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Volume 26, Number 11—November 2020
Research Letter

Large Outbreak of Guillain-Barré Syndrome, Peru, 2019

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César V. Munayco, Ronnie G. Gavilan, Gladys Ramirez, Manuel Loayza, Maria L. Miraval, Erin Whitehouse, Radhika Gharpure, Jesus Soares, Hans Vasquez Soplopuco, and James SejvarComments to Author 
Author affiliations: Centro Nacional de Epidemiología Prevención y Control de Enfermedades, Lima, Peru (C.V. Munayco, G. Ramirez, M. Loayza); Instituto Nacional de Salud, Lima (R.G. Gavilan, M.L. Miraval, H.V. Soplopuco); Centers for Disease Control and Prevention, Atlanta, Georgia, USA (E. Whitehouse, R. Gharpure, J. Soares, J. Sejvar)

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Outbreaks of Guillain-Barré syndrome (GBS) are uncommon. In May 2019, national surveillance in Peru detected an increase in GBS cases in excess of the expected incidence of 1.2 cases/100,000 population. Several clinical and epidemiologic findings call into question the suggested association between this GBS outbreak and Campylobacter.

Guillain-Barré syndrome (GBS) is the most common form of acute flaccid paralysis worldwide (1). It is characterized by motor weakness, areflexia, sensory abnormalities, and cytoalbuminologic dissociation in cerebrospinal fluid (2). An upper respiratory or gastrointestinal illness typically precedes GBS (3). Campylobacter jejuni infection is the most frequently identified precipitant of GBS and usually is associated with the acute motor axonal neuropathy form of GBS (4).

During the week of May 26, 2019, the Peruvian Ministry of Health surveillance system detected several cases of suspected GBS that exceeded the expected incidence of 1.2 cases/100,000 persons/year (i.e., 29 cases/year) (1). Since 2016, hospitals in Peru have reported suspected GBS cases to a passive surveillance system ( In early May 2019, when the system was modified to an active surveillance system because of increasing incidence, the National Center of Epidemiology, Prevention, and Disease Control solicited cases. Examining physicians classified cases in accordance with the Brighton Collaboration case definition for GBS (5). The Instituto Nacional de Salud tested serum, urine, nasal swab samples, and feces for infectious pathogens using molecular panels for multipathogen detection (bioMérieux, and conventional microbiology assays.


Cases of Guillain-Barré syndrome classified by Brighton Collaboration criteria (5) and date of illness onset, Peru, May–July 2019.

Figure. Cases of Guillain-Barré syndrome classified by Brighton Collaboration criteria (5) and date of illness onset, Peru, May–July 2019.

During May 20–July 27, 2019, we identified 683 suspected or confirmed GBS cases in Peru. The largest outbreaks of GBS have involved »30–50 cases, except for large GBS outbreaks associated with Zika virus infection; thus, this outbreak was extremely unusual because of its size. Of the cases, 32 (6.9%) were Brighton level 1, 188 (27.5%) were Brighton level 2, and 463 (67.7%) were Brighton level 3. We classified Brighton levels 1 and 2 cases as confirmed, and Brighton level 3 cases as suspected (Figure; Appendix Figures 1, 2). Nine of Peru’s 24 departments reported GBS cases, which resulted in an annualized incidence of 30.9 cases/100,000 persons/year (Table).

Of the 683 GBS patients, 287 (42.0%) had descending muscle weakness and 446 (65.3%) had ascending muscle weakness. Of 530 patients for whom data on antecedent illness were complete in the 4 weeks before neurologic symptom onset, 219 (41.3%) reported respiratory and gastrointestinal infections, 195 (36.8%) reported only a respiratory infection, 3 (0.6%) reported only a gastrointestinal infection, and 113 (21.3%) did not report any infection. Of 426 patients for whom hospitalization data were available, 64 (15.0%) required mechanical ventilation. Of 147 patients who had an electrodiagnostic exam, 100 (68.0%) had acute motor axonal neuropathy.

Clinical samples received by Instituto Nacional de Salud were as follows: serum (622 samples), urine (191), cerebrospinal fluid (230), nasal and pharyngeal swab samples (394), and feces (362) (Appendix Tables 1–3). We detected Campylobacter spp. in 19 (5.2%) fecal samples. Fecal cultures yielded 8 isolates confirmed as C. jejuni biotype I by Gram stain (6). Isolates were highly related by core-genome multilocus sequence typing and were sequence type 2993, Penner serotype HS:41.

This GBS outbreak was unusual because of the large number of cases. The incidence rate was nearly 25 times higher than expected (1) and higher than previously described GBS outbreaks. The rapid increase in numbers, followed by an equally precipitous decrease, might suggest a point-source exposure. The outbreak affected many geographically disparate regions, including some that differed substantially in geoclimatic properties.

General demographic features, such as slight male predominance and greater incidence with increased age, are typical for GBS (7). However, in many patients, a descending, rather than the more common ascending, paralysis developed (8). The clinical significance of this observation is unclear. Electrophysiologically, most cases appeared to have the acute motor axonal neuropathy phenotype of GBS, which has been closely associated with antecedent C. jejuni infection (9).

PCR and culture detected the C. jejuni outbreak reported here. Genetic analysis confirmed the clonality of these isolates recovered from affected regions of Peru and identified genotype sequence type 2993, which has been associated with GBS outbreaks in China (10). These results support the hypothesis that this unprecedented GBS outbreak was related to an antecedent Campylobacter outbreak with point source. However, diarrheal illnesses shortly before or during the GBS outbreak were not reported; previous GBS outbreaks associated with Campylobacter mostly have occurred in the context of larger outbreaks of symptomatic diarrheal illness (10). Because of the wide distribution of outbreaks in many geographically separated regions, we questioned how all areas were exposed to C. jejuni within a short time frame.

Limitations of our investigation included nonsystematic testing of samples and incomplete data on variables, such as hospitalization and clinical features. Epidemiologic investigations are ongoing to determine the potential antigenic source of the presumed infection, testing for Campylobacter-specific IgM and antiganglioside antibodies, additional isolate sequencing, and active surveillance for new cases.

Dr. Munayco is a physician, researcher, and epidemiologist at the Uniformed Services University of the Health Sciences; director of the unit of epidemiological research and evaluation of sanitary interventions at Centro Nacional de Epidemiología, Prevención y Control de Enfermedades, Ministry of Health; and professor in the School of Medicine at Universidad Peruana de Ciencias Aplicadas. His primary research interests include public health, mathematical modeling of communicable and noncommunicable diseases, health economics, social determinants and inequality, and monitoring and evaluation of health interventions and public policies.



We thank Mary Reyes, Gabriela Soto, Andree Valle, and Johans Arica for data management and quality control of the data. We also thank laboratory professionals from Regional and National Laboratories of Reference of Instituto Nacional de Salud for conducting the laboratory tests for respiratory viruses and gastrointestinal pathogens.



  1. Sejvar  JJ, Baughman  AL, Wise  M, Morgan  OW. Population incidence of Guillain-Barré syndrome: a systematic review and meta-analysis. Neuroepidemiology. 2011;36:12333. DOIPubMedGoogle Scholar
  2. Ansar  V, Valadi  N. Guillain-Barré syndrome. Prim Care. 2015;42:18993. DOIPubMedGoogle Scholar
  3. Govoni  V, Granieri  E. Epidemiology of the Guillain-Barré syndrome. Curr Opin Neurol. 2001;14:60513. DOIPubMedGoogle Scholar
  4. Nachamkin  I, Arzarte Barbosa  P, Ung  H, Lobato  C, Gonzalez Rivera  A, Rodriguez  P, et al. Patterns of Guillain-Barre syndrome in children: results from a Mexican population. Neurology. 2007;69:166571. DOIPubMedGoogle Scholar
  5. Sejvar  JJ, Kohl  KS, Gidudu  J, Amato  A, Bakshi  N, Baxter  R, et al.; Brighton Collaboration GBS Working Group. Guillain-Barré syndrome and Fisher syndrome: case definitions and guidelines for collection, analysis, and presentation of immunization safety data. Vaccine. 2011;29:599612. DOIPubMedGoogle Scholar
  6. Lior  H. New, extended biotyping scheme for Campylobacter jejuni, Campylobacter coli, and “Campylobacter laridis”. J Clin Microbiol. 1984;20:63640. DOIPubMedGoogle Scholar
  7. Hughes  RA, Cornblath  DR. Guillain-Barré syndrome. Lancet. 2005;366:165366. DOIPubMedGoogle Scholar
  8. Hughes  RA, Rees  JH. Clinical and epidemiologic features of Guillain-Barré syndrome. J Infect Dis. 1997;176(Suppl 2):S928. DOIPubMedGoogle Scholar
  9. Zhang  M, He  L, Li  Q, Sun  H, Gu  Y, You  Y, et al. Genomic characterization of the Guillain-Barre syndrome-associated Campylobacter jejuni ICDCCJ07001 Isolate. PLoS One. 2010;5:e15060. DOIPubMedGoogle Scholar
  10. Zhang  M, Li  Q, He  L, Meng  F, Gu  Y, Zheng  M, et al. Association study between an outbreak of Guillain-Barre syndrome in Jilin, China, and preceding Campylobacter jejuni infection. Foodborne Pathog Dis. 2010;7:9139. DOIPubMedGoogle Scholar




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DOI: 10.3201/eid2611.200127

Original Publication Date: October 13, 2020

Table of Contents – Volume 26, Number 11—November 2020

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Cesar V. Munayco, Calle Daniel Olaechea 199, Jesus Maria, Lima, Peru

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