Stages and syndromes of neuroborreliosis

Oschmann, Patrick; Dorndorf, W.; Hornig, C. R.; Schäfer, Claudia; Wellensiek, H. J.; Pflughaupt, K. W.

doi:10.1007/s004150050216

Cited by 198 publications

(161 citation statements)

References 17 publications

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“…[47][48][49][50][51] In most cases of encephalomyelitis, MR imaging is very helpful in assessing the presence of rare tumefactive white matter lesions that may mimic a neoplastic process. 47,48,51 Tumefactive lesion biopsies are characterized by microgliosis and spirochetes morphologically compatible with B burgdorferi yet paradoxically without an inflammatory infiltrate.…”

Section: Cns Lnbmentioning

confidence: 99%

Lyme Neuroborreliosis: Manifestations of a Rapidly Emerging Zoonosis

Hildenbrand¹,

Craven²,

Jones³

et al. 2009

AJNR Am J Neuroradiol

170

118

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SUMMARY:Lyme disease has a worldwide distribution and is the most common vector-borne disease in the United States. Incidence, clinical manifestations, and presentations vary by geography, season, and recreational habits. Lyme neuroborreliosis (LNB) is neurologic involvement secondary to systemic infection by the spirochete Borrelia burgdorferi in the United States and by Borrelia garinii or Borrelia afzelii species in Europe. Enhanced awareness of the clinical presentation of Lyme disease allows inclusion of LNB in the imaging differential diagnosis of facial neuritis, multiple enhancing cranial nerves, enhancing noncompressive radiculitis, and pediatric leptomeningitis with white matter hyperintensities on MR imaging. The MR imaging white matter appearance of successfully treated LNB and multiple sclerosis display sufficient similarity to suggest a common autoimmune pathogenesis for both. This review highlights differences in the epidemiology, clinical manifestations, diagnosis, and management of Lyme disease in the United States, Europe, and Asia, with an emphasis on neurologic manifestations and neuroimaging.

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Section: Cns Lnbmentioning

confidence: 99%

Lyme Neuroborreliosis: Manifestations of a Rapidly Emerging Zoonosis

Hildenbrand¹,

Craven²,

Jones³

et al. 2009

AJNR Am J Neuroradiol

170

118

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“…This can be followed by a complex of cardiac, neurological, or arthritic disorders (1)(2)(3). The three main genospecies of B. burgdorferi can present with somewhat different clinical manifestations: B. burgdorferi sensu stricto often causes arthritis, Borrelia garinii neuroborreliosis, and Borrelia afzelii has been preferentially associated with acrodermatitis chronica atrophicans (3,4).…”

mentioning

confidence: 99%

The Complement Regulator Factor H Binds to the Surface Protein OspE of Borrelia burgdorferi

Hellwage

Meri

Heikkilä

et al. 2001

Journal of Biological Chemistry

327

309

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Spirochete bacteria of the Borrelia burgdorferi sensu lato complex cause Lyme borreliosis. The three pathogenic subspecies Borrelia garinii, Borrelia afzelii, and Borrelia burgdorferi sensu stricto differ in their disease profiles and susceptibility to complement lysis. We investigated whether complement resistance of Borreliae could be due to acquisition of the main soluble inhibitors of the alternative complement pathway, factor H and the factor H-like protein 1. When exposed to nonimmune EDTA-plasma, the serum-resistant B. afzelii and B. burgdorferi sensu stricto strains bound factor H/factor H-like protein 1 to their surfaces. Assays with radiolabeled proteins showed that factor H bound strongly to the B. burgdorferi sensu stricto strain. To identify factor H ligands on the borrelial surface, we analyzed a panel of outer surface proteins of B. burgdorferi sensu stricto with the surface plasmon resonance technique. The outer surface lipoprotein OspE was identified as a specific ligand for factor H. Using recombinant constructs of factor H, the binding site for OspE was localized to the C-terminal short consensus repeat domains 15-20. Specific binding of factor H to B. burgdorferi sensu stricto OspE may help the pathogen to evade complement attack and phagocytosis.

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“…CNS manifestations frequency is generally low. This condition is reported more often in Europe and almost always accompanied by CSF pleocytosis and cranial neuritis [12].…”

Section: Central Nervous System Disordersmentioning

confidence: 99%

Diagnosis and Treatment Algorythm in Lyme Neuroborreliosis

Ţilea

Bălaşa

Fodor

et al. 2016

Acta Medica Marisiensis

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Lyme neuroborreliosis is an infection of the nervous system caused by spirochetes of the Borrelia burgdorferi sensulato group. Neurological clinical manifestations usually present a steady evolution and are different in patients from Europe compared to those from America, possibly due to vector agents and different bacterial species. Various diagnostic markers were studied in consideration of a clear or possible diagnosis of the disease, because evolution and complications depend on early diagnosis and initiation of therapy. The isolation of the bacterium is difficult, microscopic examination and the bacterial dezoxiribonucleic acid amplification shows low sensitivity. However, the diagnosis of Lyme neuroborreliosis is mainly based on serological methods that have a satisfactory sensitivity and specificity. A correct diagnosis can be performed by strictly respecting clinical guidelines and protocols and carefully interpreting the serological tests. The presence of anti-borrelia burgdorferi antibodies in the cerebrospinal fluid with evidence of intrathecal antibody production is the gold standard diagnosis of Lyme neuroborreliosis. Early administration of antibiotic treatment (third generation cephalosporins, cyclins, aminopenicillins) can produce the remission of neurological symptoms, the eradication of spirochetes in acute phase of the disease, thus avoiding the development of the chronic disease. Introduction Lyme neuroborreliosis (LNB) is a clinical manifestation of Lyme borreliosis (LB), which affects the central nervous system (CNS) and peripheral nervous system (PNS) caused by spirochetes of the genus Borrelia burgdorferi (Bb) sensulato complex and spread by the bite of ticks of the genus Ixodes. Nerve structures are affected by spirochetes both in acute and late phase of the disease. A distinction between early (acute) and late (chronic) phase of LNB can be made. The acute phase occurs in less than 6 months after contacting an infected arthropod and chronic LNB sets in more than 6 months or even years later after the initial infection [1,2].The clinical manifestations of LNB are various and different in patients from Europe compared to those from America, probably due to different vector agents and bacterial species of the two continents. According to Steere the frequency of neurological manifestations in case of LB is about 15-25% [3].

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Stages and syndromes of neuroborreliosis

Cited by 198 publications

References 17 publications

Lyme Neuroborreliosis: Manifestations of a Rapidly Emerging Zoonosis

Lyme Neuroborreliosis: Manifestations of a Rapidly Emerging Zoonosis

The Complement Regulator Factor H Binds to the Surface Protein OspE of Borrelia burgdorferi

Diagnosis and Treatment Algorythm in Lyme Neuroborreliosis

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