SANFORD J P, HUNTER B W, SOUDA L L
J Exp Med. 1962 Feb 1;115(2):383-410. doi: 10.1084/jem.115.2.383.
Hematogenous pyelonephritis was produced in rats utilizing multiple strains of Escherichia coli, a strain of Klebsiella pneumoniae, and a strain of Proteus mirabilis. Three patterns of hematogenous pyelonephritis occurred which represent an interrelationship between an immune response to the infecting bacteria and the development of obstructive uropathy as a consequence of infection. First, the course of pyelonephritis due to strains of Escherichia coli was acute, self-limited, and associated with the development of circulating agglutinins. Following healing, this pattern of infection was associated with acquired resistance to reinfection with the same bacterial strain. Second, the course of pyelonephritis due to a strain of Klebsiella pneumoniae type C was chronic. This infection was not associated with the production of circulating agglutinins against encapsulated strains. Acquired resistance to reinfection by the homotypic strain could not be demonstrated following eradication of infection but was produced by the passive transfer of concentrated antiserum. Third, pyelonephritis due to Proteus mirabilis was associated with circulating agglutinins and resistance to reinfection with the same organism following eradication of infection, yet the course was chronic. The chronicity appeared to be the consequence of obstructive uropathy resulting from calculi which developed during the course of the infection. Resistance to reinfection was demonstrated in infections with strains of E. coli and P. mirabilis. The resistance is associated with specific immunity as demonstrated by the observation that: (a) it is type-specific, (b) it is of at least 3 months' duration, and (c) it can be passively transferred by means of rabbit antiserum. Since K. pneumoniae failed to evoke capsular antibodies in the rat, resistance to infection with K. pneumoniae was produced only by means of passively transferred concentrated rabbit antiserum and not by prior infection. Immunity can be demonstrated to have a significant role in the pathogenesis of experimental hematogenous pyelonephritis only in the absence of obstructive uropathy.
利用多种大肠杆菌菌株、一株肺炎克雷伯菌和一株奇异变形杆菌在大鼠中诱发血源性肾盂肾炎。出现了三种血源性肾盂肾炎模式,它们代表了对感染细菌的免疫反应与感染导致的梗阻性尿路病发展之间的相互关系。首先,由大肠杆菌菌株引起的肾盂肾炎病程是急性的、自限性的,且与循环凝集素的产生有关。愈合后,这种感染模式与对同一菌株再感染的获得性抵抗力有关。其次,由C型肺炎克雷伯菌菌株引起的肾盂肾炎病程是慢性的。这种感染与针对包膜菌株的循环凝集素的产生无关。感染根除后,未证明对同型菌株再感染有获得性抵抗力,但通过浓缩抗血清的被动转移可产生这种抵抗力。第三,奇异变形杆菌引起的肾盂肾炎与循环凝集素以及感染根除后对同一生物体再感染的抵抗力有关,但其病程是慢性的。慢性似乎是感染过程中形成的结石导致梗阻性尿路病的结果。在大肠杆菌和奇异变形杆菌菌株感染中证明了对再感染的抵抗力。这种抵抗力与特异性免疫有关,如下观察结果所示:(a) 它是型特异性的,(b) 持续时间至少为3个月,(c) 可通过兔抗血清被动转移。由于肺炎克雷伯菌未能在大鼠中诱发包膜抗体,因此对肺炎克雷伯菌感染的抵抗力仅通过浓缩兔抗血清的被动转移产生,而不是通过先前感染产生。只有在没有梗阻性尿路病的情况下,才能证明免疫在实验性血源性肾盂肾炎的发病机制中起重要作用。