Perkins S E, Yan L L, Shen Z, Hayward A, Murphy J C, Fox J G
Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge 02139, USA.
Antimicrob Agents Chemother. 1996 Jun;40(6):1486-90. doi: 10.1128/AAC.40.6.1486.
Helicobacter pylori causes gastritis and peptic ulcers and is linked to gastric cancer. Domestic cats from a commercial source were found to be naturally infected with H. pylori, and studies were undertaken to eradicate H. pylori from infected cats by using triple antimicrobial therapy. Eight cats infected with H. pylori were used in the study. Six cats received a 21-day course of oral amoxicillin, metronidazole, and omeprazole, and two cats served as controls. Two weeks and 4 weeks posttreatment (p.t.), all six treated cats were negative at several sites (saliva, gastric juice, and gastric mucosa) for H. pylori by culture. However, as determined by PCR with primers specific for the 26-kDa product, the majority of cats at 2 and 4 weeks p.t. had gastric fluid samples which were positive for H. pylori and three of three cats at 2 weeks p.t. had dental plaque which was positive for H. pylori. At 6 weeks p.t., all six cats had H. pylori-negative cultures for samples from several gastric sites taken at necropsy, and only one cat had H. pylori cultured from gastric juice. PCR analysis revealed that five of six cats had H. pylori DNA amplification products from plaque, saliva, and/or gastric fluid samples. Negative bacterial cultures for cats for which there was demonstrable PCR amplification of H. pylori DNA may reflect the inability of in vitro culture techniques to isolate small numbers of H. pylori organisms, focal colonization at sites not cultured, or a failure of the antibiotics to successfully eradicate H. pylori from extragastric sites which allowed subsequent recolonization of the stomach after cessation of therapy. Alternatively, the treatment strategy may have induced in vivo viable but nonculturable coccoid forms of H. pylori. The H. pylori cat model should allow further studies to test these hypotheses as well as the efficacies of other combined therapeutic regimens. Also, because 100% of these cats were naturally infected with H.pylori, this model should prove useful in exploring mechanisms whereby human populations in underdeveloped countries, which have H. pylori infection rates approaching 100%, have a high rate of recurrence of H. pylori infection after use of prescribed antibiotic therapies that successfully eradicate H. pylori in individuals in developed countries.
幽门螺杆菌可引发胃炎和消化性溃疡,还与胃癌有关。研究发现,来自商业渠道的家猫自然感染了幽门螺杆菌,并开展了相关研究,以通过三联抗菌疗法根除感染猫体内的幽门螺杆菌。该研究使用了8只感染幽门螺杆菌的猫。6只猫接受了为期21天的口服阿莫西林、甲硝唑和奥美拉唑治疗,另外2只猫作为对照。治疗后2周和4周,通过培养发现,所有6只接受治疗的猫在唾液、胃液和胃黏膜等多个部位均未检测到幽门螺杆菌。然而,通过针对26 kDa产物的特异性引物进行PCR检测发现,大多数治疗后2周和4周的猫的胃液样本中幽门螺杆菌呈阳性,治疗后2周的3只猫中有3只的牙菌斑中幽门螺杆菌呈阳性。治疗后6周,尸检时采集的来自多个胃部位点的样本培养显示,所有6只猫的幽门螺杆菌均为阴性,只有1只猫的胃液中培养出幽门螺杆菌。PCR分析显示,6只猫中有5只的牙菌斑、唾液和/或胃液样本中存在幽门螺杆菌DNA扩增产物。对于幽门螺杆菌DNA有可证实的PCR扩增但细菌培养为阴性的猫,可能反映出体外培养技术无法分离少量幽门螺杆菌、在未培养的位点存在局部定植,或者抗生素未能成功根除胃外部位的幽门螺杆菌,从而在治疗停止后导致胃部再次定植。或者,治疗策略可能诱导了幽门螺杆菌在体内形成存活但不可培养的球形体。幽门螺杆菌猫模型应有助于进一步研究以验证这些假设以及其他联合治疗方案的疗效。此外,由于这些猫100%自然感染幽门螺杆菌,该模型在探索机制方面应会很有用,即那些幽门螺杆菌感染率接近100%的欠发达国家的人群,在使用能成功根除发达国家个体体内幽门螺杆菌的规定抗生素疗法后,幽门螺杆菌感染复发率很高的机制。