The study reports a significant outbreak of subacute tiamulin-monensin toxicosis in a flock of 21,044 commercial brown pullets, aged 11-16 weeks, on a farm in Spain. The outbreak occurred after the administration of monensin (120 ppm) in feed and tiamulin (150 ppm) in drinking water. Within 24 hours of tiamulin treatment, the pullets' feed and water consumption drastically declined, followed by a progressive increase in mortality, which peaked at 1.75% and reached a cumulative mortality of 4.3% over a 13-day period. The affected pullets, accounting for 8% of the flock, displayed symptoms such as marked apathy, muscle weakness, flaccid paralysis, and prostration. These symptoms indicate a severe impact of the tiamulin-monensin combination on the pullets' overall health and well-being.
Necropsy examinations of 18 deceased pullets revealed significant gross and histopathological changes. The most notable findings included myocardial and vastus intermedius muscle pallor, with 72% of the pullets exhibiting myocardial pallor and 100% showing pallor in the vastus intermedius muscle. Histopathological examination confirmed monophasic myocardial and myocyte degeneration and necrosis in all examined pullets. Additionally, fibrosis and granulomatous infiltration surrounding and infiltrating affected muscle fibers were observed in a low number of animals (11%). The study suggests that tiamulin enhances monensin toxicity through biochemical interactions, making the combination of 150 ppm tiamulin and 120 ppm monensin highly toxic to pullets. The withdrawal of tiamulin-monensin 24 hours after the onset of symptoms led to an increase in feed and water consumption and a decrease in mortality, highlighting the need for careful administration of these substances in poultry production. The study's findings emphasize the importance of considering tiamulin-monensin toxicosis in the differential diagnosis of cardiomuscular disorders in pullets and layers.
Link:
https://pubmed.ncbi.nlm.nih.gov/40392440/