Diagnosis of Amanita toxicosis in a dog with acute hepatic necrosis.

Poisoning with amanitin-containing hepatotoxic mushrooms demands extensive efforts from clinicians, toxicologists, and pathologists. Presumptive diagnoses are established by positive identification of the suspect mushroom along with the occurrence of consistent clinical signs. If the animal dies, hepatic lesions may suggest exposure to amanitin-containing mushrooms; however, lesions are nonspecific. A 15-week-old female Dachshund was presented to the referring veterinarian for acute onset of lethargy that quickly progressed to sternal recumbency. Despite supportive care, the dog remained lethargic and died approximately 12 hours after initial presentation. A pale tan liver was noted at necropsy. Microscopically, the liver showed panlobular coagulative necrosis of hepatocytes. A presumptive diagnosis of amanitin poisoning was based on suspect history of exposure to mushrooms, clinical signs, and pathologic findings. Exposure to amanitin was confirmed through detection of alpha-amanitin in the liver by liquid chromatography/mass spectrometry. The objective of this case report is to illustrate the essential components to a successful diagnostic work-up of a suspect case of hepatotoxic mushroom poisoning. Although hepatotoxic mushroom poisoning has been documented in dogs before, confirmatory techniques for biologic specimens have not been used previously in diagnostic investigations.

Angiostrongylus cantonensis infection in captive Geoffroy's tamarins (Saguinus geoffroyi).

CASE DESCRIPTION: 3 Geoffroy's tamarins (Saguinus geoffroyi) in a zoo in east central Alabama developed neurologic signs shortly after a tamarin kept in the same enclosure was found dead. CLINICAL FINDINGS: Neurologic abnormalities varied among animals and were progressive. One female tamarin with a head tilt, nystagmus, mild ataxia, and paresis of a thoracic limb had gram-positive cocci present in an ear canal with otitis media and interna suspected. Another female with mild ataxia attributed to previous tail amputation developed seizures, and a male tamarin with tail tip trauma also developed ataxia. TREATMENT AND OUTCOME: The tamarin with suspected otitis received cephalexin and prednisolone, but neurologic signs worsened, and the patient died. Preliminary examination of necropsy samples revealed severe meningoencephalitis in both deceased tamarins. Prednisolone and phenobarbital treatment was initiated for the tamarin with seizures, but rapid neurologic deterioration led to euthanasia. Further histologic examination of the 3 deceased tamarins revealed meningitis and acute perivascular hemorrhage in the meninges. Parasites morphologically consistent with Angiostrongylus (Parastrongylus) cantonensis were present in the lungs of 1 animal and in the meninges of 2. The surviving tamarin received cephalexin for tail tip trauma and prednisolone and albendazole for presumed meningoencephalitis and parasitic infection but had permanent neurologic deficits. CLINICAL RELEVANCE: To our knowledge, these represent the first cases of A cantonensis infection in Geoffroy's tamarins and the first report of its presence in the United States not associated with a major shipping port. The presence of a mature worm in the lungs of 1 tamarin suggested completion of the parasite life cycle, previously reported only in rats.