The clinical, neuropathologic, and magnetic resonance (MR) imaging features in four cats with necrosis of the hippocampus and piriform lobe are described. All cats had acute generalized seizures and behavioral changes including aggression, salivation, polyphagia, and disorientation. Routine hematologic, serum chemistry, and cerebrospinal fluid analyses were normal. MR imaging abnormalities were restricted to the area of the hippocampus and piriform lobe. The lesions were T2-hyperintense, T1-hypointense, and were characterized by various degrees of contrast enhancement. Lesions were consistent with necrotizing encephalitis. Two cats were euthanized and underwent postmortem examination within a week after MR imaging due to the lack of response to antiepileptic drug therapy and progressive neuropathy. The remaining two cats lived for about four months and were then euthanized because of persistent behavioral and neurologic signs; only one of these cats underwent postmortem examination with histopathologic examination. Histopathological findings were typical of severe, diffuse, bilateral symmetric necrosis, and degeneration of neurons in the hippocampus and piriform lobe, but an etiologic agent was not apparent. This apparently unique feline syndrome, now reported in Switzerland and Italy, has no known cause at this time.
The anaerobic metabolism of indoleacetate (indole-3-acetic acid [IAA]) in the denitrifying betaproteobacterium Azoarcus evansii was studied. The strain oxidized IAA completely and grew with a generation time of 10 h. Enzyme activities that transformed IAA were present in the soluble cell fraction of IAA-grown cells but were 10-fold downregulated in cells grown on 2-aminobenzoate or benzoate. The transformation of IAA did not require molecular oxygen but required electron acceptors like NAD + or artificial dyes. The first products identified were the enol and keto forms of 2-oxo-IAA. Later, polar products were observed, which could not yet be identified. The first steps likely consist of the anaerobic hydroxylation of the N-heterocyclic pyrrole ring to the enol form of 2-oxo-IAA, which is catalyzed by a molybdenum cofactor-containing dehydrogenase. This step is probably followed by the hydrolytic ring opening of the keto form, which is catalyzed by a hydantoinase-like enzyme. A comparison of the proteome of IAA- and benzoate-grown cells identified IAA-induced proteins. Owing to the high similarity of A. evansii with strain EbN1, whose genome is known, we identified a cluster of 14 genes that code for IAA-induced proteins involved in the early steps of IAA metabolism. These genes include a molybdenum cofactor-dependent dehydrogenase of the xanthine oxidase/aldehyde dehydrogenase family, a hydantoinase, a coenzyme A (CoA) ligase, a CoA transferase, a coenzyme B 12 -dependent mutase, an acyl-CoA dehydrogenase, a fusion protein of an enoyl-CoA hydratase and a 3-hydroxyacyl-CoA dehydrogenase, a beta-ketothiolase, and a periplasmic substrate binding protein for ABC transport as well as a transcriptional regulator of the GntR family. Five predicted enzymes form or act on CoA thioesters, indicating that soon after the initial oxidation of IAA and possibly ring opening, CoA thioesters are formed, and the carbon skeleton is rearranged, followed by a CoA-dependent thiolytic release of another CoA thioester. We propose a scheme of an anaerobic IAA metabolic pathway that ultimately leads to 2-aminobenzoyl-CoA or benzoyl-CoA.
Alveolar echinococcosis is a rare metacestodal infection of humans and domestic animals with Echinococcus multilocularis and predominantly affects the liver. In humans, diagnosis is based on serology, ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI), techniques that have not yet been validated for the diagnosis of alveolar echinococcosis in dogs. Therefore, the purpose of this retrospective study was to describe the radiographic, ultrasonographic, and CT appearance of canine alveolar echinococcosis. Eleven dogs with confirmed alveolar echinococcosis (PCR or histology from biopsy material of metacestode tissue) diagnosed between 1995 and 2003 were included in the study. The age of the dogs at initial presentation ranged from 7 months to 10.5 years. Abdominal radiographs were made in nine animals, abdominal ultrasonography was performed in 10 dogs, and two CT studies in one dog, respectively. The history, clinical presentation, and laboratory findings for the 11 dogs were unspecific, the most frequent clinical finding being nonpainful progressive abdominal distention. All radiographed dogs had large liver masses; they contained small mineralizations in five. The most frequent ultrasonographic finding was multiple large cavitary masses with or without wall mineralizations. Seven animals received surgical and subsequent medical therapy with albendazole (10mg/kg) and all went into clinical remission. This study reviewed for the first time imaging findings associated with alveolar echinococcosis. The disease has to be included in the list of differential diagnoses in dogs with large, cavitary liver masses, particularly when mineralization is noted.
Background: The diagnosis of feline pancreatic disease is difficult, because clinical abnormalities and routine noninvasive diagnostic tests are unreliable.Objective: The purpose of this study was to investigate by Doppler ultrasonography if vascularity and blood volume differs in the otherwise ultrasonographically normal and diseased feline pancreas.Animals: Thirty-six client owned cats. Methods: The pancreas was examined with B-mode and contrast-enhanced color and power Doppler ultrasonography. Doppler images were analyzed with a computer program: parameter fractional area represents a vascularity index and colorweighted fractional area assesses blood volume.Results: Based on the B-mode findings, the pancreas was considered normal in 11 clinically healthy cats and diseased in 25 cats of which 4 were clinically healthy and 21 had clinical signs consistent with pancreatic disease. Histologic or cytologic samples were taken in all diseased pancreata. Fifteen samples were of diagnostic quality: purulent or mixed cellular inflammation (8), nodular hyperplasia (4), and neoplasia (3) were identified. Vascularity and blood volume for all Doppler methods was significantly higher in cats with pancreatic disease. Significantly higher Doppler values were detected with power Doppler than with color Doppler, and with postcontrast color and power Doppler than with precontrast Doppler technologies.Conclusion: Contrast-enhanced Doppler ultrasonography appears feasible in the feline pancreas. Significant differences were found between normal cats and those with evidence of pancreatic pathology. Further studies are needed to evaluate its use for the differentiation of pancreatic disorders and in cats suspected to have pancreatic disease but without B-mode ultrasonographic changes of the pancreas.
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