Butler T, Johnston K H, Gutierrez Y, Aikawa M, Cardaman R
Infect Immun. 1985 Jan;47(1):294-300. doi: 10.1128/iai.47.1.294-300.1985.
The dysgonic fermenter-2 bacterium is a newly recognized fastidious gram-negative bacillus that causes bacteremia and sometimes endocarditis in immunocompromised persons after they are bitten by dogs. To develop an experimental model of this infection, we placed polyethylene catheters across the aortic valves of New Zealand white rabbits, which were inoculated intravenously the next day with dysgonic fermenter-2 bacteria. After 1 week, the rabbits were killed and the endocardial vegetations were homogenized for quantitative culture. Large inocula (1.3 X 10(10) to 2.1 X 10(10) viable bacteria) were required to produce infected vegetations. All infected rabbits had negative blood cultures at the time of autopsy and most developed serum agglutinins against dysgonic fermenter-2 bacteria. Three daily injections of methylprednisolone (30 mg/kg), starting the day before inoculation, significantly increased the incidence of endocarditis and the number of bacteria per gram of infected vegetation (P less than 0.05). Treatment with methylprednisolone prolonged the initial bacteremia and caused significant increases in the numbers of bacteria per gram of blood, spleen, and liver compared with those of untreated controls (P less than 0.05). Rabbits that had previously undergone splenectomy showed prolongation of the initial bacteremia but no significant increase in the incidence of infected vegetations. These results showed that the dysgonic fermenter-2 bacterium is a pathogen that causes endocarditis in rabbits but that it requires a large inoculum and produces blood culture-negative infections. Treatment with methylprednisolone enhances infection by prolonging the initial bacteremia and probably by diminishing bactericidal activity in the vegetations.
迟缓发酵菌-2是一种新发现的苛求性革兰氏阴性杆菌,可在免疫功能低下者被狗咬伤后引起菌血症,有时还会引发心内膜炎。为建立这种感染的实验模型,我们将聚乙烯导管穿过新西兰白兔的主动脉瓣,次日经静脉接种迟缓发酵菌-2。1周后,处死兔子,将心内膜赘生物匀浆进行定量培养。需要大量接种物(1.3×10¹⁰至2.1×10¹⁰活细菌)才能产生感染性赘生物。所有受感染的兔子在尸检时血培养均为阴性,且大多数产生了针对迟缓发酵菌-2的血清凝集素。从接种前一天开始,每天注射3次甲泼尼龙(30mg/kg),显著增加了心内膜炎的发生率以及每克感染赘生物中的细菌数量(P<0.05)。与未治疗的对照组相比,甲泼尼龙治疗延长了初始菌血症时间,并导致每克血液、脾脏和肝脏中的细菌数量显著增加(P<0.05)。先前接受过脾切除术的兔子初始菌血症时间延长,但感染赘生物的发生率没有显著增加。这些结果表明,迟缓发酵菌-2是一种可在兔子中引起心内膜炎的病原体,但它需要大量接种物,且会导致血培养阴性感染。甲泼尼龙治疗通过延长初始菌血症时间并可能通过降低赘生物中的杀菌活性来增强感染。