Outbreak of Monensin Sodium Poisoning in Horses Associated with Consumption of Mineral Supplement Based on Sugarcane Molasses
Background: Sodium monensin is a molecule of the group of ionophores antibiotics (IAs) of the polyether carboxylic type produced from the fermentation of Streptomyces cinnamonensis. Cases of IA poisoning in animals usually occur accidentally. Fatal poisoning in horses, a non-target species and with particular sensitivity usually occurs by the consumption of these products from the toxic dose of 2-3 mg/kg. This report aims to describe the epidemiological and clinical-pathological aspects of an outbreak of ionophore antibiotic poisoning in horses due to the consumption of mineral supplementation indicated for ruminants based on sugarcane molasses.
Case: Two horses were necropsied. During necropsy, fragments of various organs were collected and fixed in 10% buffered formalin, routinely processed for histology and stained with hematoxylin and eosin. The information obtained from the animal trainer was that 19 horses received approximately 25 kg of low moisture mixture based on sugarcane molasses, enriched with macro and micro minerals, vitamins and additives containing 1000 mg of monensin/kg in the trough. One day after receiving the product, five horses began to develop ataxia, reluctance to move, difficulty of accompanying the herd and arising. Out of the five, three died after three days of evolution, one after six days (equine 1) and another after 15 days (equine 2) [morbidity 26.31%]. At necropsy, diffuse pallor was observed in the gluteus medius, quadriceps femoris, semimembranosus, biceps brachii and deep pectoral muscles. Microscopically the muscle fibers were tumefied with hypereosinophilic sarcoplasm of homogeneous appearance and with loss of striations, pynotic or absent nuclei (necrosis). Multifocal areas of fibers with sarcoplasmic fragmentation were observed, with clusters of irregular eosinophilic debris, flake (floct necrosis) or granule (granular necrosis) aspects and focal muscle fibers with granular to crystalline basophilic material (mineralization) and marked multifocal infiltrate, predominantly of macrophages, plasma cells and eosinophils with occasional multinucleated giant cells. In the heart there was focally a extensive area of necrosis and a discrete eosinophil infiltrate.
Discussion: The diagnosis of ionophore antibiotic intoxication in horses was established by epidemiological and clinical-pathological aspects. In the horses affected in this outbreak, the intoxication was due to the ingestion of sugarcane molasses containing proportions of monensin, which is not indicated for equines, becoming an unusual source for this animal species. The clinical signs reported in the intoxication under study are mostly locomotors and are directly linked to poor distribution of sodium, potassium and calcium ions in muscle cells, leading to ionic disorders that modify the muscle neurotransmission by deregulating contraction and altering movement. Usually, death of horses poisoned with IAs is related to heart failure due to degenerative cardiomyopathy. However, due to the subtlety of the histological lesions in the heart, we believe that the cause of death may also be related to a possible respiratory failure owing to a degenerative myopathy of the diaphragmatic muscle. The anatomopathological changes found in the skeletal muscles of equine intoxicated with molasses are similar to those described in this species by other authors. Compounds based on sugarcane molasses formulated for cattle containing monensin should be considered as a potential source of poisoning for horses and as a cause of degenerative myopathy, which may be an alert for caring about the handling and feeding of these animals.
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