monensin has been researched along with Swine-Diseases* in 11 studies
11 other study(ies) available for monensin and Swine-Diseases
Article | Year |
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Control of proliferative enteropathy in growing/fattening pigs using growth promoters.
The aim of this study was to evaluate the effect of different antibiotics used as growth promoters on the control of porcine intestinal adenomatosis when administered in weaning, growing and fattening pig diets, according to Annex I of the European Union directive (70/524/EEC and its subsequent amendments to date) for the use of feed additives. On a farm with a previous history of proliferative enteropathy outbreaks, 648 weaned piglets (23 days old) were divided into nine experimental groups according to bodyweight and sex ratio, each group comprising four pens with 18 pigs in each pen. One group served the trial as a negative (unmedicated) control: another (the positive control) received monensin via feed at 100 p.p.m. up to the end of the growing phase (107 days old) and 50 p.p.m. up to slaughter age (156 days old). The remaining seven groups were offered feed with the addition of the following antibiotics: virginia-mycin (50-20 p.p.m.), avilamycin (40-20 p.p.m.), spiramycin (50-20 p.p.m.), zinc bacitracin (50-10 p.p.m.), avoparcin (40-20 p.p.m.), tylosin (40-20 p.p.m.) and salinomycin (60-30 p.p.m.), respectively. The performance of the pigs in the positive control group was very satisfying and among the highest in the trial, verifying earlier field studies. As a general conclusion it seems that all tested growth promoters had a beneficial effect compared with the untreated control, indicated by the decrease of mortality rate, the elimination of diarrhoeal incidence and the enhancement of growth performance, although the proliferative enteropathy control achieved by each substance was not always satisfactory. More specifically, the antibiotic growth promoters tested can be scaled according to their total efficacy as follows: 1. Salinomycin, tylosin, spiramycin; 2. Virginiamycin, zinc bacitracin, avilamycin; and 3. Avoparcin. Finally, it is considered that part of the growth promotion efficacy of the tested substances is due to their potential capacity to control porcine intestinal adenomatosis; thus, in future growth performance trials, the disease background of the trial farms must be examined, especially for porcine enteropathy challenges. Topics: Abattoirs; Animals; Anti-Bacterial Agents; Antibiotic Prophylaxis; Bacitracin; Bacterial Infections; Disease Outbreaks; Female; Food, Fortified; Glycopeptides; Greece; Growth Substances; Ileitis; Ileum; Intestinal Mucosa; Male; Monensin; Oligosaccharides; Pyrans; Spiramycin; Swine; Swine Diseases; Tylosin; Virginiamycin | 1998 |
Sensitivity of strains of Serpulina hyodysenteriae isolated in Hungary to chemotherapeutic drugs.
The sensitivity of 332 strains of Serpulina hyodysenteriae isolated in Hungary between 1978 and 1992 was tested against seven chemotherapeutic drugs frequently used for the treatment of swine dysentery, and the changes in the patterns of resistance were also monitored. All the strains remained sensitive to carbadox, with minimum inhibitory concentrations (MIC) of only 0.05 to 0.40 microgram/ml at present. The susceptibility of the strains to dimetridazole has gradually decreased, but about half of the strains are still sensitive, with large numbers of "moderately sensitive' strains; the MIC values varied within wide limits (0.1 to 50 micrograms/ml). Most of the strains were resistant to tylosin, with MIC values from 0.1 to 100 micrograms/ml. The number of strains resistant to lincomycin has gradually increased, but about half of the strains remain sensitive; the MIC values ranged from 0.2 to 100 micrograms/ml. Recently, tiamulin has proved the most effective antibiotic, but some resistant strains have already emerged (MIC values 0.05 to 50 micrograms/ml). Monensin was good for the prevention of swine dysentery, but resistance may evolve quickly; the MIC values ranged from 0.4 to 25 micrograms/ml. For sedecamycin, the MIC values (6.25 to 100 micrograms/ml) were much higher than expected. Topics: Animals; Anti-Bacterial Agents; Brachyspira hyodysenteriae; Carbadox; Dimetridazole; Diterpenes; Dose-Response Relationship, Drug; Drug Resistance, Microbial; Dysentery; Hungary; Lincomycin; Macrolides; Microbial Sensitivity Tests; Monensin; Spirochaetales Infections; Swine; Swine Diseases; Tylosin | 1996 |
Monensin toxicosis in swine.
Topics: Animals; Monensin; Muscle Fibers, Skeletal; Muscle, Skeletal; Myocardium; Necrosis; Poisoning; Swine; Swine Diseases | 1996 |
Outbreaks of proliferative haemorrhagic enteropathy on two pig farms.
Clinical signs of proliferative haemorrhagic enteropathy (PHE) including anaemia, dysentery and sudden death were observed in finisher pigs and young breeding stock on 2 farms. On farm A, PHE occurred 12 months after repopulation of the farm. Other outbreaks of PHE occurred after the withdrawal of therapeutic concentrations of in-feed antibacterial agents (farm A), or after monensin sodium (100 g/t) replaced olaquindox (100 g/t) in feed (farm B). The outbreaks, the possible sources of contamination and the role of antibacterial feed additives in the treatment and control of PHE are described. Topics: Anemia; Animal Feed; Animals; Anti-Bacterial Agents; Antiprotozoal Agents; Bacterial Infections; Disease Outbreaks; Drug Therapy, Combination; Dysentery; Enteritis; Epithelium; Female; Gastrointestinal Hemorrhage; Intestine, Large; Intestine, Small; Male; Monensin; Pregnancy; Quinoxalines; Swine; Swine Diseases; Victoria | 1995 |
[Clinico-biochemical and hematological studies in acute monensin poisoning in swine].
Investigations were carried out with pigs divided into four groups and treated with monensin-Na at rates of 20, 30, and 50 mg/kg, once only, through a nose-pharyngeal tube. The total change in the clinical status was followed up. Most characteristic were found to be the changes setting in with the posture and locomotive apparatus--prolonged lying, pareses, etc. Blood was checked in the dynamic course of the disease at the 4th and the 24th hour as well as on the 6th day following monensin-Na treatment. The amount of haemoglobin and the erythrocyte count rose in the early stage of intoxication, and came back to normal after the 24 th hour. Leukocytosis with neutrophilia was also found. The serum level of selenium, calcium, vitamins A, B1, and C dropped substantially, while that of phosphorus and magnesium rose. The morphologic changes were found to be localized in the parenchymal organs and in the skeletal muscles. Featuring were diffuse hyperaemia, haemorrhages, granular degeneration, and focal necrosis. Topics: Acute Disease; Animals; Blood Cell Count; Blood Chemical Analysis; Dose-Response Relationship, Drug; Hemoglobins; Monensin; Swine; Swine Diseases; Time Factors | 1987 |
Monensin toxicosis in swine: potentiation by tiamulin administration and ameliorative effect of treatment with selenium and/or vitamin E.
Modulation of acute monensin toxicosis in swine was evaluated in 2 studies. In study 1, 56 weanling male pigs were allotted to 14 groups of 4 each. Pigs in 7 groups were given tiamulin in the drinking water (to supply 7.7 mg/kg of body weight/day) for 3 days before and for 2 days after monensin administration. Monensin was given as a single oral dose (at 0, 7.5, 15, 25, 50, 75, or 100 mg/kg) to pigs in groups with or without tiamulin exposure. Prominent acute clinical signs of monensin toxicosis (hypermetria, hind limb ataxia, paresis, knuckling of hind limbs, and recumbency) developed by 2 to 6 hours after dosing in pigs given 15 or 25 mg of monensin/kg with tiamulin exposure, but not in pigs given the 15 or 25 mg of monensin/kg without tiamulin exposure. Also, the extent of monensin-induced skeletal muscle damage at 4 days after monensin dosing was enhanced in pigs given 7.5, 15, or 25 mg of monensin/kg and exposed to tiamulin. In study 2, 48 weanling male pigs were allotted to 8 groups of 6 each. Four groups of pigs were given 20 mg of monensin/kg orally, and 4 groups were given 100 mg of monensin/kg orally. For each monensin dose, a group was treated 24 hours before monensin administration with (i) selenium (Se)-vitamin E preparation, 0.25 mg of Se and 68 IU of d-alpha-tocopheryl acetate (vitamin E)/kg, IM; (ii) vitamin E only, 68 IU of d-alpha-tocopheryl acetate/kg; (iii) Se only, 0.25 mg of Se/kg; or (iv) vehicle.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Animals; Anti-Bacterial Agents; Diterpenes; Drug Synergism; Male; Monensin; Selenium; Swine; Swine Diseases; Vitamin E | 1987 |
Enhanced myotoxicity and involvement of both type I and II fibers in monensin-tiamulin toxicosis in pigs.
Simultaneous administration of monensin and tiamulin to pigs resulted in enhanced myotoxicity. Skeletal muscles of tongue, diaphragm and legs were preferentially affected, whereas the masseter, longissimus thoracis and cardiac muscles, including the left auricle, were spared. Histochemical examination revealed an involvement of both type I and II fibers of skeletal muscles. Topics: Animals; Anti-Bacterial Agents; Diterpenes; Drug Synergism; Food Additives; Furans; Histocytochemistry; Male; Monensin; Muscles; Muscular Diseases; Swine; Swine Diseases; Weaning | 1985 |
Acute monensin toxicosis in swine: effect of graded doses of monensin and protection of swine by pretreatment with selenium-vitamin E.
Topics: alpha-Tocopherol; Animals; Cattle; Cattle Diseases; Drug Combinations; Female; Furans; Male; Monensin; Muscles; Myocardium; Necrosis; Selenious Acid; Selenium; Swine; Swine Diseases; Tocopherols; Vitamin E | 1983 |
Clinical, clinicopathologic, and pathologic alterations of monensin toxicosis in swine.
Topics: Animals; Aspartate Aminotransferases; Creatine Kinase; Female; Furans; Heart Atria; Male; Monensin; Muscles; Myocardium; Necrosis; Swine; Swine Diseases | 1983 |
Monensin-tiamulin interaction risk to pigs.
Topics: Animal Feed; Animals; Diterpenes; Drug Interactions; Furans; Monensin; Swine; Swine Diseases | 1981 |
Monensin--tiamulin interactions in pigs.
Topics: Animals; Anti-Bacterial Agents; Diterpenes; Drug Interactions; Female; Furans; Male; Monensin; Muscular Diseases; Swine; Swine Diseases | 1981 |