Canine and Feline Epilepsy. Luisa De Risio
Poisonous Plants
Seizures have been reported following exposure to the plants listed in Box 4.7 (Barr, 2006).
Several of these plants cause vomiting. The gastric content from vomitus or lavage fluids can be submitted for plant material identification. Treatments for toxic plant ingestion include decontamination and symptomatic and supportive care (including AEMs) (see Table 4.1, Chapters 12 and 24). Detailed information on geographic distribution of these plants and clinical presentation, treatment and prognosis following exposure is beyond the scope of this book and can be found elsewhere (Barr, 2006).
Box 4.7. Poisonous plants.
Amaryllis (Amaryllis spp.)
Angel’s trumpet (Brugmansia spp.)
Aralia, balfour aralia, dinner plate aralia, ming aralia, geranium-leaf aralia, wild coffee, coffee tree (Polyscias spp.)
Black locust (Robinia pseudoacacia)
Bleeding heart, Dutchman’s breeches, squirrel corn, staggerweed (Dicentra spp.)
Box, common box, boxwood (Buxus sempervirens)
Broom (Cytisus spp.)
Candelabra cactus, false cactus, mottled spurge, dragon bones (Euphorbia lactea)
Castor bean (Ricinus communis)
Chinaberry tree (Melia azedarach)
Croton (Croton tiglium)
English ivy, Irish ivy, common ivy (Hedera helix)
Euphorbium (Euphorbia resinifera)
Golden chain tree (Laburnum anagyroides)
Golden corydalis, bulbous corydalis, scrambled
eggs, fitweed, fumitory (Corydalis spp.)
Meadow saffron, autumn crocus (Colchicum autumnale)
Mediterranean thistle (Atractylis gummifera)
Milkweed, butterfly weed (Asclepias spp.)
Mimosa, silk tree (Albizia julibrissin)
Pencil tree, milkbush, Indian tree, rubber euphorbia, finger tree, naked lady (Euphorbia tirucalli)
Persian violet, alpine violet, sowbread (Cyclamen spp.)
Sago palm, leatherleaf palm, Japanese fern palm (Cycas revoluta, Cycas spp.)
Sandbox tree, monkey pistol (Hura crepitans)
Schefflera, umbrella tree, rubber tree, starleaf (Schefflera spp.)
Sea onion (Urginea maritima)
Spurge, creeping spurge, donkey tail (Euphorbia myrisinites)
Squill, starry hyacinth, autumn scilla, hyacinth scilla, Cuban lily, Peruvian jacinth, hyacinth of Peru, bluebell (Scilla spp.)
Snowdrop (Galanthus nivalis)
Tobacco, tree tobacco (Nicotiana spp.)
Tung oil tree (Aleurites spp.)
Water hemlock, cowbane (Cicuta spp.)
White cedar (Thuja occidentalis)
Yellow jessamine, Carolina jessamine (Gelsemium sempervirens)
Yesterday today and tomorrow (Brunfelsia spp.)
Zamia (Macrozamia spp.)
Zulu potato, climbing onion (Bowiea volubilis)
Blue-green algae (cyanobacteria)
Overview
Blue-green algae (cyanobacteria) are commonly found growing in fresh and salt water in temperate areas worldwide. Under certain climatic and nutritional conditions cyano-bacteria reproduce explosively, resulting in algae blooms that accumulate at the water surface and sometimes produce hepatotoxins and/or neurotoxins. Dogs can be exposed by drinking or ingesting contaminated water while swimming (Edwards et al., 1992; Gugger et al., 2005; Puschner et al., 2010; Elford et al., 2012; Faassen et al., 2012). Cats seem to be affected less commonly than dogs.
Mechanism of action
Blue-green algae Anabaena, Aphanizomenon, Lyngbya and Oscillatoria can produce the neurotoxins anatoxin-a (a potent postsynaptic depolarizing neuromuscular blocking agent) and anatoxin-as (a potent acetylcholinesterase inhibitor) (Hooser and Talcott, 2006).
Clinical presentation
Clinical signs often occur very rapidly (10 min to a few hours) after oral exposure and include salivation, lacrimation, urination and defecation, muscle rigidity, muscle tremors, seizures, appendicular paralysis, respiratory paralysis and death within 30 to 60 min of the onset of clinical signs.
Diagnosis
Confirmation of exposure can be achieved by detection of the algae in gastric contents or suspect water source and detection of the toxins in stomach contents or liver.
Management
Treatment includes decontamination (bathing if the animal went into the contaminated water, gastric lavage, activated charcoal and/ or a cathartic) (Table 4.1), AEMs in seizuring animals (see Table 4.1 and Chapters 12 and 24) and aggressive supportive care including intravenous fluid therapy, atropine (in animals exposed to anatoxin-as neurotoxin) and respiratory support (Hooser and Talcott, 2006).
Prognosis
The prognosis for animals that show clinical signs is guarded to poor.
Mycotoxins
Penitrem A and roquefortine
Overview
The mycotoxins penitrem A (produced by Penicillium crustorum) and roquefortine (produced predominately by Penicillium roqueforti as well as other Penicillium species including P. crustorum) can be found in mould-contaminated cheese, bread, rice, walnuts and decaying organic matter such as silage, garbage and compost. Absorption after oral ingestion is rapid. Dogs are more commonly affected than cats, probably because of their tendency to scavenge and ingest rotting material (Barker et al., 2013).
Mechanism of action
The exact mechanism of action of these mycotoxins is unknown; however, results of in vitro studies indicate that penitrem A may antagonize the release or action of glycine in the CNS and interfere with the release of glutamate, aspartate and gamma-aminobutyric acid in central and peripheral synapses (Young et al.,