Effects of the accidental feeding of lasalocid sodium to broiler breeder chickens

Abstract

Lasalocid sodium was accidentally introduced into the feed of several broiler breeder chicken farms at levels between 115 and 150 ppm. On one farm, leg weakness and ataxia were observed in a few cockerels. A reduction in egg production and a sharp decrease in fertility and hatchability were observed in all the flocks receiving the contaminated feed. Many piping chicks were unable to hatch and there was an increase in the number of weak ataxic chicks at the hatchery. Histological examination of the muscle tissues of the affected cockerels, the piping chicks unable to hatch and the one-day-old chicks with leg weakness and ataxia revealed severe muscle damage. Increasing levels of lasalocid were detected in the yolk of eggs collected from the affected flocks.

The Protective Effect of Silybin against Lasalocid Cytotoxic Exposure on Chicken and Rat Cell Lines

“…This drug is characterized by a narrow safety margin, since the accidental lasalocid poisoning cases among animals have been reported [1–4]. The clinical syndrome of lasalocid poisoning in animals includes skeletal muscle lesions, neurological signs, and increase serum enzymes,s which results from muscles and liver's damages [1–4]. The toxicological monitoring of eggs and chicken edible tissues (liver, muscles) revealed that the concentration of lasalocid is much higher than its maximum residue limits (MRL) [5, 6].…”

The residue levels of narasin in eggs of laying hens fed with unmedicated and medicated feed

“…Nonetheless, residues of coccidiostats have been detected in eggs. These have been attributed either to contamination of unmedicated feed at the feed manufac-turer [1 -3] or accidental feeding of salinomycin [4] or lasalocid [5] to the laying hens.…”

Intoxicação espontânea por antibióticos ionóforos em ovinos no Rio Grande do Sul

“…Casos de intoxicação por AI usualmente são resultado da suplementação com ração ou outro tipo de alimento contendo AI (Nation et al 1982, Newsholme et al 1983, Blanchard et al 1993, Gava et al 1997, Jones 2001, Dedoussi et al 2007), da ingestão acidental de rações contendo esses compostos por espécies não-alvo (Perelman et al 1993, Baird et al 1997, Shlosberg et al 1997, Segev et al 2004) ou em situações onde há o envolvimento de substâncias que potencializam a ação dos AI, retardando a eliminação pelo organismo ). Nos casos deste surto, os ovinos tiveram acesso a um aditivo alimentar para frangos contendo 250g/kg de narasina.…”

“…Não foram observadas alterações macroscópicas e as alterações histológicas observadas foram discretas e refletem o pouco tempo decorrido desde a ingestão do AI até a morte dos ovinos. Considera-se que a causa da morte em casos de intoxicação por AI é decorrente ou da paralisia dos músculos respiratórios (secundária à degeneração de miofibras ou de neuropatia periférica) ou de alterações nos mecanismos contráteis do miocárdio (Gaide et al 1984, Perelman et al 1993. Os ovinos afetados neste surto apresentaram marcado edema pulmonar, o que pode ter contribuído ou mesmo causado a morte desses animais.…”