Concurrent Guillain-Barré syndrome, transverse myelitis and encephalitis post-Zika: A case report and review of the pathogenic role of multiple arboviral immunity

Abstract

We review post-infectious and post-vaccination neurological syndromes involving peripheral and central nervous system (CNS) and report an illustrative case of simultaneous occurrence of Guillain-Barré syndrome (GBS), confirmed by nerve conduction velocities, plus MRI-demonstrated transverse myelitis (TM) and acute encephalitis [acute disseminated encephalomyelitis] (ADEM+GBS) affecting a 24-year-old woman from Cúcuta, Colombia, who developed acute Zika virus (ZIKV) infection confirmed by serum reverse transcriptase-polymerase chain reaction (RT-PCR) and convalescent ZIKV IgG antibodies. With intensive care treatment, respiratory support, steroids, and intravenous immunoglobulin (IVIg), patient survived with residual flaccid paraparesis. She had preexisting immunity against Chikungunya virus (CHIKV) and Dengue virus (DENV) acquired before the arrival of ZIKV in Colombia. From reports in the Caribbean, Central and South America we review 19 cases of ZIKV-associated TM, encephalitis and ADEM occurring after a mean latent period of 10.5 days (range 1-96) post-infection. Although GBS and ADEM are usually considered post-infectious and associated with development of antibodies against peripheral nerve and CNS epitopes, we postulate that our case of ADEM+GBS is para-infectious, induced by acute ZIKV neurotropism boosted by active immunity against other arboviruses. Animal models of ZIKV demonstrated strong viral neurotropism enhanced by passive immunity with antibodies against arboviruses such as West Nile virus, CHIKV, or DENV. These considerations are relevant to prevent potential ZIKV vaccine-induced reactions involving central and peripheral nervous system.cycle where transmission to humans occurs mainly by female Aedes mosquitoes-also carriers of DENV and Chikungunya (CHIKV), an alphavirus of the family Togaviridae. In addition, sexual transmission of ZIKV has been demonstrated with virus isolations from urine, semen, blood, maternal milk and tears. Zika infection is manifested by fever, maculopapular rash, conjunctivitis and rare uveitis, arthralgias, muscle pain and headache, but about 80% of infections are asymptomatic [2]. Nonetheless, ZIKV is neuroinvasive and capable of causing numerous neurological manifestations [2].According to the World Health Organization (WHO) [3], a major

Identifying the culprits in neurological autoimmune diseases

“…Another virus that has recently gained attention is the Zika virus (ZIKV), which is among the Flaviviruses. From December 2015 to July 2016, hundreds of cases of ZIKV-related GBS were reported [ 126 ]. This led the World Health Organization to name Zika a worldwide public health emergency, mainly due to its viral neurotropism that was causing microcephaly, GBS, and other neurological disorders [ 127 ].…”

“…This led the World Health Organization to name Zika a worldwide public health emergency, mainly due to its viral neurotropism that was causing microcephaly, GBS, and other neurological disorders [ 127 ]. ZIKV infection can produce a characteristic post-infectious GBS, together with a concurrent para-infection of the nervous system heightened by pre-existing arboviral and herpesvirus immunity [ 126 ]. Nevertheless, the mechanisms underlying the host-pathogen neuro-immune interactions remain unknown.…”

Zika virus infection as a cause of congenital brain abnormalities and Guillain-Barré syndrome: A living systematic review

“…Traveller/non-traveller populations: In studies included in this update, we found additional evidence of GBS in both travellers and non-travellers with ZIKV infection. Ten publications report on 11 travellers 218, 220, 222– 224, 227, 229, 232– 234 , while 34 publications report GBS due to ZIKV in 402 non travellers 4, 44, 118, 219, 221, 225, 226, 228, 230, 231, 235– 237, 239– 247, 249, 251, 253– 260, 262, 263 .…”

A to Z of Zika Virus: A Comprehensive Review for Clinicians

“…A mean latency period of 10.5 days (range = 1-96 days) was found in review of 19 cases of TM, encephalitis, and ADEM. 70 Several cases of TM and ADEM associated with ZIKV infection have been reported. [71][72][73][74][75][76] In one report of TM after ZIKV infection, anti-myelin oligodendrocyte glycoprotein antibody against the myelin sheath was detected, favoring an autoimmune-mediated neurotoxicity.…”