Miles A A, Pillow J, Khimji P L
Br J Exp Pathol. 1976 Apr;57(2):217-42.
The infectivity of 16 strains of Klebsiella spp. and its modification by systemic and local ferric iron were tested in the skin of the guinea-pig. The in vivo proliferation of 11 strains was enhanced in varying degrees by Fe+++ (E + strains); 5 strains (Eo) were not enhanceable even by large doses of Fe+++. Of 10 strains examined in detail, 6 were E + and 4 were E0. Guinea-pig and human sera were consistently bacteriostatic for E + strains and bactericidal for Eo strains. Both Fe+++ and microbial iron-chelators abolished the bacteriostasis of E + strains but did not affect the lethal effect on Eo strains. Both effects were diminished by heating the sera to 56 degrees for 30 min and by the anticomplementary substance Liquoid; neither appeared to be due to specific antibody. Virulence, as measured in the skin and by intravenous injection, was roughly associated with degree of enhanceability by iron, the EO strains being among the least virulent. The volume of plasma exudate entering the skin during the first 5 h was sufficient to kill a large proportion of the infecting doses of Eo strains and to inhibit the growth of infecting doses of E + strains. Enhancement of the latter by Fe+++ is predominantly the result of inhibition of the non-specific bacteriostasis exerted by the extravascular plasma. Lesions by E + strains aged 4 h or more are insusceptible to systemic Fe+++ and only moderately susceptible to large doses of local Fe+++. The insusceptibility appears to be due to segregation of the infecting bacilli within exudate leucocytes. Klebsiella infections accordingly provide another example of an initial decisive period of action of the antibacterial defences-in this case non-specific and humoral-which cease to be locally effective after the first few hours. Besides enhancing lesions due to E + strains, systemic Fe+++ has an opposite, apparently anti-inflammatory action on klebsiella lesions, slightly decreasing their size. It was evident with all the strains tested, whether dead or alive, but not in E + lesions in circumstances when they were susceptible to enhancement by the Fe+++.
在豚鼠皮肤中测试了16株克雷伯菌属菌株的感染性及其受全身和局部三价铁影响的情况。11株菌株（E+菌株）的体内增殖在不同程度上被Fe+++增强；5株菌株（E0）即使大剂量的Fe+++也无法增强其增殖。在详细检测的10株菌株中，6株为E+菌株，4株为E0菌株。豚鼠血清和人血清对E+菌株始终具有抑菌作用，对E0菌株具有杀菌作用。Fe+++和微生物铁螯合剂均消除了E+菌株的抑菌作用，但不影响对E0菌株的致死作用。将血清加热至56摄氏度30分钟以及使用抗补体物质Liquoid后，这两种作用均减弱；两者似乎均不是由特异性抗体引起的。通过皮肤和静脉注射测量的毒力大致与铁增强能力的程度相关，E0菌株的毒力最低。在前5小时内进入皮肤的血浆渗出液量足以杀死大部分感染剂量的E0菌株，并抑制感染剂量的E+菌株的生长。Fe+++对后者的增强作用主要是抑制血管外血浆施加的非特异性抑菌作用的结果。4小时及以上的E+菌株引起的损伤对全身Fe+++不敏感，仅对大剂量局部Fe+++中度敏感。这种不敏感性似乎是由于感染的杆菌在渗出白细胞内分离所致。因此，克雷伯菌感染提供了抗菌防御初始决定性作用时期的另一个例子——在这种情况下是非特异性和体液性的——在最初几个小时后不再具有局部有效性。除了增强E+菌株引起的损伤外，全身Fe+++对克雷伯菌损伤具有相反的、明显的抗炎作用，使其大小略有减小。在所有测试的菌株中，无论死活，这种情况都很明显，但在E+菌株损伤对Fe+++增强敏感的情况下则不明显。
