Kass E M, Szaniawski W K, Levy H, Leach J, Srinivasan K, Rives C
Department of Dermatology, New York Medical College, NY.
N Engl J Med. 1994 Dec 15;331(24):1612-7. doi: 10.1056/NEJM199412153312403.
Rickettsialpox is caused by Rickettsia akari, which is transmitted from rodents to humans by bloodsucking mites. The initial skin lesion forms an eschar and is followed by the development of fever, malaise, myalgia, and 5 to 40 maculopapules and papulovesicles. The disease, which responds to tetracycline, can be mistaken for chickenpox. The diagnosis has been based on an increase in serum antibody titers against R. akari over a period of three to eight weeks. We discuss a more rapid technique that uses direct immunofluorescence to identify R. akari in paraffin-embedded tissue, and we describe the histopathological findings of lesional skin.
We studied 13 patients (age, 11 months to 58 years) who were seen at Lincoln Hospital in New York City from 1980 to 1989 and were suspected of having rickettsialpox. In nine patients serum samples were obtained during the acute and convalescent phases of the illness for indirect fluorescent-antibody testing. Punch-biopsy specimens of skin lesions were examined by microscopy and by direct fluorescent-antibody testing with an anti-R. rickettsii globulin conjugated with fluorescein isothiocyanate.
The diagnosis was confirmed in all 13 patients by indirect or direct fluorescent-antibody techniques. Direct fluorescent-antibody testing of eschars from seven patients was positive in five patients, but negative in two patients who had serologically confirmed rickettsialpox. In contrast, direct fluorescent-antibody testing of papulovesicles from nine patients was positive in only one patient. Histopathological analysis of the eschars revealed extensive necrosis and inflammation. In biopsy specimens of papulovesicles, dermal edema, subepidermal vesicles, and vascular changes were present.
The combination of direct fluorescent-antibody testing of an eschar from the presumed site of inoculation and histopathological examination of papulovesicles for distinctive features represents an improved method of diagnosing rickettsialpox.
立克次体痘由小蛛立克次体引起，通过吸血螨从啮齿动物传播给人类。最初的皮肤损害形成焦痂，随后出现发热、不适、肌痛以及5至40个斑丘疹和丘疹水疱。该疾病对四环素治疗有效，可能被误诊为水痘。诊断一直基于在三至八周内血清抗小蛛立克次体抗体滴度的升高。我们讨论一种更快速的技术，该技术使用直接免疫荧光法在石蜡包埋组织中鉴定小蛛立克次体，并描述皮损的组织病理学发现。
我们研究了1980年至1989年在纽约市林肯医院就诊的13例患者（年龄11个月至58岁），这些患者被怀疑患有立克次体痘。9例患者在疾病的急性期和恢复期采集血清样本进行间接荧光抗体检测。对皮肤损害进行打孔活检标本，通过显微镜检查以及用异硫氰酸荧光素偶联的抗立氏立克次体球蛋白进行直接荧光抗体检测。
通过间接或直接荧光抗体技术在所有13例患者中均确诊。对7例患者的焦痂进行直接荧光抗体检测，5例呈阳性，但2例血清学确诊为立克次体痘的患者呈阴性。相比之下，对9例患者丘疹水疱进行直接荧光抗体检测，仅1例呈阳性。焦痂的组织病理学分析显示广泛坏死和炎症。在丘疹水疱的活检标本中，存在真皮水肿、表皮下水疱和血管改变。
对接种部位假定的焦痂进行直接荧光抗体检测与对丘疹水疱进行具有特征性的组织病理学检查相结合，是诊断立克次体痘的一种改进方法。
