Abstract
Guillain-Barré syndrome (GBS) is associated with various types of preceding infections including Campylobacter jejuni and cytomegalovirus, but there is also an association with arthropod borne viruses (arboviruses), such as Zika virus, that are endemic in tropical regions. Here we present the clinical characteristics of 12 GBS patients from Suriname that were hospitalized between the beginning of 2016 and half 2018. Extensive diagnostic testing was performed for pathogens that are commonly associated with GBS, but also for arboviruses, in order to identify the preceding infection that might have led to GBS. With this extensive testing algorithm, we could identify a recent infection in six patients of which four of them had evidence of a recent Zika virus or dengue virus infection. These results suggest that arboviruses, specifically Zika virus but possibly also dengue virus, might be important causative agents of GBS in Suriname. Furthermore, we found that more accessibility of intravenous immunoglobulins or plasma exchange could improve the treatment of GBS in Suriname.
Highlights
Guillain-Barré syndrome (GBS) is an immune-mediated polyradiculoneuropathy, characterized by a rapidly progressive symmetrical limb weakness and decreased or absent deep tendon reflexes [1]
The highest peak of GBS patients, in the first quarter of 2016, coincided with the peak of the Zika virus (ZIKV) outbreak in Suriname and South America in the first months of 2016 [19, 20]
We performed extensive diagnostic testing for preceding infections that are commonly associated with GBS and arboviruses that are endemic in Suriname and are possibly associated with GBS
Summary
Guillain-Barré 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 3–7% [2]. There are 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 extensive differential diagnosis. Proven effective treatment of GBS are intravenous immunoglobulins and plasma exchange [1, 3]
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