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(searched for: doi:10.1371/journal.pone.0000344)
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Ahed J. Alkhatib
Published: 10 May 2022
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, Ubaid Ahmad, , Obed Boadi Amissah, Asaf Khan, Zohaib Noor, Nasib Zaman
Published: 23 December 2021
Clinical Immunology Communications, Volume 2, pp 1-5; https://doi.org/10.1016/j.clicom.2021.12.002

The publisher has not yet granted permission to display this abstract.
Oana Mosora, , Rodica Balasa, Raluca Fodor, Smaranda Maier, Zoltan Bajko, Adina Stoian, Anca Motataianu
The Journal of Critical Care Medicine, Volume 7, pp 302-307; https://doi.org/10.2478/jccm-2021-0030

Abstract:
Acute Motor Axonal Neuropathy (AMAN) is an immune-mediated disorder of the peripheral nervous system, part of the spectrum of the Guillain-Barre syndrome (GBS). An infectious event most often triggers it reported a few weeks before the onset. The reported case is of a 56 years-old woman who developed acute motor axonal neuropathy three weeks after respiratory infection with influenza A virus subtype H1N1. Despite early treatment with plasmapheresis and intravenous immunoglobulins, the patient remained tetraplegic, mechanically ventilated for five months, with repetitive unsuccessful weaning trails. The probable cause was considered to be phrenic nerve palsy in the context of acute motor axonal neuropathy. This case highlights that acute motor axonal neuropathy is a severe and life-threatening form of Guillain-Barre syndrome associated with significant mortality and morbidity. Neurological and physical recovery strongly depend on the inter-professional effort in an intensive care unit and neurology professionals.
Published: 15 September 2021
by MDPI
BioMed, Volume 1, pp 80-92; https://doi.org/10.3390/biomed1010006

Abstract:
Coronavirus disease 2019 (COVID-19) interacts with the nervous system directly and indirectly by affecting the activation of the immune system. Guillain–Barré syndrome (GBS) is triggered by an inappropriate immune system activation that overlaps with the neurotoxic mechanism of an invading pathogen. Here, we discuss the complexity of an abnormal immune system response leading to the generation of autoimmunity in the setting of acute viral infection. A 67-year-old male patient with COVID-19 developed a sensory motor acute polyneuropathy with respiratory failure. Several serum inflammatory and neurodegeneration markers were collected during hospital days 1, 3, 8, and 67 and compared to healthy individuals. Neural cell adhesion molecule 1 (NCAM-1) and neurofilament light chain (NfL) values were highly variable when compared to healthy individuals, but not to the reference COVID-19 group. We focused our attention on NCAM-1 as a possible target for antibodies directed at COVID-19 in silico.
, Belen Castillo-Cano, Mar Martín-Perez, Ana Llorente-García, Dolores Montero-Corominas
Published: 24 June 2021
Vaccine, Volume 39, pp 4306-4313; https://doi.org/10.1016/j.vaccine.2021.06.029

The publisher has not yet granted permission to display this abstract.
, , Felix Schweiger, Beatrix Schweiger, Jörg Spitz
Published: 7 April 2021
Frontiers in Immunology, Volume 12; https://doi.org/10.3389/fimmu.2021.655739

Abstract:
Vitamin D3 (cholecalciferol) is a secosteroid and prohormone which is metabolized in various tissues to the biologically most active vitamin D hormone 1,25(OH)2D3 (calcitriol). 1,25(OH)2D3 has multiple pleiotropic effects, particularly within the immune system, and is increasingly utilized not only within prophylaxis, but also within therapy of various diseases. In this context, the latest research has revealed clinical benefits of high dose vitamin D3 therapy in autoimmune diseases. The necessity of high doses of vitamin D3 for treatment success can be explained by the concept of an acquired form of vitamin D resistance. Its etiology is based on the one hand on polymorphisms within genes affecting the vitamin D system, causing susceptibility towards developing low vitamin D responsiveness and autoimmune diseases; on the other hand it is based on a blockade of vitamin D receptor signaling, e.g. through pathogen infections. In this paper, we review observational and mechanistic evidence for the acquired vitamin D resistance hypothesis. We particularly focus on its clinical confirmation from our experience of treating multiple sclerosis patients with the so-called Coimbra protocol, in which daily doses up to 1000 I.U. vitamin D3 per kg body weight can be administered safely. Parathyroid hormone levels in serum thereby provide the key information for finding the right dose. We argue that acquired vitamin D resistance provides a plausible pathomechanism for the development of autoimmune diseases, which could be treated using high-dose vitamin D3 therapy.
, Benedikt Schoser, Gilbert Wunderlich, Peter Berlit, Gereon R. Fink
Published: 26 March 2021
Der Nervenarzt, Volume 92, pp 540-547; https://doi.org/10.1007/s00115-021-01094-0

The publisher has not yet granted permission to display this abstract.
International Journal of Molecular Sciences, Volume 22; https://doi.org/10.3390/ijms22062992

Abstract:
A growing body of preclinical evidence indicates that certain cannabinoids, including cannabidiol (CBD) and synthetic derivatives, may play a role in the myelinating processes and are promising small molecules to be developed as drug candidates for management of demyelinating diseases such as multiple sclerosis (MS), stroke and traumatic brain injury (TBI), which are three of the most prevalent demyelinating disorders. Thanks to the properties described for CBD and its interesting profile in humans, both the phytocannabinoid and derivatives could be considered as potential candidates for clinical use. In this review we will summarize current advances in the use of CBD and other cannabinoids as future potential treatments. While new research is accelerating the process for the generation of novel drug candidates and identification of druggable targets, the collaboration of key players such as basic researchers, clinicians and pharmaceutical companies is required to bring novel therapies to the patients.
, Emanuele Spina, , , , , the Italian Peripheral Nervous System Association (ASNP)
Journal of the Peripheral Nervous System, Volume 26, pp 148-154; https://doi.org/10.1111/jns.12435

Abstract:
Background and aims To develop recommendations for vaccination for coronavirus‐19 (COVID‐19) in patients with inflammatory neuropathies. Methods Key questions were formulated in order to perform a literature review on the safety and efficacy of vaccines in patients with inflammatory neuropathies. Based on the best evidence and expert opinion, a list of recommendations was formulated to inform decision on vaccination for COVID‐19 in patients with inflammatory neuropathies and increase adherence to vaccination programmes. Results Recommendations addressing safety and efficacy of vaccination in patients with inflammatory neuropathies were formulated. No data are currently available on the safety and efficacy of COVID‐19 vaccines in patients with inflammatory neuropathies or other immune‐mediated conditions. There is only sparse data on the safety of previous available vaccines in patients with inflammatory neuropathies, but studies on other autoimmune disorders indicate that these are safe and mostly efficacious. Patients with inflammatory neuropathies might be at increased risk for severe illness from COVID‐19. Interpretation Patients with inflammatory neuropathies should be encouraged to adhere to the vaccination campaign for COVID‐19. These recommendations provide guidance on the management of vaccinations for COVID‐19 in patients with inflammatory neuropathies. More research is needed regarding the safety and efficacy of vaccination in patients with inflammatory neuropathies and other immune conditions.
Journal of Clinical Neurology, Volume 17, pp 257-264; https://doi.org/10.3988/jcn.2021.17.2.257

Abstract:
Guillain-Barré syndrome (GBS) is rare, but its symptoms are severe and they occasionally lead to long-term disability. Country-specific epidemiological evidence is useful for detecting potential problems at the population level. This study investigated the epidemiological and economic characteristics of GBS in South Korea. The Korean National Health Insurance Service claims data from 2010 to 2016 were used to identify incident cases as newly hospitalized patients with a primary diagnosis of GBS (the 10th revision of the International Classification Disease code of G61.0). New cases were defined as patients not having claim records for GBS within one year prior to the hospital admission for GBS. The incidence rate increased by 45.6% between 2010 and 2016, from 1.28 to 1.82 per 100,000 population. All age groups other than <20 years showed increasing trends. The incidence rate was highest in those aged 65 years to 74 years. Approximately 72% of the incident GBS cases had antecedent infection within 42 days before GBS was diagnosed. Children younger than 10 years constituted the highest proportion of antecedent infections (93.7%). The average length of stay per GBS hospitalization was 33.5 days. Patients had an average of 7.48 outpatient visits for GBS treatment per year. The economic burden from a societal perspective of treating GBS during the first year was USD 16,428. The increasing incidence trend and substantial economic burden of GBS strongly advocate the development of effective strategies for preventing and managing GBS.
Abstract:
Objective: To determine whether hospital-diagnosed and community-treated infections are important Guillain-Barré syndrome (GBS) risk factors, we investigated the magnitude and duration of associated GBS risk.Methods: We conducted a nationwide population-based case–control study of all patients with first-time hospital-diagnosed GBS in Denmark between 1987 and 2016 and 10 matched population controls per case. Hospital-diagnosed infections were determined in the 1987–2016 period and community antibiotic prescriptions in the 2004–2016 period. We used conditional logistic regression to examine the relative risk of GBS associated with having a recent infection.Results: Hospital-diagnosed infections within 60 days were observed in 4.3% of 2,414 GBS cases vs 0.3% of 23,909 controls, with a matched odds ratio (OR) of 13.7 (95% confidence interval [CI], 10.2–18.5). The strongest association with subsequent GBS was observed for lower respiratory tract infection, gastrointestinal tract infection, and septicemia. Community antibiotic prescriptions within 60 days were observed in 22.4% of 1,086 GBS cases and 7.8% of 10,747 controls, with a matched OR of 3.5 (95% CI, 3.0–4.1). The risk of GBS declined considerably with time since infection, with high ORs of 21.3 (95% CI, 14.5–31.2) and 4.7 (95% CI, 3.9–5.7) observed within the first month after a hospital-diagnosed infection and a community antibiotic prescription, respectively. However, GBS risk remained increased 2.4-fold (95% CI, 1.1–5.5) and 1.5-fold (95% CI, 1.2–2.0) even in the fifth month after infection.Conclusion: There is a strong, temporal association between community antibiotic use and especially infections necessitating hospitalization and risk of subsequent GBS.
, Julia Pakpoor, Christina Mousele, Menelaos Pipis, , Mark Foster, Christopher J Record, Ryan Y S Keh, Janev Fehmi, Ross W Paterson, et al.
Published: 14 December 2020
Brain, Volume 144, pp 682-693; https://doi.org/10.1093/brain/awaa433

Abstract:
Reports of Guillain-Barré syndrome (GBS) have emerged during the Coronavirus disease 2019 (COVID-19) pandemic. This epidemiological and cohort study sought to investigate any causative association between COVID-19 infection and GBS. The epidemiology of GBS cases reported to the UK National Immunoglobulin Database was studied from 2016 to 2019 and compared to cases reported during the COVID-19 pandemic. Data were stratified by hospital trust and region, with numbers of reported cases per month. UK population data for COVID-19 infection were collated from UK public health bodies. In parallel, but separately, members of the British Peripheral Nerve Society prospectively reported incident cases of GBS during the pandemic at their hospitals to a central register. The clinical features, investigation findings and outcomes of COVID-19 (definite or probable) and non-COVID-19 associated GBS cases in this cohort were compared. The incidence of GBS treated in UK hospitals from 2016 to 2019 was 1.65–1.88 per 100 000 individuals per year. GBS incidence fell between March and May 2020 compared to the same months of 2016–19. GBS and COVID-19 incidences during the pandemic also varied between regions and did not correlate with one another (r = 0.06, 95% confidence interval: −0.56 to 0.63, P = 0.86). In the independent cohort study, 47 GBS cases were reported (COVID-19 status: 13 definite, 12 probable, 22 non-COVID-19). There were no significant differences in the pattern of weakness, time to nadir, neurophysiology, CSF findings or outcome between these groups. Intubation was more frequent in the COVID-19 affected cohort (7/13, 54% versus 5/22, 23% in COVID-19-negative) attributed to COVID-19 pulmonary involvement. Although it is not possible to entirely rule out the possibility of a link, this study finds no epidemiological or phenotypic clues of SARS-CoV-2 being causative of GBS. GBS incidence has fallen during the pandemic, which may be the influence of lockdown measures reducing transmission of GBS inducing pathogens such as Campylobacter jejuni and respiratory viruses.
Dorothy L. Butler, Jeffrey C. Gildersleeve
Published: 16 October 2020
Abstract:
SARS-CoV-2 is a deadly virus that is causing the global pandemic coronavirus disease 2019 (COVID-19). Our immune system plays a critical role in preventing, clearing, and treating the virus, but aberrant immune responses can contribute to deleterious symptoms and mortality. Many aspects of immune responses to SARS-CoV-2 are being investigated, but little is known about immune responses to carbohydrates. Since the surface of the virus is heavily glycosylated, pre-existing antibodies to glycans could potentially recognize the virus and influence disease progression. Furthermore, antibody responses to carbohydrates could be induced, affecting disease severity and clinical outcome. In this study, we used a carbohydrate antigen microarray with over 800 individual components to profile serum anti-glycan antibodies in COVID-19 patients and healthy control subjects. In COVID-19 patients, we observed abnormally high IgG and IgM antibodies to numerous self-glycans, including gangliosides, N-linked glycans, LacNAc-containing glycans, blood group H, and sialyl Lewis X. Some of these anti-glycan antibodies are known to play roles in autoimmune diseases and neurological disorders, which may help explain some of the unusual and prolonged symptoms observed in COVID-19 patients. The detection of antibodies to self-glycans has important implications for using convalescent serum to treat patients, developing safe and effective SARS-CoV-2 vaccines, and understanding the risks of infection. In addition, this study provides new insight into the immune responses to SARS-CoV-2 and illustrates the importance of including host and viral carbohydrate antigens when studying immune responses to viruses.
Published: 31 July 2020
by MDPI
Abstract:
We aimed to analyze the incidence of Guillain-Barré syndrome (GBS) and its association with influenza vaccination (IV) in the elderly population. This study included 2470 patients hospitalized with GBS (G61.0) between 2014 and 2016 based on the Korean National Health Insurance Service (NHIS) claims data. We reviewed every medical claim in the 42 days preceding GBS diagnosis looking for precedent causes of GBS. To assess the relationship between IV and the development of GBS, data from the NHIS and the National Vaccination Registry were combined and analyzed. Using a self-controlled case series (SCCS) approach, we calculated the incidence rate ratio by setting the risk period as 42 days following vaccination. The annual background incidence of GBS was estimated at 4.15 per 100,000 persons. More than half of the patients with newly developed GBS had a previous infection or surgery. The incidence of GBS within 42 days of IV was estimated at 0.32 per 100,000 vaccinated persons. SCCS analysis showed that the risk of GBS was not significantly higher. While GBS can potentially develop from various infections, no association was found between GBS and IV. These results will contribute to developing an evidence-based vaccine policy that includes a clear causality assessment of adverse events.
Published: 24 July 2020
Abstract:
Background: Reports of Guillain-Barré Syndrome (GBS) have emerged during the Coronavirus Disease 2019 (COVID-19) pandemic. This epidemiological and cohort study sought to investigate any causative association between COVID-19 infection and GBS.Methods: The epidemiology of GBS cases reported via the UK National Immunoglobulin Database were studied from 2016-2019 and compared to cases reported during the COVID-19 pandemic. For the cohort study, members of the British Peripheral Nerve Society reported all cases of GBS during the pandemic. The clinical features, investigation findings and outcomes of COVID-19 (definite or probable) and non-COVID-19 associated GBS cases were compared.Results: The UK GBS incidence from 2016-2019 was 1.65-1.88 per 100,000 people per year. GBS and COVID-19 incidence varied between regions and did not correlate (r = 0.06, 95% CI −0.56 to 0.63, p=0.86). GBS incidence fell between March and May 2020 compared to the same months of 2016-2019. Forty-seven GBS cases were included in the cohort study (13 definite, 12 probable COVID-19 and 22 non-COVID-19). There were no significant differences in the pattern of weakness, time to nadir, neurophysiology, CSF findings or outcome. Intubation was more frequent in the COVID-19+ve cohort (7/13, 54% vs 5/22, 23% in COVID negative) thought to be related directly to COVID-19 pulmonary involvement.Conclusions: This study finds no epidemiological or phenotypic clues of SARS-CoV-2 being causative of GBS. GBS incidence has fallen during the pandemic which may be the influence of lockdown measures reducing transmission of GBS inducing pathogens such as Campylobacter jejuni and respiratory viruses.
, Katharina M. Busl
Critical Care Explorations, Volume 2; https://doi.org/10.1097/cce.0000000000000107

Abstract:
Objectives: Endemic and pandemic viral respiratory infections have recently emerged as a critical topic of investigation given the recent severe acute respiratory syndrome coronavirus-2 outbreak. Data from such outbreaks indicate that severe systemic comorbidities including acute neurologic illness are associated with illness and lead to significant outcome differences. Herein, we will discuss the neurologic manifestations of severe viral respiratory infections including coronavirus, influenza, respiratory syncytial virus, metapneumovirus, and enterovirus. Data Sources: PubMed and EMBASE were searched by two independent investigators up to March 2020. Study Selection: Data selection included preclinical and clinical studies detailing neurologic manifestations of viral respiratory infections. Data Extraction and Synthesis: Two independent investigators reviewed and extracted the data. Conclusions: Neurologic manifestations including seizures, status epilepticus, encephalitis, critical illness neuromyopathy, acute disseminated encephalomyelitis, acute necrotizing encephalitis, Guillan-Barré syndrome, transverse myelitis, and acute flaccid myelitis have all been associated with severe viral respiratory infections. Having an understanding of the direct neurotropism of such viruses is imperative to understanding pathogenesis, clinical presentation, and potential treatment paradigms aimed at improving morbidity and mortality.
Published: 27 March 2020
by MDPI
Abstract:
While the weight of epidemiological evidence does not support a causal link with influenza vaccination evaluated over the last 30 years, Guillain–Barré syndrome (GBS) has been considered a vaccine-associated adverse event of interest since 1976. To investigate the existence of GBS risk after vaccination against seasonal influenza, a systematic review and meta-analysis have been conducted based on 22 eligible epidemiological studies from 1981 to 2019 reporting 26 effect sizes (ESs) in different influenza seasons. The primary result of our meta-analysis pointed to no risk of vaccine-associated GBS, as documented by a pooled ES of 1.15 (95% CI: 0.97–1.35). Conversely, an obvious high risk of GBS was observed in patients with previous influenza-like illness (ILI), as demonstrated by a pooled ES of 9.6 (95% CI: 4.0–23.0) resulting from a supplementary analysis. While the meta-analysis did not confirm the putative risk of vaccine-associated GBS suggested by many epidemiological studies, vaccination against seasonal influenza reduced the risk of developing ILI-associated GBS by about 88%. However, to obtain strong evidence, more epidemiological studies are warranted to establish a possible coincidence between vaccination and ILI prior to GBS onset.
, , Jérémie Rudant, Yann Mikaeloff, Pascale Tubert-Bitter, , , Joël Coste,
Abstract:
Objective: To evaluate the risk of Guillain-Barré syndrome (GBS) following seasonal influenza vaccination based on French nationwide data.Methods: All cases of GBS occurring in metropolitan France between September 1 and March 31 from 2010 to 2014 were identified from the French national health data system. Data were analyzed according to the self-controlled case series method. The risk period started 1 day after the patient received vaccine (D1) until 42 days after vaccination (D42). The incidence of GBS during this risk period was compared to that of the control period (D43–March 31). The incidence rate ratio (IRR) was estimated after adjusting for seasonality and presence or not of acute infections.Results: Between September and March, of the 2010/2011 to 2013/2014 influenza vaccination seasons, 3,523 cases of GBS occurred in metropolitan France and were included in the study. Among them, 15% (527 patients) had received influenza vaccination. A total of 140 patients developed GBS during the 42 days following influenza vaccination. The crude risk of developing GBS was not significantly increased during the 42 days following influenza vaccination (IRR, 1.02; 95% confidence interval [CI], 0.83–1.25; p = 0.85). This result remained nonsignificant after adjustment for calendar months and the incidence of acute gastrointestinal and respiratory tract infections (IRR, 1.10; 95% CI, 0.89–1.37; p = 0.38). In contrast, the risk of GBS was fourfold higher after acute respiratory tract infection (IRR, 3.89; 95% CI, 3.52–4.30; p< 0.0001) or gastrointestinal infection (IRR, 3.64; 95% CI, 3.01–4.40; p< 0.0001).Conclusions: No association between seasonal influenza vaccination and GBS was shown during the 42 days following vaccination.
Published: 24 February 2020
by MDPI
Abstract:
South Korea operates a National Vaccine Injury Compensation Program (VICP) for people who experience adverse events following immunization (AEFI). To run this program rationally, it is a prerequisite to confirm whether adverse events were caused by immunization. Guillain–Barré syndrome (GBS), a severe neurological disease with limb pain and muscle weakness as cardinal symptoms, is attracting attention as an AEFI. However, algorithm or guidelines for assessing the causality between vaccination and the incidence of GBS are lacking. We aimed to develop guidelines for causality assessment of GBS as an AEFI and suggest using these guidelines in alignment with the VICP. We systematically searched for other previously published algorithms or guidelines and found a WHO-AEFI guideline used worldwide; however, it only provides general instructions and is not tailored to specific adverse events. We translated and locally adapted the structure of this guideline and then added contents related to GBS. The GBS-specific guideline consists of four steps: case ascertainment of GBS, checklist (including (1) order of incidence, (2) temporal proximity, (3) evidence for other causes and (4) published evidence), an algorithm, and final classification. We listed key information on confirming GBS and whether any other causes of GBS were present. For real world application of the guideline along with the VICP, we collaborated with a panel of neurologists, epidemiologic investigators, and committee members from the VICP. To ensure transparency and a scientific approach, regular updates and collaboration with neurologists are essential. We expect that this guideline will contribute to logical causality assessment and compensation decisions for GBS and will provide the basic structure for causality assessment of other AEFIs.
Nicola Principi,
Published: 1 September 2019
Vaccine, Volume 37, pp 5544-5550; https://doi.org/10.1016/j.vaccine.2018.05.119

Abstract:
Guillain–Barré syndrome (GBS) is an acute, immune-mediated polyradiculoneuropathy. Infections and vaccines have been hypothesized to play a role in triggering GBS development. These beliefs can play a role in reducing vaccination coverage. In this report, data concerning this hypothesis are discussed. It is shown that an association between vaccine administration and GBS has never been proven for most of debated vaccines, although it cannot be definitively excluded. The only exception is the influenza vaccine, at least for the preparation used in 1976. For some vaccines, such as measles/mumps/rubella, human papillomavirus, tetravalent conjugated meningococcal vaccine, and influenza, the debate between supporters and opponents of vaccination remains robust and perception of vaccines’ low safety remains a barrier to achieving adequate vaccination coverage. Less than 1 case of GBS per million immunized persons might occur for these vaccines. However, in some casesimmunization actually reduces the risk of GBS development. In addition, the benefits of vaccination are clearly demonstrated by the eradication or enormous decline in the incidence of many vaccine-preventable diseases. These data highlight that the hypothesized risks of adverse events, such as GBS, cannot be considered a valid reason to avoid the administration of currently recommended vaccines.
Ben Cantan, Charles-Edouard Luyt,
Seminars in Respiratory and Critical Care Medicine, Volume 40, pp 488-497; https://doi.org/10.1055/s-0039-1693497

Abstract:
Critically ill patients are admitted to an intensive care unit (ICU) for multiple reasons. In this study, we aim to analyze the current evidence and findings associated with influenza and other emergent viral infections, namely, herpes simplex virus type 1 (HSV-1), Epstein-Barr virus (EBV), and cytomegalovirus (CMV).Among medical conditions, community-acquired respiratory infections are the most frequent reason for ventilatory support in ICUs. Community-acquired pneumonia in a severe form including the need of invasive mechanical ventilation and/or vasopressors is associated with high mortality rates. However, after the pandemic that occurred in 2009 by H1N1 influenza, the number of cases being admitted to ICUs with viral infections is on the rise. Patients in whom an etiology would not have been identified in the past are currently being tested with more sensitive viral molecular diagnostic tools, and patients being admitted to ICUs have more preexisting medical conditions that can predispose to viral infections. Viral infections can trigger the dysregulation of the immune system by inducing a massive cytokine response. This cytokine storm can cause endothelial damage and dysfunction, deregulation of coagulation, and, consequently, alteration of microvascular permeability, tissue edema, and shock. In severe influenza, this vascular hyperpermeability can lead to acute lung injury, multiorgan failure, and encephalopathy. In immunocompetent patients, the most common viral infections are respiratory, and influenza should be considered in patients with severe respiratory failure being admitted to ICU. Seasonality and coinfection are two important features when considering influenza as a pathogen in critically ill patients.Herpesviridae (HSV, CMV, and EBV) may reactivate in ICU patients, and their reactivation is associated with morbidity/mortality. However, whether a specific treatment may impact on outcome remains to be determined.
Kuo-Hsuan Chang, Rong-Kuo Lyu, Wan-Ting Lin, , Huang-Shen Lin, Shang-Hung Chang
Published: 24 July 2019
Frontiers in Neurology, Volume 10; https://doi.org/10.3389/fneur.2019.00768

Abstract:
Lines of evidence suggest trivalent influenza vaccination may be associated with Guillain–Barre syndrome (GBS), an immune-mediated acute inflammatory neuropathy. On the other hand, this vaccination protects against influenza infection, which has been demonstrated as a trigger of GBS. To clarify the net effect of trivalent influenza vaccines on GBS, we conducted a retrospective nationwide nested case–control study using the database of the Taiwan National Health Insurance program. We identified 182 hospitalized patients with GBS aged ≥50 years from 2007 to 2015 as the cases, and 910 hospitalized patients, matched by gender, age, date of hospitalization, comorbidities, and medications, as the control subjects. Nearby and remote exposures of vaccination were defined as subjects who had received trivalent influenza vaccine 42 (nearby exposure) and 90 days (remote exposure) before the date of hospitalization, respectively. We found 7 (3.85%) GBS patients and 26 (2.86%) matched control subjects who demonstrated nearby exposures of influenza vaccine (odds ratio: 1.46, 95% confidence interval: 0.56–3.78). Seventeen (9.34%) GBS patients were exposed to influenza vaccines remotely, while the number of remote exposure of influenza vaccines in matched control subjects was 72 (7.91%, odds ratio: 1.26, 95% confidence interval: 0.67–2.38). These results do not support an association between trivalent influenza vaccine and GBS among the patients aged ≥50 years.
Rosario Sanz Fadrique, Luis Martín Arias, , Natalia Jimeno Bulnes, Pilar García Ortega
Published: 29 June 2019
Abstract:
Guillain-Barré Syndrome (GBS) as a consequence of influenza vaccination is a relevant topic, yet to be clarified, which raises concern both amongst health care personnel and the general population. Every study and pharmacovigilance system point to need of further research and the importance of continuous monitoring of safety regarding influenza vaccines. The aim of the present study is to investigate the publication of new data since the realisation of our meta-analysis of GBS and influenza vaccines (published in 2015). A systematic revision of PubMed, Embase, and Web of Knowledge (WOS) databases has been carried out. These report observational studies assessing GBS risk after the administration of influenza vaccines from May 2014 up to July 20th, 2017. The research yielded 107 articles. Only three studies met established inclusion criteria and referred to an estimation GBS risk after some influenza vaccine. Two studies investigated GBS risk by the pandemic A/H1N1 vaccine, while only one looked into season vaccines. The present systematic review, conducted after the publication of our previous meta-analysis, seems to confirm its previous results. Therefore, GBS should be considered an infrequent adverse effect of influenza vaccination, which should not negatively influence its acceptance. Unfortunately, very few of the systematically surveyed studies meeting inclusion criteria. This fact sharply contrasts with the current consensus as to the need of continuously monitoring the safety of influenza vaccines.
Published: 1 June 2019
Vaccine, Volume 37, pp 3856-3865; https://doi.org/10.1016/j.vaccine.2019.05.041

Abstract:
The U.S. Food and Drug Administration and the Centers for Medicare & Medicaid Services have been actively monitoring the risk of Guillain-Barré syndrome (GBS) following influenza vaccination among Fee-for-Service (FFS) Medicare beneficiaries every season since 2008. We present our evaluation of the GBS risk following influenza vaccinations during the 2017-2018 season. We implemented a multilayered approach to active safety surveillance that included near real-time surveillance early in the season, comparing GBS rates post-vaccination during the 2017-2018 season with rates from five prior seasons using the Updating Sequential Probability Ratio Test (USPRT), and end-of-season self-controlled risk interval (SCRI) analyses. We identified approximately 16 million influenza vaccinations. The near real-time surveillance did not signal for a potential 2.5-fold increased GBS risk either in days 8-21 or 1-42 post-influenza vaccination. In the SCRI analyses, we did not detect statistically significant increased GBS risks among influenza-vaccinated Medicare beneficiaries ≥65 years for either the 8-21 or 1-42-day risk windows for all seasonal vaccines combined, high-dose vaccine, or standard-dose vaccines; we did detect an increased GBS risk in days 8-21 post-vaccination for individuals vaccinated with the adjuvanted vaccine (OR: 3.75; 95% CI: 1.01, 13.96), although this finding was not statistically significant after multiplicity adjustment (p = 0.146). Our multilayered surveillance approach-which allows for early detection of elevated GBS risk and provides reliable end-of-season SCRI estimates of effect size-did not identify an increased GBS risk following 2017-2018 influenza vaccinations. The slightly increased GBS risk with the adjuvanted vaccine, which was not statistically significant following multiplicity adjustment, is consistent with the package inserts of all U.S.-licensed influenza vaccines, which warn of a potential low increased GBS risk. The benefits of influenza vaccines in preventing morbidity and mortality heavily outweigh this potential risk.
Published: 16 April 2019
Case Reports in Neurology, Volume 11, pp 117-123; https://doi.org/10.1159/000499701

Abstract:
Herpes simplex virus type 2 (HSV-2) is the most common cause of genital herpes with a seroprevalence of 20–30% in developed countries and 80% worldwide. In addition to neonatal encephalitis and meningitis, HSV-2 is associated with radiculomyelitis marked by pain, paresis, sphincter disturbances, sensory loss, or ascending necrotizing myelitis. We report the case of a patient with a lengthy psychiatric history who presented with lower extremity pain and weakness. Cervical, thoracic, and lumbar MRI scans with and without gadolinium contrast revealed no significant stenosis, neural compression, or other abnormal findings, and the brain MRI with and without gadolinium contrast was normal. The initial diagnosis was conversion disorder due to myriad psychological stressors. Polymerase chain reaction (PCR) of CSF detected HSV-2 and a lymphocytic pleocytosis, and the diagnosis of radiculomyelitis was confirmed. She was treated with i.v. acyclovir for 3 weeks followed by valacyclovir. The patient attained no improvement of her symptoms within 8 months; however, she reported decreased pain and improved strength of the lower extremities by 17 months. Neurologists should be aware of the association between HSV-2 and radiculomyelitis, particularly in the setting of a patient with psychiatric comorbidities. Recognition of HSV-2 through PCR of CSF and prompt treatment with acyclovir may prevent devastating neurological sequelae.
, Muhammad Dain Yazid, Ruszymah Bt Hj Idrus, Srijit Das,
Published: 19 March 2019
Frontiers in Neurology, Volume 10; https://doi.org/10.3389/fneur.2019.00087

Abstract:
Demyelinating diseases represent a spectrum of disorders that impose significant burden on global economy and society. Generally, the prognosis of these diseases is poor and there is no available cure. In recent decades, research has shed some light on the biology and physiology of Schwann cells and its neuroprotective effects in the peripheral nervous system (PNS). Insults to the PNS by various infectious agents, genetic predisposition and immune-related mechanisms jeopardize Schwann cell functions and cause demyelination. To date, there are no effective and reliable biomarkers for PNS-related diseases. Here, we aim to review the following: pathogenesis of various types of peripheral demyelinating diseases such as Guillain-Barre syndrome, Chronic Inflammatory Demyelinating Polyradiculoneuropathy, Anti-Myelin Associated Glycoprotein Neuropathy, POEMS syndrome, and Charcot-Marie-Tooth disease; emerging novel biomarkers for peripheral demyelinating diseases, and Schwann cell associated markers for demyelination.
Fatima Kudaeva, Mark Speechley, Neil Klar, Orit Schieir, , Louis Bessette, , , , Edward Keystone, et al.
Published: 15 March 2019
ACR Open Rheumatology, Volume 1, pp 63-69; https://doi.org/10.1002/acr2.1009

The publisher has not yet granted permission to display this abstract.
, Nico Golfrè Andreasi, Paolo De Martin, Vittorio Govoni, , Edward Cesnik, Maura Pugliatti, Ilaria Casetta
Published: 7 January 2019
Neurological Sciences, Volume 40, pp 603-609; https://doi.org/10.1007/s10072-018-3688-4

Abstract:
Guillain-Barré syndrome (GBS) is an acute/subacute autoimmune inflammatory polyradiculoneuropathy. Previous epidemiological studies carried out in the province of Ferrara, Italy, from 1981 to 2002 indicated that GBS incidence had tendency of increase in the period considered.
, , Maria Regina Fernandes De Oliveira
Tropical Medicine & International Health, Volume 24, pp 132-142; https://doi.org/10.1111/tmi.13181

Abstract:
Objective To describe the factors associated with the development of Guillain‐Barré syndrome, both infectious and non‐infectious, during and after the A(H1N1) influenza pandemic in 2009 and the recent Zika virus epidemic in the Americas. Method Systematic review of literature on factors associated with the development of the Guillain‐Barré syndrome published between 2007 and 2017 listed in EBSCO, MEDLINE, and LILACS databases. The quality of the studies was evaluated using the Newcastle Ottawa Scale. Results 34 articles met inclusion criteria and were selected for analysis. Their quality was considered good in relation to most of the items evaluated. Many etiological agents had results of association with Guillain‐Barré syndrome, among them Campylobacter jejuni, influenza vaccine ‐ both pandemic and seasonal vaccines, respiratory infection, gastrointestinal infection among others. The etiological agents found are in most part the same reported prior to the study period. The association with surgeries, chikungunya virus (CHIKV), Zika virus and quadrivalent human papillomavirus vaccine stand out as new etiological agents in the list of the various possible agents that trigger Guillain‐Barré syndrome reported in the study period. There were no Brazilian studies identified during this period. Conclusions The results of the review reaffirmed Campylobacter jejuni as the major trigger of GBS, whereas the association of influenza vaccines and GBS is less clear: Zika virus infection in association with GBS was found in only one study.
, W. Gu, M.E. Wise, J. J. Sejvar, , B. E. Mahon
Epidemiology and Infection, Volume 146, pp 1740-1745; https://doi.org/10.1017/s0950268818001802

Abstract:
Guillain Barré syndrome (GBS), which is triggered by autoantibodies produced in response to antigenic stimuli such as certain infections and vaccinations, is the most common cause of acute flaccid paralysis worldwide. Campylobacter, the most common bacterial enteric infection in the USA, is reported to be the most commonly diagnosed antecedent of GBS, yet little information is available about the risk of post-Campylobacter GBS. Data collected through active, population-based surveillance in the Emerging Infections Program during the 2009–2010 novel Influenza A (H1N1) vaccination campaign allowed us to compare confirmed and probable GBS cases to non-cases to determine whether antecedent Campylobacter infection (or a diarrhoeal illness consistent with campylobacteriosis) was more common among cases and to assess the risk of GBS following Campylobacter infection. We estimate that 8–12% of GBS cases in the USA are attributable to Campylobacter infection (or a diarrhoeal illness consistent with campylobacteriosis), with 434–650 cases of post-diarrhoeal GBS annually and about 49 cases of GBS per 100 000 Campylobacter infections. These results provide updated estimates for post-Campylobacter GBS incidence in the USA and highlight an important benefit of effective measures to prevent Campylobacter infections.
, , Luis F. Castillo-Medina, Yhojan Rodríguez, Yovana Pacheco, Susan Halstead, Hugh J. Willison, ,
Frontiers in Molecular Neuroscience, Volume 11; https://doi.org/10.3389/fnmol.2018.00116

Abstract:
Zika virus (ZIKV) is an emerging flavivirus rapidly spreading throughout the tropical Americas. Aedes mosquitoes is the principal way of transmission of the virus to humans. ZIKV can be spread by transplacental, perinatal, and body fluids. ZIKV infection is often asymptomatic and those with symptoms present minor illness after 3 to 12 days of incubation, characterized by a mild and self-limiting disease with low-grade fever, conjunctivitis, widespread pruritic maculopapular rash, arthralgia and myalgia. ZIKV has been linked to a number of central and peripheral nervous system injuries such as Guillain-Barré syndrome (GBS), transverse myelitis (TM), meningoencephalitis, ophthalmological manifestations, and other neurological complications. Nevertheless, mechanisms of host-pathogen neuro-immune interactions remain incompletely elucidated. This review provides a critical discussion about the possible mechanisms underlying the development of autoimmune neurological conditions associated with Zika virus infection.
, Robert S. Hagan, Frederick G. Hayden, William A. Fischer
Influenza and Other Respiratory Viruses, Volume 11, pp 372-393; https://doi.org/10.1111/irv.12470

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, Juliane M. A. S. Malta, Elisabeth R. Krow-Lucal, Jadher Percio, , Alexander Vargas, Tatiana M. Lanzieri, Priscila L. Leite, J. Erin Staples, Marc X. Fischer, et al.
PLOS Neglected Tropical Diseases, Volume 11; https://doi.org/10.1371/journal.pntd.0005869

Abstract:
In mid-2015, Salvador, Brazil, reported an outbreak of Guillain-Barré syndrome (GBS), coinciding with the introduction and spread of Zika virus (ZIKV). We found that GBS incidence during April–July 2015 among those ≥12 years of age was 5.6 cases/100,000 population/year and increased markedly with increasing age to 14.7 among those ≥60 years of age. We conducted interviews with 41 case-patients and 85 neighborhood controls and found no differences in demographics or exposures prior to GBS-symptom onset. A higher proportion of case-patients (83%) compared to controls (21%) reported an antecedent illness (OR 18.1, CI 6.9–47.5), most commonly characterized by rash, headache, fever, and myalgias, within a median of 8 days prior to GBS onset. Our investigation confirmed an outbreak of GBS, particularly in older adults, that was strongly associated with Zika-like illness and geo-temporally associated with ZIKV transmission, suggesting that ZIKV may result in severe neurologic complications. Shortly following the introduction of Zika virus (ZIKV), a type of flavivirus transmitted by mosquitoes, into Brazil in early 2015, the Brazil Ministry of Health began receiving increased reports of a paralyzing condition known as Guillain-Barré syndrome (GBS). The areas with the greatest number of GBS cases appeared to correlate geographically and temporally with the areas reporting the highest rate of ZIKV infections. This association had been previously observed during a ZIKV outbreak in French Polynesia, however, this had not been systematically examined in a case-control investigation for the ZIKV outbreak in South America. In this investigation, the authors found that the occurrence of GBS in the affected population was nearly four times higher than would be expected, and the risk for GBS was particularly elevated among older adults. GBS was associated with ZIKV-like symptoms and with a combination of ZIKV-like symptoms plus laboratory evidence of a recent flavivirus infection. Taken together, these findings provide strong support for and greater understanding of the link between ZIKV and GBS.
, , Carmen Laurino, Beniamino Palmieri
Published: 20 July 2017
EPMA Journal, Volume 8, pp 295-311; https://doi.org/10.1007/s13167-017-0101-y

Abstract:
Autoimmune diseases, including multiple sclerosis and type 1 diabetes mellitus, affect about 5% of the worldwide population. In the last decade, reports have accumulated on various autoimmune disorders, such as idiopathic thrombocytopenia purpura, myopericarditis, primary ovarian failure, and systemic lupus erythematosus (SLE), following vaccination. In this review, we discuss the possible underlying mechanisms of autoimmune reactions following vaccinations and review cases of autoimmune diseases that have been correlated with vaccination. Molecular mimicry and bystander activation are reported as possible mechanisms by which vaccines can cause autoimmune reactions. The individuals who might be susceptible to develop these reactions could be especially not only those with previous post-vaccination phenomena and those with allergies but also in individuals who are prone to develop autoimmune diseases, such as those with a family history of autoimmunity or with known autoantibodies, and the genetic predisposed individuals.Further research is encouraged into the direct associations between vaccines and autoimmune conditions, and the biological mechanisms behind them.
Sammy Searcy, Oluwaseun O. Akinduro, Andrew Spector, Jang W. Yoon, ,
Published: 8 May 2017
Neurocritical Care, Volume 28, pp 388-394; https://doi.org/10.1007/s12028-017-0406-7

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, Wei Hua, Thomas E. MaCurdy, , Armen Avagyan, Jeffrey Kelman, Christopher M. Worrall, Robert Ball, Michael Nguyen
Published: 1 May 2017
Vaccine, Volume 35, pp 2986-2992; https://doi.org/10.1016/j.vaccine.2017.03.087

Abstract:
Conducting near real-time surveillance using USPRT has proven to be an excellent method for near real-time GBS surveillance after influenza vaccination, as demonstrated by our surveillance efforts during the 2010/11-2013/14 influenza seasons. In the 2010/2011 influenza season, in addition to the 2009 H1N1 influenza pandemic, using near real-time surveillance we were able to observe a signal early in the influenza season and the method has now become routine.
Mohamed Kazamel, , Eduardo E. Benarroch, Mrinal M. Patnaik,
Published: 18 March 2017
Muscle & Nerve, Volume 57, pp 150-156; https://doi.org/10.1002/mus.25581

Abstract:
Introduction: Autosomal dominant haploinsufficiency of GATA2 causes monocytopenia and natural killer cell lymphopenia, resulting in predisposition to mycobacterial, fungal, and viral infections. Methods: Herein we report on the clinical, serologic, electrophysiologic, and pathologic evaluations of a 29-year-old woman with GATA2 haploinsufficiency and active Epstein–Barr virus (EBV) infection complicated by subacute painful neuropathy. Results: Nerve conduction and electromyography studies showed predominantly demyelinating sensorimotor polyradiculoneuropathy. Lumbar spine MRI showed thickening and enhancement of the cauda equina nerve roots. Serum and cerebrospinal fluid anti-IgG and IgM EBV capsid and nucleic acid antibodies were positive. Sural nerve biopsy showed microvasculitis and an increased frequency of fibers with segmental demyelination. Intravenous immunoglobulin and steroids improved the patient's neuropathy. Conclusion: GATA2 mutation–related immunodeficiency may predispose to EBV-associated subacute demyelinating polyradiculoneuropathy by both viral susceptibility and immune dysregulation. In patients who present in this manner, immunodeficiency syndromes should be considered when lymphomatous infiltration is excluded. Immunotherapy can be helpful. Muscle Nerve 57: 150–156, 2018
K. Gaardbo Kuhn, G. Falkenhorst, H.-D. Emborg, T. Ceper, M. Torpdahl, , S. Ethelberg,
Epidemiology and Infection, Volume 145, pp 701-709; https://doi.org/10.1017/s0950268816002788

Abstract:
SUMMARY: Following an unusually heavy rainfall in June 2009, a community-wide outbreak ofCampylobactergastroenteritis occurred in a small Danish town. The outbreak investigation consisted of (1) a cohort study using an e-questionnaire of disease determinants, (2) microbiological study of stool samples, (3) serological study of blood samples from cases and asymptomatic members of case households, and (4) environmental analyses of the water distribution system. The questionnaire study identified 163 cases (respondent attack rate 16%). Results showed a significant dose-response relationship between consumption of tap water and risk of gastroenteritis.Campylobacter jejunibelonging to two relatedflaAtypes were isolated from stool samples. Serum antibody levels againstCampylobacterwere significantly higher in cases than in asymptomatic persons. Water samples were positive for coliform bacteria, and the likely mode of contamination was found to be surface water leaking into the drinking-water system. This geographically constrained outbreak presented an ideal opportunity to study the serological response in persons involved in aCampylobacteroutbreak. The serology indicated that asymptomatic persons from the same household may have been exposed, during the outbreak period, toCampylobacterat doses that did not elicit symptoms or alternatively had been exposed toCampylobacterat a time prior to the outbreak, resulting in residual immunity and thus absence of clinical signs.
Published: 18 April 2016
BMC Genomics, Volume 17, pp 1-18; https://doi.org/10.1186/s12864-016-2612-7

Abstract:
Campylobacter is the leading cause of foodborne diarrhoeal illness in humans and is mostly acquired from consumption or handling of contaminated poultry meat. In the absence of effective licensed vaccines and inhibitors, selection for chickens with increased resistance to Campylobacter could potentially reduce its subsequent entry into the food chain. Campylobacter intestinal colonisation levels are influenced by the host genetics of the chicken. In the present study, two chicken populations were used to investigate the genetic architecture of avian resistance to colonisation: (i) a back-cross of two White Leghorn derived inbred lines [(61 x N) x N] known to differ in resistance to Campylobacter colonisation and (ii) a 9th generation advanced intercross (61 x N) line. The level of colonisation with Campylobacter jejuni following experimental infection was found to be a quantitative trait. A back-cross experiment using 1,243 fully informative single nucleotide polymorphism (SNP) markers revealed quantitative trait loci (QTL) on chromosomes 7, 11 and 14. In the advanced intercross line study, the location of the QTL on chromosome 14 was confirmed and refined and two new QTLs were identified located on chromosomes 4 and 16. Pathway and re-sequencing data analysis of the genes located in the QTL candidate regions identified potential pathways, networks and candidate resistance genes. Finally, gene expression analyses were performed for some of the candidate resistance genes to support the results. Campylobacter resistance in chickens is a complex trait, possibly involving the Major Histocompatibility Complex, innate and adaptive immune responses, cadherins and other factors. Two of the QTLs for Campylobacter resistance are co-located with Salmonella resistance loci, indicating that it may be possible to breed simultaneously for enhanced resistance to both zoonoses.
, Christos Karadedos, Ioannis Chiotis, Nikolaos Chaliasos, Sophia Tsabouri
Jornal de Pediatria (Versão em Português), Volume 92, pp 113-121; https://doi.org/10.1016/j.jpedp.2016.01.007

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, Christos Karadedos, Ioannis Chiotis, Nikolaos Chaliasos,
Published: 1 March 2016
Jornal de Pediatria, Volume 92, pp 113-121; https://doi.org/10.1016/j.jped.2015.06.007

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