Pediatric Exposures to Veterinary Pharmaceuticals.

OBJECTIVE: To describe the epidemiology of veterinary pharmaceutical-related exposures to children based on calls to a regional poison control center. METHODS: A retrospective analysis of pediatric (≤19 years of age) exposures to pharmaceutical products intended for animal use, managed by a regional poison control center from 1999 through 2013, was conducted. Case narratives were reviewed and coded for exposure-related circumstances and intended species. Descriptive statistics were generated. RESULTS: From 1999 through 2013, the Central Ohio Poison Center received 1431 calls that related to a veterinary pharmaceutical exposure for children ≤19 years of age. Most of the pediatric calls (87.6%) involved children ≤5 years of age. Exploratory behavior was the most common exposure-related circumstance (61.4%) and ingestion accounted for the exposure route in 93% of cases. Substances commonly associated with exposures included: veterinary drugs without human equivalent (17.3%), antimicrobial agents (14.8%), and antiparasitics (14.6%). Based on substance and quantity, the majority of exposures (96.9%) were not expected to result in long-term or lasting health effects and were managed at home (94.1%). A total of 80 cases (5.6%) were referred to a health care facility, and 2 cases resulted in a moderate health effect. CONCLUSIONS: Children ≤5 years of age are most at risk for veterinary pharmaceutical-related exposures. Although most exposures do not result in a serious medical outcome, efforts to increase public awareness, appropriate product dispensing procedures, and attention to home storage practices may reduce the risk of veterinary pharmaceutical exposures to young children.

Accidental and experimental Closantel intoxication in Uruguayan sheep / Intoxicação acidental e experimental por Closantel em ovinos no Uruguai

An outbreak of Closantel intoxication in sheep in Uruguay is described. The outbreak occurred in a group of 1300 weaning lambs treated orally with a 10% solution of Closantel. One hundred forty eight lambs showed clinical signs of intoxication and 14 died. The clinical signs included mydriasis, nystagmus, and negative pupillary reflex, bilateral blindness, bump into objects, and lateral movement of the head. No macroscopic lesions were observed. The histological lesions of the retina were cytoplasmic vacuolization in ganglion cells and in cells of the inner and outer nuclear layers with different degrees of atrophy. Vacuolization and axonal degeneration were observed in the optic nerve, with multifocal areas of fibrosis and infiltration by lymphocytes and Gitter cells. To reproduce the intoxication, four sheep were given two, four and 10 times the therapeutic dose of Closantel (0.1g/kg of BW). Only the animals receiving 10 times the recommended dose showed clinical signs. The histological examination of the lesions in experimental sheep showed similar results to those described in the accidental outbreak, except for the absence of optic nerve fibrosis and inflammation, characterizing an acute phase. Axonal myelin sheaths loss, fibroblasts and collagen fibers were observed in the ultrastructural study of the optic nerve of accidental intoxicated animals. The optic nerve of experimentally intoxicated animals had vacuoles that separated the myelin sheaths of axons. To prevent outbreaks it is suggested to weigh the animals before Closantel administration to avoid errors in dose calculation.

Descreve-se um surto de intoxicação por Closantel em ovinos no Uruguai. O surto ocorreu em um lote de 1300 cordeiros que foram dosados com uma solução de Closantel 10%, por via oral. Do total, 148 apresentaram sinais clínicos de intoxicação e 14 morreram. Os sinais clínicos incluíam midríase, nistagmo, reflexo pupilar negativo, cegueira bilateral, pressão da cabeça contra objetos e desvio lateral da cabeça. Lesões macroscópicas não foram observadas. Histologicamente havia vacuolização citoplasmática das células ganglionares e nas células das camadas nuclear interna e externa. Na retina havia, também, diferentes graus de atrofia. Vacuolização e degeneração axonal foram observados no nervo óptico, com áreas multifocais de fibrose e infiltrado de linfócitos e células Gitter. Quatro ovinos receberam experimentalmente duas, quatro e 10 vezes a dose terapêutica de Closantel (0,1 g/kg de peso vivo). Apenas os animais que receberam 10 vezes a dose recomendada apresentaram sinais clínicos. O exame histológico nos ovinos experimentais mostrou resultados semelhantes aos do surto, com exceção da ausência de fibrose e infiltrado inflamatório do nervo óptico, caracterizando um quadro agudo. Foram observadas a perda da bainha de mielina dos axônios e a presença de fibroblastos e fibras colágenas no estudo ultra-estrutural do nervo óptico de animais intoxicados espontaneamente. No nervo óptico de animais intoxicados experimentalmente havia vacúolos que separavam as bainhas de mielina dos axônios. Para evitar surtos, sugere-se pesar os animais antes da administração de Closantel para evitar erros no cálculo da dose.

[Doramectin intoxication in 3 kittens]. / Doramectin-Intoxikation bei drei Katzenwelpen.

This case report describes 3 kittens with suspected doramectin toxicity. In a litter of 7 kittens treated with doramectin, 3 developed neurological symptoms. One kitten showed mild apathy and tremors, while a second one additionally presented behavioral changes and seizures that had to be treated with diazepam. Both kittens recovered completely. A third kitten was presented to us in coma 3 days following treatment with doramectin. Subsequently, this kitten developed behavioral changes such as aggression, hyperesthesia, tremors, and seizures and died 36 hours after presentation. Histopathologic examination of the brain showed cytotoxic edema and polioencephalomalacia. The doramectin dosage of the deceased kitten was 380 µg/kg.

Outcomes of the California ban on pharmaceutical lindane: clinical and ecologic impacts.

INTRODUCTION: There are increasing concerns over the presence and implications of pharmaceutical agents in water. In 2002, California banned pharmaceutical use of lindane because of concerns about water quality, as lindane treatment for head lice and scabies was found to be a significant factor adversely affecting wastewater quality. OBJECTIVES: In this article we describe the effects the ban has had on wastewater quality, unintentional exposures, and clinical practice. This is the first time that a pharmaceutical has been outlawed to protect water quality. As such, this ban provides a rare opportunity to evaluate the possible or potential outcomes of future public health interventions aimed at reducing pharmaceutical water contamination. METHODS: We compiled data on lindane in wastewater treatment plant effluent for several large plants in California and one outside of California. Data on exposures to lindane were obtained from records of the California Poison Control System. We assessed the impact on clinical practice via a survey of 400 pediatricians RESULTS: Wastewater treatment plant monitoring showed that lindane declined in California after the ban. Similarly, unintentional exposure calls declined. Most physicians were aware of the ban (81%) and had used lindane previously (61%), but they did not notice any difficulties with the ban (78%). CONCLUSIONS: The California experience suggests that elimination of pharmaceutical lindane produced environmental benefits, was associated with a reduction in reported unintentional exposures, and did not adversely affect head lice and scabies treatment. This ban serves as a model for governing bodies considering limits on the use of lindane or other pharmaceuticals.

Suspected ivermectin toxicosis in a miniature mule foal causing blindness.

A 9-week-old miniature mule foal presented to the Veterinary Medical Teaching Hospital for acute blindness, ataxia, and depression following an overdose of an over-the-counter ivermectin-based de-worming medication. Ophthalmic examination and electrodiagnostic evaluation eliminated outer retinal abnormalities as the primary cause of the bilateral blindness, implicating instead a central neurologic effect of the drug. With symptomatic and supportive care, the foal recovered fully and regained its vision.