OBJECTIVE To compare ammonia concentrations in arterial blood, venous blood, and CSF samples of dogs with and without extrahepatic portosystemic shunts (EHPSS). ANIMALS 19 dogs with congenital EHPSS and 6 healthy control dogs. PROCEDURES All dogs underwent a physical examination and then were anesthetized for transsplenic portal scintigraphy to confirm the presence or absence of EHPSS. While dogs were anesthetized, arterial and venous blood samples and a CSF sample were simultaneously collected for determination of ammonia concentration, which was measured by use of a portable blood ammonia analyzer (device A) and a nonportable biochemical analyzer (device B). Results were compared between dogs with EHPSS and control dogs. RESULTS Arterial, venous, and CSF ammonia concentrations for dogs with EHPSS were significantly greater than those for control dogs. For dogs with EHPSS, ammonia concentrations in both arterial and venous blood samples were markedly increased from the reference range. There was a strong positive correlation between arterial and venous ammonia concentrations and between blood (arterial or venous) and CSF ammonia concentrations. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that blood and CSF ammonia concentrations in dogs with EHPSS were greater than those for healthy dogs and were strongly and positively correlated, albeit in a nonlinear manner. This suggested that the permeability of the blood-brain barrier to ammonia may be abnormally increased in dogs with EHPSS, but further investigation of the relationship between blood or CSF ammonia concentration and clinical signs of hepatic encephalopathy or the surgical outcome for dogs with EHPSS is warranted.

Objective—To investigate clinical use of proton magnetic resonance spectroscopy (1H MRS) and to compare metabolic brain bioprofiles of dogs with and without hepatic encephalopathy. Animals—6 dogs with hepatic encephalopathy and 12 control dogs. Procedures—Conventional MRI and single-voxel 1H MRS were performed with a 3-T magnet. Images for routine MRI planes and sequences were obtained. Single-voxel 1H MRS was performed with a point-resolved sequence with a short echo time (35 milliseconds) and voxel of interest placement at the level of the basal ganglia. Metabolites of interest included the glutamine-glutamate complex (sum quantification of glutamate and glutamine), myoinositol, N-acetyl aspartate, total choline, and creatine. Data were analyzed with postprocessing fitting algorithm software, and metabolite concentration relative to water and ratios with creatine as the reference metabolite were calculated. Results—Compared with control dogs, dogs with hepatic encephalopathy had specific changes, which included significantly higher concentration relative to water of the glutamine-glutamate complex and significantly lower concentration of myoinositol. Choline and N-acetyl aspartate concentrations were also slightly lower in dogs with hepatic encephalopathy than in control dogs. No differences in creatine concentration were detected between groups. Conclusions and Clinical Relevance—1H MRS aided in the diagnosis of hepatic encephalopathy in dogs, and findings supported the assumption that ammonia is a neurotoxin that manifests via glutamine-glutamate complex derangements. Use of 1H MRS may provide clinically relevant information in patients with subclinical hepatic encephalopathy, equivocal results of bile acids tests, and equivocal ammonia concentrations or may be helpful in monitoring efficacy of medical management.

A 2-year old castrated male Alaskan malamute was referred with primary complaints of marked anemia, hemeglobinuria and depression. Laboratory tests revealed canine babesiois with severe anemia. The dog was treated by blood transfusion and beneril (diminazene aceturate, 3.5 mg/kg IM). Two days after Beneril injection, the dog suddenly showed ataxia progressing to paresis. MRI revealed irregularly diffused lesions in the cerebellum. The case was tentatively diagnosed as cerebellar encephalopathy caused by diminazene toxicity. The dog successfully recovered following steroid therapy.

Early epidemiological information indicated that bovine spongiform encephalopathy (BSE) originated from scrapie in sheep. The question arose if scrapie in North America would induce a BSE-like disease in cattle. Six years ago, we reported that brain tissue from sheep with scrapie caused a neurologic disease when injected directly into the brains of cattle, but the disease induced was different from BSE as it occurs in the United Kingdom and Europe. Here, we report that cattle fed raw brain or meat and bone meal and tallow prepared from sheep with scrapie remained normal for 8 years after exposure. This work indicates that cattle are highly resistant to North American scrapie by the oral route.

The primary objective of this study was to determine whether or not Spiroplasma mirum would be capable of producing lesions of transmissible spongiform encephalopathy (TSE) when inoculated in raccoons (Procyon lotor) and, if that was possible, to compare the clinicopathological findings with those of transmissible mink encephalopathy (TME) in the same experimental model. For this purpose, 5 groups (n 5 5) of raccoon kits were inoculated intracerebrally with either S. mirum and/or TME. Two other groups (n 5 5) of raccoon kits served as sham-inoculated controls. All animals inoculated with TME, either alone or in combination, showed clinical signs of neurologic disorder and were euthanized within 6 mo post-inoculation (MPI). None of the carcasses revealed gross lesions. Spongiform encephalopathy was observed by light microscopy and the presence of abnormal disease-causing prion protein (PrPd) was detected by immunohistochemistry (IHC) and Western blot (WB) techniques in only the raccoons administered TME. Raccoons inoculated with Spiroplasma, but not administered TME agent, were euthanized at 30 MPI. They did not show clinical neurologic signs, their brains did not have lesions of spongiform encephalopathy, and their tissues were negative for S. mirum by polymerase chain reaction (PCR) and for PrPd by IHC and WB techniques. The results of this study indicate that Spiroplasma mirum does not induce TSE-like disease in raccoons.