Roberts-Thomson I C
Department of Gastroenterology, Queen Elizabeth Hospital, Woodville, South Australia.
Clin Infect Dis. 1993 Mar;16 Suppl 2:S98-104. doi: 10.1093/clinids/16.supplement_2.s98.
Wide variation has been observed in the natural history of human and murine giardiasis, which could be due to factors associated with the parasite or with the host. In humans, prolonged infections with Giardia duodenalis have been associated with hypogammaglobulinemia, protein-calorie malnutrition, and prior gastrectomy. The duration of infection or severity of symptoms may also be influenced by the humoral immune response and by other factors such as ABO blood group and HLA antigen type. Elimination of Giardia muris is impaired in hypothymic mice, B-cell-deficient mice expressing the xid gene, and in mice deficient in mast cells. Prolonged infections also occur following depletion of helper/inducer T cells and suppression of antibody production with antisera to IgM. However, quantitative or qualitative defects in immune function do not appear to account for prolonged cyst excretion in C3H/He, C3H/HeJ, and A/J mice. The defect in these strains is influenced by several genes and may involve intermediate or late stages of macrophage activation leading to impaired elimination of the parasite.
在人类和鼠类贾第虫病的自然病史中观察到了广泛的差异,这可能归因于与寄生虫或宿主相关的因素。在人类中,十二指肠贾第虫的长期感染与低丙种球蛋白血症、蛋白质 - 热量营养不良以及既往胃切除术有关。感染持续时间或症状严重程度也可能受体液免疫反应以及其他因素如ABO血型和HLA抗原类型的影响。在胸腺发育不全的小鼠、表达xid基因的B细胞缺陷小鼠以及肥大细胞缺陷的小鼠中,鼠贾第虫的清除受到损害。在用抗IgM抗血清耗尽辅助/诱导性T细胞并抑制抗体产生后,也会发生长期感染。然而,免疫功能的定量或定性缺陷似乎并不能解释C3H/He、C3H/HeJ和A/J小鼠中囊肿排泄延长的现象。这些品系中的缺陷受多个基因影响,可能涉及巨噬细胞激活的中期或后期阶段,导致寄生虫清除受损。