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食源性甲型肝炎暴发:急性和迁延性疾病的临床及实验室特征

Foodborne outbreak of hepatitis A: clinical and laboratory features of acute and protracted illness.

作者信息

Routenberg J A, Dienstag J L, Harrison W O, Kilpatrick M E, Hooper R R, Chisari F V, Purcell R H, Fornes M F

出版信息

Am J Med Sci. 1979 Sep-Oct;278(2):123-37.

PMID:517565
Abstract

During a 1974 foodborne outbreak of viral hepatitis type A among Navy recruits, we evaluated clinical and laboratory features prospectively in 130 affected persons. The ratio of anicteric to icteric persons identified during the outbreak was 1:3.5 but illness was relatively mild in this population of young adults. Infrequently reported in association with type A hepatitis, rash and arthralgias (but not arthritis) were reported by 14 and 10% of affected persons, respectively. Fourteen weeks after onset of acute illness, 8.5% of patients had persistently elevated aminotransferase activities and underwent percutaneous liver biopsy. Morphologic features included piecemeal necrosis, but clinical, biochemical, and histological evidence of disease resolved within five months to one year after the outbreak. Fecal shedding of hepatitis A virus began during the preicteric stage, did not persist beyond the second day of jaundice (even in patients with protracted illness), and was not detected in anicteric patients. Feces and serum obtained during the late incubation period, but not urine, were infectious in chimpanzees. Antibody to hepatitis A virus developed during convalescence, and serum anticomplementary activity was noted during acute illness. Failure of T-lymphocytes to bind sheep erythrocytes and form rosettes was observed, was found to be modulated in several cases by an intrinsic lymphocyte defect and in others by the presence in serum of an extrinsic immunoregulatory serum lipoprotein, "rosette inhibitory factor," which persisted in patients with slow resolution.

摘要

在1974年海军新兵中发生的一次甲型病毒性肝炎食源性暴发期间,我们对130名感染者的临床和实验室特征进行了前瞻性评估。暴发期间确诊的无黄疸者与黄疸者的比例为1:3.5,但在这群年轻成年人中疾病相对较轻。皮疹和关节痛(而非关节炎)与甲型肝炎相关的情况较少见,分别有14%和10%的感染者报告出现此类症状。急性病发作14周后,8.5%的患者转氨酶活性持续升高并接受了经皮肝活检。形态学特征包括桥接坏死,但疾病的临床、生化和组织学证据在暴发后5个月至1年内消失。甲型肝炎病毒的粪便排出始于黄疸前期,在黄疸出现后第二天之后不再持续(即使是病程迁延的患者),在无黄疸患者中未检测到。潜伏期后期采集的粪便和血清(而非尿液)在黑猩猩中具有传染性。甲型肝炎病毒抗体在恢复期产生,急性病期间观察到血清抗补体活性。观察到T淋巴细胞不能结合绵羊红细胞并形成玫瑰花结,在一些病例中发现这是由内在淋巴细胞缺陷调节的,而在其他病例中是由血清中存在的一种外源性免疫调节血清脂蛋白“玫瑰花结抑制因子”调节的,该因子在恢复缓慢的患者中持续存在。

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