Nilsson K, Wallménius K, Hartwig S, Norlander T, Påhlson C
Department of Medical Sciences, Section of Clinical Microbiology, Uppsala University, Uppsala, Sweden; Department of Medical Sciences, Section of Infectious Diseases, Uppsala University, Uppsala, Sweden; Centre of Clinical Research, Falu Hospital, Falun, Sweden.
Eur J Neurol. 2014 Feb;21(2):206-14. doi: 10.1111/ene.12218. Epub 2013 Jun 21.
Sixty patients with facial palsy and 67 with sudden deafness were retrospectively or prospectively examined for serological evidence of rickettsial infection; in six cases where cerebrospinal fluid was available, patients were also examined for presence of rickettsial DNA.
Rickettsial antibodies were detected in single or paired serum samples using immunofluorescence with Rickettsia helvetica as the antigen and in four cases also using western blot. Using PCR and subsequent direct cycle sequencing, the nucleotide sequences of the amplicons (17 kDa protein gene) in cerebrospinal fluid were analysed.
Five out of 60 (8.3%) patients with facial palsy and eight of 67 (11.9%) with hearing loss showed confirmative serological evidence of infection with Rickettsia spp. An additional three and four patients in the facial palsy and hearing loss groups, respectively, showed evidence of having a recent or current infection or serological findings suggestive of infection. In four cases, the specificity of the reaction was confirmed by western blot. An additional 70 patients were seroreactive with IgG or IgM antibodies higher than or equal to the cut-off of 1:64, whereas 37 patients were seronegative. Only two of 127 patients had detectable antibodies to Borrelia spp. In three of six patients, rickettsial DNA was detected in the cerebrospinal fluid, where the obtained sequences (17 kDa) shared 100% similarity with the corresponding gene sequence of Rickettsia felis.
These results highlight the importance of considering Rickettsia spp. as a cause of neuritis, and perhaps as a primary cause of neuritis unrelated to neuroborreliosis.
对60例面瘫患者和67例突发性耳聋患者进行回顾性或前瞻性检查,以寻找立克次体感染的血清学证据;在6例可获取脑脊液的病例中,还对患者进行了立克次体DNA检测。
使用以瑞士立克次体为抗原的免疫荧光法检测单份或双份血清样本中的立克次体抗体,4例还使用了蛋白质印迹法。采用聚合酶链反应(PCR)及随后的直接循环测序法分析脑脊液中扩增子(17 kDa蛋白基因)的核苷酸序列。
60例面瘫患者中有5例(8.3%),67例听力损失患者中有8例(11.9%)显示有立克次体属感染的确证血清学证据。面瘫组和听力损失组分别还有另外3例和4例患者显示有近期或当前感染的证据或提示感染的血清学结果。4例中,蛋白质印迹法证实了反应的特异性。另外70例患者的IgG或IgM抗体血清反应阳性,高于或等于1:64的临界值,而37例患者血清反应阴性。127例患者中只有2例检测到针对疏螺旋体属的抗体。6例患者中有3例在脑脊液中检测到立克次体DNA,所获得的序列(17 kDa)与猫立克次体的相应基因序列有100%的相似性。
这些结果凸显了将立克次体属视为神经炎病因的重要性,或许还可作为与神经莱姆病无关的神经炎的主要病因。