IONOPHOR ANTIBIOTIC POISONING IN SWINE HE RDS

Citation
G. Salyi et al., IONOPHOR ANTIBIOTIC POISONING IN SWINE HE RDS, Magyar allatorvosok lapja, 49(3), 1994, pp. 140-146
Citations number
NO
Categorie Soggetti
Veterinary Sciences
Journal title
ISSN journal
0025004X
Volume
49
Issue
3
Year of publication
1994
Pages
140 - 146
Database
ISI
SICI code
0025-004X(1994)49:3<140:IAPISH>2.0.ZU;2-7
Abstract
Ionophor antibiotic (monesin, narasin, salinomycin maduramycin) poison ings were diagnosed in 9 cases. In one each cases, poisoning was cause d by overdose of Dizenzin (containing monensin) and Salocin (containin g salinomycin) and drug-incompatibility due to the simultaneous applic ation of salinomycin and tiamulin. In the other cases, the cause of po isoning was suspected due to the overdose of premixes, as well as feed ing premixes or feeds by swine produced for chickens. In all the cases , the clinical symptoms were characterized by motor disturbances, firs t of all weakness of the posterior body half and laying in more severe cases. Besides these symptoms, signs of circulatory disturbances, dys pnoea, as well as discharge of red-brown urine were also observed. The gross-pathological investigation revealed - first of all - discoloura tion of mass extremity muscles, sometime of the heart muscle greyish-w hite paleness of certain muscle fibres, as well as lung oedema were ob served. The histopathological examinations revealed Zenker-type necros is of muscle fibres in the acute stage of poisoining (Figs 1a and 1b). In subacute and chronic stages, some of the necrotic muscle fibres sh owed calcification and signs of reparation and regeneration (Figs 2 an d 3). Ionophor antibiotics - in high amounts in most cases - were demo nstrated by chemical methods in the gastric content of swine died duri ng the acute phase of the poisoning and also in the feed samples. In c ase of simultaneous application of salinomycin and tiamulin their tota l quantities were relatively small (approx. 7.2 mg/body-mass kg/day). It was also proposed that their toxic effect was increased by the T-2 toxin contamination of feeds and/or selenium vitamin E deficiency of p igs.