Anand B S, Kumar M, Chakravarti R N, Sehgal A K, Chhuttani P N
Trans R Soc Trop Med Hyg. 1980;74(5):565-9. doi: 10.1016/0035-9203(80)90139-x.
It is well established that infection with Giardia lamblia can cause malabsorption although the pathogenesis of this is unknown. Transport studies were made on the intestinal segments of male albino rats infected with Giardia cysts obtained from human stools to investigate this pathogenesis. The results were compared with those seen in a normal group and in a control group that was fed with a Giardia-free stool suspension. There was a significant fall in the transport of glucose and glycine, both of which were actively absorbed. On the other hand, potassium, which diffuses passively in a bidirectional manner across the bowel wall, was not affected. Furthermore, it was observed that the transport mechanism was deranged in the presence of an entirely normal small intestinal mucosa, as judged by light microscopy. It is concluded that Giardia trophozoites interfere with the active transport mechanisms of the small intestinal mucosa. This defect could result either from structural damage to the substrate carriers or from an alteration in cell maturation.
虽然贾第虫感染导致吸收不良的发病机制尚不清楚，但贾第虫感染可引起吸收不良这一点已得到充分证实。为了研究这一发病机制，对感染了从人类粪便中获取的贾第虫囊肿的雄性白化大鼠的肠段进行了转运研究。将结果与正常组和喂食无贾第虫粪便悬液的对照组的结果进行了比较。葡萄糖和甘氨酸的转运显著下降，这两种物质都是主动吸收的。另一方面，以双向方式被动扩散穿过肠壁的钾不受影响。此外，通过光学显微镜观察发现，在小肠黏膜完全正常的情况下，转运机制也发生了紊乱。得出的结论是，贾第虫滋养体干扰了小肠黏膜的主动转运机制。这种缺陷可能是由于底物载体的结构损伤或细胞成熟的改变所致。
