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T2 MYCOTOXICOSIS IN SWINE FOLLOWING TOPICAL APPLICATION, INTRAVASCULAR ADMINISTRATION AND INHALATION EXPOSURE.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
T2 MYCOTOXICOSIS IN SWINE FOLLOWING TOPICAL APPLICATION, INTRAVASCULAR ADMINISTRATION AND INHALATION EXPOSURE./
作者:
PANG, FEI VICTOR.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 1986,
面頁冊數:
308 p.
附註:
Source: Dissertations Abstracts International, Volume: 47-07, Section: B.
Contained By:
Dissertations Abstracts International47-07B.
標題:
Veterinary services. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=8623386
ISBN:
9798206550658
T2 MYCOTOXICOSIS IN SWINE FOLLOWING TOPICAL APPLICATION, INTRAVASCULAR ADMINISTRATION AND INHALATION EXPOSURE.
PANG, FEI VICTOR.
T2 MYCOTOXICOSIS IN SWINE FOLLOWING TOPICAL APPLICATION, INTRAVASCULAR ADMINISTRATION AND INHALATION EXPOSURE.
- Ann Arbor : ProQuest Dissertations & Theses, 1986 - 308 p.
Source: Dissertations Abstracts International, Volume: 47-07, Section: B.
Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1986.
This item must not be added to any third party search indexes.
Studies were conducted to characterize the clinical signs, pathologic changes and pulmonary and systemic immunity of T-2 toxicosis in swine following a single, topical (15 mg/kg), intravascular (0.6 to 5.4 mg/kg) or inhalation (8 or 9 mg/kg; 20 to 30 percent retention) exposure. Topical T-2 application caused severe dermal injury and adverse systemic effects, including anorexia, posterior weakness, persistent fever and reduced body weight gain; neutrophilia, decreased serum glucose, albumin and alkaline phosphatase activity, and increased serum globulin; lower cell-mediated immune responses; and minimal pancreatic and lymphoid necrosis. Significant amounts of T-2 toxin and its metabolites were detected in dosed areas of the skin and subcutaneous fat. Thus, the skin and subcutaneous fat may act as a depot and site of metabolism for T-2 toxin from which the toxin and its metabolites are slowly absorbed. Intravascular injection of T-2 toxin caused degeneration and necrosis of lymphoid tissues, gastrointestinal mucosa, pancreas, myocardium, bone marrow, adrenal cortex and kidney. There was a dose-dependent increase in lesion severity except for the pancreatic changes. The lymphoid and gastrointestinal necrosis of T-2 treated pigs are similar to those of other species. The pancreas and heart should also be considered as target organs in the pig. Inhalation exposure to T-2 toxin caused vomiting, cyanosis, anorexia, lethargy, lateral recumbency and even death. Elevated rectal temperature and poor body weight gain; neutrophilia, lymphopenia, decreased serum protein, and a transient increase followed by a prominent decrease in serum alkaline phosphatase activity; lower cell-mediated and humoral systemic immune responses; markedly reduced phagocytic ability of alveolar macrophages and mitogen-induced blasto-genesis of pulmonary lymphocytes; interstitial pneumonia, and necrosis of lymphoid tissues, gastrointestinal mucosa, pancreas and myocardium were also found. The majority of these alterations occurred early after dosing and were transient. In many respects, the effects of T-2 toxin on pigs dosed by inhalation are similar those following intravascular injection.
ISBN: 9798206550658Subjects--Topical Terms:
3433982
Veterinary services.
T2 MYCOTOXICOSIS IN SWINE FOLLOWING TOPICAL APPLICATION, INTRAVASCULAR ADMINISTRATION AND INHALATION EXPOSURE.
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Studies were conducted to characterize the clinical signs, pathologic changes and pulmonary and systemic immunity of T-2 toxicosis in swine following a single, topical (15 mg/kg), intravascular (0.6 to 5.4 mg/kg) or inhalation (8 or 9 mg/kg; 20 to 30 percent retention) exposure. Topical T-2 application caused severe dermal injury and adverse systemic effects, including anorexia, posterior weakness, persistent fever and reduced body weight gain; neutrophilia, decreased serum glucose, albumin and alkaline phosphatase activity, and increased serum globulin; lower cell-mediated immune responses; and minimal pancreatic and lymphoid necrosis. Significant amounts of T-2 toxin and its metabolites were detected in dosed areas of the skin and subcutaneous fat. Thus, the skin and subcutaneous fat may act as a depot and site of metabolism for T-2 toxin from which the toxin and its metabolites are slowly absorbed. Intravascular injection of T-2 toxin caused degeneration and necrosis of lymphoid tissues, gastrointestinal mucosa, pancreas, myocardium, bone marrow, adrenal cortex and kidney. There was a dose-dependent increase in lesion severity except for the pancreatic changes. The lymphoid and gastrointestinal necrosis of T-2 treated pigs are similar to those of other species. The pancreas and heart should also be considered as target organs in the pig. Inhalation exposure to T-2 toxin caused vomiting, cyanosis, anorexia, lethargy, lateral recumbency and even death. Elevated rectal temperature and poor body weight gain; neutrophilia, lymphopenia, decreased serum protein, and a transient increase followed by a prominent decrease in serum alkaline phosphatase activity; lower cell-mediated and humoral systemic immune responses; markedly reduced phagocytic ability of alveolar macrophages and mitogen-induced blasto-genesis of pulmonary lymphocytes; interstitial pneumonia, and necrosis of lymphoid tissues, gastrointestinal mucosa, pancreas and myocardium were also found. The majority of these alterations occurred early after dosing and were transient. In many respects, the effects of T-2 toxin on pigs dosed by inhalation are similar those following intravascular injection.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=8623386
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