Abstract:Guillain-Barré syndrome (GBS) can occur at all stages of human immunodeficiency virus (HIV) infection. HIV, cytomegalovirus (CMV), and varicella zoster virus (VZV) are the main infectious agents in HIV-positive GBS cases. These cases include acute and chronic HIV infection, immune reconstitution inflammatory syndrome (IRIS) shortly after anti-retroviral therapy (ART), those with ART interruption, or those with cerebrospinal fluids (CSF) HIV escape. The mechanisms are involved in both humoral and cellular immun… Show more
“…The differentiating feature that prompts the clinician to consider HIV is the presence of lymphocytic pleocytosis in the CSF, instead of the expected albuminocytologic dissociation of non-HIV-GBS cases [66]. GBS-phenotype may also be part of the immune reconstitution inflammatory syndrome [67].…”
Section: Infectious Neuropathies Presenting With Gbs-like Phenotypesmentioning
Purpose of eview
The aim of this review is to discuss the presentation, diagnosis, and management of polyneuropathy (PN) in selected infections. Overall, most infection related PNs are an indirect consequence of immune activation rather than a direct result of peripheral nerve infection, Schwann cell infection, or toxin production, though note this review will describe infections that cause PN through all these mechanisms. Rather than dividing them by each infectious agent separately, we have grouped the infectious neuropathies according to their presenting phenotype, to serve as a guide to clinicians. Finally, toxic neuropathies related to antimicrobials are briefly summarized.
Recent findings
While PN from many infections is decreasing, increasing evidence links infections to variants of GBS. Incidence of neuropathies secondary to use of HIV therapy has decreased over the last few years.
Summary
In this manuscript, a general overview of the more common infectious causes of PN will be discussed, dividing them across clinical phenotypes: large- and small-fiber polyneuropathy, Guillain-Barré syndrome (GBS), mononeuritis multiplex, and autonomic neuropathy. Rare but important infectious causes are also discussed.
“…The differentiating feature that prompts the clinician to consider HIV is the presence of lymphocytic pleocytosis in the CSF, instead of the expected albuminocytologic dissociation of non-HIV-GBS cases [66]. GBS-phenotype may also be part of the immune reconstitution inflammatory syndrome [67].…”
Section: Infectious Neuropathies Presenting With Gbs-like Phenotypesmentioning
Purpose of eview
The aim of this review is to discuss the presentation, diagnosis, and management of polyneuropathy (PN) in selected infections. Overall, most infection related PNs are an indirect consequence of immune activation rather than a direct result of peripheral nerve infection, Schwann cell infection, or toxin production, though note this review will describe infections that cause PN through all these mechanisms. Rather than dividing them by each infectious agent separately, we have grouped the infectious neuropathies according to their presenting phenotype, to serve as a guide to clinicians. Finally, toxic neuropathies related to antimicrobials are briefly summarized.
Recent findings
While PN from many infections is decreasing, increasing evidence links infections to variants of GBS. Incidence of neuropathies secondary to use of HIV therapy has decreased over the last few years.
Summary
In this manuscript, a general overview of the more common infectious causes of PN will be discussed, dividing them across clinical phenotypes: large- and small-fiber polyneuropathy, Guillain-Barré syndrome (GBS), mononeuritis multiplex, and autonomic neuropathy. Rare but important infectious causes are also discussed.
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