A Neurologist's View of Lyme Disease and Other Tick-Borne Infections

Halperin, John J.

doi:10.1055/s-0039-1692143

Cited by 7 publications

(4 citation statements)

References 45 publications

(44 reference statements)

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“…B. burgdorferi are known to cause both peripheral and central nervous system pathology, collectively termed Lyme neuroborreliosis (Halperin, 2019). The central nervous system contains a diverse repertoire of myeloid cells, including microglia found in the brain parenchyma and non-parenchymal macrophages that can be found in the perivascular areas, the meninges and the choroid plexus (Prinz et al, 2011).…”

Section: Microgliamentioning

confidence: 99%

Immune Response to Borrelia: Lessons from Lyme Disease Spirochetes

Wooten¹,

Baumgarth²

2022

Current Issues in Molecular Biology

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The mammalian host responds to infection with Borrelia spirochetes through a highly orchestrated immune defense involving innate and adaptive effector functions aimed toward limiting pathogen burdens, minimizing tissue injury, and preventing subsequent reinfection. The evolutionary adaptation of Borrelia spirochetes to their reservoir mammalian hosts may allow for its persistence despite this immune defense. This review summarizes our current understanding of the host immune response to B. burgdorferi sensu lato, the most widely studied Borrelia spp. and etiologic agent of Lyme borreliosis. Pertinent literature will be reviewed with emphasis on in vitro, ex vivo and animal studies that influenced our understanding of both the earliest responses to B. burgdorferi as it enters the mammalian host and those that evolve as spirochetes disseminate and establish infection in multiple tissues. Our focus is on the immune response of inbred mice, the most commonly studied animal model of B. burgdorferi infection and surrogate for one of this pathogen's principle natural reservoir hosts, the white-footed deer mouse. Comparison will be made to the immune responses of humans with Lyme borreliosis. Our goal is to provide an understanding of the dynamics of the mammalian immune response during infection with B. burgdorferi and its relation to the outcomes in reservoir (mouse) and non-reservoir (human) hosts.Curr. Issues . caister.com/cimb caister.com/cimb 145 Curr. Issues Mol. Biol. Vol. 42 Immune Response to Borrelia Bockenstedt et al.

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Section: Microgliamentioning

confidence: 99%

Immune Response to Borrelia: Lessons from Lyme Disease Spirochetes

Wooten¹,

Baumgarth²

2022

Current Issues in Molecular Biology

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“…In contrast, chronic sensory axonal neuropathy is a late manifestation of European LNB, which is frequently associated with acrodermatitis chronica atrophicans (ACA). Typically observed months to years after the tick bite, ACA starts with a diffuse reddish or purplish discoloration of the skin of the involved limb, which evolves to marked skin atrophy (Halperin, 2019). Our patient did not recall any erythema, which is identified in up to 60% of patients with LNB in the course of the disease (Ogrinc et al, 2016).…”

Section: Discussionmentioning

confidence: 56%

Peripheral neuropathy due to neuroborreliosis: Insensitivity for CXCL13 as early diagnostic marker

Gubanova

Lang

Latzko

et al. 2021

International Journal of Infectious Diseases

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The case of a 69-year-old woman with peripheral neuropathy caused by Lyme neuroborreliosis (LNB) in an endemic region in Eastern Austria is reported. The patient had noticed transient numbness of her left leg. On initial examination, she had patchy sensory disturbances of the left lower leg, but ancillary examinations of nerve conduction and cerebrospinal fluid (CSF), including the B-cell chemokine CXCL13, were normal. A re-tap performed 54 days later, following clinical progression with foot drop, widespread lower leg paresthesia, and pain, revealed an increased cell count, autochthonous IgM production, synthesis of Borrelia-specific IgM, and elevated CXCL13. Neurophysiological examinations disclosed an incomplete conduction block, mixed axonal and demyelinating sensorimotor neuropathy, and subacute neurogenic damage of muscles innervated by the peroneal nerve. This case study presents rare evidence of very early diagnostic findings in peripheral neuropathy caused by LNB. These are characterized by insensitivity of CXCL13 in CSF to aid earlier diagnosis and the development of an intrathecal immune response against Borrelia at a later stage. These findings reinforce the need for a re-tap to confirm the diagnosis and facilitate appropriate treatment in this rare manifestation of LNB.

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“…The most common causes are idiopathic (eg Bell's palsy), infectious (eg Herpes zoster oticus), traumatic (eg temporal bone fracture), metabolic (eg diabetes mellitus), neoplasmatic (eg acoustic neuroma) and paraneoplastic manifestations. One of the commonly missed causes is Lyme borreliosis (LB) 1‐4 . It should always be considered, especially in the areas endemic for tick‐borne diseases, for example in Central and Eastern Europe, where incidence of LB is high.…”

Section: Introductionmentioning

confidence: 99%

“…One of the commonly missed causes is Lyme borreliosis (LB). [1][2][3][4] It should always be considered, especially in the areas endemic for tick-borne diseases, for example in Central and Eastern Europe, where incidence of LB is high.It is worth mentioning that the annual incidence of LB in Poland has been increasing systematically. The number of registered patients…”

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confidence: 99%

Assessment of anti‐HSV antibodies in patients with facial palsy in the course of neuroborreliosis

et al. 2020

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Aim There are many causes of facial nerve palsy. The most common causes are neuroborreliosis (NB), idiopathic paralysis or Herpes simplex virus (HSV) reactivation. The aim of this study was to characterize patients with facial palsy in the course of NB and to determine whether HSV‐1 reactivation takes place during the acute phase of NB. Methods A retrospective analysis of 66 patients with facial nerve palsy was performed. In 38 patients, facial palsy was caused by Borrelia burgdorferi sl infection. Immunological tests for HSV‐1, tick‐borne encephalitis virus and B burgdorferi sl in serum and cerebrospinal fluid (CSF) were performed. Results In this analysis, 55.2% of NB patients had right nerve palsy and 21% bilateral palsy; 15.8% of patients had erythema migrans (EM). Lymphocytic meningitis was diagnosed in 92% of patients and Bannwarth's syndrome was diagnosed in 47% of patients. IgM anti‐HSV‐1 antibodies were detected in four patients with NB and two patients with facial nerve palsy of other origin. IgM anti‐HSV‐1 antibodies were detected in the CSF of three patients (7.9%) with NB, and one of them had bilateral VII paresis and EM simultaneously. Treatment with ceftriaxone or doxycycline led to complete recovery. Conclusions Neuroborreliosis should always be considered as a cause of peripheral facial nerve palsy. Peripheral facial nerve palsy is a significant symptom in the course of NB, especially in patients accompanied by meningitis. Pathomechanism of facial nerve paresis has not been well explained so far and may depend on two independent mechanisms in NB, including HSV‐1 reactivation.

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A Neurologist's View of Lyme Disease and Other Tick-Borne Infections

Cited by 7 publications

References 45 publications

Immune Response to Borrelia: Lessons from Lyme Disease Spirochetes

Immune Response to Borrelia: Lessons from Lyme Disease Spirochetes

Peripheral neuropathy due to neuroborreliosis: Insensitivity for CXCL13 as early diagnostic marker

Assessment of anti‐HSV antibodies in patients with facial palsy in the course of neuroborreliosis

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