Fundoscopic findings in a cat with acute ivermectin toxicity: A case report

Introduction

Ivermectin is a semi-synthetic macrocyclic lactone commonly used as an antiparasitic drug. Toxicity develops when the drug penetrates the blood-brain barrier and enhances the activity of gamma-aminobutyric acid (GABA), leading to neurological and ocular manifestations such as hypersalivation, tremors, ataxia, dilated pupils with reduced pupillary response, blindness, and in severe cases, death (Merola et. al., 2012) [1] . Most reported cases of ivermectin toxicosis involve animals that were accidentally or deliberately exposed to formulations not intended for their species (Muhammad et al., 2004, Kenny et al., 2008) [2,3] . The risk of toxicosis is especially high when high-concentration ivermectin formulations intended for large animals are administered to small animal species. Mechanisms underlying blindness in animals with ivermectin toxicosis are unknown. Previous studies have suggested that both intracranial (Plummer et al., 2006) [4] and retinal (Kenny et al., 2008) [3] mechanisms may contribute to the clinical manifestations of ivermectin toxicity. Gamma-aminobutyric acid (GABA), the principal inhibitory neurotransmitter in the mammalian retina, plays a critical role in the modulation and processing of visual signals. Therefore, disruption of GABA-mediated neurotransmission may contribute to the visual disturbances observed in affected animals. Ophthalmic examination may reveal multifocal areas of retinal oedema, retinal folds, and mild separation of the retina (Epstein et al., 2013; Merola et al., 2009) [5,6] . Electroretinography (ERG) commonly demonstrates decreased amplitudes of both a-and b-waves, indicating impaired retinal function. However, visual deficits observed in affected animals may also be associated with involvement of the central nervous system (Pollio et al., 2018) [7] . Intravenous lipid emulsion (ILE) therapy has been advocated in the management of lipophilic toxicants, including ivermectin. Its therapeutic effect is believed to occur through the "lipid sink" phenomenon, whereby the lipid phase sequesters circulating toxin molecules, ultimately lowering their bioavailability and limiting distribution to target tissues (Epstein et al., 2013) [5] . This report aims to describe the fundoscopic findings in a cat with suspected ivermectin toxicity. Although intravenous lipid emulsion (ILE) therapy was advised, the animal was not presented for subsequent treatment or follow-up assessment. Furthermore, due to the emergency nature of the case, comprehensive hematological and biochemical analyses were not available.

Materials and Methods

A one-and-a-half-year-old female non-descript intact cat weighing 4 kg was presented to the Department of Veterinary Surgery and Radiology, MR College Of Veterinary Science and Research Centre, Jhajjar, Haryana, India with the complaint of sudden onset of tremors, obtundation, blindness, and dilated pupils. The cat had no relevant medical history. One day before presentation, the owner reportedly administered ivermectin, both orally and via injection, in an attempt to treat a suspected mite infestation. Neuroophthalmic test (Menace response, PLR, Palpebral reflex, Corneal reflex), Aqueous tear tests (Schirmer's strip test reading in mm), intraocular pressure and fundoscopic examination was done. Rebound tonometer (icare Tonovet plus) was used to measure intraocular pressure (IOP). A magnetised pin, which had a plastic tip at its end, was placed in the instrument. After selecting the canine option, proper holding of the instrument was detected by the light source present on the instrument (it should be parallel to the ground). The instrument takes six readings and averages them. Fundoscopic examination was conducted without pharmacological mydriasis, as the pupils were already adequately dilated, allowing satisfactory visualization of the ocular fundus (Fig. 1). Monocular indirect ophthalmoscopy was performed in the cat using a 20-diopter indirect condensing lens (Volk) and a Finoff transilluminator (Heine). The animal was restrained in sternal recumbency in a darkened room, with assistance provided to gently maintain eyelid opening. The light source was positioned at the examiner's temple and directed toward the patient's eye. After identification of the tapetal reflex (Fig. 1), the condensing lens was held in front of the eye to facilitate examination of the ocular fundus. Fundus images were captured using the iPhone 13 camera.

Results and Discussion

A one-and-a-half-year-old, female non-descript intact cat weighing 4 kg was presented with the complaint of sudden "T" Tapetum; "NT" Non-Tapetum; "RV" Retinal Vein; "RA" Retinal Arteries; "OC" Optic Cup; "AC" Area Centralis Fundoscopic examination of the cat showed a hyperreflective tapetum with normal retinal vasculature and no visible abnormality of the optic disc (Fig. 2). In contrast, more pronounced retinal changes have been described in other reports of ivermectin toxicosis. Two affected dogs presented with blindness and mild obtundation, and ophthalmic examination revealed retinal edema and retinal folds (Kenny et al., 2008) [3] . Fundoscopy in those cases demonstrated multifocal fold-like grey opacities in the non-tapetal retina and linear dark lesions within the tapetal region. Small multifocal bullous retinal detachments were also noted dorsolateral to each optic disc, while the optic nerve heads and retinal vasculature remained normal (Arad et al., 2025) [8] . Parenteral fluid therapy with an isotonic crystalloid solution (0.9% normal saline) was administered for three consecutive days. Cefotaxime was given at a dose of 25 mg/kg body weight intravenously twice daily for five days. Diazepam was administered intramuscularly at 0.5 mg/kg body weight as a single dose. Dexamethasone was given intravenously at 0.5 mg/kg body weight for three days. In addition, vitamin C, vitamin B12, folic acid, and nicotinamide were administered intravenously at a dose of 0.5 ml for five days. Intravenous lipid emulsion (20%) therapy was advised as part of the treatment protocol at a dose of 1.5 ml/kg body weight administered over 10 minutes, followed by a continuous rate infusion (CRI) of 0.25 ml/kg for 30 minutes once daily for three days, as previously described for the management of ivermectin toxicosis in cats (Rajpurohit et al., 2024) [9] . However, the owner did not present the animal for further treatment, and therefore lipid emulsion therapy and follow-up evaluation could not be performed.

Conclusion

This case highlights the occurrence of acute neurological and ophthalmic manifestations associated with suspected ivermectin toxicosis in a young cat. The clinical findings of tremors, obtundation, blindness, and fixed mydriasis with absent menace, dazzle, and pupillary light reflexes were consistent with neurotoxic effects. Despite these functional deficits, fundoscopic examination revealed no structural abnormalities of the retina or optic disc. Early recognition of these clinical signs is important for the diagnosis and management of ivermectin toxicosis in cats.

References

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