Rickettsial infections are an unlikely cause of peripheral facial palsy in Southern Jutland, Denmark.

INTRODUCTION: Several infectious aetiologies have been associated with peripheral facial palsy, among others Herpes viridae and Borrelia burgdorferi and, rarely, cases of rickettsiosis. In this study, we prospectively included 19 patients with peripheral facial palsy from the Department of Neurology, University Hospital of Southern Denmark, and 29 healthy controls to examine infectious causes and risk factors of peripheral facial palsy. METHODS: Patients and controls completed a questionnaire regarding exposures, and the patients' medical files were examined. Serum from patients and controls were tested for antibodies against B. burgdorferi, Rickettsia felis and Rickettsia helvetica. Cerebrospinal fluids were tested using polymerase chain reaction for the presence of herpes simplex virus 1 and 2, herpes zoster virus and spotted fever group rickettsial DNA and for intrathecal production of antibodies against B. burgdorferi with an antibody index test. RESULTS: One patient was diagnosed with peripheral facial palsy associated with neuroborreliosis with a positive antibody index test but had a negative serological analysis. No patients had evidence of herpes or rickettsial infection. Fourteen out of the 19 patients had symptom onset in the winter months. Preceding myalgia was the only significant difference in symptoms between patients and controls (p = 0.011). CONCLUSION: Rickettsiosis is unlikely as a common cause of facial palsy in Southern Jutland, Denmark. FUNDING: The study was supported financially by the Knud and Edith Eriksen Mindefond and the Region of Southern Denmark. TRIAL REGISTRATION: The study population and the control group were approved by the Regional Committees on Health Research Ethics for Southern Denmark (S-20170136 and S-20170049) and by the Danish Data Protection Agency (17/31901 and 18/28928). All participants provided informed consent before their enrollment in the study.

Acute facial nerve palsy in children in a Lyme disease-endemic area in the Netherlands.

We assessed the prevalence of Lyme neuroborreliosis in children with acute facial nerve palsy in a Lyme-endemic region and patient characteristics associated with this. All children visiting one of three participating hospitals between January 2010 and December 2016 were included in the study. Of 104 children referred to the hospital with facial nerve palsy, 43% had Lyme neuroborreliosis and 57% idiopathic facial palsy. Characteristics significantly associated with Lyme neuroborreliosis were headache (55% versus 18%), meningeal irritation (21% versus 5%), presentation in summer months (69% versus 37%), and a previous tick bite (33% versus 7%).

Metagenomic next-generation sequencing of viruses, bacteria, and fungi in the epineurium of the facial nerve with Bell's palsy patients.

Bell's palsy (BP) represents a major cause leading to facial paralysis in the world. The etiology of BP is still unknown, and virology is the prevailing theory. The purpose of this study is to explore the pathogenic microorganisms that may be related to BP, and it is of great significance to study the pathogenesis and treatment of BP. Metagenomic next-generation sequencing (mNGS) detection was performed in the epineurium of the facial nerve of 30 BP patients who underwent facial nerve epineurium decompression. A total of 84 pathogenic microorganisms were detected in 30 clinical samples, including 4 viruses, 10 fungi, and 70 bacteria. The species with the highest detection frequency in virus was human betaherpesvirus 7 (HHV-7). The species with the highest detection frequency in Fungi was Malassezia restricta. The species with the highest detection frequency in Bacteria was Pseudomonas aeruginosa. In this study, mNGS method was firstly used to detect the pathogenic microorganisms in the epineurium of the facial nerve with BP patients. We have for the first time identified HHV-7 and aspergillus in the epineurium of the facial nerve of BP patients. These results suggest that these two pathogenic microorganisms should be considered in the pathogenesis of BP.

[Acute abdominal pain caused by neuroborreliosis]. / Acute buikpijn bij neuroborreliose.

BACKGROUND: Lyme disease is a multisystem disease which can present itself in several ways. When the nervous system is involved, it is called Lyme neuroborreliosis. Both central and peripheral nervous systems can be affected. CASE DESCRIPTION: A 39-year-old man visited the emergency department multiple times with severe abdominal-pain attacks with motoric unrest. Extensive diagnostic work-up was done, which was initially inconclusive. Lyme neuroborreliosis was suspected when he developed a facial-nerve palsy during admission; the abdominal pain was thought to be caused by thoracic radiculoneuropathy. Serologic testing for antibodies against Borrelia burgdorferi was positive, confirming the diagnosis. The patient was treated with intravenous ceftriaxone. CONCLUSION: This case shows abdominal pain being caused by radiculoneuropathy at thoracic level, an uncommon presentation of Lyme neuroborreliosis. Often, this diagnosis is only made when neurological paralysis occurs. Information regarding skin lesions or a recent tick bite can lead to earlier recognition of the diagnosis.

Bell's palsy and sudden deafness associated with Rickettsia spp. infection in Sweden. A retrospective and prospective serological survey including PCR findings.

BACKGROUND AND PURPOSE: Sixty patients with facial palsy and 67 with sudden deafness were retrospectively or prospectively examined for serological evidence of rickettsial infection; in six cases where cerebrospinal fluid was available, patients were also examined for presence of rickettsial DNA. METHODS: Rickettsial antibodies were detected in single or paired serum samples using immunofluorescence with Rickettsia helvetica as the antigen and in four cases also using western blot. Using PCR and subsequent direct cycle sequencing, the nucleotide sequences of the amplicons (17 kDa protein gene) in cerebrospinal fluid were analysed. RESULTS: Five out of 60 (8.3%) patients with facial palsy and eight of 67 (11.9%) with hearing loss showed confirmative serological evidence of infection with Rickettsia spp. An additional three and four patients in the facial palsy and hearing loss groups, respectively, showed evidence of having a recent or current infection or serological findings suggestive of infection. In four cases, the specificity of the reaction was confirmed by western blot. An additional 70 patients were seroreactive with IgG or IgM antibodies higher than or equal to the cut-off of 1:64, whereas 37 patients were seronegative. Only two of 127 patients had detectable antibodies to Borrelia spp. In three of six patients, rickettsial DNA was detected in the cerebrospinal fluid, where the obtained sequences (17 kDa) shared 100% similarity with the corresponding gene sequence of Rickettsia felis. CONCLUSIONS: These results highlight the importance of considering Rickettsia spp. as a cause of neuritis, and perhaps as a primary cause of neuritis unrelated to neuroborreliosis.

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.

Bell's palsy may have relations to bacterial infection.

Bell's palsy is the most common acute facial paralysis with its causes still unclear. At present, the most widely accepted causes are viral infections, trauma, surgery, diabetes, local infections, tumor, immunological disorders, or drugs. Unclear causes lead to unidentified treatments. Most therapeutic methods are simply symptomatic treatment. Fortunately, the pathomechanism of Bell's palsy is relative clear, involving herpes simplex virus (HSV) reactivation within the geniculate ganglion, followed by inflammation and entrapment of the nerve in the bony foramen. This makes symptomatic treatment possible. But the therapeutic effects are not quite satisfactory. Therefore, novel etiological and therapeutic concepts are urgently needed. According to our clinical observation and some facts that do not favor the viral infections theory, we can conclude that all Bell's palsy is not related to viral infections, some even may have relations to bacterial infection. As far as blood routine examination is concerned, though lymphocyte increasing can be seen in most patients with Bell's palsy, there are cases with normal lymphocyte but increased neutrophil. Also, antibiotic treatment in these patients could accelerate recovery to some extent. These results indicate that Bell's palsy in these patients may be caused by bacterial infection.

Nuclear bilateral Bell's palsy and ageusia associated with Mycoplasma pneumoniae pulmonary infection.

This case report describes a case of nuclear bilateral Bell's palsy and ageusia associated with Mycoplasma pneumoniae infection. Magnetic resonance imaging evidenced T2-weighted hyper-intense protuberantial lesions. Such topography leading to a nuclear palsy contrasts with previously reported infectious diplegia involving only peripheral facial nerves, and has not yet been described in the spectrum of M. pneumoniae post-infectious neurological manifestations.

Frequent detection of Mycoplasma pneumoniae in Bell's palsy.

The cause of Bell's palsy (BP) remains unknown despite various hints to an infectious etiology. Mycoplasma pneumoniae is a common pathogen of the respiratory tract causing pharyngitis, tracheobronchitis or pneumonia. Neurological complications are the most frequent extrapulmonary manifestation. So far, only a few case reports suggested an association between cranial nerve palsy and M. pneumoniae infection. Patients with a BP who were admitted to the Department of Otorhinolaryngology or Neurology of the University of Wuerzburg between 2000 and 2002 were tested serologically for the presence of antibodies against Borrelia burgdorferi, herpes viruses (HSV-1/2, VZV) and M. pneumoniae. The diagnosis of mycoplasmal infection was made when at least one of the following criteria was met: a threefold rise or more in the titer of antibody of M. pneumoniae in paired sample or a microparticle agglutination assay (MAG) of > or =1:40 and the detection of IgA and/or IgM antibodies in the acute phase serum. Ninety-one consecutive patients could be included. Fifteen patients showed a reactivation of a VZV ( n=12) or of a HSV-1 ( n=3) infection. In six cases the immunoblot revealed specific antibody bands for B. burgdorferi. In 24 patients (26.4%) a seroconversion of M. pneumoniae could be detected. Only two patients complained of mild respiratory symptoms. According to our results, M. pneumoniae is frequently associated with Bell's palsy. Thus, a routine screening for this pathogen, even in the absence of respiratory symptoms, is necessary.

Annualized incidence and spectrum of illness from an outbreak investigation of Bell's palsy.

BACKGROUND: There are limited clinical and epidemiological data on patients diagnosed with Bell's palsy. While investigating an apparent clustering of Bell's palsy, we sought to characterize the spectrum of illness in patients with this diagnosis. METHODS: A telephone survey of persons with idiopathic facial (Bell's) palsy in the Greater Toronto Area (GTA, population = 4.99 million) and Nova Scotia (population = 0.93 million) from August 1 to November 15, 1997 collected information on subject demographics, neurological symptoms, constitutional symptoms, medical investigation and management. Information regarding potential risks for exposure to infectious agents, past medical history, and family history of Bell's palsy was also collected. Subjects with other secondary causes of facial palsy were excluded. RESULTS: In the GTA and Nova Scotia, 222 and 36 patients were diagnosed with idiopathic facial (Bell's) palsy, respectively. The crude annualized incidence of Bell's palsy was 15.2 and 13.1 per 100,000 population in the GTA and Nova Scotia, respectively. There was no temporal or geographical clustering, and symptomatology did not differ significantly between the two samples. The mean age was 45 years, with 55% of subjects being female. The most common symptoms accompanying Bell's palsy were increased tearing (63%), pain in or around the ear (63%), and taste abnormalities (52%). A significant number of patients reported neurological symptoms not attributable to the facial nerve. CONCLUSION: No clustering of cases of Bell's palsy was observed to support an infectious etiology for the condition. Misdiagnosis of the etiology of facial weakness is common. Patients diagnosed with Bell's palsy have a variety of neurological symptoms, many of which cannot be attributed to a facial nerve disorder.

No evidence of acute Chlamydia pneumoniae infection in patients with Bell's palsy.

The cause of Bell's palsy remains unknown even though available evidence suggests that infection could be a factor. In recent studies, Chlamydia pneumoniae has been associated with neurologic diseases such as multiple sclerosis. In the present study, the association of C pneumoniae with Bell's palsy was studied with the use of serology and polymerase chain reaction to test tear fluid and peripheral blood mononuclear cells from 21 patients with Bell's palsy and 21 control subjects. C pneumoniae DNA was detected from tear fluid samples in 1 patient with Bell's palsy and in 2 healthy control subjects. Whether this indicates earlier disease or subclinical infection remains to be studied. However, an association between Bell's palsy and acute C pneumoniae infection could not be shown.

Living with Lyme disease.

The occurrence of Lyme disease is rising steadily in the United States. The majority of health care providers are unfamiliar with this complex syndrome. Nurses lack accurate clinical information to provide comprehensive nursing care to these patients. The progression of Lyme disease is addressed through three stages. Untreated or poorly managed, Lyme disease may become a chronic, debilitating illness. The author's personal story is interwoven and serves to highlight the pathophysiology of the disease and the emotional and physical costs to the patient.