From the Departamento de Medicina (A.P.R., M.A.C., C.C.C., J.A.D., M.A.T., J.T.A., H.F.U.), Servicio de Neurología y Neuropsiquiatría, Hospital Cayetano Heredia, Lima, Perú; Department of Neurology (S.E.L.) and Department of Neurology and Department of Immunology (B.C.J.), Erasmus MC, University Medical Center Rotterdam, Netherlands; Institute of Infection, Immunity and Inflammation (S.K.H., D.G., H.J.W.), University of Glasgow, United Kingdom; Departamento de Enfermedades Infecciosas Tropicales y Dermatológicas (A.L.), Hospital Cayetano Heredia, Lima, Perú; U.S. Naval Medical Research Unit-6 (M.G., M.R., J.D.R., R.M.), Lima, Peru; Center for Computational Biology (D.P., R.M.S., S.L.S.), Department of Computer Science, Whiting School of Engineering, Johns Hopkins University, Baltimore, MD; and Department of Pathology (P.J.S.), Department of Neurology (D.R.C.), and Department of Neurology and Department of Pathology (C.A.P.), Johns Hopkins University School of Medicine, Baltimore, MD.
Neurol Neuroimmunol Neuroinflamm. 2021 Feb 5;8(2). doi: 10.1212/NXI.0000000000000952. Print 2021 Mar.
To identify the clinical phenotypes and infectious triggers in the 2019 Peruvian Guillain-Barré syndrome (GBS) outbreak.
We prospectively collected clinical and neurophysiologic data of patients with GBS admitted to a tertiary hospital in Lima, Peru, between May and August 2019. Molecular, immunologic, and microbiological methods were used to identify causative infectious agents. Sera from 41 controls were compared with cases for antibodies to and gangliosides. Genomic analysis was performed on 4 isolates.
The 49 included patients had a median age of 44 years (interquartile range [IQR] 30-54 years), and 28 (57%) were male. Thirty-two (65%) had symptoms of a preceding infection: 24 (49%) diarrhea and 13 (27%) upper respiratory tract infection. The median time between infectious to neurologic symptoms was 3 days (IQR 2-9 days). Eighty percent had a pure motor form of GBS, 21 (43%) had the axonal electrophysiologic subtype, and 18% the demyelinating subtype. Evidence of recent infection was found in 28/43 (65%). No evidence of recent arbovirus infection was found. Twenty-three cases vs 11 controls (OR 3.3, confidence interval [CI] 95% 1.2-9.2, < 0.01) had IgM and/or IgA antibodies against . Anti-GM1:phosphatidylserine and/or anti-GT1a:GM1 heteromeric complex antibodies were strongly positive in cases (92.9% sensitivity and 68.3% specificity). Genomic analysis showed that the strains were closely related and had the Asn51 polymorphism at gene.
Our study indicates that the 2019 Peruvian GBS outbreak was associated with infection and that the strains linked to GBS circulate widely in different parts of the world.
确定 2019 年秘鲁格林-巴利综合征（GBS）暴发的临床表型和感染诱因。
我们前瞻性地收集了 2019 年 5 月至 8 月期间在秘鲁利马的一家三级医院住院的 GBS 患者的临床和神经生理数据。采用分子、免疫和微生物方法来确定致病感染因子。将 41 例对照者的血清与病例进行比较，以检测针对 和神经节苷脂的抗体。对 4 株 分离株进行了基因组分析。
纳入的 49 例患者的中位年龄为 44 岁（四分位间距 [IQR] 30-54 岁），28 例（57%）为男性。32 例（65%）有前驱感染症状：24 例（49%）腹泻，13 例（27%）上呼吸道感染。感染至神经系统症状的中位时间为 3 天（IQR 2-9 天）。80%的患者为纯运动型 GBS，21 例（43%）为轴索性电生理亚型，18%为脱髓鞘亚型。在 28/43（65%）例中发现近期 感染的证据。未发现近期虫媒病毒感染的证据。23 例病例与 11 例对照（比值比 [OR] 3.3，95%置信区间 [CI] 1.2-9.2， < 0.01）的 IgM 和/或 IgA 抗体对 呈阳性。抗 GM1：磷脂酰丝氨酸和/或抗 GT1a：GM1 异源复合物抗体在病例中呈强阳性（92.9%的敏感性和 68.3%的特异性）。基因组分析显示，这些 株密切相关，并且在 基因上具有 Asn51 多态性。
我们的研究表明，2019 年秘鲁 GBS 暴发与 感染有关，与 GBS 相关的 株在世界不同地区广泛传播。
