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Acute phase protein response in an experimental model of ovine caseous lymphadenitisAbstract: The concentration in serum of Hp, SAA and AGP in 6 sheep challenged with 2 × 105 cells of C. pseudotuberculosis showed significant increases (P < 0.05) compared to 3 unchallenged control sheep. By day 7 post infection. (p.i.) the Hp and SAA concentrations reached mean (± SEM) values of 1.65 ± 0.21 g/L and 18.1 ± 5.2 mg/L respectively. Thereafter, their concentrations fell with no significant difference to those of the control sheep by day 18 p.i.. In contrast, the serum AGP concentration in infected sheep continued to rise to a peak of 0.38 ± 0.05 g/L on day 13 p.i., after which a slow decline occurred, although the mean concentration remained significantly higher (P < 0.05) than the control group up to 29 days p.i.. Specific IgG to phospholidase D of C. pseudotuberculosis became detectable at 11 days p.i. and continued to rise throughout the experiment.The serum concentrations of Hp, SAA and AGP were raised in sheep in an experimental model of CLA. An extended response was found for AGP which occurred at a point when the infection was likely to have been transforming from an acute to a chronic phase. The results suggest that AGP could have a role as a marker for chronic conditions in sheep.Caseous Lymphadenitis (CLA) is a chronic disease of sheep and goats caused by Corynebacterium pseudotuberculosis and is characterised by the formation of pyogranulomas within the superficial lymph nodes draining the site of infection. Subsequent dissemination of this facultatively intracellular organism via the lymphatic or blood systems can also result in the formation of similar abscesses within the internal organs and other internal and external lymph nodes, most frequently the mediastinal lymph node and lungs [1,2]. As lesions progress they become encased within fibrous capsules, the inflammatory immune response decreases, and continued slow expansion of the abscess may then occur [3]. It is known that cytokines are involved in the host response to infection, with inflammator
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