Smith N C, Wallach M, Miller C M, Morgenstern R, Braun R, Eckert J
Institut für Parasitologie, Universität Zürich, Switzerland.
Infect Immun. 1994 Apr;62(4):1348-57. doi: 10.1128/iai.62.4.1348-1357.1994.
Vaccination of broiler chickens against Eimeria infection is problematic because of the need to ensure that birds are protected from the time of hatching. We have therefore investigated the feasibility of protecting hatchling broilers via maternal transfer of protective antibodies from hens to their offspring. Oral infection of broiler breeder hens with 20,000 sporulated Eimeria maxima oocysts caused production of antibodies which were passed into the egg yolk and subsequently to hatchlings. The level of specific antibodies in the yolks to unsporulated oocysts, sporulated oocysts, merozoites, and gametocytes was assessed by enzyme-linked immunosorbent assays. The levels in yolks of antibodies to all developmental stages peaked 3 to 4 weeks after infection of the hens. Groups of 10 hatchlings were challenged at 3 days of age by oral infection with 100 sporulated E. maxima oocysts. In the first experiment, the mean 4-day (days 6 to 9 post-infection) total number of oocysts excreted in the feces of chicks from eggs collected 3 weeks after infection of the hens was (0.6 +/- 0.4) x 10(6) (mean +/- standard error) compared with (9.9 +/- 1.4) x 10(6) for the progeny of uninfected hens, which represents a greater than 90% reduction. However, oocyst excretion by chicks from eggs collected 7 or 8 weeks after infection of the hens was only 47 or 68% lower than control values, reflecting declining levels of protective antibodies. In a second experiment, in which the hens were somewhat older and pretreated by intramuscular injection of saline in the emulsifying agent, Arlacel A, the period for which protective antibodies were transferred to hatchlings was prolonged. Thus, oocyst excretion by challenged hatchlings from eggs collected for an 8-week period after infection of the hens was more than 90% lower than oocyst excretion by control chicks, and even hatchlings of eggs collected 19 weeks after infection of the hens showed a 60% reduction in oocyst output. In both experiments, the levels of immunoglobulin G (IgG) antibodies to all developmental stages in yolks or hatchling sera were very strongly correlated with maternally derived immunity to E. maxima. In contrast, parasite-specific IgM or IgA was not detectable, either in egg yolk or egg white. These results demonstrate the ability of IgG antibodies to protect against E. maxima in poultry, thus raising the possibility of using protective maternally derived IgG antibodies to identify potentially protective parasite antigens and indicating the feasibility of using maternal immunization as a means for parasite control.
给肉鸡接种疫苗以预防艾美耳球虫感染存在问题,因为需要确保雏鸡从孵化时起就受到保护。因此,我们研究了通过母鸡将保护性抗体母源传递给后代来保护雏鸡的可行性。用20,000个孢子化的巨型艾美耳球虫卵囊经口感染肉种鸡,可产生抗体,这些抗体进入蛋黄,随后传递给雏鸡。通过酶联免疫吸附测定法评估蛋黄中针对未孢子化卵囊、孢子化卵囊、裂殖子和配子体的特异性抗体水平。母鸡感染后3至4周,蛋黄中针对所有发育阶段的抗体水平达到峰值。10只雏鸡组成的小组在3日龄时经口感染100个孢子化的巨型艾美耳球虫卵囊进行攻毒。在第一个实验中,母鸡感染3周后收集的鸡蛋所孵出的雏鸡,感染后第4天(感染后第6至9天)粪便中排出的卵囊总数平均为(0.6±0.4)×10⁶(平均值±标准误差),而未感染母鸡的后代为(9.9±1.4)×10⁶,减少了90%以上。然而,母鸡感染7或8周后收集的鸡蛋所孵出的雏鸡的卵囊排泄量仅比对照值低47%或68%,这反映了保护性抗体水平的下降。在第二个实验中,母鸡年龄稍大且预先通过肌肉注射含乳化剂阿拉塞A的生理盐水进行处理,保护性抗体传递给雏鸡的时间延长。因此,母鸡感染后8周期间收集的鸡蛋所孵出的经攻毒雏鸡的卵囊排泄量比对照雏鸡低90%以上,甚至母鸡感染19周后收集的鸡蛋所孵出的雏鸡的卵囊产量也降低了60%。在两个实验中,蛋黄或雏鸡血清中针对所有发育阶段的免疫球蛋白G(IgG)抗体水平与对巨型艾美耳球虫的母源免疫力密切相关。相比之下,在蛋黄或蛋清中均未检测到寄生虫特异性IgM或IgA。这些结果证明了IgG抗体在家禽中预防巨型艾美耳球虫的能力,从而增加了利用母源保护性IgG抗体鉴定潜在保护性寄生虫抗原的可能性,并表明了利用母源免疫作为控制寄生虫手段的可行性。