Shapiro E D, Gerber M A, Holabird N B, Berg A T, Feder H M, Bell G L, Rys P N, Persing D H
Department of Pediatrics, Yale University School of Medicine, New Haven, Conn. 06510-8064.
N Engl J Med. 1992 Dec 17;327(25):1769-73. doi: 10.1056/NEJM199212173272501.
Borrelia burgdorferi, which causes Lyme disease, is transmitted by deer ticks (lxodes dammini) in the northeastern and midwestern United States. Although deer-tick bites are common in areas in which the disease is endemic, there is uncertainty about how to manage the care of persons who are bitten.
To assess the risk of infection with B. burgdorferi and the efficacy of prophylactic antimicrobial treatment after a deer-tick bite, we conducted a double-blind, placebo-controlled trial in an area of southeastern Connecticut in which Lyme disease is endemic. Children and adults who had been bitten by deer ticks were randomly assigned to receive either amoxicillin or placebo for 10 days. Subjects were followed for one year for clinical manifestations of Lyme disease. Serum samples obtained at enrollment and six weeks and three months later were tested for antibodies against B. burgdorferi.
Of the 387 subjects, 205 (53 percent) were assigned to receive amoxicillin and 182 (47 percent) to receive placebo. Of 344 deer ticks submitted and analyzed by the polymerase chain reaction, 15 percent were infected with B. burgdorferi. Erythema migrans developed in two subjects, both of whom had received placebo. There were no asymptomatic seroconversions and no late manifestations of Lyme disease. The risk of infection with B. burgdorferi in the placebo-treated subjects was 1.2 percent (95 percent confidence interval, 0.1 to 4.1 percent), which was not significantly different (P = 0.22) from the risk in the amoxicillin-treated subjects (0 percent; 95 percent confidence interval, 0 to 1.5 percent).
Even in an area in which Lyme disease is endemic, the risk of infection with B. burgdorferi after a recognized deer-tick bite is so low that prophylactic antimicrobial treatment is not routinely indicated.
引起莱姆病的伯氏疏螺旋体通过美国东北部和中西部的鹿蜱(达敏硬蜱)传播。尽管在该病流行地区鹿蜱叮咬很常见,但对于如何处理被叮咬者的护理存在不确定性。
为了评估伯氏疏螺旋体感染风险以及鹿蜱叮咬后预防性抗菌治疗的疗效,我们在康涅狄格州东南部莱姆病流行地区进行了一项双盲、安慰剂对照试验。被鹿蜱叮咬的儿童和成人被随机分配接受阿莫西林或安慰剂治疗10天。对受试者随访一年以观察莱姆病的临床表现。在入组时、六周后和三个月后采集的血清样本检测抗伯氏疏螺旋体抗体。
387名受试者中,205名(53%)被分配接受阿莫西林治疗,182名(47%)接受安慰剂治疗。在提交并通过聚合酶链反应分析的344只鹿蜱中,15%感染了伯氏疏螺旋体。两名受试者出现了游走性红斑,两人均接受了安慰剂治疗。没有无症状血清转化,也没有莱姆病的晚期表现。安慰剂治疗组伯氏疏螺旋体感染风险为1.2%(95%置信区间,0.1%至4.1%),与阿莫西林治疗组风险(0%;95%置信区间,0至1.5%)相比无显著差异(P = 0.22)。
即使在莱姆病流行地区,如果已确认被鹿蜱叮咬,感染伯氏疏螺旋体的风险也很低,因此通常无需进行预防性抗菌治疗。