Tiamulin and monensin intoxication in commercial brown pullets.

Abstract

Tiamulin and monensin intoxication has been widely reported in broilers and many other domestic animals, causing muscular dystrophy. This study reports an outbreak of subacute tiamulin-monensin toxicosis in commercial brown pullets and provides a detailed clinicopathological description. The outbreak occurred on a floor-rearing farm in Spain of 21,044 Lohmann Brown pullets (11-16 weeks old) after monensin (120 ppm) was administered in feed and tiamulin (150 ppm) in drinking water. Within 24 h after tiamulin treatment, feed and water consumption declined drastically, and mortality increased progressively, reaching a peak of 1.75%. Cumulative mortality over a 13-day period was 4.3%. Affected pullets (8%) exhibited marked apathy, muscle weakness, flaccid paralysis, and prostration. Necropsy of 18 naturally dead pullets revealed gross myocardial (72%) and vastus intermedius (100%) muscle pallor, with histopathological examination confirming monophasic myocardial and myocyte degeneration and necrosis (100%). Fibrosis and granulomatous infiltration surrounding and infiltrating affected muscle fibers were observed in a low number of animals (11%). These findings suggest that tiamulin enhances monensin toxicity through biochemical interactions, indicating that the combination of 150 ppm tiamulin and 120 ppm monensin is highly toxic to pullets. This highlights the need for careful administration in poultry production. Twenty-four hours after tiamulin-monensin withdrawal, feed and water consumption increased and mortality decreased. Tiamulin-monensin toxicosis should be considered in the differential diagnosis of cardiomuscular disorders in pullets and layers.