Haemorrhagic septicaemia (HS) is an acute disease of cattle and buffaloes caused by Pasteurella multocida 6:B. Outbreaks of the disease have been closely associated with carrier animals that transmit the organism to susceptible animals during stressful condition. This study was conducted to determine whether goats exposed intranasally to P. multocida 6:B can transmit the organism to contact goats. Thirty-six healthy local Katjang goats were divided into four groups and goats of groups 1 and 3 were each inoculated intranasally with a 1-ml inoculum that contained 1 x 10(9) CFU/ml of live P. multocida 6:B. Following the exposure, all goats of groups 3 and 4 were injected with dexamethasone at the rate of 1 mg/kg for three consecutive days. At the end of the dexamethasone treatment, goats of groups 1 and 2 were commingled but kept separate from goats of groups 3 and 4, which were commingled in another pen. Three surviving goats from each group were killed on days 7, 14 and 21 post-exposure for postmortem examination. Naso-pharyngeal mucus and heart blood were collected on swabs. Tissues from lungs, lymph nodes and tonsils were collected for bacteriological isolation and identification. Only one goat of group 3 died 6 days post-exposure showing clinical signs and lesions typical of HS. Other goats showed mild signs of upper respiratory tract infection. Goats of all groups developed acute mild pneumonic lesions, however, those treated with dexamethasone had significantly (P < 0.05) more extensive lesion scoring based on the lesion scoring system. P. multocida 6:B was isolated from the nasal mucosa and lung lesions of exposed and contact goats not treated with dexamethasone. Exposed and contact goats treated with dexamethasone carried the organism for 21 days. P. multocida isolation from heart blood was made only from exposed and contact goats treated with dexamethasone. P. multocida was isolated from the lymph node of the goat that died during the experiment.
Redox polymerization of poly(acrylonitrile-co-acrylic acid) (poly(AN-co-AA)) is performed at 40 °C under N2 gas by varying the ratio of acrylonitrile (AN) and acrylic acid (AA) in the feed. The yield production of poly(acrylonitrile) (PAN) is 73% and poly(AN-co-AA) with a feed ratio of 93:7 is the highest yield (72%). The PAN and poly(AN-co-AA) are further chemically modify with hydroxylamine hydrochloride. The FTIR spectroscopy is used to confirm the copolymerization of poly(AN-co-AA) and chemical modification of poly(AN-co-AA). Elemental microanalysis shows that the overall trend percentage of carbon, hydrogen, and nitrogen for all feed ratios are slightly decreasing as the feed ratio of AA is increasing except for poly(AN-co-AA) 93:7. The SEM images shows that spherical diameter of poly(AN-co-AA) is smaller compared to the PAN and amidoxime (AO) OPEN ACCESSPolymers 2015, 7 1206 modified poly(AN-co-AA). The TGA (thermogravimetric analysis) analysis reveals that the poly(AN-co-AA) degrades at lower temperatures compared to the PAN but higher than AO modified poly(AN-co-AA). The case study adsorption test showed that the AO modified poly(AN-co-AA) 93:7 had the highest percentage removal of Cd 2+ and Pb 2+.
Bronchial mucous cell metaplasia (MCM) is a histologic component of chronic mucus hypersecretion. The hamster model of elastase-induced MCM appears to involve an irreversible conversion of Clara cells to mucous cells. The present study questioned whether the mucous cells seen in hamster bronchi exposed to neutrophil elastase produce and maintain a form of glycoconjugate secretory product different from that normally found in mucous cells or Clara cells. Ultrastructural cytochemistry using the gold-labeled lectin HPA revealed a difference in the cell surface and stored secretory granules of elastase-derived mucous cells compared to normal mucous cells and Clara cells at 3 weeks and 4 months following exposure. The results suggest that elastase irreversibly alters the glycoconjugate character of the Clara cells normally present so that they produce an abnormal form of mucus. Because secreted glycoconjugates can affect the rate of mucociliary clearance and receptor-mediated binding of microorganisms, this change in phenotype may be involved in the pathogenesis of diseases associated with chronic mucus hypersecretion in humans.
Chronic mucus hypersecretion (CMH), a common feature of various obstructive pulmonary diseases, is caused by a variety of airway irritants. Bronchial mucous cell metaplasia (MCM), a histological correlate of CMH, can be induced in hamster airways by a number of different irritants. Previous studies with the hamster model suggest that the secretory cell response to different agents is not stereotyped but can vary in the type of mucus glycoconjugate produced. The present ultrastructural study was conducted therefore to provide quantitative evidence of phenotypic variation in mucous cells induced independently by exposure to the metaplastic agents elastase and acid. HPA-gold lectin cytochemistry revealed an increase in N-acetyl galactosamine at the cell surface and secretory granules of mucous cells in elastase-treated vs. acid-treated animals. Although there was no quantitative difference between the acid-treated and untreated groups, a difference in the pattern of binding within granules indicated variation in the secretory product. Because mucus glycoconjugates serve as attachment sites for specific pathogens, phenotypically distinct mucous cells may promote differential microbial colonization. In humans therefore, variation in the severity and progression of CMH may be due in part to secretory cell susceptibility and response to different pathogenic stimuli.
Twenty goats of about 7 months of age were divided into five groups. The goats in groups 1 and 2 were exposed once, using an intranasal spray to 2 ml of an inoculum containing 10(6) colony-forming units/ml of living or dead Pasteurella haemolytica A2, respectively. The goats in groups 3 and 4 were similarly exposed twice at a 2-week interval. Group 5 was the untreated control. The number and size of the bronchus-associated lymphoid tissue (BALT) in goats exposed twice to either living or dead organisms were significantly (p < 0.05) increased compared with those exposed once and with the unexposed control. In vitro colonization by living P. haemolytica A2 onto the lung tissue in which the BALT had been stimulated by two exposures of either living or dead organisms was significantly (p < 0.05) reduced. The study indicates that stimulation of the respiratory mucosal immunity may prevent P. haemolytica A2 infection.
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