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Biomedical subjects

M A Breider

Publications and source records attributed to M A Breider.

At least 37 records · Page 2Linked to original sources
PubMed1991

Fine structural aspects of postnatal development of feline lung.

Lung development was studied in late prenatal, 1-, 7-, 14-, and 21-days postnatal and adult cats. Cats were born with a few alveoli, and the lungs appeared to have patches of primitive air spaces (saccules). The saccules of prenatal kittens were thick walled, very cellular, and lined by type II pneumocytes. Eosinophils were observed in the septum, intraepithelially, and in the alveolar space of growing cats. Secondary septa were flanked by a double capillary network and divided saccules into multiple shallow alveoli. Septation was irregular and time dependent and not completed by day 231 of postnatal life. Elastic fibers accumulated at the tip of the septa, seemingly playing an important role in alveolar formation. Type II pneumocytes were located at the base of the secondary septa in growing cats, thus strengthening secondary septa to withstand the stresses of respiration. Pores of Kohn were not observed in growing cats.

Animals↗
PubMed1991

Protective role of bovine neutrophils in Pasteurella haemolytica-mediated endothelial cell damage.

The purpose of this study was to determine if Pasteurella haemolytica can directly injure bovine pulmonary endothelial cells (EC) and if neutrophils have a beneficial or detrimental role in bacterium-EC interaction. Various combinations of live P. haemolytica, heat-killed P. haemolytica, anti-P. haemolytica immune serum, polymyxin B, and bovine neutrophils were added to confluent monolayers of bovine EC. Monitoring included determination of 51Cr release from EC, phase microscopy, and transmission electron microscopy. Although toxic changes were not evident at 5 h postinoculation, both live and heat-killed P. haemolytica produced extensive EC damage by 22 h postinoculation. Damage by live P. haemolytica was prevented only when both neutrophils and immune serum were used. Polymyxin B effectively prevented the toxic effect of heat-killed P. haemolytica, suggesting that lipopolysaccharide was the major toxic factor. Morphological studies showed close apposition of P. haemolytica to EC membranes, neutrophil activation, and adherence to EC but no evidence of neutrophil-associated EC membrane damage. These studies demonstrate that neutrophils and immune serum in combination are effective in preventing EC damage mediated by live P. haemolytica.

Animals↗
PubMed1991

Effect of Pasteurella haemolytica saline capsular extract on bovine pulmonary endothelial cells.

The purpose of this in vitro study was to determine whether Pasteurella haemolytica capsular extract (CE) damages bovine pulmonary endothelial cells (EC) directly or through neutrophil-mediated mechanisms. Chromium 51-labeled EC were treated with the following variables: CE (1, 10, and 100 ng of protein/ml), CE and bovine neutrophils (10(6) cells/well), and CE and polymyxin B (500 U/ml). Although only minimal damage to EC occurred by 5 hours after treatment, by 22 hours after treatment, the 10-ng and 100-ng CE dose produced severe damage to EC, as indicated by 51Cr release, cellular detachment, and loss of monolayer confluency. The component in the CE that was toxic to the EC was lipopolysaccharide, evidenced by effective neutralization of the toxic effect with polymyxin B. Neutrophils inhibited the CE-mediated EC toxicity and were activated, as indicated by shape change and adhesion to EC monolayers. We concluded that the lipopolysaccharide component of CE causes direct damage to EC, which can be attenuated by neutrophils and polymyxin B.

Animals↗
PubMed1990

Bovine pulmonary endothelial cell damage mediated by Pasteurella haemolytica pathogenic factors.

The in vitro effects of Pasteurella haemolytica components on bovine pulmonary endothelial monolayers were investigated to determine the relative role of individual bacterial factors in the pathogenesis of bovine pulmonary pasteurellosis. Bovine pulmonary endothelial monolayers were treated with P. haemolytica bacterial culture supernatant (CS) and P. haemolytica lipopolysaccharide. At 22 h postinoculation, the CS produced severe damage to the endothelial cells, indicated by high 51Cr release, extensive cellular detachment, and morphologic changes characterized by cell contraction, cytoplasmic blebbing, and loss of monolayer confluency. The neutralization of leukotoxin activity of the CS by heat inactivation was ineffective in decreasing the damage to endothelial cells; however, leukotoxin-neutralizing monoclonal antibody slightly diminished the toxic effect. P. haemolytica lipopolysaccharide by itself or as a supplement to CS produced endothelial cell damage similar to that of CS. The preincubation of CS dilutions (10(-1) and 10(-2)) or P. haemolytica lipopolysaccharide with polymyxin B almost completely eliminated cell toxicity. These studies show that P. haemolytica produces a soluble factor that is consistent with bacterial lipopolysaccharide and that is directly toxic to bovine pulmonary endothelial cells in vitro.

Animals↗
PubMed1990

Cardiovascular changes after bone marrow transplantation in dogs with mucopolysaccharidosis I.

Five dogs with mucopolysaccharidosis I, 3 of which had been treated with bone marrow transplantation (BMT), were evaluated for 20 months with electrocardiography, thoracic radiography, and M-mode and 2-dimensional echocardiography. Treated and untreated (control) dogs had widened P waves on ECG. Thoracic radiographs remained normal for all dogs throughout the study. Thickening of the mitral valve was observed on echocardiograms of dogs in both groups, but the untreated dogs appeared to have thicker valves. Concentrations of glycosaminoglycans in the mitral valves and myocardium were higher in control dogs than in treated dogs. Markedly large aortic root diameters were observed on echocardiograms in both untreated dogs, but aortic root diameters remained normal in treated dogs. Echocardiography, but not electrocardiography, was useful in monitoring heart enlargement in each dog. Dogs treated with BMT generally had less severe cardiac changes and slower disease progression than control dogs.

Animals↗
PubMed1989

Detection of Ehrlichia risticii using an avidin-biotin-immunoperoxidase staining system.

An indirect immunoperoxidase procedure using a specific anti-Ehrlichia risticii monoclonal antibody and an avidin-biotin-peroxidase staining method was used to detect E. risticii antigen in infected P388D1 murine monocytes. Several different methods of cytological fixation were used, including acetone (15 min), 95% ethanol (15 min), Bouin's fixative (5 hr), and 10% buffered neutral formalin (24 hr). The E. risticii organisms were labeled effectively and identified in cells fixed with acetone and ethanol. However, infected P388D1 cells fixed in 10% formalin or Bouin's fixative required enzymatic digestion with 1.0% trypsin for 15 min at 37 C before positive results were evident. This indirect immunoperoxidase avidin-biotin staining procedure proved to be a sensitive assay for the detection of intracellular E. risticii and may be an effective diagnostic procedure for formalin-fixed paraffin-embedded tissue.

Animals↗
PubMed1989

Long-term effects of bone marrow transplantation in dogs with mucopolysaccharidosis I.

The therapeutic effects of allogeneic bone marrow transplantation (BMT) in a canine model of mucopolysaccharidosis I (MPS I) were investigated. Long-term post-BMT pathologic and biochemical studies were performed on three groups of dogs: 1) MPS I-affected dogs that did not receive BMT, 2) MPS I-affected dogs that received total body irradiation followed by an allogeneic BMT, and 3) normal, unaffected dogs that served as BMT donors. All dogs were necropsied at approximately 20 months after BMT. The severity of MPS I-related lesions in the dogs receiving BMT was greatly diminished. These dogs had only slight cardiac valvular thickening, no meningeal thickening, no renal tubular epithelial vacuolation, decreased neuronal vacuolation, decreased corneal stromal vacuolation, and greatly diminished arterial medial thickening. The severity and incidence of degenerative arthropathy also were decreased in BMT dogs, however, vertebral lesions were similar to nontransplanted, affected dogs. Chondrocytes of both MPS I-BMT and MPS I-no BMT groups had similar marked cytoplasmic vacuolation, except for MPS I-BMT chondrocytes near the articular surface, which had more normal morphology. Ultrastructurally, the liver and kidney tissue in BMT recipients had no appreciable lysosomal accumulation of GAGs. These morphologic findings were supported by near normal levels and electrophoretic patterns of glycosaminoglycans (GAG) in most tissues of BMT recipient dogs. This study demonstrates that BMT is capable of substantially diminishing the severity of MPS I-related lesions in this canine model.

Animals↗
PubMed1989

Early renal ultrasonographic findings in dogs with experimentally induced ethylene glycol nephrosis.

Renal ultrasonographic changes were evaluated in 5 dogs administered 10 ml of commercial antifreeze (95% ethylene glycol)/kg of body weight, PO, and in 2 dogs given placebos. Studies were made prior to and after ingestion on an hourly basis over a period of 8 to 10 hours. All dogs were anesthetized immediately after toxin or placebo ingestion for the duration of the study. Renal cortical echogenicity was evaluated in comparison with that of the adjacent liver and spleen. Echogenicity of the renal medulla and definition of the corticomedullary junction were assessed. Within 4 hours after ethylene glycol administration, renal cortical echogenicity of all intoxicated dogs increased from normal to surpass that of liver and approach or equal that of the spleen. Medullary echogenicity in all intoxicated dogs progressively increased over the course of the study, with changes recognized within 5 hours after ethylene glycol administration. An ultrasonographic pattern consisting of nearly equal, marked increase in cortical and medullary echogenicity and relatively hypoechoic corticomedullary junction and central medullary regions was recognized concurrent with the development of anuria in 3 of the 5 intoxicated dogs. Mild, transient increases in cortical and medullary echogenicity were observed in anesthetized control dogs. However, no statistical difference (P less than 0.05) was detected between baseline, peak, and terminal echogenicity values in these dogs. Blood and urine samples were collected hourly from intoxicated dogs to coincide with ultrasonographic studies. Most clinicopathologic values derived from these samples were not statistically different (P less than 0.05) from those reported in a study that used a similar intoxication protocol in nonanesthetized dogs.

Animals↗
PubMed1988

Blastomycosis in cats: five cases (1979-1986).

Medical records of 5 cats with blastomycosis examined at the University of Tennessee Veterinary Teaching Hospital from 1979 to 1986 were reviewed. Clinical signs of blastomycosis varies depending on the organ(s) affected, but respiratory tract disease was most common, followed by CNS signs and ocular problems. A definitive diagnosis was made by identification of characteristic fungal organisms in biopsy or necropsy specimens. Two cats treated with amphotericin B did not respond to treatment and died or were euthanatized. The lungs, brain, eyes, and lymph nodes commonly were affected, but one cat had only cutaneous and regional lymph node involvement. The respiratory tract appeared to be a common primary site of infection, with dissemination to other organ systems. The typical host response was a pyogranulomatous cellular infiltrate with numerous fungal organisms evident.

Animals↗
PubMed1988

Experimental bovine respiratory tract disease with Haemophilus somnus.

Eight calves were inoculated into the bronchus with H. somnus. Thirteen calves were inoculated with bovine respiratory syncytial virus (BRSV) and 8 days later with H. somnus. All calves developed necrotizing, suppurative, lobular bronchopneumonia and pleuritis. Clinical signs of disease and pneumonic lesions were significantly more severe in calves that were sequentially inoculated with BRSV followed by H. somnus. Pneumonic lesions in the inoculated calves were similar to those described for naturally occurring H. somnus-associated respiratory tract disease. Control calves inoculated with BRSV alone or sham-inoculated with medium did not develop clinical signs of respiratory tract disease. The BRSV-inoculated control calves developed minimal pneumonic lesions.

Animals↗
PubMed1988

Long-term neurological effects of bone marrow transplantation in a canine lysosomal storage disease.

A naturally occurring disease in Plott hound dogs, caused by deficiency of the lysosomal enzyme alpha-L-iduronidase, was used to study the feasibility of bone marrow transplantation therapy in a neurodegenerative storage disease. Three long-term survivors of transplantation with littermate marrow at 5 months of age (before clinical signs) had CNS enzyme activity, glycosaminoglycan storage, and light microscopic and ultrastructural changes evaluated 594, 628, and 740 days after treatment. Iduronidase activity in small amounts (1-3% of donor values) was detectable in brain tissue. Cerebrospinal fluid had higher iduronidase activity after transplantation (7-15% of donor values). Enzyme activity within the CNS resulted in significant reductions in stored glycosaminoglycans and resolution, to a large extent, of light microscopic and ultrastructural lesions observed in affected, untreated littermate control dogs.

Animals↗
PubMed1988

Pulmonary lesions induced by Pasteurella haemolytica in neutrophil sufficient and neutrophil deficient calves.

The role of neutrophils in the development of peracute lung lesions of bovine pneumonic pasteurellosis was investigated. Eight calves were divided into two groups of four calves each. Group I was treated with intravenous phosphate-buffered saline and served as the neutrophil sufficient calves. Group II was treated with intravenous hydroxyurea which produced a state of neutropenia. When peripheral blood neutrophil numbers dropped below 300 cells/microL in group II, all calves were challenged with an intrabronchial bolus of Pasteurella haemolytica in the log phase of growth. An acute inflammatory process occurred in both groups of calves indicated by a rise in body temperature. While pulmonary lesions occurred in both groups by six hours postinoculation, they varied in pathological characteristics. Pulmonary lesions in the neutrophil sufficient calves consisted of fibrinopurulent alveolitis-bronchiolitis with associated alveolar septal necrosis, interlobular edema, and intravascular thrombi. The neutrophil deficient calves had extensive intra-alveolar edema, interlobular edema, intraalveolar hemorrhage, atelectasis, and focal areas of alveolar septal necrosis. These results show that P. haemolytica can induce severe pulmonary tissue damage through both neutrophil dependent and neutrophil independent mechanisms.

Agranulocytosis↗
PubMed1987

Influence of interferon in natural resistance of mice to Sendai virus pneumonia.

The influence of interferon (IFN) on the natural resistance to Sendai virus was investigated in resistant (C57BL/6NCr) and susceptible (DBA/2NCr) mouse strains. After inoculation with strain 52 Sendai virus, the pulmonary titers of Sendai virus were similar in both mice strains, indicating that the quantity of virus in the lungs may not be a major factor in determination of resistance. The pulmonary IFN titers were higher in DBA/2 mice, indicating that increased susceptibility of DBA/2 mice is not a result of inadequate production of IFN. Treatment of both strains with exogenous IFN before and during viral infection induced an increased survival time in C57BL/6 mice, but eventual mortality was the same in both mouse strains. Administration of anti-IFN antibodies to both mouse strains during Sendai infection decreased mortality equally in both strains, compared with mortality in control mice. Seemingly, the difference in resistance to Sendai virus in DBA/2 and C57BL/6 mice was probably not a result of the beneficial effects of IFN. On the contrary, administration of anti-IFN antibodies decreased the susceptibility of both mouse strains.

Animals↗
PubMed1985

Chronic eosinophilic pancreatitis and ulcerative colitis in a horse.

A generalized debilitating disease in a horse was believed to be related to hypersensitivity to migrating strongyle larvae. The clinical signs included weight loss, diarrhea, and ulcers on all 4 coronary bands. The mare's condition deteriorated rapidly, so the mare was euthanatized and necropsied. The major histopathologic findings were chronic multifocal eosinophilic pancreatitis, hepatic portal fibrosis, biliary hyperplasia, and chronic ulcerative eosinophilic colitis. This case was similar to previously reported cases of chronic eosinophilic gastroenteritis in horses. Although the etiologic agent was not evident, the distribution and character of the lesions were consistent with a hypersensitivity response to migrating parasitic larvae, most probably Strongylus equinus.

Animals↗
PubMedDate not supplied

Treatment of mycotic rhinitis with itraconazole in three horses.

Itraconazole, a third-generation azole, was evaluated for treatment of resistant nasal mycotic infections in horses. Two horses with Aspergillus spp nasal granulomas and 1 horse with Conidiobolus coronatus nasal infection were treated with itraconazole (3 mg/kg PO bid). One of the horses with nasal aspergillosis was also treated by surgical resection of the nasal septum. The treatment time for the horses ranged from 3 to 4.5 months. No adverse effects were noted in any of the horses during the treatment period. Peak and trough serum itraconazole concentrations were < 0.5 micrograms/mL in all 3 horses. Itraconazole (3 mg/kg PO bid) appears to be effective in the treatment of nasal Aspergillus spp infections in horses because the fungal infection was eliminated in both horses. One horse still had excessive nasal sounds during exercise and was retired from training, whereas the other horse returned to normal. The nasal C. coronatus infection appeared resistant to itraconazole treatment in the affected horse because the granulomas were still present after 4.5 months of treatment.

Animals↗
PubMedDate not supplied

Gastric gland degeneration induced in monkeys by the CCK-B/gastrin receptor antagonist CI-988.

Gastric effects of subchronic treatment with the cholecystokinin-B (CCK-B)/gastrin receptor antagonist CI-988 were investigated in cynomolgus monkeys. In preliminary range-finding studies, CI-988 was given orally to 1 monkey per sex for 14 days at doses of 50, 100, 200, and 500 mg/kg/day. Subchronic studies of CI-988 were subsequently conducted using 5 monkeys per sex at doses of 0, 5, 25, and 75 mg/kg for 4 or 13 wk. High-dose monkeys were dosed initially at 100 mg/kg, but the dose was not well tolerated and was decreased to 75 mg/kg after 8 days of treatment. One male monkey at 75 mg/kg was euthanatized in extremis on day 23. In the range-finding study, minimal to moderate, multifocal to diffuse degeneration of gastric glands, primarily in the fundic region, was observed at 100 mg/kg and above, with frank gastric mucosal atrophy occurring at 200 and 500 mg/kg. Minimal to mild gastric gland degeneration was also observed in the subchronic study after 4 wk at 25 and 75 mg/kg, but histopathologic gastric changes were remarkably absent after 13 wk. Mucosal height in the stomach fundus was decreased 19.8% in 75-mg/kg males at week 4, and although gastric mucosa appeared histologically normal after 13 wk, mucosal height remained 28.6% less than that of controls. In females at 75 mg/kg, fundic mucosal height was decreased 7% and 5% at weeks 4 and 13, respectively, but decreases were not statistically significant. Mean serum gastrin concentrations were increased 10-fold in males only after 4 wk at 75 mg/kg, but were comparable to controls during week 13. CI-988-induced gastric gland degeneration is consistent with antagonism of gastrin's trophic activity toward gastric mucosa. Notwithstanding decrements in gastric mucosal height, disappearance of mild histopathologic findings despite continued treatment with the ligand suggests some degree of adaptation to subchronic CCK-B/gastrin inhibition, although the mechanism of accommodation has yet to be delineated.

Administration, Oral↗