目的　探讨氯硝柳胺和 o,o’-二乙基 - o’’- (邻氯苯乙腈肟 )硫代磷酸酯 (代号 B0 0 2 )合用的灭螺增效机理。　方法　采用肉眼观察、组织学、组织化学、酶组织化学方法对经氯硝柳胺和 B0 0 2分别处理后的钉螺软体进行了观察。　结果　氯硝柳胺对钉螺肝、睾丸、卵巢等各组织、器官都有损伤作用。B0 0 2使钉螺软体肿胀、外伸 ,失去附着能力 ,对外界反应能力降低 ,呈麻痹状态 ;头足部呈现明显病理性改变 ,糖元含量减少 ,神经节和足肌中的胆碱酯酶 (CHE)、一氧化氮合成酶 (NOS)活性降低。　结论　 B0 0 2干扰钉螺神经介质的传递 ,使得头足部肌肉失去张力 ,对外界刺激反应消失 ,增加与氯硝柳胺接触介面 ,导致钉螺对氯硝柳胺的吸收增加 ,加剧了钉螺的损伤和死亡 Aim To investigate the snail synergism mechanism of niclosamide and o, o’-diethyl-o ’’ - (o -chloroacetonitrile oxime) phosphorothioate (code B0 0 2) Methods The snail mollusks treated with niclosamide and B0 0 2 were observed by naked eye, histology, histochemistry and enzymatic histochemistry. Results niclosamide on snail liver, testes, ovaries and other tissues and organs have an injury. B0 0 2 to snail soft body swelling, stretching, loss of attachment, the ability to respond to the outside world reduced, paralysis; head and foot showed significant pathological changes, glycogen content decreased, ganglion and foot muscle cholinesterase (CHE), nitric oxide synthase (NOS) activity decreased. Conclusion B0 0 2 interference snail transmission of nerve mediators, the head and foot muscles lose tension, the external response to the disappearance of stimuli, increased contact with niclosamide interface, resulting snail snail nicotine absorption increased, exacerbated the snail injury And death