La bursite infectieuse aviaire (IBD) est une des causes majeures de pertes économiques pour l’industrie aviaire. La vaccination est le principal outil de contrôle de cette maladie et les oiseaux susceptibles doivent être vaccinés aussitôt que le niveau des anticorps maternels (MA) anti-IBDV est suffisamment bas. L’estimation du moment de vaccination est habituellement déterminée par la formule de Deventer qui utilise le titre initial de MA anti-IBDV et la demi-vie des anticorps pour prédire l’évolution du titre. Dans la présente étude, l’effet du gain de poids sur la vitesse de disparition des MA a été étudié dans le but de l’utiliser pour prédire la détermination du moment de la vaccination. L’analyse des taux d’anticorps neutralisants par ELISA a montré que les poussins avec une forte croissance avaient un taux de disparition plus rapide des MA que ceux à faible croissance. Une formule pour la prédiction du moment de vaccination contre le IBDV, basée sur le gain de poids et le niveau des MA a été développée et vérifiée. La prédiction du moment de vaccination avec cette formule a montré une haute corrélation avec les titres de MA mesurés par ELISA. Le virus de l’anémie infectieuse aviaire (CIAV) est une cause importante d’immunosuppression chez le poulet augmentant la pathogénicité des infections secondaires et en entraînant une réponse humorale suboptimale et une forte mortalité. D’autre part, l’infections sub-clinique du au CIAV provoque une immunosuppression qui facilite la coinfection par d’autre virus tel que le IBDV. Les effets de la coinfection à J1 avec une souche vaccinale de CIAV CAV-VAC® (Intervet) et à J14 avec une souche faiblement virulente de IBDV isolée au Québec, sur l’état de santé des poussins, sur la persistance virale et sur la réponse immunitaire ont été étudiés autant chez des poussins de 1 jour d’âge exempts d’agents pathogènes specifique (SPF) que ceux provenant d’élevages commerciaux. Les résultats ont montré que l’inoculation de la souche vaccinale du CIAV a entraîné une infection sub-clinique, une persistance virale dans la rate et le thymus, une altération de la thymopoièse et une réponse humorale temporaire chez les poussins SPF. Ces effets ont aussi été mis en évidence chez des poussins d’élevage commerciaux malgré des taux élevés de MA. Lors de l’infection avec la souche de IBDV chez des poussins déjà vaccinés contre le CIAV, la persistance du CIAV dans les organes lymphoïdes a été aggravée par une présence de réponses humorales temporaires contre les deux virus et une altération des populations lymphocytaires dans les organes lymphoïdes. Par contre, la présence des MA contre le CIAV a limité temporairement ces effets. Ces travaux ont mis en évidence des désordres immunitaires cellulaires et humoraux et une persistance virale chez des poussins vaccinés contre le CIAV et co-infectés avec le IBDV. / Infectious bursal disease (IBD) is one of the major causes of economic losses in the chicken industry. Vaccination is the main tool against the disease, and the susceptible birds should be vaccinated as soon as the maternal antibody (MA) becomes low enough to allow the vaccine to break through. Estimation of vaccination time is currently performed by Deventer formula which uses initial anti-IBDV titer and antibody half-life to predict the titer. Considering the increased growth rate of chicken in the last decades and the wide variations of MA, we have examined the effects of chick’s weight gain on MA decline and the use of weight in predicting IBD vaccination time. The virus neutralization test and ELISA results demonstrated that fast-growing birds had a faster rate of antibody decline whereas slow-growing birds demonstrated a slower rate. Based on the effect of weight-gain on maternal antibody decline, a new formula for predicting IBD vaccination time was introduced and tested. The predicted IBD vaccination time made by this weight formula showed higher correlation with the measured ELISA titers in the experiment. Chicken infectious anemia virus (CIAV) is another cause of immunosuppression in chicken which is characterized by increased pathogenicity of secondary infectious agents, sub-optimal antibody responses and mortality. CIAV subclinical infections can result in immunosuppression and enhancement of pathogenicity of co-infecting agents such as infectious bursal disease virus (IBDV). Effects of pathogenic CIAV and IBDV coinfection on chick’s health and immune responses are investigated in different studies. In this study, newly hatched specific pathogen free (SPF) and commercial chicks were vaccinated with CAV-VAC® (Intervet) vaccine and /or inoculated with a low-virulent Québec isolate of IBDV at 14 days post CIAV vaccination. Inoculation of the CIAV vaccinal strain at hatch resulted in subclinical infection associated with viral persistency in spleen and thymus, alteration of thymopoiesis and transient humoral response in SPF chicks. Subclinical infection, viral persistency and lack of antibody responses were also shown in CIAV inoculated commercial chicks with high MA. Infection of the low-virulent IBDV in the CIAV vaccinated SPF chicks lead to extended viral persistence of CIAV in lymphoid organs, transient immune responses to both CIAV and IBDV, and alteration of lymphocytes subpopulation in the lymphoid organs. In the coinfected commercial chicks, presence the CIAV in the lymphoid organs was controlled by MA in the first 1-2 weeks after hatch. Thereafter, the immune disorders, viral persistence and lack of humoral responses almost similar to the coinfected SPF chicks were recorded.

Made available in DSpace on 2015-05-14T13:00:13Z (GMT). No. of bitstreams: 1 arquivototal.pdf: 2275378 bytes, checksum: fcb4196c739d83997818dc074daf738f (MD5) Previous issue date: 2010-03-11 / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES / The pharmacological effects of carvacrol, a monoterpenoid phenol, on the cardiovascular system were studied in normotensive rats, using in vivo and in vitro techniques. In superior mesenteric artery rings isolated from rats with functional endothelium carvacrol (10-8 - 3 ₓ 10-4 M) concentration-dependently relaxed phenylephrine-induced contractions (pD2 = 4.59  0.02, MR = 103.03  1.5%, N=8) and this effect was not altered after removal of the endothelium (pD2 = 4.36  0.02, MR = 111.03  4.8%, N=8), suggesting that the vasorelaxant response induced by carvacrol appears to be independent of vascular endothelium. Furthermore, carvacrol antagonized the vasoconstriction induced by high K+ solution (Tyrode with 80 mM of KCl) (pD2 = 4.12  0.01, MR = 94.38  3.97%, N=6), inhibited contraction elicited by CaCl2 in depolarizing (KCL 60 mM) nominally without Ca2+ medium out carvacrol also antagonized the contractions induced by the L-type Ca2+ channel agonist, S(-)-Bay K 8644 (pD2 = 4.537  0.023, MR = 9.8  3.58%, N=6), indicating that the vasodilatation involve probably the inhibition of Ca2+ influx through L-type voltage-dependent calcium channels (Cav type-L). Additionally, carvacrol antagonized the contractions induced by CaCl2 in nominally without Ca2+ medium in the presence of PHE and nifedipine, suggesting a possible inhibition of calcium influx by store operated channels (SOC), receptor operated channels (ROC) and/or TRP channels. Interestingly, in a depolarizing (KCL 60 mM) nominally without Ca2+ medium and in the presence of nifedipine, carvacrol also inhibited the contraction induced by CaCl2, suggesting a probable inhibition of SOC and/or TRP channels. To evaluate the involvement of TRP channels in the vasorelaxant effect induced by carvacrol, non-selective inhibitors were used. No change in the relaxation response was observed in the presence of ruthenium red (pD2= 4.31  0.029, N=6), however, the effect induced by carvacrol was potentiated by La3+ (pD2 = 5.231  0,04, N=6), Gd3+ (pD2 = 4.97  0.02, N=6) or Ni2+ (pD2 = 5.079  0.02, N=6), furthermore, Mg2+ (pD2 = 4.168  0.021; MR = 81.12  4.03%, N=6) attenuated the relaxation elicited by carvacrol, suggesting that monoterpenoid may to action on TRPC1, TRPC3, TRPC6 and TRPM7 channels. Carvacrol also induced hypotension and bradycardia in non-anesthetized normotensive rats. In conclusion, these results suggest that carvacrol induced vasorelaxant effect in superior mesenteric artery rats isolated probably inhibiting Ca2+ influx by Cav, SOC (TRPC1), ROC (TRPC1 or TRPC6) and TRPM7 channels. Moreover, the effects induced by carvacrol in normotensive non-anesthetized rats showed a hypotensive and bradycardic activity. / Os efeitos farmacológicos de carvacrol, um fenol monoterpenóide, sobre o sistema cardiovascular, foi estudado em ratos normotensos, usando técnicas in vivo e in vitro. Carvacrol (10-8 - 3 ₓ 10-4 M) induziu vasorelaxamento dos anéis de artéria mesentérica superior isolada de rato pré-contraídos com 10 μM FEN (pD2 = 4,59  0,02, Emáx = 103,03  1,5%) na presença do endotélio funcional e esse efeito não foi alterado após a remoção do endotélio (pD2 = 4,36  0,02, Emáx = 111,03  4,8%), sugerindo, portanto, que a resposta vasorelaxante induzida por carvacrol parece ser independente do endotélio vascular. Interessantemente em anéis pré-contraídos com KCl 80 mM (pD2 = 4,12  0,01, Emáx = 94,38  3,97%), observou-se uma diminuição na sua potência e na sua eficácia farmacológica, sugerindo um passo comum na via que seria um aumento citosólico dos níveis de cálcio. Adicionalmente, carvacrol antagonizou, de maneira dependente de concentração, as contrações induzidas por CaCl2 em meio despolarizante nominalmente sem Ca2+ e induziu relaxamento das contrações induzidas pelo S(-)-Bay K 8644 (pD2 = 4,537  0,023, Emáx = 91,8  3,58%) com uma diminuição na sua eficácia farmacológica, sugerindo uma inibição do influxo de cálcio por canais de Ca2+ tipo-L. Além disso, antagonizou as contrações induzidas por CaCl2 em meio nominalmente sem cálcio, na presença de FEN e nifedipina, sugerindo uma provável inibição do influxo de cálcio por SOC, ROC e/ou canais TRP. Como também, em um meio despolarizante e nominalmente sem cálcio na presença de nifedipina esse mesmo antagonismo foi observado, ressaltando a provável inibição dos SOC e/ou canais TRP. Para avaliar a participação dos canais TRP, as preparações foram incubadas com La3+ (pD2 = 5,231  0,04) , Gd3+ (pD2 = 4,97  0,02) e Ni2+ (pD2 = 5,079  0,02) onde seu efeito foi potencializado sugerindo sua ação sobre os canais TRPC e ao utilizar magnésio (pD2 = 4,168  0,021 e Emáx = 81,12  4,03%) tanto sua potência quanto sua eficácia farmacológica foi atenuada, sugerindo inibição do canal TRPM7. Nos estudos in vivo, em ratos normotensos não anestesiados, carvacrol produziu hipotensão e bradicardia. Em conclusão, esses resultados sugerem que carvacrol induz efeito vasorelaxante em anéis de artéria mesentérica superior isolada de rato por inibir provavelmente TRPM7, como também inibir o influxo de cálcio por Cav, SOC, ROC e ou TRPC1 e 6. Além disso, os efeitos induzidos por carvacrol em ratos normotensos não anestesiados mostrou uma atividade hipotensora e bradicárdica.

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