Confirmed cases of Neuroborreliosis with involvement of peripheral nervous system: Description of a cohort.

The manifestations of borreliosis in the peripheral nervous system (PNS) remain poorly described. As the symptoms of neuroborreliosis can be reversed with timely introduction of antibiotics, early identification could avoid unnecessary axonal loss. Our aim was to describe the characteristics of confirmed neuroborreliosis cases involving the PNS diagnosed between 2007 and 2017 in our neuromuscular disease center in a nonendemic area (La Pitié-Salpêtrière Hospital, Paris, France).Neuroborreliosis was defined as follows: compatible neurological symptoms without other cause of neuropathy; cerebrospinal fluid and serum analysis (positive serological tests with ELISA, confirmed by Western Blot); and improvement of symptoms with adapted antibiotherapy. All the patients consulting in our center between 2007 and 2017 underwent electrophysiological study.Sixteen confirmed cases of neuroborreliosis involving the PNS were included: 10 cases of meningoradiculoneuritis, 4 of axonal neuropathy, and 2 of demyelinating neuropathy (one acute and one chronic). Only 4 (25%) patients reported tick bites. Meningoradiculoneuritis was characterized by lymphocytic meningitis, intense pain, cranial nerve palsy, and contrast enhancement of nerve roots on imagery. The patients with axonal neuropathy presented sensory symptoms with intense pain but no motor deficit and meningitis was rare. Nerve biopsy of 1 patient revealed lymphocytic vasculitis. Electrophysiological testing showed sensory or sensorimotor axonal neuropathy (3 subacute and 1 chronic) of the lower limbs, with asymmetrical neuropathy in 1 patients, symmetrical neuropathy in one and monomelic sensory mononeuritis multiplex in another. We also found 1 case of acute demyelinating neuropathy, treated with antibiotherapy and immunoglobulins, and 1 chronic demyelinating neuropathy. Overall, diaphragmatic paralysis was frequent (18.6%). Antibiotherapy (mostly ceftriaxone 3-4 weeks) resulted in symptom resolution.This series gives an updated overview of the peripheral complications of neuroborreliosis to help identify this disease so that timely treatment could avoid axonal loss.

Lyme neuroborreliosis epidemiology in Sweden 2010 to 2014: clinical microbiology laboratories are a better data source than the hospital discharge diagnosis register.

BackgroundIn a study from 2013 that prioritised communicable diseases for surveillance in Sweden, we identified Lyme borreliosis as one of the diseases with highest priority. In 2014, when the present study was designed, there were also plans to make neuroborreliosis notifiable within the European Union.AimWe compared possibilities of surveillance of neuroborreliosis in Sweden through two different sources: the hospital discharge register and reporting from the clinical microbiology laboratories.MethodsWe examined the validity of ICD-10 codes in the hospital discharge register by extracting personal identification numbers for all cases of neuroborreliosis, defined by a positive cerebrospinal fluid-serum anti-Borrelia antibody index, who were diagnosed at the largest clinical microbiology laboratory in Sweden during 2014. We conducted a retrospective observational study with a questionnaire sent to all clinical microbiology laboratories in Sweden requesting information on yearly number of cases, age group and sex for the period 2010 to 2014.ResultsAmong 150 neuroborreliosis cases, 67 (45%) had received the ICD-10 code A69.2 (Lyme borreliosis) in combination with G01.9 (meningitis in bacterial diseases classified elsewhere), the combination that the Swedish National Board of Health and Welfare recommends for neuroborreliosis. All 22 clinical laboratories replied to our questionnaire. Based on laboratory reporting, the annual incidence of neuroborreliosis in Sweden was 6.3 cases per 100,000 in 2014.ConclusionThe hospital discharge register was unsuitable for surveillance of neuroborreliosis, whereas laboratory-based reporting was a feasible alternative. In 2018, the European Commission included Lyme neuroborreliosis on the list of diseases under epidemiological surveillance.

Impact of serodiagnosis on the management of Lyme borreliosis at Angers University Hospital.

INTRODUCTION: Lyme borreliosis (LB) is an emerging arthropod-borne disease the diagnosis of which is made on clinical and biological data. We assessed the Angers University Hospital physicians' management of LB, in case of positive serology, and estimated their compliance to European recommendations (EUCALB). METHODS: We retrospectively included 75 cases with positive ELISA serologies confirmed by Western-Blot, performed at the Angers University Hospital between 2008 and 2012. RESULTS AND DISCUSSION: There were 4 cases of early localized phase, 26 of early-disseminated phase (including 17 cases of neuroborreliosis), and one case of late phase. The curative management complied with EUCALB guidelines in 28 cases out of 31. CONCLUSION: Serology remains a reference diagnostic tool for LB, as long as the practitioner is aware of the main clinical and biological criteria.

Microbiologic findings in acute facial palsy in children.

OBJECTIVE: Microbiologic causes of facial palsy in children were investigated. STUDY DESIGN: Prospective clinical study. SETTING: Tertiary referral center. PATIENTS: Forty-six children aged 0 to 16 years with peripheral facial palsy. INTERVENTIONS: Paired serum samples and cerebrospinal fluid were tested to find indications of microbes associated with facial palsy. The microbes tested were herpes simplex virus 1 and 2, varicella-zoster virus, human herpesvirus-6, Mycoplasma pneumoniae, Borrelia burgdorferi, influenza A and B virus, picorna, cytomegalovirus, parainfluenza virus, respiratory syncytial virus, coxsackie B5 virus, adenovirus, and enterovirus, Chlamydia psittaci, and Toxoplasma gondii. Besides the routine tests in clinical practice, serum and cerebrospinal fluid samples were tested with a highly sensitive microarray assay for DNA of herpes simplex virus 1 and 2; human herpes virus 6A, 6B, and 7; Epstein-Barr virus, cytomegalovirus, and varicella zoster virus. RESULTS: Incidence for facial palsy was 8.6/100,000/children/year. Cause was highly plausible in 67% and probable in an additional 11% of cases. Borrelia burgdorferi caused facial palsy in 14 patients (30%), varicella zoster virus in 5 (11%) (one with concomitant adenovirus), influenza A in 3 (6%), herpes simplex virus 1 in 2 (4%) (one with concomitant enterovirus), otitis media in 2 (4%), and human herpesvirus 6 in 2 (4%). Mycoplasma pneumoniae, neurofibromatosis, and neonatal age facial palsy affected 1 child (2%) each. CONCLUSION: Microbiologic etiology association of pediatric facial palsy could frequently be confirmed. Borreliosis was the single most common cause; hence, cerebrospinal fluid sampling is recommended for all pediatric cases in endemic areas. Varicella zoster virus accounted for 11% of the cases, being the second most common factor.

[Neuroborreliosis]. / Neuroborreliose.

Neuroborreliosis is easily diagnosed by means of clinical symptoms and laboratory findings. Guiding symptoms are radicular pain and pareses of the extremities and the facial nerve. There is a great number of further less frequently occurring neurological symptoms, which can be attributed to a borrelial infection only by appropriate investigations of the CSF. Radiculitis is cured adequately by oral doxycycline while symptoms of the central nervous system are probably better treated intravenously by ceftriaxone, cefotaxime or penicillin G. Post-Lyme syndrome is a diffuse description of non-specific complaints, which are not the explicit result of a former infection with B. burgdorferi. As further antibiotics do not help and the CSF is unremarkable in most patients, a persistent infection with B. burgdorferi s.l. in all probability can be excluded.

[Borreliosis as the cause of disability pensions in Norway]. / Borreliose som årsak til uførepensjon i Norge.

BACKGROUND: Borreliosis is a bacterial infection transferred by tick-bites. Neuroborreliosis is the most frequent disseminated form of the disorder in Norway. Registers exist in Norway on all reported communicable diseases (The Norwegian Surveillance System for Communicable Diseases [MSIS]) and disability pension diagnoses (The Norwegian Directorate of Labour and Welfare). MATERIAL AND METHODS: Geographic distributions of borreliosis and changes over time are presented. Disability pensions (coded by International Classification of Diseases [ICD]) in the period 1998-2005, in which borreliosis was used as the primary or secondary diagnosis (ICD-10), were compared with MSIS-data for borreliosis on municipal and county levels. RESULTS: Borreliosis was the cause of disability pensions in 55 cases. The Vestfold and Agder counties had the highest number of cases. Larvik municipality had 9 cases, Arendal had four and Kristiansand had nine cases. The annual rates of new disability pensions caused by borreliosis were low but increasing in the period 1998-2005. The disability pension rates tended to reflect changes in the number of MSIS-reported cases, with pensions changing 1-2 years after MSIS-changes. Most MSIS-reported cases are in the Agder and Telemark counties. INTERPRETATION: Disability pension are rarely caused by borreliosis. The annual incidence of disability pensions seems to reflect the number of MSIS-reported cases of borreliosis. The Agder and Vestfold counties have the highest incidence.

[Heterogeneity of Borrelia burgdorferi: etiopathogenetic relevance and clinical implications]. / Heterogenität von Borrelia burgdorferi: Atiopathogenetische Relevanz und klinische Implikationen.

Of the ten different species of Borrelia (B.) burgdorferi sensu lato which have been characterized to date, only B. burgdorferi sensu stricto, B. garinii and B. afzelii have been identified as pathogenic in humans. It was suggested that different species possess different organotropisms and may preferentially cause distinct clinical manifestations of Lyme disease. Molecular analyses revealed a strong association of B. afzelii with the late cutaneous manifestation acrodermatitis chronica atrophicans, whereas B. garinii was predominantly identified in clinical samples from patients with neuroborreliosis. PCR-based analyses of samples from European patients with Lyme arthritis had given controversial results, but B. burgdorferi sensu stricto appears to be the major pathogen. The identity of the infecting species seems to be a major determinant in the pathogenesis of Lyme arthritis, although its complex immunopathological background and its clinical heterogeneity clearly indicate concomitant factors. Thus, characterization of the infecting organism at the species level on the one hand and linkage of clinical data with pathogenetically relevant immune parameters on the other, shall lead to a more precise understanding of the pathogenesis and the individual clinical course of Lyme borrelioses.

[Diagnosis and therapy of neuroborreliosis. On the hunt for the "great imitator"]. / Diagnostik und Therapie der Neuroborreliose. Auf der Jagd nach dem "grossen imitator".

Neurological manifestations are characteristic of stage 2 and stage 3 borreliosis. In stage 2, some 15% of the patients have neurological symptoms expressed as a triad of aseptic meningitis, cranial neuritis and radiculitis. Stage 3--chronic neuroborreliosis affects some 5% of untreated patients. The condition has its onset at the earliest 6 months after the infection, and is characterized by encephalopathic symptoms, such as fatigue, sleep and memory disturbances, and depressive states. Further manifestations of this stage may be Lyme polyneuropathy, in rare cases also progressive borrelia encephalomyelitis and cerebrovascular neuroborreliosis. The treatment of choice is intravenous administration of cephalosporins over 2-4 weeks. The success of treatment should be assessed on the basis of the clinical course rather than on laboratory results. Patience is required in the treatment of the post-Lyme syndrome, characterized by residual symptoms, recurrences or a relapsing course.

[Neuroborreliosis]. / La neuroborréliose.

Lyme disease, or borreliosis, is an endemic affection in Belgium. It is transmitted by a spirochete, Borrelia burgdorferi. The particularity of the infecting genomic group, Borrelia garinii, implies that half of the reported cases of Lyme disease in our country have neurologic manifestations. Due to the marked clinical heterogeneity and the difficult serologic diagnosis, neuroborreliosis is often part of the differential diagnosis in neurology. The antibiotic treatment is necessary because it decreases the risk of more advanced stages of the disease. We hope that a vaccination will soon be available in Belgium.

[Neurologic syndromes in Lyme disease]. / Neurologiczne postacie choroby z Lyme.

Lyme borreliosis, multisystem disease, when involve neurologic system is named neuroborrelosis. Symptomatology of neuroborreliosis is rich and various. Difficulties in recognition are connected usually with long period from tick bite to late neurological signs. Any headache and psychiatric disorder in the course of Lyme disease could be an early manifestation of invasion of the CNS by the spirochaetes. Each part of neurologic system could be involved. The most common clinical picture of neuroborreliosis is meningitis with cranial or peripheral neuropathies connected with radiculalgia, less common are encephalitis and myelitis, neuropathies and polyneuropathies, encephalopathies. Encephalomyelitis is the most serious form of neuroborreliosis. From the pathophysiologic point of view all cranial and peripheral neuropathies are forms of mononeuritis multiplex. Vasculitis and autoimmunology processes are present. Encephalopathy is due to neuroimmunomodulators, like lymphokines and by toxico-metabolic effect could be connected with each form of systemic borreliosis. Spheroplast L-form of borrelia could be responsible for difficulties with their eradication. Diagnosis of neuroborreliosis is based on culturing of B. burgdorferi from CSF, detection of specific antispirochaetal antibodies produced in subarachnoid space, detection of activated lymphocytes, other antigens detection in CSF (also after dissociation of complexes) or borrelial DNA sequences.