Seroepidemiological studies on domestic animal and human diseases infected with enterohemorrhagic Escherichia coli.

为调查某养殖场产志贺毒素大肠杆菌（STEC）感染犊牛的频率，采用聚合酶链式反应（PCR）检测志贺毒素基因。2月龄以下犊牛、2 ~ 8月龄牛和1岁以上成年牛的患病率分别为39.4%、79%和40.8%。0-8月龄犊牛粪便标本中产大肠杆菌的检出频率在不同牛种（荷斯坦牛、日本黑牛，F1: HxB）中无显著差异。研究了奶牛通过初乳对产志毒素大肠杆菌的被动免疫。采用酶联免疫吸附试验（ELISA）测定了牛初乳和犊牛血清中的抗体滴度。结果表明，产后初乳对产志贺毒素大肠杆菌的抗体效价最高。首次食用高抗体滴度的初乳可提高新生牛犊在出生后4-9小时的血清抗体滴度，这表明初乳（和奶牛血清）中的抗体滴度与新生牛犊之间存在相关性。由此可见，通过初乳对产大肠杆菌感染产生了被动免疫。提出了一种保护新生牛犊免受产志贺毒素大肠杆菌感染的新方法。我们评估了促炎细胞因子如γ干扰素（IFN-γ）或肿瘤坏死因子-α (TNF-α)介导Stx1或Stx2致死率的可能性。注射Stx1 400ng后3 ~ 4 d内小鼠全部死亡，Stx2的致死剂量比Stx1低40倍。给药400 ng Stx1或10 ng Stx2后1 ~ 6 h，小鼠血清和脾脏中均未见IFN-γ和TNF-α的产生。然而，当小鼠注射133 ng Stx1或3.3 ng Stx2时，与C57BL/6小鼠相比，IFN-γ缺陷小鼠和TNF-α缺陷小鼠明显存活，这表明无法检测到的IFN-γ和TNF-α都参与了Stx的致死。本研究使用细胞因子基因敲除小鼠直接证实IFN-γ和TNF-α参与Stx1和Stx2的致死性。少

To investigate the frequency of Shiga toxin-producing Escherichia coli (STEC) infected calves at a breeding farm, the plymerase chain reaction (PCR) was used for detection of genes for Shiga toxin (s). The prevalence rates in calves less than 2 months of age, cattle 2-8 months age, and adults greater than 1 year of age were 39.4, 79, and 40.8%, respectively. Detection frequency of STEC in the fecal specimens from calves aged 0-8 months was not different among the breeds of cattle (Holstein, Japanese black cattle, F1 : HxB).Passive immunity against STEC from cows to newborn calves through colostrum was studied. Antibody titers in colostrum and sera from cows and newborn calves were determined by enzyme-linked immunosorbent assay (ELISA). The obtained results indicate that antibody titer to STEC in colostrum from cows soon after parturition was the highest one. The first consumption of colostrum with high antibody titer elevated serum antibody titer from newborn calves at 4-9 hours after … More birth, suggesting a correlation between antibody titer in colostrum (and sera of cows) and newborn calves. From this result, passive immunity to STEC infection is found to be occurred in newborn claves through colostrum. Suggests a new way to protect newborn calves against STEC infection.We assess that possibility of proinflammatory cytokines such as gamma interferon (IFN-γ) or tumor necrosis factor-alpha (TNF-α) mediate lethality of Stx1 or Stx2. All of mice died within 3 to 4 days after injection with 400 ng of Stx1, a lethal dose of Stx2 was lower 40-times than that of Stx1. When mice were given 400 ng of Stx1 or 10 ng of Stx2, IFN-γand TNF-α production in the sera and spleens was not observed 1 h to 6 h after injection. However, when mice were injected with 133 ng of Stx1 or 3.3 ng of Stx2, IFN-γ -deficient mice and TNF-α-deficient mice significantly survived, compared with C57BL/6 mice, suggesting that undetectable levels of both IFN-γ and TNF-α are involved in lethality of Stx. The present study using cytokine-gene knockout mice directly demonstrated that both IFN-γ and TNF-α are involved in lethality of Stx1 and Stx2. Less