Anibal Guillermo Armién

Spontaneous and Experimental Glycoprotein Storage Disease of Goats Induced by Ipomoea carnea subsp fistulosa (Convolvulaceae)

Spontaneous and experimental poisoning with the swainsonine-containing and calystegine-containing plant Ipomoea carnea subsp fistulosa is described. Three of 8 goats presenting with emaciation, weakness, symmetrical ataxia, posterior paresis, proprioceptive deficits, abnormal posture, abnormal postural reaction, and muscle hypertonia were necropsied. I fistulosa was suspected to be the cause of the neurologic disease in all cases. An experiment was conducted to confirm the diagnosis using 12 goats and diets containing 3 different concentrations of the plant. All goats fed I fistulosa developed neurological signs that were similar to those observed in the spontaneous intoxication. Muscle atrophy and pallor were the only macroscopic changes observed in spontaneous and in experimental intoxication. Histological lesions of spontaneous and experimental animals were similar. The most prominent lesion was cytoplasmic vacuolation in neurons of the central and the autonomous nervous system, pancreatic acinar cells, hepatocytes, Kupffer cells, follicular epithelial cells of the thyroid gland, and macrophages of the lymphatic tissues. Neuronal necrosis, axonal spheroids formation, and astrogliosis were additionally observed in the brain. Ultrastructurally, the cytoplasmic vacuoles consisted of distended lysosomes surrounded by a single-layered membrane. Nonreduced end-rests or sequence of α-Man, α-Glc, β(1–4)-GlcNAc, and NeuNAc on lysosomal membrane were revealed by lectin histochemistry. Samples of plants used in the experimental trial contained swainsonine and calystegine and their intermediary derivate. We conclude that I fistulosa induces a glycoprotein storage disease primarily based on the inhibition of the lysosomal α-mannosidase by the alkaloid swainsonine.

Comparative skeletal muscle histopathologic and ultrastructural features in two forms of polysaccharide storage myopathy in horses.

Polysaccharide storage myopathy (PSSM) has been found in more than 35 different horse breeds through identification of abnormal storage of polysaccharide in muscle biopsies. A dominant mutation in the glycogen synthase 1 gene (GYS1) accounts for a substantial proportion of PSSM cases in at least 17 breeds, including Quarter Horses, but some horses diagnosed with PSSM by muscle histopathologic analysis are negative for the mutation. We hypothesized that a second distinct form of glycogen storage disease exists in GYS1 -negative horses with PSSM. The objectives of this study were to compare the histopathologic features, ultrastructure of polysaccharide, signalment, history, and presenting complaints of GYS1 -negative Quarter Horses and related breeds with PSSM to those of GYS1 -positive horses with PSSM. The total histopathologic score in frozen sections of skeletal muscle stained with hematoxylin and eosin, periodic acid Schiff (PAS) and amylase-PAS stains from 53 GYS1-negative horses did not differ from that of 52 GYS1 -positive horses. Abnormal polysaccharide was fine granular or homogenous in appearance (49/53; 92%), often amylase-sensitive (28/53; 53%), more commonly located under the sarcolemma, and consisting of β glycogen particles in GYS1 -negative horses. However, in GYS1 -positive horses, abnormal polysaccharide was usually coarse granular (50/52; 96%), amylase-resistant (51/52; 98%), more commonly cytoplasmic, and consisting of β glycogen particles or, in some myofibers, filamentous material surrounded by β glycogen particles. Retrospective analysis found that GYS1 -negative horses (n = 43) were younger at presentation (4.9 ± 0.6 years vs. 6.7 ± 0.3 years for GYS1 -positive horses) and were more likely to be intact males than GYS1 -positive horses (n = 160). We concluded that 2 forms of PSSM exist and often have distinctive abnormal polysaccharide. However, because evaluation of the histologic appearance of polysaccharide can be subjective and affected by age, the gold standard for diagnosis of PSSM at present would appear to be testing for the GYS1 mutation followed by evaluating muscle biopsy for characteristic abnormal polysaccharide in those horses that are negative for the mutation.

Clinical Findings, Lesions, and Viral Antigen Distribution in Great Gray Owls (Strix nebulosa) and Barred Owls (Strix varia) with Spontaneous West Nile Virus Infection

Abstract West Nile Virus (WNV) infection manifests itself clinically and pathologically differently in various species of birds. The clinicopathologic findings and WNV antigen tissue distribution of six great gray owls (Strix nebulosa) and two barred owls (Strix varia) with WNV infection are described in this report. Great gray owls usually live in northern Canada, whereas the phylogenetically related barred owls are native to the midwestern and eastern United States and southern Canada. Naturally acquired WNV infection caused death essentially without previous signs of disease in the six great gray owls during a mortality event. Lesions of WNV infection were dominated by hepatic and splenic necrosis, with evidence of disseminated intravascular coagulation in the great gray owls. WNV antigen was widely distributed in the organs of the great gray owls and appeared to target endothelial cells, macrophages, and hepatocytes. The barred owls represented two sporadic cases. They had neurologic disease with mental dullness that led to euthanasia. These birds had mild to moderate lymphoplasmacytic encephalitis with glial nodules and lymphoplasmacytic pectenitis. WNV antigen was sparse in barred owls and only present in a few brain neurons and renal tubular epithelial cells. The cause of the different manifestations of WNV disease in these fairly closely related owl species is uncertain.

Clinical and Morphologic Changes in Ewes and Fetuses Poisoned by Ipomoea Carnea Subspecies Fistulosa

Intoxication with Ipomoea carnea has been reported in goats, sheep, and cattle in tropical regions worldwide. The disease has been characterized only in goats; therefore, the present study was conducted in sheep. Nine animals were fed feed rations that contained 3 different concentrations of Ipomoea carnea subsp. fistulosa. Individual intake varied between 10.5 and 135.2 g of fresh plant per kilogram of body weight (BW) per day. Animals first showed clinical signs between day 43 and day 63. The maximum survival time was 133 days. Sheep presented with weight loss and neurologic abnormalities. Neurologic signs were dominated by marked depression, abnormal behavior, and musculoskeletal weakness, with poorly defined motor and proprioceptive deficits. In mature animals, cytoplasmic vacuolation, consistent with accumulation of secondary lysosomes, affected neurons, astrocytes, exocrine pancreatic acinar epithelia, hepatocytes and Kupffer cells, renal tubular epithelia, thyroid follicular epithelia, cortical adrenal epithelia, endothelia and perivascular cells, and macrophages in lymph nodes and spleen. In the central nervous system, there was axonal degeneration and astrogliosis. Abortion was observed as early as day 22 of the trial. In fetal tissues and placenta of chronically poisoned ewes, cytoplasmic vacuolation was histologically detected in neurons, exocrine pancreatic acinar epithelia, hepatocytes, renal tubular epithelia, and thyroid follicular epithelia. All the sheep developed a glycoprotein storage disease, with lysosomal accumulation of N-glycosidically linked oligosaccharides, which was indistinguishable from that induced by the alkaloid swainsonine alone.

Estudos complementares sobre a toxidez de Lantana camara (Verbenaceae) em bovinos

An outbreak of poisoning by Lantana camara var. aculeata in cattle was diagnosed in the county of Quatis, State of Rio de Janeiro. The animals, after travelling by foot, were put, hungry, for a few days, on a pasture highly infested by the plant. The toxicity of the plant was proved experimentally in cattle; also experiments to see how far the plant has cumulative properties, were performed. The plant caused lethal poisoning when given as a single dose of 40 g/kg; 20 g/kg caused severe poisoning, 10 g/kg slight or no poisoning and 5 g/kg failed to provoke symptoms. A lethal result was produced also when 10 g/kg per day was given over 4 days. The administration of 5 g/kg per day caused severe poisoning when fed over 5 days to two calves. The dose of 2.5 g/kg fed daily over 7 or 9 days also produced severe poisoning in two calves; in another calf, severe symptoms were produced only after feeding 2.5 g/kg per day for 19 days; still another calf showed no symptoms after 32 days of feeding 2,5 g/kg per day, although twice the lethal dose had been fed by this time. A dose of 1.25 g/kg per day over 34 days also failed to produce any symptoms.

Surto de intoxicação por narasina em suínos

An outbreak of narasin poisoning in swine is described. The diagnosis was based on the history, clinical-pathological findings, the reproduction of the disease by the administration of the feed originally given to the animals and by chemical analysis which showed doses sufficiently high to cause poisoning. Inspite that the clinical-pathological picture of the natural and experimental poisoning was of the same nature, there were some differences. In the natural outbreak lethality was high, but in the experiments none of the animals died. In the natural cases besides the lesions in the muscles, also lesions of the heart muscle fibres were seen, not detected in the esperimental animals. It is suggested that these differences could be due to the stress to which the animals were submitted in the piggery by the great number of animals per box, whereas the experimental animals were kept individually.

Renal infection by a new coccidian genus in big brown bats (Eptesicus fuscus).

Abstract A novel coccidian parasite from the kidney of big brown bats (Eptesicus fuscus) is described. This coccidian (Nephroisospora eptesici nov. gen., n. sp.) was associated with a generally mild, focal or multifocal, well-demarcated cortical renal lesion less than 1 mm in diameter. The lesion represented cystic, dilated tubules with hypertrophied tubular epithelial cells and was present in the kidneys of 29 of 590 bats. Numerous coccidian parasites in various stages of development were present within the tubular epithelial cells and within the cyst lumina. Oocysts were collected from cystic dilated tubules. Thin-walled, sporulated ellipsoidal oocysts measuring an average of 18.9 × 20.8 µm were present in kidney tissue. The oocysts contained 2 sporocysts with 4 sporozoites. A polar body and a prominent oocyst residuum were present in the oocysts, but no micropyle, sporocyst residuum, or Stieda bodies were detected. Analysis of the 18S rRNA gene sequence put the parasite in the Sarcocystidae. The parasite is closely related to Besnoitia, Hammondia, Neospora, and Toxoplasma. Ultrastructural features, such as the presence of an apical complex in merozoites, support the identification of a coccidian. A new genus and species, Nephroisospora eptesicii, is proposed for this unusual coccidian in which the entire cycle is completed in the kidney of a single host; it has a membrane-like oocyst wall, sporogony occurs in the host rather than in the abiotic environment, and the positioning of the parasite by nucleic acid sequence indicates it to be closely allied to Sarcocystis and Besnoitia.

Neuronal Storage Disease in a Group of Captive Humboldt Penguins (Spheniscus humboldti)

A neuronal storage disease affecting 5 captive Humboldt penguins is described. One bird died after 3 days of lethargy and anorexia. The 4 remaining birds died after a slowly progressing course of disease with signs that included lethargy, weakness, and neurologic dysfunction. Neurologic signs included dysphagia and ataxia. Gross lesions in the first animal to die consisted of hepatosplenomegaly indicative of avian malaria, which was confirmed histologically. The 4 remaining animals were mildly to moderately emaciated. Moderate to marked vacuolation of the neuronal perikarya was observed in Purkinje cells, neurons of the brainstem nuclei, and motorneurons of the spinal cord in all birds. By electron microscopy the vacuoles represented multilayered concentric lamellar structures. These findings were indicative of sphingolipidosis. All animals had been prophylactically treated for avian malaria, aspergillosis, and possible bacterial infections with chloroquine, itraconazole, and enrofloxacin. circumstantial evidence implicates chloroquine therapy as the possible cause of the storage disease.