Simpson K W, Strauss-Ayali D, McDonough P L, Chang Y F, Valentine B A
Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
J Vet Intern Med. 1999 Nov-Dec;13(6):507-15. doi: 10.1892/0891-6640(1999)013<0507:gfidwn>2.3.co;2.
The association of Helicobacter pylori with gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship of Helicobacter spp. infection to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter infection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquired Helicobacter spp. infection were studied before and after (4 and 29 days) the attempted eradication of Helicobacter spp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific-pathogen-free, Helicobacter-free Beagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection with Helicobacter felis- and H bizzozeronii-like organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin-stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P = .09) toward higher meal-stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin-stimulated maximal acid output (mmol HCI/kg0.75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P < .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA with Helicobacter-specific primers indicated persistence of Helicobacter DNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression of Helicobacter spp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquired Helicobacter spp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastric Helicobacter spp. in dogs.
幽门螺杆菌与胃炎、消化性溃疡及胃肿瘤的关联已使人们对人类胃部疾病的认识发生了根本性变化。幽门螺杆菌属感染与犬类胃部疾病的关系尚不清楚。本研究的目的是确定幽门螺杆菌感染是否会影响犬类的胃分泌轴。对8只自然感染幽门螺杆菌属的比格犬在尝试用阿莫西林、甲硝唑和法莫替丁（AMF）联合根除幽门螺杆菌属之前及之后（4天和29天）进行了研究。6只无特定病原体、未感染幽门螺杆菌的比格犬作为对照。感染犬体内螺旋状生物体的电子显微镜外观表明同时感染了猫幽门螺杆菌和类比氏幽门螺杆菌。未受刺激时的胃pH值以及空腹、餐后和蛙皮素刺激后的血浆胃泌素在感染犬和未感染犬中相似，不过在感染犬中，60分钟时观察到餐后胃泌素呈升高趋势（P = 0.09）。五肽胃泌素刺激后的最大酸排量（mmol HCl/kg0.75/小时）和可滴定酸度（mmol HCl/mL）在感染犬和未感染犬中相似，但在最大酸排量期间，未感染犬的胃pH值更低（P < 0.01）。感染犬和未感染犬均存在轻度胃部炎症。AMF治疗4天后，8只感染犬中有6只未检测到胃螺旋状生物体，但AMF治疗29天后，8只犬中螺旋状生物体均再次出现。用幽门螺杆菌特异性引物分析胃DNA表明，抗生素治疗后4天和29天幽门螺杆菌DNA持续存在。AMF对幽门螺杆菌属的短暂抑制并未影响胃酸分泌、血浆胃泌素和黏膜炎症。这些发现表明，自然感染幽门螺杆菌属不会明显扰乱犬类的胃分泌功能，并且用阿莫西林、甲硝唑和法莫替丁治疗会抑制而非根除犬类胃部的幽门螺杆菌属。
