completely effective. Antimicrobial therapy is effective in decreasing the duration and severity of diarrhoea and in reducing the likelihood of relapses, complications, and death. An antimicrobial drug for the treatment of acute infectious diarrhoeal disease must be relatively specific, effective, and safe, and it should not promote the development of resistant bacteria. Furazolidone (Furoxone) has been used for 30 years for the specific and symptomatic treatment of bacterial or protozoal diarrhoea and enteritis caused by susceptible organisms. Its effectiveness has often been shown to be comparable or superior to that of other drugs. In addition, the toxicity of furazolidone is relatively low, and it minimizes the development of resistant organisms. These characteristics should contribute to the continued use of furazolidone as a rational choice in the treatment of acute infectious diarrhoeal diseases that occur worldwide.

Adolescent↗
PubMed1984

Issues in clinical parasitology: the treatment of giardiasis.

Giardiasis is the most common pathogenic parasitic infection in the United States. The choice of a therapeutic agent for treatment of the infection is unclear; of the three drugs commonly used, metronidazole and furazolidone have been shown to be carcinogenic in animal studies, while quinarcrine causes frequent side effects. In order to evaluate the usefulness of these three drugs, eight randomized trials of effectiveness were evaluated. The trials suffered from unclear methods, variability in study populations and total dosage of medication used, inaccuracy in determining outcomes, and inadequate sample sizes. Both metronidazole and quinacrine were more effective than furazolidone (p less than 0.001), but quinacrine caused frequent side effects which may have been responsible for poor compliance. With regard to the carcinogenicity of these compounds, it appears likely that there is no large short-term risk from the use of metronidazole, but long-term follow-up studies have not been done and no clinical studies have been done regarding the risk of furazolidone or quinacrine. The lack of clear confidence in animal studies is evident in the fact that the Food and Drug Administration has approved ongoing studies with drugs related to metronidazole.

Carcinogens↗
PubMed1983

[Nitrofuran poisoning in veal calves].

Prolonged administration of furazolidone to calves may give rise to chronic furazolidone poisoning: retardation of growth, thrombocytopenia and leucopenia, occasionally changing into haemorrhagic diathesis. In acute nitrofuran poisoning neurological signs are observed as a consequence of monoamine oxidase inhibition. Five incidents of acute nitrofuran poisoning on veal calf farms are reported in the present paper, each with a mortality rate varying frm 46.7 per cent ot 70 per cent. Ten times the recommended dose of furazolidone or furadoltone was administered in each case.

Acute Disease↗
PubMed1980

[Drug resistance of Salmonella strains isolated from poultry].

A study was carried out to investigate the sensitivity of 326 salmonella strains with regard to the antibiotics: penicillin, oxacillin, ampicillin, carbenicillin, tetracycline, streptomycin, kanamycin, gentamicin, erythromycin and chloramphenicol and furazolidone. A tendency towards an increase of the salmonella strains resistant to tetracycline was observed. Such a tendency was not found with chloramphenicol, streptomycin, kanamycin, gentamicin, carbenicillin and furazolidone. An idea is endorsed, namely, that an increased use of large-spectre antibiotics for prophylaxis ends and treatment in poultry-raising has not brought about the development of a sufficient medicinal resistance with salmonellas. Medicinal preparations are recommended for keeping down the salmonelloses with poultry--namely, a mixture of chloramphenicol and furazolidone. It is pointed out that on the basis of these studies a good effect is to be expected also of the implementation of gentamicin, kanamycin and carbenicillin.

Animals↗
PubMed1996

N-[5-nitro-2-furfurylidene]-3-amino-2-oxazolidinone activation by the human intestinal cell line Caco-2 monitored through noninvasive electron spin resonance spectroscopy.

The pathways participating in the metabolism of the nitrofuran antimicrobial drug N-[5-nitro-2-furfurylidene]-3-amino-2-oxazolidinone (furazolidone) in intact cells were investigated in the human intestinal cell line Caco-2. One-electron reduction of furazolidone led to the formation of a free radical intermediate that could be monitored in dense cell suspensions by noninvasive electron spin resonance spectroscopy. The effects of enzyme inhibitors on the kinetics of radical production and decay were used to estimate the relative contribution of different enzymes to the reductive activation of the drug. Although many enzymes are known to reduce nitrofurans in vitro (e.g., xanthine oxidase, aldehyde oxidase, DT-diaphorase, mitochondrial redox chain components), their contributions were insignificant in living Caco-2 cells. The first reducing equivalent required for the formation of the nitroanion derivative of furazolidone appeared to be provided essentially by the microsomal cytochrome P450 reductase. This was confirmed through studies of the NADPH-dependent radical formation by microsomes. Differentiated Caco-2 cells, an established enterocyte model, showed only modestly increased radical formation and the same enzyme-specificity pattern as undifferentiated cells. Consistently, only a small increase in P450 reductase activity was found in differentiated cells, in contrast to the 10-fold increase seen in typical differentiation marker enzymes. With the electron spin resonance method that we describe, it is possible to distinguish between sites of bioactivation of redox active drugs in intact cells.

Animals↗
PubMed1976

[The development of antibiotics resistance among Salmonella bacteria of animal origin in the Federal Republic of Germany and Berlin (West). 3rd Communication: 1972 Annual Report (author's transl)].

2273 Salmonella strains received from veterinary laboratories in the Federal Republic of Germany including Berlin (West) in 1972 were examined for their resistance against tetracyclines, ampicillin, chloramphenicol, kanamycin, nitrofurazone, and furazolidone. 13.3% of the strains studied were found to be resistant to one or more of these antibacterial substances. The proportion of resistant strains was 37.5% for S. typhimurium (excluding var. copenhagen), 3.1% for S. typhimurium var. copenhagen and 57% for S. panama. 79.8% of resistant strains were found to belong to these types. From 303 resistant strains found, resistance determinants were present in 87.4% to tetracyclines, in 37.2% to ampicillin, in 15.8% to chloramphenicol, in 4.6% to kanamycin, in 0.9% to furazolidone, and in 1.3% to nitrofurazone. 16 combinations of resistance determinants were found to occur 95.0% of strains transmitted resistance to E. coli K-12. A transmission of resistance determinants to furazolidone and nitrofurazone could not be demonstrated. Resistance patterns differed considerably from one serotype to another.

Ampicillin↗
PubMed1976

[The development of antibiotics resistance among slamonella bacteria of animal origin in the Federal Republic of Germany and Berlin (West). 4th Communication: 1973 Annual Report (author's transl)].

2894 salmonella strains received from veterinary laboratories in the Federal Republic of Germany including Berlin (West) in 1973 were examined for their resistance against tetracyclines, ampicillin, chloramphenicol, kanamycin, nitrofurazone, and furazolidone. 24.4% of the strains studied were found to be resistant to one or more of these antibacterial substances. The proportion of resistant strains was 63.9% for S. typhimurium (excluding var. copenhagen), 6.5% for S. typhimurium var. copenhagen and 51% for S. panama. 81.3% of resistant strains were found to belong to these types. From 708 resistant strains found, resistance determinants were present in 92.9% to tetracyclines in 27.9% to ampicillin, in 22.0% to chloramphenicol, in 13.6% to kanamycin, in 1.4% to furazolidone, and in 1.7% to nitrofurazone. 20 combinations of resistance determinants were found to occur 90.9% of strains transmitted resistance to E. coli K-12. A transmission of resistance determinants to furazolidone and nitrofurazone could not be demonstrated. As in the preceding years, there was a clear difference of resistance patterns from one serotype to another.

Ampicillin↗
PubMed1982

Studies on the induction of sex-linked recessive lethal mutations in Drosophila melanogaster by nitroheterocyclic compounds.

24 nitroheterocyclic compounds were investigated for their capacity to induce sex-linked recessive lethals in Drosophila, by the adult feeding technique, and in some cases injection or larval-feeding methods. Out of 9 5-nitroimidazoles, ZK 26.173 and ZK 25.095 (moxnidazole) were clearly active whereas nimorazole and ronidazole were marginally mutagenic. Out of 10 5-nitrofurans, nitrovin, furazolidone and furaltadone were unambiguously mutagenic, whereas nitrofurantoin was a borderline case. Nitrofurans were active at lower molar concentrations than nitroimidazoles. Out of a group of 5 related nitro compounds (2 nitrothiophenes, picrolonic acid, niridazole and 4-NQO), only 4-NQO was clearly mutagenic, when fed to larvae. Experiments with germ-free flies showed that, for ZK 26.173 and furazolidone, the gut flora of Drosophila do not play a role in the activation of the compounds to mutagenic metabolites. Furazolidone, 4-NAO, ZK 26.173, ZK 25.095 and furaltadone were tested in mal and cin strains, both of which lack xanthine dehydrogenase and aldehyde oxidase. The latter enzyme and xanthine oxidase are known to carry out nitro reduction in mammalian tissues. For ZK 26.173, the mutation frequencies were drastically reduced in the enzyme-deficient strains, indicating the involvement of one of these enzymes in the activation of this substance.

Animals↗
PubMed2001

Antibiotic resistance in Salmonella enterica subsp. enterica strains isolated in Poland from 1998 to 1999.

A total of 326 Salmonella enterica subsp. enterica strains representing 29 serotypes, isolated from human stool specimens during 1998-1999 in sanitary-epidemiological units in Poland were tested for antibiotic susceptibility by a standard disk diffusion method. The antibiotics used were ampicillin, cefotaxime, chloramphenicol, tetracycline, streptomycin, gentamicin, kanamycin, nalidixic acid, ciprofloxacin, furazolidone, cotrimoxazole, sulphonamides and trimethoprim. In addition, 201 strains belonging to the five most commonly isolated serotypes (S. Enteritidis, S. Typhimurium, S. Hadar, S. Infantis and S. Virchow) also had minimal inhibitory concentrations (MICs) determined for amoxycillin/clavulanic acid. Selected strains were screened for production of extended spectrum beta-lactamases (ESBLs). There were 49.4% of Salmonella enterica subsp. enterica strains resistant to two or more antibiotics, with the highest prevalence of multiple resistant strains among serotypes Typhimurium, Hadar and Virchow. Resistance to ampicillin, streptomycin, tetracycline, nalidixic acid, furazolidone and sulphonamides occurred most frequently. Over 93% of S. Virchow strains were resistant to furazolidone. No strains resistant to ciprofloxacin by disk-diffusion method were detected but 31.3% of isolates of the 201 strains representing the five most common serotypes had reduced ciprofloxacin susceptibility (MICs ranging 0.125-0.5 mg/l). One strain (S. Mbandaka) was resistant to cefotaxime and produced ESBL.

Anti-Bacterial Agents↗
PubMed2001

Induction of rat liver cytochrome P450 isoenzymes CYP 1A and CYP 2B by different fungicides, nitrofurans, and quercetin.

The genotoxic activity of environmental xenobiotics is manifested either in their direct interaction with cellular genetic material or in provoking secondary events, among which reactive oxygen species (ROS) production is a common phenomenon. Both pathways can be mediated by the activity of the cytochrome P450 monooxygenase system. We studied induction of the CYP 1A or CYP 2B monooxygenases in rat liver by the fungicides: thiram, captan, captafol, dodine and the drugs: nitrofurazone, furazolidone and the plant flavonoid: quercetin. A cytochrome P450 induction assay (CYPIA test) was used. S9 prepared from livers of rats treated with the test compounds were used to activate ethidium bromide (EtBr) (CYP 1A isoenzyme) or cyclophosphamide (CPA) (CYP 2B isoenzyme) in the Ames test. It was found that among the tested compounds, the most potent inducer of CYP 1A was furazolidone (3 x 80 mg/kg). Less potent was thiram (1 x 100mg/kg), as well as quercetin (3 x 80 mg/kg), and captafol (1 x 30 mg/kg). On the other hand, thiram (1 x 100 mg/kg), captafol (1 x 30 mg/kg), and quercetin (3 x 80 mg/kg) were most potent in the CYP 2B isoenzyme induction, while furazolidone (3 x 80 mg/kg), and nitrofurazone (3 x 80 mg/kg) appeared to be less potent in this respect. Captan and dodine (3 x 80 mg/kg) did not affect the activity of any of the cytochrome P450 isoenzymes.

Animals↗
PubMed1983

Comparative in vitro activities of ten antimicrobial agents against bacterial enteropathogens.

The in vitro susceptibilities of 50 strains of Salmonella spp., 80 strains of Shigella spp., and 50 enterotoxigenic Escherichia coli, 14 Yersinia enterocolitica, 6 Aeromonas hydrophila, 4 Plesiomonas shigelloides, 9 Vibrio parahaemolyticus, and 30 Campylobacter jejuni strains that were recently isolated from worldwide sources were determined for 10 antimicrobial agents. The antimicrobial agents tested included ampicillin, bicozamycin, doxycycline, enoxacin (CI-919), erythromycin, furazolidone, amdinocillin, norfloxacin, trimethoprim, and trimethoprim-sulfamethoxazole. Ampicillin resistance occurred frequently in strains of Salmonella and Shigella spp. and enterotoxigenic E. coli strains. The most active agents against all of the bacteria tested were enoxacin and norfloxacin. Furazolidone and amdinocillin were also highly active against the majority of strains. Trimethoprim and trimethoprim-sulfamethoxazole were inhibitory at low concentrations against all test except C. jejuni isolates. The in vitro results of this study confirm the high prevalence of bacterial resistance to ampicillin. However, this work also identifies four antimicrobial agents, enoxacin, furazolidone, norfloxacin, and amdinocillin, that would be appropriate for further testing in clinical trials.

Anti-Bacterial Agents↗
PubMed2003

Analysis of antimicrobial susceptibility and virulence factors in Helicobacter pylori clinical isolates.

BACKGROUND: In this study, we evaluated the prevalence of primary resistance of Brazilian H. pylori isolates to metronidazole, clarithromycin, amoxicillin, tetracycline, and furazolidone. In addition, the vacA, iceA, cagA and cagE genotypes of strains isolated from Brazilian patients were determined and associated with clinical data in an effort to correlate these four virulence markers and antibiotic resistance. METHODS: H. pylori was cultured in 155 H. pylori-positive patients and MICs for metronidazole, clarithromycin, amoxicillin, tetracycline, and furazolidone were determined by the agar dilution method. Genomic DNA was extracted, and allelic variants of vacA, iceA, cagA and cagE were identified by the polymerase chain reaction. RESULTS: There was a strong association between the vacA s1/cagA -positive genotype and peptic ulcer disease (OR = 5.42, 95% CI 2.6-11.3, p = 0.0006). Additionally, infection by more virulent strains may protect against GERD, since logistic regression showed a negative association between the more virulent strain, vacA s1/cagA-positive genotype and GERD (OR = 0.26, 95% CI 0.08-0.8, p = 0.03). Resistance to metronidazole was detected in 75 patients (55%), to amoxicillin in 54 individuals (38%), to clarithromycin in 23 patients (16%), to tetracycline in 13 patients (9%), and to furazolidone in 19 individuals (13%). No significant correlation between pathogenicity and resistance or susceptibility was detected when MIC values for each antibiotic were compared with different vacA, iceA, cagA and cagE genotypes. CONCLUSION: The analysis of virulence genes revealed a specific association between H. pylori strains and clinical outcome, furthermore, no significant association was detected among pathogenicity and resistance or susceptibility.

Adult↗
PubMedDate not supplied

[HELICOBACTER PYLORI INFECTION ERRADICATION IN DISPEPTIC PATIENTS WITH AND WITHOUT PEPTIC ULCER]

BACKGROUND: Helicobacter pylori (HP) infection is very prevalent worldwide, and has been associated with the presence of duodenal ulcer, gastric ulcer and chronic active gastritis. It is also speculated that HP may have a role in gastric cancer development. Triple drug schemes have been shown to be the most effective approach to erradicate HP infection. Nevetheless, high rates of resistance against some antibiotics as well as high costs affect the effectiveness of these therapies. The goal of the present study is to assess the effectiveness of the combination of tetracycline, furazolidone and bismuth in erradicating HP, as well as the changes in the histology.METHODS: Patients with diagnosis of HP infection, found in their antral gastric biopsies (hematoxylin and eosin staining (H-E)), were included. They received the following scheme for 10 days: tetracycline 500 mg qid., furazolidone 100 mg qid., and colloidal bismuth subcitrate 120 mg qid. Patients were instructed to come back for follow-up 6 to 8 weeks after starting the therapy. At that time a control upper endoscopy was performed and 3 antral biopsies were taken. Biopsies were stained with H-E and read by experienced pathologists. In both, the biopsy before treatment and the control biopsy, the following parameters were looked for: presence and density of HP; presence, depth and grade of chronic gastritis (lymphoplasmocytic infiltrate); presence and grade of inflammatory activity (polymorphonuclear inflitrate); presence of glandular atrophy; presence, grade (partial or total) and extent (focal or multifocal) of mucinous damage (epithelial damage); presence of intestinal metaplasia; and presence of lymphoid follicles.RESULTS: Fifty-nine patients (30 men and 29 women) completed per protocol. Mean age was 43 +/- 18 (range: 14-73). HP erradication was achieved in 54 patients (91.5%). Control biopsies showed improvement in the following parameters: presence and density of HP (p<0.001); presence, depth and grade of chronic gastritis (p<0.001); presence and grade of inflammatory activity (p<0.001); presence, grade and extent of mucinous damage (p<0.001); and presence of lymphoid follicles (p<0.001). Neither the presence of glandular atrophy nor the presence of intestinal metaplasia showed any significant change. Patients who did not erradicate HP showed no significant difference in any of the parameters.CONCLUSIONS: The triple drug scheme including tetracycline, furazolidone and bismuth is effective in HP erradication. Erradication of HP is followed by an improvement in the following histologic parameters: presence, depth and grade of chronic gastritis (LMN infiltrate); presence and grade of inflammatory activity (PMN infiltrate); presence, grade and extent of mucinous damage; and presence of lymphoid follicles. This scheme is a cost-effective alternative for the therapy of HP infection in low income populations with a high prevalence of infection with this bacteria.

Journal Article↗
PubMed1987

[In vitro effect of 10 antimicrobial agents on the fermentative capacity of the intestinal bacteria].

Using a technique previously described a study was done on the in vitro effect of 10 antimicrobials on the fermentative capacity of human fecal bacteria. The antimicrobials were: 5 antibiotics, oxytetracycline, chloramphenicol, neomycin, paramomycin and lincomycin; and 5 chemotherapeutic agents, bismuth subnitrate, cotrimoxazole, furazolidone, norfloxacin and metronidazole. The study was done with 162 stool samples, 27 to investigate the effect of bismuth subnitrate, and 135 to investigate the effect of the remaining 9 antimicrobials (15 for each one of them). The quantities of antimicrobials used were calculated to reproduce in vitro minimal inhibitory concentrations against fecal bacteria and/or concentrations reached by the respective antimicrobials or their active metabolites in the colonic contents or the stools after regular oral doses. For greater simplicity and clarity, whenever two concentrations of an antimicrobial were reproduced they were denominated low concentration and high concentration as it corresponded. Oxytetracycline, neomycin, paramomycin, cotrimoxazole and norfloxacin did not significantly affect fermentation by fecal bacteria. Chloramphenicol, lincomycin, bismuth subnitrate and furazolidone did not seem to affect significantly fermentation when the variations, increases and decreases produced in it, where evaluated as a whole. But, when increases and decreases were evaluated separately it was found that: chloramphenicol, at low concentration, increase fermentation significantly with 11 from 15 stool samples and diminished it although not significantly with the remaining 4 samples, and at high concentration, increased fermentation significantly with 8 from the 15 samples and diminished it although not significantly with the remaining 7 samples; lincomycin, at low concentrations, increased fermentation with 6 from 15 stool samples and diminished it with the remaining 9 samples although not significantly, and at high concentration, increased it significantly with 9 from the 15 samples and diminished it although not significantly with the remaining 6 samples; bismuth subnitrate, at low concentration, increased fermentation although not significantly with 5 from 27 stool samples and diminished it significantly with the remaining 22 samples, and at high concentration, increased it although not significantly with 2 from 10 stool samples and diminished it significantly with the remaining 8 samples; and furazolidone, at a unique concentration, increased fermentation significantly with 9 from 15 stool samples and diminished it although not significantly with the remaining 6 samples.(ABSTRACT TRUNCATED AT 400 WORDS)

Anti-Bacterial Agents↗
PubMed1983

[Sensitivity of Pasteurella multocida strains to antibiotics and chemotherapeutic agents].

The disk diffusion method was employed to test the sensitivity of a total of 330 Pasteurella multocida strains to streptomycin and kanamycin, of 309 strains to erythromycin, of 315 strains to chloramphenicol, of 240 strains to tetracycline, of 213 strains to gentamycin, of 211 strains to ampicillin, of 209 strains to neomycin, of 199 strains to novobiocin, of 169 to spectinomycin, of 162 to borgal, and of 67 strains to furazolidon. All tested strains were isolated from birds with cholera and from mammals with pneumonia, showing 100 per cent sensitivity to ampicillin, chloramphenicol, erythromycin, tetracycline, gentamycin, and borgal, 88.2 per cent to spectinomycin, 86.6% to furazolidon, 74.2% to neomycin, 52.7% to kanamycin, 23.7% to streptomycin, 32.7% to novobiocin. 13.9 per cent of the P. multocida strains only were resistant to streptomycin. Strains of intermediate sensitivity were as follows: 67.3%--to novobiocin, 62.4%--to streptomycin, 47.3%--to kanamycin, 25.8%--to neomycin, 13.4%--to furazolidon, and 11.8%--to spectinomycin. Ninety-seven strains (42 from birds, 23 from pigs, and 32 from rabbits) were tested for sensitivity in solid media to lowest inhibiting concentrations of tetracycline--4 micrograms/cm3, gentamycine--6 micrograms/cm3, chloramphenicol--12.5 micrograms/cm3, kanamycin--6 micrograms/cm3, erythromycin--8 micrograms/cm3, ampicillin--8 micrograms/cm3, and imekil--0.8 microgram. All tested strains were sensitive to these concentrations. For the treatment and prophylaxis of birds (fowl cholera) and mammals (pasteurellosis) a wide set of antibiotics and chemotherapeutic agents can be used.

Anti-Bacterial Agents↗