A limitation is that the small sample size of this study and the period of recruitment of the patients (partially during the ZIKV outbreak) does not allow us to generalize the results found in this study with respect to amongst others the incidence of GBS in Suriname and the exact contribution of the different pathogens in causing GBS

A limitation is that the small sample size of this study and the period of recruitment of the patients (partially during the ZIKV outbreak) does not allow us to generalize the results found in this study with respect to amongst others the incidence of GBS in Suriname and the exact contribution of the different pathogens in causing GBS. of them experienced evidence of a recent Zika computer virus BMPS or dengue computer BMPS virus contamination. These results suggest that arboviruses, specifically Zika computer virus but possibly also dengue computer virus, might be important causative brokers of GBS in Suriname. Furthermore, we found that more convenience of intravenous immunoglobulins or plasma exchange could improve the treatment of GBS in Suriname. Keywords: Guillain-Barr syndrome, Suriname, Zika computer virus, dengue computer virus, arthropod borne viruses Introduction Guillain-Barr syndrome (GBS) is an immune-mediated polyradiculoneuropathy, characterized by a rapidly progressive symmetrical limb weakness and decreased or absent deep tendon reflexes (1). GBS can be a life-threatening disease because of respiratory and autonomic failure, and has an estimated mortality of 3C7% (2). The exact pathogenesis BMPS of GBS is usually unknown, but it is usually thought that preceding infections or vaccinations may trigger the production of autoantibodies to components of peripheral nerves due to molecular mimicry, leading to peripheral nerve injury (1). You will find multiple clinical variants and electrophysiological GBS subtypes, such as acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor and sensory axonal neuropathy (AMSAN) and Miller Fisher syndrome (1). Diagnosis of GBS is based on clinical characteristics but can be supported by investigation of cerebrospinal fluid (CSF) and nerve conduction studies (3). Diagnosis and classification of GBS can be challenging because of the heterogeneity of the syndrome and the considerable differential diagnosis. Proven effective treatment of GBS are intravenous immunoglobulins and plasma exchange (1, 3). Multiple pathogens are associated with GBS such as ((were assessed with use of commercial ELISA packages (ZIKV and DENV; Euroimmun, HEV; Wantai Biological, serology was performed with an indirect IgG ELISA and antibody class capture ELISAs for IgM and IgA antibodies at the Department of Medical Microbiology, Reinier de Graaf Gasthuis, Delft, the Netherlands. Neutralizing antibodies against ZIKV and TFIIH DENV-2 [used as a representation of total DENV immunity (15)], were decided with an in-house micro-neutralization test (VNT) as previously explained (9). Sera were tested in triplicates and the geometric mean of the highest final serum dilution was reported as titer. For both ZIKV and DENV-2, the cut-off of BMPS a positive VNT was a final serum dilution >1:32. For ZIKV diagnosis, a reverse transcriptase polymerase chain reaction (RT-PCR) was performed on plasma or, when available, urine using the primer/probe set explained by Lanciotti et al. (16). Case Definitions for Preceding Infections For the interpretation of the serological and molecular assessments performed in these patients, a variation was made between confirmed recent infections, probable recent infections and possible recent infections. A recent contamination was considered confirmed if one serum or urine sample was RT-PCR positive, or if IgM antibodies against the specific pathogens were present and there was a more than four-fold increase of IgG- or neutralization titer in paired samples. Presence of IgM antibodies with an increasing IgG- or neutralization titer in paired samples was considered a probable recent infection. Presence of IgM but with no increase in IgG or neutralization titer in paired samples was considered a possible recent infection. When paired blood samples were not available, presence of IgM in a single blood sample was considered a possible recent infection. Specifically for CMV, presence of anti-CMV IgM in combination with a rising IgG titer with low avidity was considered a confirmed recent CMV contamination. The combination of CMV IgM with IgG with high avidity was considered as reactivation of CMV antibodies and not a recent contamination (17). Presence of IgM against EBV in combination with IgG against EBV nuclear antigen (EBNA) was considered a non-recent contamination (18). Results Participant Enrolment In total, 27 patients with suspected GBS were enrolled in this study. Of these 27 patients, 15 were excluded because during admission another diagnosis than GBS was made or because the availability of clinical data or blood samples was insufficient, illustrated by the flowchart in Physique 1A. The number of GBS patients recruited per quarter of a 12 months is usually displayed in Physique 1B. The highest peak of GBS patients, in the first quarter of 2016, coincided with the peak of the ZIKV outbreak in Suriname and South America BMPS in the first months of 2016 (19, 20). Open in a separate window Physique 1 (A) Flowchart of patient recruitment and exclusion. (B) Quantity of GBS patients recruited in this study per quarter of.