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Narasin poisoning in the dromedary camel (Camelus dromedarius)

Narasin poisoning in the dromedary camel (Camelus dromedarius) Narasin poisoning was reported in 15 camels, 7 adults and 8 young, after accidental access to poultry feed medicated with 60 g narasin per ton. Fourteen camels died between 3 and 20 days, and one young animal survived the dose after developing a chronic course of a disease. The main clinical signs of narasin toxicity in the dromedary include: weakness of hind limbs, lack of coordination, oedema of dependent parts, inappetence, ruminal atony, myoglobinuria, profound depression, tachycardia, sternal recumbency and death. The lesions were mainly in the heart and skeletal muscles and consisted of multifocal degeneration and necrosis of heart and skeletal muscle fibres with areas of regeneration and lung oedema. There was high enzyme activity for creatine kinase (CK), lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase and an increase in urea concentration and white blood cells, neutrophil and platelet counts. Cardiac markers, troponin T, CK-MB and C-reactive protein, showed slight or no changes terminally. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Comparative Clinical Pathology Springer Journals

Narasin poisoning in the dromedary camel (Camelus dromedarius)

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References (30)

Publisher
Springer Journals
Copyright
Copyright © 2012 by Springer-Verlag London Limited
Subject
Medicine & Public Health; Pathology; Hematology; Oncology
eISSN
1618-565X
DOI
10.1007/s00580-011-1403-4
Publisher site
See Article on Publisher Site

Abstract

Narasin poisoning was reported in 15 camels, 7 adults and 8 young, after accidental access to poultry feed medicated with 60 g narasin per ton. Fourteen camels died between 3 and 20 days, and one young animal survived the dose after developing a chronic course of a disease. The main clinical signs of narasin toxicity in the dromedary include: weakness of hind limbs, lack of coordination, oedema of dependent parts, inappetence, ruminal atony, myoglobinuria, profound depression, tachycardia, sternal recumbency and death. The lesions were mainly in the heart and skeletal muscles and consisted of multifocal degeneration and necrosis of heart and skeletal muscle fibres with areas of regeneration and lung oedema. There was high enzyme activity for creatine kinase (CK), lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase and an increase in urea concentration and white blood cells, neutrophil and platelet counts. Cardiac markers, troponin T, CK-MB and C-reactive protein, showed slight or no changes terminally.

Journal

Comparative Clinical Pathology – Springer Journals

Published: Jan 10, 2012

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