Mycotoxins are produced by specific fungus and only certain species of Aspergillus spp, Claviceps spp and Penicillium spp produce tremorgenic mycotoxins, the latter of which is most frequently seen in dogs. The principal toxins involved are roquefortine and penitrem A, produced as a byproduct of mold growth, but consumption of more than one toxin is common in clinical cases.
Penicillium crustosum may be isolated from several types of food, including meat, fruit, cereal and cereal products, cheese, spices, and nuts. Fungal synthesis of mycotoxins is factor-dependent. For example, an ambient temperature of 25°C and a pH of 5.7 optimize production of penitrem A by P. crustosum.
Tremorgenic mycotoxicosis can occur rapidly (within 2 - 3 hours) following ingestion of moldy rice, walnuts, dairy products and other spoiled food, often eaten indiscriminately by dogs. However, some dogs may vomit before any of these clinical signs appear.
After ingestion, the tremorgenic mycotoxins present in contaminated food are thought to cross the blood-brain barrier due to lipophilic properties. These mycotoxins alter central presynaptic release of the excitatory neurotransmitters glutamate and aspartate, and the inhibitory neurotransmitter gamma-aminobutyric acid, causing most of the clinical signs.
Clinically affected dogs present with acute abdominal pain, muscle tremors and fasciculation, ptyalism, vomiting, fever, tachycardia, mydriasis, nystagmus, hyperesthesia and seizures. In dogs which have died from mycotoxicosis, the lungs and large and small intestine are often hemorrhagic and edematous.
In the brain, lesions are isolated to the cerebellum, characterized by degeneration of Purkinje cells.
In order to differentiate from organophosphate toxicity, which has similar clinical symptoms, vomitus should be chemically tested for presence of organochlorine, organophosphor and carbamate insecticides. Biochemical detection of penetrim A needs to be distinguished from roquefortine C, a mycotoxin found in blue-vein cheese, that is relatively innocuous.
Treatment is usually supportive, with induction of vomiting to excavate the stomach. Apomorphine is usually given but gastric lavage may be required if severe intoxication is evident.
Supportive therapy includes intravenous fluid replacement, parenteral atropine and muscle relaxants such as diazepam, methocarbamol and anesthesia induction in severe cases with thiopentone followed by mechanical ventilation support.
Most affected dogs recover within a 24 - 48 hour period, although ataxia has been reported to persist up to three years in some cases.
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