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- Author or Editor: Francis D. Galey x
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Abstract
Case Description—A 4-month-old American Paint filly was evaluated because of sudden onset of ataxia that progressed to recumbency. Five additional horses from the same and neighboring premises developed signs of poor performance, generalized weakness, ataxia, and recumbency; 2 of those horses were also evaluated. A new batch of a commercial feed supplement had been introduced to the horses' diet on each farm within the preceding 3 days.
Clinical Findings—Other than recumbency, findings of physical and neurologic examinations of the foal were unremarkable. The other 2 horses had generalized weakness and mild ataxia, and 1 horse also had persistent tachycardia. The foal had mild leukocytosis with neutrophilia, hyperglycemia, and mildly high serum creatine kinase activity. Results of cervical radiography, CSF analysis, and assessments of heavy metals and selenium concentrations in blood and vitamin E concentration in serum were within reference limits. Feed analysis revealed high concentrations of the ionophore antimicrobial salinomycin.
Treatment and Outcome—The 5 affected horses survived, but the foal was euthanized. At necropsy, a major histopathologic finding was severe vacuolation within neurons of the dorsal root ganglia, which was compatible with ionophore toxicosis. The surviving horses developed muscle atrophy, persistent weakness, and ataxia.
Clinical Relevance—In horses, ionophore toxicosis should be considered as a differential diagnosis for acute weakness, ataxia, recumbency, or sudden death. Furthermore, ionophore toxicosis should be considered as a cause of poor performance, weakness, muscle wasting, and cardiac arrhythmias in horses. Surviving horses may have impaired athletic performance.
Abstract
Objective—To compare efficacy and safety of meso- 2,3-dimercaptosuccinic acid (DMSA) and Ca EDTA for treatment of experimentally induced lead toxicosis in cockatiels ( Nymphicus hollandicus).
Animals—137 (69 females, 68 males) healthy cockatiels between 6 months and 8 years old.
Procedure—Lead toxicosis was induced by placing lead shot in the gastrointestinal tract. Treatment with Ca EDTA (40 mg/kg of body weight, IM, q 12 h), DMSA (40 or 80 mg/kg, PO, q 12 h), and sodium sulfate salts (SSS; 0.5 mg/kg, PO, q 48 h) was initiated 4 days after induction of lead toxicosis. Blood lead concentrations were determined, using atomic absorption spectrophotometry. Number of birds surviving and blood lead concentrations were compared among groups.
Results—In Phase II of the study, administration of DMSA and Ca EDTA significantly decreased blood lead concentrations when used alone or in combination in birds with lead toxicosis. Addition of SSS did not result in further decreases in lead concentrations. Eight of 12 (66.7%) birds without lead toxicosis given 80 mg of DMSA/kg did not survive to the end of the study . Lesions related to treatment with chelating agents were not detected during necropsy.
Conclusions and Clinical Relevance—DMSA and Ca EDTA are effective chelating agents in cockatiels. Because DMSA is administered orally, it may be easier than other chelating agents for bird owners to administer at home. However, the narrow margin of safety of DMSA indicates that this agent should be used with caution. (Am J Vet Res 2000;61:935–940)
Summary
Staggers was diagnosed in sheep and cattle from the northern California coast. The diagnosis was made on the basis of history of ingestion of perennial ryegrass (Lolium perenne) stubble, clinical signs of transient ataxia, which was aggravated by stimulation, and nearly complete recovery after removal of ryegrass as the primary forage. Morbidity was high, but death did not occur in any affected animals. The toxic endophyte, Acremonium lolii, was in most lower leaf sheaths from the ryegrass. Injection of extracts of the ryegrass from affected farms into mice induced signs of toxicosis. Additionally, ryegrass from all 3 farms contained the tremorgenic mycotoxin, lolitrem-B.
