Recently, a technique was described for amplification of Rhodococcus equi-specific chromosomal and vapA DNA from blood and tracheal wash fluids. It was hypothesized that this technique would be more sensitive than standard culture techniques or serology for diagnosis of R. equi pneumonia in foals. Tracheal wash fluid, nasal swabs, whole blood samples, and serum samples from 56 foals with pneumonia were analyzed. Final clinical diagnosis was determined by the attending clinician on the basis of final interpretation of all available information about each foal, including clinical presentation, diagnostic test results, response to therapy, and outcome. Clinical diagnosis was used as a final reference standard for calculation of sensitivity, specificity, and predictive values for PCR, serology using an agar gel immunodiffusion test, and tracheal wash fluid culture. PCR of tracheal wash fluid using primers that recognized the vapA virulence plasmid of R. equi had a diagnostic sensitivity of 100% and specificity of 90.6%. Sensitivity and specificity were 57.1 and 93.8%, respectively, for standard microbiologic culture of tracheal wash fluid and 62.5 and 75.9%, respectively, for serology. PCR of tracheal wash fluid is more sensitive and specific for diagnosis of R. equi pneumonia than are other available diagnostic tests.Rhodococcus equi is a gram-positive, pleomorphic coccobacillus that causes pneumonia and enteritis in foals less than 6 months of age and has been associated with a variety of suppurative processes in immune-suppressed humans (19). The organism is worldwide in distribution and commonly isolated from soil and environmental samples (2,4,23). Strains of R. equi isolated from sick foals uniformly contain an 85-to 90-kb plasmid that carries the gene responsible for expression of a 15-to 17-kDa antigen of undetermined function (vapA) (24,25). Environmental strains of R. equi not associated with equine disease do not contain this plasmid.The onset of clinical signs of R. equi pneumonia in foals is often insidious, and the infection is not recognized until severe abscessation has occurred and prognosis is poor. Culture of the organism from tracheal wash (TW) fluid is currently considered the "gold standard" for diagnosis (7). However, it can be difficult to reliably grow R. equi from a single TW sample, possibly because of prior antibiotic administration (12,14) or the presence of multiple pathogenic bacterial species (5, 21). Hillidge reported that only 7 of 11 foals (62%) with positive R. equi cultures at necropsy, and 57 of 89 foals (64%) with radiographic evidence of lung abscessation, yielded R. equi on culture of TW (10). Other studies reported a 100% positive result on cultures of TW fluid from foals later confirmed to have R. equi pneumonia at necropsy (14,17).Recently, a technique was described for amplification of R. equi-specific chromosomal and vapA DNA from blood and TW fluids (20). It was hypothesized that this technique would be more sensitive than standard culture techniques or serology for dia...

Prolonged phenylbutazone administration caused hypoalbuminemia, neutropenia, changes in RDC arterial blood flow, and changes in VFA production. Veterinarians should monitor serum albumin concentrations and neutrophil counts and be cautious when making dosing recommendations for phenylbutazone treatment of horses.

Persistent hyperammonemia was diagnosed in 2 Morgan fillies with clinical signs that developed early in the postweaning period. Diagnostic evaluation, including routine serum chemistries, CBC, liver biopsy, hepatic ultrasonography, liver function test, and necropsy findings did not support a toxic, developmental, or infectious cause. Abnormal serum amino acid and urine orotic acid concentrations suggest that the foals may have had an inherited disorder, described in ncephalopathy, a clinical syndrome characterized by E dysfunction of the cerebral cortex, may occur as a consequence of hepatic insufficiency in horses of all ages.' Toxic hepatopathy associated with ferrous fumarate administration and Tyzzer's disease can cause acute fulminant disease with severe central nervous system (CNS) derangement in foals.2 Portosystemic shunts and biliary atresia are developmental anomalies that can cause variable neurologic signs, such as poor growth, and even death in foals.'~' Acute hepatic necrosis (Theiler's disease) causes similar signs in horses 2 years of age and older.6 Pyrrolizidine alkaloid intoxication and chronic active hepatitis can cause progressive weight loss and gradually developing CNS disturbances in adult horses.6 Several other causes of hepatic insult with the possibility of related CNS abnormalities include biliary obstruction, advanced neoplasia, hyperlipemia, aflatoxicosis, parasitism, and various bacterial This article describes 2 cases of encephalopathy in weanling foals that shared the same sire and whose mothers were sisters. Both foals were developmentally normal and healthy until approximately 2 to 3 weeks postweaning, when they began exhibiting abnormal behavior, unthriftiness, and poor growth. Hyperammonemia was persistently detected throughout the clinical course. Serum biochemical values, liver function tests, biopsy, ultrasonography, contrast study, and ultimately necropsy and histopathology could not explain the persistent hyperammonemia and progressively deteriorating condition, which ultimately led to humane euthanasia.An amino acid profile from the serum of both foals and the urine of one suggests that the weanlings may have had an inherited disorder described in humans as hyperornithinemia, hyperammonemia, and homocitrullinuria (HHH) syndrome. The disorder is thought to be caused by a defective mitochondrial transporter protein, such that the urea cycle mitochondrial step requiring ornithine for complete urea synthesis is deficient, thus causing hyperammonemia and hyperornithinemia. Materials and Methods Horse 1A 6-month-old Morgan filly was admitted to the veterinary teaching hospital (VTH) after 6 days of depression, respiratory wheezing, and anorexia. The referring veterinarian had administered systemic antimicrobials and vitamin supplementation PO for 4 days with no observed clinical improvement. The foal had been weaned at 5 months of age, and the owner reported 2 episodes of an "epileptic seizure" approximately 2 to 3 weeks after weaning. Clinical abnormalities observed on physi...

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