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Biomedical subjects

B G Bang

Publications and source records attributed to B G Bang.

36 records · Page 2Linked to original sources
PubMed1975

Acute newcastle viral infection of the upper respiratory tract of the chicken. II. The effect of diets deficient in vitamin A on the pathogenesis of the infection.

Keratotic and squamous changes characteristic of vitamin A deficiency were minimal even in chicks which were malnourished and growth stunted and had no vitamin A in their diet. However, when these chicks were infected with Newcastle disease virus (NDV), keratotic changes appeared, most markedly in areas regenerating after infection. In chicks raised on full nutrient diets lacking only vitamin A, keratotic changes appeared in several areas of nasal mucosa but were absent from the mucosa of the inner (under) surface of the maxillary turbinate. Following NDV infection, such changes did appear in the inner lining epithelia. It is suggested that depletion of vitamin A causes regenerating epithelial cells to keratinize. Other effects of combined lack of vitamin A plus NDV infection were exhaustion of lymphoid cells from cranial bone marrow and exhaustion of lymphoid cell systems locally from the nose and paranasal glands.

Acute Disease↗
PubMed1974

Acute Newcastle viral infection of the upper respiratory tract of the chicken. I. A model for the study of environmental factors on upper respiratory tract infection.

Acute Newcastle disease virus infection following intranasal inoculation of chicks with a mesogenic strain of the virus produced a localized infection of the middle turbinate which was histologically demonstrable 18 hours after inoculation. There was destruction of mucous cells of individual acini in the under surface of the middle turbinate, and the infection rapidly spread to ciliated and goblet cells and to neighboring acini. By day 2 there was simultaneous remodeling of the mucosa, continued destruction and inflammatory infiltration and frequent loss of cartilage basophilia. By day 3 polymorphonuclear cells almost disappeared, epithelial mitoses commenced, and lymphocyte infiltration intensified; the plasma cells normally present along the lateral nasal gland ducts were often destroyed, very occasionally the glands themselves were destroyed. By days 5 and 6 inflammation greatly decreased, and by day 8 the mucociliated epithelium was essentially normal. The infection is sequentially comparable to acute mild rhinitis of man.

Administration, Intranasal↗
PubMed1972

Lymphocyte depression induced in chickens on diets deficient in vitamin A and other components.

Chickens maintained from time of hatching to age of 30 days on a diet lacking vitamin A, and on 2 diets lacking vitamin A and other nutritional components showed depletion of lymphocyte and plasma cell populations in nasal, paranasal and bursal lymphoepithelial tissues. Effects were significant with all diets but most severe with the most deprived diet. Infection of these birds with Newcastle disease virus showed further depletion of plasma cells, subnormal inflammatory response, keratinization of bursal epithelia and postsloughing metaplasia of nasal mucociliated epithelia. The bursae of infected chickens on the diet lacking only vitamin A were completely devoid of lymphocytes 6 days after Virus inoculation. Infected chickens on the most deprived diet showed atrophy of areas of intranasal epithelia which indicated failure of basal cells to synthesize replacement cells.

Animals↗
PubMed1972

Mucous hypersecretion induced in isolated mucociliated epithelial cells by a factor in heated serum.

A factor in the serum of the marine coelomate, Sipunculus nudus, induced by injecting a mixture of a marine bacterial vibrio and a solution of dried cholera toxin, will, after heating to 85 to 90 C, cause intensive continuous hypersecretion of mucus in isolated free-swimming mucociliated cells from another Sipunculus. The factor, released from coleomic cells into the serum, is heat stable to 90 C, withstands several freeze-thawings, is induced only by specific stimuli, is rapidly released into the serum, persists for different time spans depending on the stimulus, and is not present in normal heated sera. It is proposed that in nature this factor is balanced by a heat labile inhibitory factor. Cholera toxin alone is a feeble stimulus. The marine vibrio alone is a powerful stimulus to mucus secretion but lethal for the host. In combination with cholera toxin, the vibrio is nonlethal.

Animals↗
PubMed1969

Experimentally induced changes in nasal mucous secretory systems and their effect on virus infection in chickens. I. Effect on mucosal mrphology and function.

The domestic chicken was used as an experimental model in which to demonstrate morphological and functional relationships of nasal organ systems, principally of mucous systems. Mucous secretions of olfactory, respiratory, lacrimal, and accessory areas were found to have clear histochemical differences, yet were sufficiently miscible in normal circumstances to form an unbroken, synchronously moving sheet. Changes induced experimentally in host physiology did not all affect the mucous components of given areas in the same way or to the same degree. Mucosal changes were produced by the following methods: Topically administered cocaine 20%, in a single application, temporarily paralyzed the cilia, and the consequently reduced traction apparently held mucus in the acini and effected a temporary lag in mucus excretion. Three successive applications caused acute acinar depletion and ciliary paralysis. Hexylcaine chloride 5% immediately desquamated all intranasal epithelia, damaged the proximal portion of the acini, and induced acinar exhaustion and mucosal inflammation-effects not overcome within 5(1/2) days. Internal dehydration produced progressively viscous mucus, severe acinar gaping with mucus anchored in the acini, a heavy surface sheet, and deceleration or arrest of mucociliary flow. Avitaminosis A induced reduction in the height (about 50%) of all mucosae and acini, especially the inner lining of the maxillary concha, caused an actual 50% reduction in the number of cells per acinus, and retarded the mucociliary flow rate about 50%. Pilocarpine induced initial hypersecretion, later exhaustion, and, still later, slow production of densely staining mucus in the acinar cells; also acinar gaping. Breeding in a germfree environment produced a greatly reduced mucosal depth throughout the nasal fossa, an extraordinary reduction in the number of cells per acinus, relative reduction in the number of acinar neck cells, and concomitant increase in ciliated cells in that region. Exposure to a temperature of -20 degrees C for 1 hr caused blanching of all secretory cells, acinar gaping, and temporary reduction of mucosal depth.

Amino Alcohols↗
PubMed1967

Laryngotracheitis virus in chickens. A model for study of acute nonfatal desquamating rhinitis.

Infectious laryngotracheitis can be produced in chickens as an experimental model of severe nonfatal rhinitis and sinusitis. Inoculated intranasally into unanesthetized baby chicks it remains limited to the nasal fossa, produces acute desquamation of all nasal epithelia, results in functional recovery of the respiratory epithelium, but leaves important residual abnormalities. From the earliest recognizable lesions through 4(1/2) months' convalescence, the principal changes are as follows: 1. Initial lesions, or small syncytia of intranuclear "inclusions", first identifiable in the mucociliated cells of the shallowest portion of the epithelium at about 21 hr postinoculum (the inner surface of the maxillary conchal scroll). 2. Acute sloughing, (about 3 to 7 days), marked by: (a) spread of lesions from cell to cell via multinucleated "giant cells" which progressively slough and desquamate respiratory, olfactory, and sinus epithelia, epithelial neural elements and blood vessels; (b) appearance of numbers of eosinophilic leukocytes along the basement membrane at the sites of lesions just previous to sloughing; intensive infiltration of the submucosa with small lymphocytes after sloughing begins; (c) histochemical change in the intracellular mucus of the cells which comprise the syncytia: this mucus stains with Alcian blue alone when stained with AB-PAS; and (d) all cartilages of the maxillary conchae become flaccid, and the cell nuclei and matrix lose both basophilic and Alcian blue staining properties, effects which recede by about the 8th day. 3. Repair (about 8 to 21 days), marked by rapid initial spread of a sheet of epithelial cells over the infiltrated subrmucosa, appearance of numbers of plasma cells circulating in the tissues, formation of encapsulated secondary nodules, and mucosal adhesions. 4. Convalescence (about 1 to 4(1/2) months when experiments terminated), marked by functional restoration of the mucociliary lining of the nasal fossa. However, at 4(1/2) months eight specimens all show complete metaplasia of the olfactory organ (end nerves, supporting cells, and glands of Bowman) to mucociliated epithelium, all show abnormal formation and alignment of mucous acini, and about 50% have severe persistent sinusitis.

Animals↗
PubMedDate not supplied

Mucociliary transport in chickens infected with Newcastle disease virus and exposed to sulfur dioxide.

Mucociliary transport was studied in the nasal mucous membranes and sinuses of 3-week-old chickens which were either exposed to sulfur dioxide (SO2), infected intranasally with the mesogenic strain of Newcastle disease virus (NDV), or exposed to SO2 after NDV infection. A newly developed apparatus was used to follow intranasal transport rates over time in the same animal, and to follow sinus transport rates over time in a separate group of animals. Intermittent exposure to concentrations of 1.4-66.0 ppm SO2 produced peaks of increased intranasal transport time, with intervening recovery periods. This suggests a homeostatic mechanism. Transport was also decelerated in the sinus when concentrations of SO2 were above 10 ppm. NDV infection produced decelerated intranasal transport rates but did not decelerate sinus rates. Combined NDV and SO2 interacted to produced persistent deceleration of the intransal transport rate. In the sinus, the combination seemed to conteract the decelerating effect of SO2 alone, suggesting a separate mechanism of homeostasis.

Animals↗
PubMedDate not supplied

Effect of SO2 on nasal secretory cells.

Quantitative histochemical analysis of the secretory cells producing the different types of glycoproteins were examined in the chicken nasal cavity with and without moderate levels of SO2 exposure for 14 days. On the nasal maxillary concha of chickens, the number of acinar gland cells containing glycoproteins was significantly reduced on the 1st, 7th and 14th days of exposure to 11.8 ppm of SO2, but not on the 5th day of exposure. There was no histochemical modification in the intracellular glycoproteins of the acinar cells. The number of goblet cells in the same region increased greatly and showed a change of intracellular glycoproteins from neutral to acid between the 5th and 7th day of exposure.

Animals↗