Allen P C
USDA, Agricultural Research Service, Livestock and Poultry Sciences Institute, Parasite Biology and Epidemiology Laboratory, BARC-East, Beltsville, Maryland 20705, USA.
Poult Sci. 2000 Sep;79(9):1251-8. doi: 10.1093/ps/79.9.1251.
Reduced weight gains and feed conversions are major sources of economic losses from avian coccidiosis. Experiments were conducted to determine possible involvement of up-regulation of cyclooxygenase (COX) activity during coccidia infections that might contribute to reduced weight gain. In a series of trials, young (3 to 5 wk of age) cockerels infected with Eimeria acervulina, a duodenal parasite, received oral treatments with indomethacin (IM), an inhibitor of both COX-1 and COX-2, or nimesulide (NIM), a specific inhibitor of COX-2. Infection doses varied with experiment (from 10(5) to 10(6) oocysts per chick). Effects of infection on weight gain, duodenal lesions, plasma carotenoids, and levels of NO2+ NO3- were determined at 6 d postinoculation. Total oocysts were enumerated in feces collected from 5 through 8 d postinoculation from separate replicate groups. In no trials did treatment with IM reverse effects of infection on weight gain or significantly reduce lesion scores. However, in all trials, IM treatment reduced oocyst output per chick (Trial 1, 15%; Trial 2, 19%; Trial 3, 53%; Trial 4, 29%; Trial 5, 28.5%). Supplementation of feed with 400 and 100 ppm NIM significantly reduced weight gain of, and increased oocyst output from, infected chicks, whereas supplementation with 50 ppm NIM had no beneficial effects on weight gain or lesion scores, but reduced oocyst shedding. The inability of the IM and NIM treatments to reverse infection-associated weight gain suppression suggests that this pathological effect is not linked to increased prostanoid synthesis as a result of COX-2 up-regulation during infection. The inhibitory effects of IM treatment on oocyst shedding suggest that COX-2 products may have immunosuppressive effects in coccidia infection at local sites of infection. The stimulating effects of high-dose NIM treatments on oocyst shedding suggest that this compound may inhibit synthesis of other prostanoids as well.
体重增加减少和饲料转化率降低是禽球虫病造成经济损失的主要原因。开展实验以确定球虫感染期间环氧化酶（COX）活性上调可能对体重增加减少产生的影响。在一系列试验中，感染十二指肠寄生虫堆型艾美耳球虫的3至5周龄小公鸡接受了吲哚美辛（IM，一种COX-1和COX-2的抑制剂）或尼美舒利（NIM，一种COX-2的特异性抑制剂）的口服治疗。感染剂量因实验而异（每只鸡10⁵至10⁶个卵囊）。在接种后6天测定感染对体重增加、十二指肠病变、血浆类胡萝卜素以及NO₂+NO₃⁻水平的影响。从单独重复组接种后5至8天收集的粪便中计数总卵囊数。在所有试验中，IM治疗均未逆转感染对体重增加的影响，也未显著降低病变评分。然而，在所有试验中，IM治疗均降低了每只鸡的卵囊产量（试验1，15%；试验2，19%；试验3，53%；试验4，29%；试验5，28.5%）。在饲料中添加400 ppm和100 ppm的NIM显著降低了感染小鸡的体重增加，并增加了其卵囊产量，而添加50 ppm的NIM对体重增加或病变评分没有有益影响，但减少了卵囊排出。IM和NIM治疗无法逆转与感染相关的体重增加抑制，这表明这种病理效应与感染期间COX-2上调导致的类前列腺素合成增加无关。IM治疗对卵囊排出的抑制作用表明，COX-2产物可能在感染局部部位的球虫感染中具有免疫抑制作用。高剂量NIM治疗对卵囊排出的刺激作用表明，该化合物可能也抑制其他类前列腺素的合成。
