Objective—To determine the usefulness of retina samples for detection of disease-associated prion protein by use of a commercially available enzyme immunoassay (EIA) intended for rapid identification of sheep and cattle with transmissible spongiform encephalopathies (TSEs).
Samples—Retina, brainstem at the level of the obex, and retropharyngeal lymph node samples obtained from 15 TSE-inoculated sheep (scrapie [n = 13] or transmissible mink encephalopathy passaged through a bovid ); retina and brainstem samples obtained from 11 TSE-inoculated cattle (transmissible mink encephalopathy passaged through a bovid  or classical BSE ); and negative control tissue samples obtained from 2 sheep and 2 cattle that were not inoculated with TSEs.
Procedures—Tissue samples were homogenized and analyzed for detection of abnormally folded disease-associated prion protein with a commercially available EIA and 2 confirmatory assays (western blot analysis or immunohistochemical analysis).
Results—Retina sample EIA results were in agreement with results of brainstem sample EIA or confirmatory assay results for negative control animals and TSE-inoculated animals with clinical signs of disease. However, TSE-inoculated animals with positive confirmatory assay results that did not have clinical signs of disease had negative retina sample EIA results. Retina sample EIA results were in agreement with brainstem sample immunohistochemical results for 4 TSE-inoculated sheep with negative retropharyngeal lymph node EIA results.
Conclusions and Clinical Relevance—Results of this study suggested that retina samples may be useful for rapid EIA screening of animals with neurologic signs to detect TSEs.
A 15-year-old sexually intact female ring-tailed lemur (Lemur catta) was evaluated for a heart murmur and progressive radiographic cardiomegaly.
The lemur was clinically normal at the time of initial evaluation. Results of transthoracic echocardiography performed when the animal was anesthetized indicated mitral valve stenosis and severe left atrial dilation. Three months later, signs of left-sided congestive heart failure (CHF; coughing, exercise intolerance, and tachypnea) were observed and confirmed by the presence of radiographic pulmonary edema.
TREATMENT AND OUTCOME
Medical treatment that consisted of aspirin, benazepril, furosemide, pimobendan, spironolactone, and ultimately torsemide in lieu of furosemide successfully controlled the lemur's clinical signs for 33 months after the development of CHF. Euthanasia was then elected on the basis of perceived poor quality of life because tachypnea became refractory to progressively higher dosages of diuretic. Necropsy confirmed mitral stenosis with severe left atrial dilation and chronic pulmonary congestion.
The present report described the long-term medical management of CHF secondary to mitral stenosis in a lemur. Mitral stenosis was suspected to be a congenital defect, similar to the cause of mitral stenosis reported for dogs and cats, rather than to be an acquired change in association with rheumatic heart disease as commonly occurs for people. The lemur's CHF was well managed for 33 months with treatment, including pimobendan, which was well tolerated.