Page 1126 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Nervous system 1101

VetBooks.ir Aetiology/pathophysiology although signs of hepatic dysfunction may be pres-
ent. Results of CSF analysis are frequently normal;
Intoxication of horses is caused by ingestion of corn
contaminated with Fusarium moniliforme and, occa-
present. The liquefactive necrosis seen grossly at
sionally, Fusarium tricinctum. Cool humid conditions elevations in protein and cell count are sometimes
favour the growth of the fungus and therefore this necropsy is usually diagnostic.
intoxication is most common in the late autumn
and early spring, with a worldwide occurrence. The Management
fungi produce the toxins (B1, B2 and B3) that are There is no specific treatment. Supportive care,
thought to be responsible for the condition. The removal of contaminated feed and elimination of
pathophysiology is not fully understood, but it is toxins by use of activated charcoal (2.2 kg/500 kg
thought that fumonisin (B1) plays a major role. This body weight in 4 litres of water q12 h for 24–36
toxin interferes with sphingolipid metabolism, dis- hours) are recommended.
rupting endothelial cell walls and basement mem-
branes. Liquefactive necrosis and malacia of the Prognosis
white matter of one or both cerebral hemispheres The prognosis is poor. Mortality rates of 40–84%
results. Lesions can be seen in other organs, primar- have been reported.
ily the liver. Fumonisins have also been implicated in
the aetiology of porcine pulmonary oedema, human METALDEHYDE TOXICOSIS
oesophageal cancer, hepatotoxicity in animals and
disease in poultry. Definition/overview
Metaldehyde toxicosis is uncommon in horses and
Clinical presentation may result from inadvertent ingestion or malicious
Clinical signs are seen on average 3 weeks after ini- poisoning.
tial ingestion of contaminated corn. Initial signs are
related to cerebral disease and include depression, Aetiology/pathophysiology
circling, aimless wandering, blindness and finally Metaldehyde is a polycyclic polymer of acetaldehyde
recumbency, paddling, coma and death. Morbidity in and is an ingredient in slug and snail baits. These
outbreaks has been reported as 14–100%. The clini- baits usually contain oats, bran, rice, soybeans, sor-
cal course is usually short (1–3 days), but may be pro- ghum or apples in addition to metaldehyde, and
longed in animals that recover, and survivors usually are readily consumed by horses. The CNS is pri-
have permanent neurological dysfunction. Horses marily affected, but the exact mechanism of action
with uncomplicated leucoencephalomalacia are not is unknown. Studies in mice have indicated that
usually febrile, which helps distinguish them from excitatory neurotransmitter levels are increased and
those affected by arboviral encephalomyelitides. inhibitory neurotransmitter levels are decreased.
The exact toxic dose in horses is not known. The
Differential diagnosis reported oral lethal dose in horses ranges from 60
EPM, verminous migrans, hepatic encephalopathy, to 100 mg/kg, which is less than the lethal dose
rabies, metabolic derangements, trauma, lightning reported for other species including ruminants,
strike and cerebral abscess should be considered, dogs, laboratory animals and poultry.
depending on the presentation.
Clinical presentation
Diagnosis Clinical signs are reported to begin within 15 min-
Clinical presentation and history of possible expo- utes of ingestion in the horse and include ataxia,
sure to contaminated feed should raise suspicion of hyperesthesia, muscular twitching and agitation.
leucoencephalomalacia, particularly if multiple ani- Convulsive spasms are commonly seen. Limb move-
mals are affected. Definitive diagnosis is difficult ments resembling stringhalt, tachycardia, tachy-
ante mortem. Haematology is usually unremarkable, pnoea, weak pulse and profuse sweating are other