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Biomedical subjects

M N Novilla

Publications and source records attributed to M N Novilla.

32 records · Page 2Linked to original sources
PubMed1979

Disseminated granulomas caused by an unidentified protozoan in sandhill cranes.

Oral granulomas were observed in 31 (33%) of 95 captive sandhill cranes (Grus canadensis) at the Patuxent Wildlife Research Center. Necropsy of six of the afflicted cranes revealed granulomatous nodules throughout many of their organ systems. Intracellular protozoan organisms morphologically resembling schizogonic stages were observed within the granulomas by light and electron microscopy. Sexual and asexual stages of coccidia were seen in sections of the intestines of 4 of 5 cranes examined microscopically, and Eimerian oocysts were seen in fecal flotation specimens from 3 of 4 birds.

Animals↗
PubMed1979

Heart failure associated with unusual hepatic inclusions in a Deckert's rat snake.

A juvenile Deckert's rat snake, Elaphe obsoleta deckerti, was presented with a circumferential enlargement of the body in the region of the heart. The heart was enlarged approximately twice normal size. Focal mineralized lesions were present in the tunica media of the right aorta and the right atrioventricular valve. The normal sinusoid architecture of the liver was disrupted with deeply eosinophilic to lightly basophilic granules of variable size in the cytoplasm and light eosinophilic intranuclear inclusions. Similar appearing intracytoplasmic granules were seen in the glomeruli and kidney tubules.

Animals↗
PubMed1978

Lymphocyte responsiveness to mitogens and quantitation of T and B lymphocytes in canine malignant lymphoma.

Two canine malignant lymphoma cases were studied, one from the time of detection of enlarged palpable lymph nodes through the terminal stage and another at the terminal stage. Hematologic and histopathologic studies were confirmative of leukemia. The lymphocyte subpopulations, T and B cells, were quantitated as identified by the presence or absence of surface immunoglobulin and erythrocyte-antibody-complement-rosette formation. The average number of B cells in the peripheral blood lymphocytes throughout the study were approximately 80%. The B cells in the lymph node lymphocytes were 82%. There was considerable fluctuation in the number of blood lymphocytes, but the percentage of T and B lymphocytes remained nearly constant. There was marked impairment in the lymphocytic response to mitogens. The results of this study indicate that the canine malignant lymphoma is predominantly a B-lymphocyte type.

Animals↗
PubMed1977

Diabetes mellitus in a black-footed ferret.

Diabetes mellitus was tentatively diagnosed in a black-footed ferret with polyuria, polydipsia, polyphagia, dehydration, and weight loss. Laboratory findings (marked hyperglycemia (724 mg/100 ml), glycosuria, and ketonuria) and the subsequent favorable response to insulin therapy confirmed the diagnosis. Although lesions were not observed in the pancreas, gross and histologic findings concomitant with diabetes mellitus included arteriosclerosis, with calcification of the aorta and other major vessels; mild necrotizing hepatitis; and mild proliferative glomerulonephritis. A perineal adenocarcinoma, with metastasis to an internal iliac lymph node, was an incidental finding. Special stains demonstrated adequate numbers of beta cell granules in the islets of Langerhans. Thus, the diabetes was apparently due to a lack of release of the synthesized insulin or to diminished effectiveness of the secreted insulin.

Adenocarcinoma↗
PubMed1976

Fatal vaccine-induced canine distemper virus infection in black-footed ferrets.

Four black-footed ferrets that were live-trapped in South Dakota and transported to the Patuxent Wildlife Research Center died within 21 days after vaccination with modified live canine distemper virus. Immunofluorescence, European ferret inoculation, virus isolation attempts, and serum-neutralization tests indicated insufficient attenuation of the vaccine for this species.

Animals↗
PubMedDate not supplied

Turkey knockdown in successive flocks.

Turkey knockdown was diagnosed in three of five flocks of hen turkeys on a single farm within a 12-mo period. The age of birds in the flocks affected ranged from 6 wk 2 days to 7 wk 4 days. The attack rate ranged from 0.02% to 0.30% with a case fatality rate in affected birds ranging from 0 to 74%. The diagnosis was made on the basis of clinical signs and histopathologic lesions associated with knockdown. The feed in all flocks contained bacitracin methylene disalicylate and monensin (Coban). Affected birds were recumbent, demonstrated paresis, and were unable to vocalize. Postmortem examination revealed few significant lesions although pallor of the adductor muscles and petechiation in adductor and gastrocnemius muscles were noted. Birds that had been recumbent for extended periods were severely dehydrated. Consistent microscopic lesions included degeneration, necrosis, and regeneration of adductor, gastrocnemius, and abdominal muscles. No lesion in cardiac tissue was noted. Results of our investigation indicated that changes in water consumption, vitamin E status, and brooder to finisher movement correlated with the occurrence of knockdown. Turkey knockdown was defined in 1993 as any condition identified in a turkey flock that has affected the neuromuscular system to a degree that a turkey is unable to walk or stand. This definition was later modified to...neuromuscular or skeletal systems to a degree that a turkey is unable to walk or stand properly. Knockdown may be associated with numerous feed, management, or disease factors alone or in combination. Dosage of monensin, feed restriction/gorging, water restriction, heat stress, copper, mycotoxins, sodium chloride in feed, and sulfa drugs have all been suggested as contributing factors; however, laboratory studies to duplicate this have not been successful. This report presents observations from a single farm at which three of five hen flocks in a single year experienced knockdown. When a flock was reported as affected, a detailed investigation was initiated within 3 hr. The fifth flock was followed on a twice weekly basis from 0 to 8 wk of age to determine if initiating events were evident, but knockdown did not occur.

Animals↗
PubMedDate not supplied

Alterations in levels of various host antioxidant factors in turkey knockdown syndrome.

Five components (selenium, glutathione peroxidase, copper, superoxide dismutase, and vitamin E) of the antioxidant system of turkey poults were examined to determine if they play any role in the knockdown (KD) syndrome. All flocks were provided with feed formulated to contain monensin at 54-60 g/ton. Flock data were analyzed as a case-control study with three treatment groups (KD-affected and unaffected turkey poults from a KD flock and poults from an unaffected flock [control]). Affected turkey poults had lower (P < 0.001) serum vitamin E levels compared with unaffected poults from KD flocks or poults from unaffected flocks. No significant differences were observed for the other parameters evaluated but there was a trend towards lower copper and superoxide dismutase values in affected birds. It appears that serum vitamin E concentrations in turkey poults may play a significant role in susceptibility to or protection against KD syndrome. Other components of the antioxidant system may also be involved, and complex interactions among several body systems may be critical.

Animals↗
PubMedDate not supplied

An immunosuppressed rat model of respiratory cryptosporidiosis.

A rat model is described in which animals develop respiratory cryptosporidiosis, a disease which is well documented in immunocompromised patients, especially those with AIDS. Our present lack of knowledge of the pathophysiology and immunology of Cryptosporidium parvum respiratory infections warrants the development of a laboratory animal model. Lewis rats immunosuppressed by subcutaneous injection of methylprednisolone acetate and inoculated intratracheally with 10(6) C. parvum oocysts developed a reproducible infection consisting of all known developmental stages in the epithelium lining airways from the trachea to the terminal bronchioles. Developmental stages were morphologically indistinguishable from those seen in gut epithelium. Infections were apparent at 4 days post-inoculation, and at 10-14 days post-inoculation, rats exhibited respiratory distress and severe weight loss and had enlarged, elastic lungs. Increased mucus production and exfoliative necrosis of the epithelium resulted in accumulation of large amounts of mucocellular exudate throughout the airways and patchy alveolitis involving alveoli emerging from respiratory bronchioles.

Animals↗
PubMedDate not supplied

Microsporidian infection in the pied peach-faced lovebird (Agapornis roseicollis).

A microsporidian infection was diagnosed in a pied peach-faced lovebird (Agapornis roseicollis) which had died after an illness of 2 days. The parasite was observed in the liver, kidney, and small intestine. Lesions were most severe in the liver, with numerous organisms adjacent to areas of hepatic necrosis. Although the organisms were seen within renal tubules and within the intestinal mucosa, inflammatory lesions in those sites were minimal. The microsporidian nature of the parasite was confirmed by morphologic studies. The genus of the organism was not determined.

Animals↗
PubMedDate not supplied

Nutritional encephalomalacia in turkeys: diagnosis and growth performance.

An outbreak of neurological disease in 2 1/2-to-3 1/2-week-old male turkey poults was diagnosed morphologically as nutritional encephalomalacia. About 20 to 30% of the flock of 6360 showed clinical signs, which included going down with legs extended or hock-sitting and inability to get up, incoordination, weakness, staggering, trembling, torticollis, and opisthotonus. The most important gross postmortem changes were found in the brain, which consisted of an enlarged and swollen cerebellum with focal and/or diffuse hemorrhages. Major histopathological alterations included congestion, hemorrhages, necrosis, and malacia associated with hyaline capillary thrombi affecting the cerebellar cortex and adjacent white matter. Except for a slightly higher mortality, flock performance compared favorably with performance of other flocks grown in the same farm as well as with the national average for market tom turkeys.

Animal Feed↗
PubMedDate not supplied

A sudden death syndrome induced in poults and chicks fed diets containing Fusarium fujikuroi with known concentrations of moniliformin.

A sudden death syndrome was induced in chicks and poults fed diets containing Fusarium fujikuroi, formulated to contain 0-330 mg/kg moniliformin (M) with or without the maximum recommended therapeutic concentration of monensin. Lesions of monensin toxicosis were not observed. Clinical signs were referable to cardiac dysfunction (sudden death, dyspnea, cyanosis, depression). Poults and chicks dying early in the study had no gross lesions or had lesions of right ventricular dilation. Treated poults and chicks dying late in the study or euthanatized at termination of the study had lesions of bilateral myocardial hypertrophy, usually concentric. Absolute heart weights and relative heart weights, expressed as a percentage of body weight, were significantly greater in treated birds than controls (P < 0.05), whereas body weights were significantly less (P < 0.05). Microscopically, lesions progressed from acute myocardial degeneration to necrosis, fibrosis, and hypertrophy. Ultrastructural findings were consistent with the gross and microscopic lesions. Serum pyruvate concentrations were a useful indicator of M-induced cardiotoxicosis. Concentrations of serum pyruvate increased with increased concentration of dietary M, but were not affected by addition of monensin to the diet. In chicks ingesting 40-300 mg/kg M, serum pyruvate concentrations were significantly greater (P > 0.05) than those in controls (controls, 0.28 +/- 0.08 mmol/liter; exposed 0.38 +/- 0.11-0.55 +/- 0.13 mmol/liter). Poults ingesting 80-330 mg/kg M had significantly greater serum pyruvate concentrations than controls (controls 0.33 +/- 0.09 mmol/liter; exposed 0.43 +/- 0.13-1.00 +/- 0.006 mmol/liter). The Vetronics System was used to evaluate electrocardiographic alterations in a limited number of chicks and poults surviving to the end of the feeding trial. Electrocardiographic alterations in poults and chicks fed diets containing > or = 40 mg/kg and > or = 160 mg/kg M, respectively, were consistent with ventricular hypertrophy, myocardial injury, and hypoxia. Electrocardiographic alterations were more striking in poults than in chicks. Altered myocardial metabolism due to M toxicosis, in conjunction with the unusual susceptibility of domestic poultry to altered cardiac metabolism, is believed to be the cause of the organ-specific lesions in these birds. These findings suggest that cardiac injury with subsequent alterations in cardiac electrical conductance may be a cause of the sudden deaths observed in poultry chronically intoxicated with dietary M.

Animals↗