Guillain–Barré syndrome, transverse myelitis and infectious diseases

Abstract

Guillain-Barré syndrome (GBS) and transverse myelitis (TM) both represent immunologically mediated polyneuropathies of major clinical importance. Both are thought to have a genetic predisposition, but as of yet no specific genetic risk loci have been clearly defined. Both are considered autoimmune, but again the etiologies remain enigmatic. Both may be induced via molecular mimicry, particularly from infectious agents and vaccines, but clearly host factor and co-founding host responses will modulate disease susceptibility and natural history. GBS is an acute inflammatory immune-mediated polyradiculoneuropathy characterized by tingling, progressive weakness, autonomic dysfunction, and pain. Immune injury specifically takes place at the myelin sheath and related Schwann-cell components in acute inflammatory demyelinating polyneuropathy, whereas in acute motor axonal neuropathy membranes on the nerve axon (the axolemma) are the primary target for immune-related injury. Outbreaks of GBS have been reported, most frequently related to Campylobacter jejuni infection, however, other agents such as Zika Virus have been strongly associated. Patients with GBS related to infections frequently produce antibodies against human peripheral nerve gangliosides. In contrast, TM is an inflammatory disorder characterized by acute or subacute motor, sensory, and autonomic spinal cord dysfunction. There is interruption of ascending and descending neuroanatomical pathways on the transverse plane of the spinal cord similar to GBS. It has been suggested to be triggered by infectious agents and molecular mimicry. In this review, we will focus on the putative role of infectious agents as triggering factors of GBS and TM.

Guillain‐Barré syndrome post renal transplant: A systematic review

“…It is common that no infectious aetiology is identified, and furthermore only a small proportion of the population who have Campylobacter jejuni or CMV infections develop GBS . Therefore, it is clear that host and environmental factors must modulate the susceptibility of individuals to develop GBS, and that more research is needed to further elucidate the pathogenesis of GBS . While this review establishes CMV infection and calcineurin inhibitor medications as potentially important triggers for GBS in renal transplant patients, this is based on associations reported in the literature, and causation cannot be established.…”

“…It is likely that the pathogenesis for GBS varies significantly between patients, and while GBS may be partly explained by molecular mimicry due to antecedent infection, it is not a sufficient cause. It is common that no infectious aetiology is identified, and furthermore only a small proportion of the population who have Campylobacter jejuni or CMV infections develop GBS . Therefore, it is clear that host and environmental factors must modulate the susceptibility of individuals to develop GBS, and that more research is needed to further elucidate the pathogenesis of GBS .…”

“…The most common viral cause of GBS is CMV. CMV is part of the herpesviridae family and is common in the general population where primary infection leads to lifelong latency of the virus in endothelial cells, smooth muscle cells, fibroblasts, and monocytes . While CMV presents as a relatively benign febrile illness in the immunocompetent host, it is a significant contributor to mortality and morbidity in immunosuppressed individuals, including solid organ transplant recipients .…”

Causality Assessment Guidelines for Adverse Events Following Immunization with a Focus on Guillain–Barré Syndrome

“…Based on a literature review and consultation with the clinician panel, we found that several conditions are known to cause GBS [18]. These include upper respiratory infection [18][19][20][21], gastrointestinal disorders [18][19][20]22], Zika/Dengue infection [23], Malaria infection [24,25], Tsutsugamushi infection [26], surgery history [27,28], campylobacter infection [29][30][31][32][33][34], cytomegalovirus infection [33][34][35][36][37][38], Epstein-Barr virus infection [33,[38][39][40][41], herpes simplex virus [39], varicella-zoster virus infection [42], mycoplasma pneumonia infection [43,44], haemophilus influenza infection [18,45], and influenza virus infection [46,47]. For each condition, the checklist asks whether the patient had the condition prior to the manifestation of GBS.…”

Zika virus infection and autonomic symptoms

“…The infection is usually asymptomatic [2] and neurological deficits, including autonomic dysfunction, are rarely observed. Regarding the pathogenesis, the potential explanation for autonomic dysfunction in these patients might be linked to the immune changes seen in the Zika virus-related Guillain-Barré syndrome [3]. According to the editorial comment by Carod-Artal, further research in this area is suggested [4].…”