Reassessing clinical presentations of emamectin benzoate poisoning: A comprehensive study.

BACKGROUND: The mechanism of emamectin benzoate (EMB-a macrocyclic lactone insecticide like abamectin) action involves the disruption of glutamate-gated chloride channels and GABA receptors in insects, leading to paralysis and death. EMB overdose can breach the blood-brain barrier, resulting in severe poisoning and altered consciousness. AIM: Review EMB poisoning presentations in patients and reevaluate clinical manifestations. MATERIALS AND METHODS: This retrospective study reviewed (August 31, 2008-August 31, 2023) medical university hospital records. We analyzed symptoms, patient characteristics, vital signs, Glasgow Coma Scale scores, laboratory findings, and outcomes. RESULTS: Ten patients (males: 6, females: 4, median age = 64.5 years) experienced EMB poisoning. Common symptoms included sore throat, gastrointestinal distress, dyspnea, and altered consciousness; two patients showed laryngeal corrosive injuries. Management involved activated charcoal administration, gastric lavage, and intensive care unit admission. DISCUSSION: Sore throat and corrosive injuries were distinctive presentations of EMB poisoning, warranting vigilance. Potential mechanisms of corrosive injury include skin and eye irritation effects of EMB, the solvents of which might exert corrosive action. CONCLUSION: EMB poisoning manifests as diverse symptoms, including sore throat, gastrointestinal symptoms, central nervous system depression, and potential aspiration pneumonia. Recognizing and promptly managing EMB poisoning are crucial for enhancing patient outcomes and minimizing complications.

Abamectin poisoning with severely abnormal electroencephalogram: A case report.

Cases of abamectin poisoning have been reported previously, but cases of severe brain dysfunction after poisoning are rarely reported, and abnormal electroencephalograms (EEGs) have not been reported. We report a case of a 46-year-old female who intentionally drank 400 mL of 5% abamectin pesticide. We describe in detail the clinical and EEG characteristics of the patient. The patient was discharged in good condition after 10 days. The study indicates that serious brain dysfunction and abnormal EEG caused by abamectin poisoning are treatable. Despite poor clinical and EEG findings at the outset, recovery is still possible. This is the first report on EEG after abamectin poisoning.

[A case report of death from acute emamectin·chlorfenapyr poisoning].

To analyze the clinical data of a case of acute emamectin·chlorfenapyr poisoning in Guangzhou 12th People's Hospital in 2019. The patient developed high fever and night sweats, and gradually became unconscious. The patient died after 5 days of treatment. The toxicity and mortality of emamectin·chlorfenapyr were high. For acute poisoning patients, in addition to conventional symptomatic treatment, early blood purification treatment should be actively carried out.

Nystagmus following acute avermectins poisoning.

BACKGROUND: Acute pesticide poisoning is a major public health problem in the world. Most pesticides are toxic to human beings, because of diverse components resulting in different reaction. OBJECTIVE: As clinicians identify various symptoms due to pesticide poisoning, it is necessary for the diagnosis and treatment for treating such toxins. Accidents associated with acute avermectins poisoning are rarely reported, especially self-induced nystagmus. In the present study, a case of human abamectin poisoning with relevant toxic effects has been reported. CONCLUSIONS: Acute avermectins poisoning-induced nystagmus may be affected due to the vestibular cerebellar system, but the exact mechanism and pharmacological basis is still worthy of further study.

[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.

Molecular cloning and characterization of a P-glycoprotein from the diamondback moth, Plutella xylostella (Lepidoptera: Plutellidae).

Macrocyclic lactones such as abamectin and ivermectin constitute an important class of broad-spectrum insecticides. Widespread resistance to synthetic insecticides, including abamectin and ivermectin, poses a serious threat to the management of diamondback moth, Plutella xylostella (L.) (Lepidoptera: Plutellidae), a major pest of cruciferous plants worldwide. P-glycoprotein (Pgp), a member of the ABC transporter superfamily, plays a crucial role in the removal of amphiphilic xenobiotics, suggesting a mechanism for drug resistance in target organisms. In this study, PxPgp1, a putative Pgp gene from P. xylostella, was cloned and characterized. The open reading frame (ORF) of PxPgp1 consists of 3774 nucleotides, which encodes a 1257-amino acid peptide. The deduced PxPgp1 protein possesses structural characteristics of a typical Pgp, and clusters within the insect ABCB1. PxPgp1 was expressed throughout all developmental stages, and showed the highest expression level in adult males. PxPgp1 was highly expressed in midgut, malpighian tubules and testes. Elevated expression of PxPgp1 was observed in P. xylostella strains after they were exposed to the abamectin treatment. In addition, the constitutive expressions of PxPgp1 were significantly higher in laboratory-selected and field-collected resistant strains in comparison to their susceptible counterpart.

Intoxicação por ivermectina em cães / Intoxicatin ivermectin in dogs

As ivermectinas são substâncias obtidas originalmente da fermentação de amostras de solo, contendo o fungo Streptomyces avermitilis (LYNN et al., 1999). É um dos antiparasitários mais utilizados mundialmente, sendo aprovado para uso em bovinos, suínos, ovinos e equinos como endectocida (SINDAN et al., 2001). Rotineiramente, o produto à base de ivermectina de uso bovino é empregado em clínica de pequenos animais, provocando intoxicações (SAKATE et al., 2002). O medicamento vem sendo usado para o tratamento da sarna sarcóptica, demodécica, notoédrica e otodécica de pequenos animais (SAKATE et al., 2002). Segundo a literatura, em caninos, a toxidade está relacionada às altas dosagens e à predisposição racial. Cães das raças Collie, Old English Sheepdog, Pastor de Shetland, Pastor Alemão, Afgan Hounds, ou seus mestiços são particularmente sensíveis, o que torna a barreira hematoencefálica desses cães mais permeável a ivermectina, ocasionando depressão do sistema nervoso central (MEALEY et al., 2006). Os sinais clínicos de intoxicação incluem ataxia, hipertermia, desorientação, sialorréia, midríase, hiperestesia, tremores, depressão, paralisia, ausência dos reflexos pupilares, cegueira, bradicardia, pulso fraco e em casos graves, coma, hipotermia e morte (SAKATE et al., 2002). Com esse trabalho, objetivou-se relatar um caso de intoxicação por ivermectina em dois cães sensíveis ao princípio ativo, desencadeando um quadro tóxico.

Toxicology of avermectins and milbemycins (macrocylic lactones) and the role of P-glycoprotein in dogs and cats.

The macrocyclic lactones (MLs) are parasiticides able to kill a wide variety of arthropods and nematodes. They have a high margin of safety for labeled indications, and ivermectin has become the best-selling antiparasitic in the world. Dogs of certain breeds and mixtures of those breeds have a defect in the ABCB1 gene (formerly MDR1 gene) that results in a lack of functional P-glycoprotein, which leads to accumulation of the MLs in the central nervous system and a higher risk of adverse effects when exposed. There is no specific antidote for ML toxicosis so the most important part of treatment is good supportive care.

Macrocyclic lactone toxicity due to abamectin in farm dogs without the ABCB1 gene mutation.

CASE HISTORY: A 5-year-old entire female Huntaway from a sheep and beef farm was one of four dogs that developed clinical signs including hypersalivation, depression, blindness and ataxia after the death of another dog. A 4-year-old female Huntaway farm dog from a second farm was observed to be sitting down more often than usual on the day after being fed part of a calf carcass that had been treated with an abamectin pour-on. CLINICAL FINDINGS: The first dog was ataxic and depressed but did respond to sound. The second dog presented with an acute onset of blindness, mydriasis, absence of a menace response, hypersalivation, gait abnormalities (e.g. high stepping gait and ataxia), and depression. Other presenting signs included muscle tremors, dehydration and difficulty eating. No abnormalities were detected from routine haematology and biochemistry. Analysis of samples of plasma from both dogs revealed concentrations of abamectin of 0.149 mg/L and 0.260 mg/L for the first and second dogs, respectively. Buccal swabs taken from the first dog for DNA testing for the ABCB1 gene mutation, gave a negative result. DIAGNOSIS: In addition to the presenting signs which suggested a toxicosis, both dogs had measurable concentrations of abamectin in plasma confirming exposure. CLINICAL RELEVANCE: Farm dogs exposed to concentrated pour-on products containing abamectin have been poisoned and recover or die. The product labels do not carry any warnings as to the risk of poisoning to dogs. This paper discusses two incidents affecting six farm dogs, but the authors are aware of more toxicoses in farm dogs exposed to abamectin.

Intravenous fat emulsion as treatment for ivermectin toxicosis in three dogs homozygous for the ABCB1-1Δ gene mutation.

OBJECTIVE: To describe the outcome of 3 cases of ivermectin toxicosis in dogs homozygous for the ABCB1-1Δ gene mutation treated with intravenous fat emulsion (IFE). SERIES SUMMARY: One Australian Shepherd and 2 Miniature Australian Shepherds were treated for naturally occurring ivermectin toxicosis with IFE. All 3 dogs were homozygous for the ABCB1-1Δ gene mutation. Serum ivermectin concentrations confirmed ivermectin exposure in each case. All 3 dogs exhibited tremors, ptyalism, and central nervous system depression, which progressed over several hours to stupor in 2 dogs, and to a comatose state requiring mechanical ventilation in the remaining dog. A 20% formulation of IFE(a) was administered as an IV bolus (1.5 mL/kg) followed by a slow IV infusion (7.5-15 mL/kg [0.25-0.5 mL/kg/m], over 30 minutes). No change was observed in the neurologic status of any patient. Lipemia visible upon blood sampling persisted for 36 hours in 1 dog however, no other adverse effects were noted. Flumazenil (0.01 mg/kg IV), followed by a constant rate infusion(CRI) of 0.01 mg/kg/h IV was administered in 1 case, without any apparent clinical benefit or adverse effect. NEW OR UNIQUE INFORMATION PROVIDED: IFE was ineffective in the treatment of ivermectin toxicosis in these ABCB1-1Δ homozygous mutant dogs. Further investigation is necessary to determine why IFE treatment was unsuccessful in these cases and whether its use can be optimized to yield better results.