Canine and Feline Epilepsy. Luisa De Risio
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Clinical presentation
Ingestion of contaminated material results in salivation, vomiting, diarrhoea, restlessness and panting, generally followed by severe generalized muscle tremors (generally 2–3 h following ingestion), seizures, ataxia, tachycardia and hyperthermia (Lowes et al., 1992; Young et al., 2003; Eriksen et al., 2010). Seizures can sometimes be triggered by auditory (e.g. loud noise), visual (e.g. bright light) and tactile stimuli. Status epilepticus can occur.
Diagnosis
The presumptive diagnosis is based on the history of ingestion of mouldy food or compost and exclusion of other aetiologies. Definitive diagnosis is made by identification of the mycotoxins by means of laboratory analysis of samples of the ingested material, gastric content, serum or urine. Liquid chromatography-mass spectrometry can be used to screen for the mycotoxins penitrem A and roquefortine in serum and urine samples.
Management
Treatment involves reducing toxin absorption (by induction of emesis and/or gastric lavage and administration of activated charcoal and an osmotic cathartic) (Table 4.1), methocarbamol to control the muscle tremors and AEMs (see Table 4.1 and Chapters 12 and 24) and supportive care (intravenous fluid therapy, convective whole body cooling and, in severely affected animals, intubation and ventilation). Emesis should be induced in asymptomatic animals that present within 15–30 min after suspected or confirmed ingestion of mouldy food or non-corrosive waste material (Barker et al., 2013). Administration of activated charcoal should be repeated over 1–3 days due to entero-hepatic recirculation of mycotoxins. Seizures may not respond to diazepam administration and it has been suggested that poor or no response to diazepam is suggestive of mycotoxicosis (Barker et al., 2013). If there is inadequate response after the first administration of diazepam, alternative AEMs such as levetiracetam, phenobarbital, propofol and ketamine (see Table 4.1 and Chapter 24) should be used.
Prognosis
The majority of dogs recover in a few days following prompt and appropriate treatment; however, severely affected animals may take several months to achieve complete resolution of neurological signs (Eriksen, 2010).
Animal-related Poisoning
Neurological signs including seizures can occur following exposure to venom of several animal species including insects (bee, wasp), spiders, reptiles and amphibians.
Toad
Overview
There are more than 200 species of Bufo toads in the world and they all have parotid glands on their dorsum that release toxic substances when the toad is attacked or threatened. These include bufotoxins and bufagenins, bufotenine, dopamine, epinephrine, norepinephrine, serotonin and indolealkylamines. Most small animals do not consume Bufo toads. Toxicosis occurs in animals that masticate or hold the toad instead of just biting and then releasing it. The toxins are rapidly absorbed through the oral mucosa and enter the systemic circulation. The toxins can also be absorbed through the gastric mucosa following ingestion, through open skin wounds and across the conjunctiva (Peterson and Roberts, 2006). Toad intoxication has been diagnosed in dogs and cats, however, dogs are more commonly affected (Roberts et al., 2000). Chances of exposure are higher when toads are most active (i.e. in the evening after high rainfall or with high temperatures).
Mechanism of action
Bufotoxins and bufagenins are digitalis-like compounds, which result in cardiac arrhythmias. In addition, bufotoxins cause vasoconstriction. Bufotenins are hallucinogenic. Epinephrine, norepinephrine and dopamine cause tachycardia, hypertension and seizures.
Clinical presentation
The toxins produced by the Bufo marinus toad (Fig. 4.6) (which is found in Florida, USA and north and north-east Australia) have been reported to result in neurological signs including seizures, ataxia, nystagmus, extensor rigidity, opisthotonos and stupor in dogs (Roberts et al., 2000). The neurological signs occur within minutes to 1 h after exposure and are preceded by oral mucous membrane hyper-aemia, hypersalivation and pawing at the mouth. Cardiac arrhythmias often occur. Severity of signs is directly proportional to toxin dose. Death may occur following prolonged seizure activity and cerebral oedema or cardiac arrest.
The European Bufo vulgaris (common toad) and the Asian Bufo gargarizans are related species to the Bufo marinus toad and can also cause poisonings, although seizures have not been described (Peterson et al., 2006).
Fig. 4.6a, b. Bufo marinus toad (courtesy of Courtney Freeman ©).
Diagnosis
No true confirmatory tests exist for Bufo toad intoxication. Clinical diagnosis is based on history of exposure and presenting signs. Digoxin serum immunoassays can identify the digitalis-like compounds produced by the toad parotid glands in the serum of the intoxicated animal.
Management
Treatment involves decontamination by thorough flushing of the oral cavity with running water for at least 5 min, AEMs (see Table 4.1; Chapters 12 and 24), detection and management of cardiac arrhythmias, intravenous fluids and diuretics to promote urinary excretion of the toxin. Emesis, gastric lavage or endoscopic removal is indicated in the rare event of toad ingestion.
Prognosis
Overall mortality is low in animals treated within a few hours of exposure (Roberts et al., 2000; Reeves, 2004).
Therapeutic Agents and Supplements
Metronidazole
Overview
Metronidazole is a nitroimidazole antibacterial and antiprotozoal agent used in the treatment of giardiasis, anaerobic infections and inflammatory bowel disease (Evans et al., 2003). Neurotoxicity from metronidazole has been reported in dogs receiving as low as 67 mg/ kg/day for an average of 3–14 days (Dow, 1989) or 60.3 mg/kg/day for 44.9 days (Evans et al., 2003), and in cats receiving 111 mg/kg/ day for 9 weeks or 58 mg/kg/day for 6 months (Caylor and Cassimatis, 2001).
Mechanism of action
The neurotoxic mechanism of metronidazole has not been identified. Proposed mechanisms include thiamine antagonism and inhibition of neuronal protein synthesis.