scholarly journals Campylobacter Species and Guillain-Barré Syndrome

1998 ◽  
Vol 11 (3) ◽  
pp. 555-567 ◽  
Author(s):  
Irving Nachamkin ◽  
Ban Mishu Allos ◽  
Tony Ho
Keyword(s):  
Molecular Mimicry ◽  
Current Knowledge ◽  
Axonal Neuropathy ◽  
Autoimmune Disorder ◽  
Acute Motor Axonal Neuropathy ◽  
Acute Inflammatory Demyelinating Polyneuropathy ◽  
Campylobacter Species ◽  
Antecedent Infection ◽  
Different Strains ◽  
Campylobacter Infection

SUMMARY Since the eradication of polio in most parts of the world, Guillain-Barré syndrome (GBS) has become the most common cause of acute flaccid paralysis. GBS is an autoimmune disorder of the peripheral nervous system characterized by weakness, usually symmetrical, evolving over a period of several days or more. Since laboratories began to isolate Campylobacter species from stool specimens some 20 years ago, there have been many reports of GBS following Campylobacter infection. Only during the past few years has strong evidence supporting this association developed. Campylobacter infection is now known as the single most identifiable antecedent infection associated with the development of GBS. Campylobacter is thought to cause this autoimmune disease through a mechanism called molecular mimicry, whereby Campylobacter contains ganglioside-like epitopes in the lipopolysaccharide moiety that elicit autoantibodies reacting with peripheral nerve targets. Campylobacter is associated with several pathologic forms of GBS, including the demyelinating (acute inflammatory demyelinating polyneuropathy) and axonal (acute motor axonal neuropathy) forms. Different strains of Campylobacter as well as host factors likely play an important role in determining who develops GBS as well as the nerve targets for the host immune attack of peripheral nerves. The purpose of this review is to summarize our current knowledge about the clinical, epidemiological, pathogenetic, and laboratory aspects of campylobacter-associated GBS.

Acute Motor Axonal Neuropathy in a 5-Month-Old Child

2019 ◽  
Vol 18 (03) ◽  
pp. 171-174
Author(s):  
Federica Sullo ◽  
Milena Motta ◽  
Pierluigi Smilari ◽  
Luigi Rampello ◽  
Filippo Greco ◽  
...  
Keyword(s):  
Axonal Neuropathy ◽  
Male Infant ◽  
Guillain Barre Syndrome ◽  
Acute Motor Axonal Neuropathy ◽  
Fisher Syndrome ◽  
Acute Inflammatory Demyelinating Polyneuropathy ◽  
Guillain Barré Syndrome ◽  
Guillain Barré ◽  
Prior Infection ◽  
Prevalent Form

AbstractGuillain–Barré syndrome (GBS) is an acute inflammatory polyneuropathy characterized by rapidly progressive, essentially symmetric weakness and areflexia in a previously otherwise healthy child. It is the most common cause of acute flaccid paralysis in children, and its reported incidence is 1 to 2/100,000 population. Prior infection is a well-established predating event in GBS. The commonly recognized variants of GBS are acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor sensory axonal neuropathy, and Miller–Fisher syndrome. AIDP is the most prevalent form. As Guillain–Barrè syndrome represents an important differential diagnosis in infancy with pronounced and progressive hypotonia, we herein report a case of AMAN in a 5-month-old male infant without known exposure to immunomodulating factors or infections.

Did Jules Dejerine describe AMAN at the end of the 19th century?

Neurology ◽  
2017 ◽  
Vol 89 (16) ◽  
pp. 1749-1753 ◽  
Author(s):  
Stéphane Mathis ◽  
Laurent Magy ◽  
Gwendal Le Masson ◽  
Jean-Michel Vallat
Keyword(s):  
19Th Century ◽  
Axonal Degeneration ◽  
Axonal Neuropathy ◽  
Northern China ◽  
Acute Motor Axonal Neuropathy ◽  
Acute Inflammatory Demyelinating Polyneuropathy ◽  
Immune Mediated ◽  
Pathologic Lesions ◽  
Motor Nerves ◽  
The 19Th Century

Guillain-Barré syndrome (GBS) is a heterogeneous group of acute immune-mediated neuropathies, including acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). AMAN is an axonal subtype of GBS that has been known since the 1990s; this term was first used to describe a summer epidemic of acute ascending paralysis observed in children in northern China (and Mexico). It is pathologically characterized by noninflammatory axonal degeneration of the motor nerves (with little or no demyelination). The French neurologist Jules Dejerine (1849–1917) conducted a clinical and pathologic description of AMAN in the late 19th century. We describe his observations, which provide us with valuable information on the course of pathologic lesions in this disease.

scholarly journals Guillain Barre Syndrome: Major Cause of Acute Flaccid Paralysis in Children and Adolescents of Nepal

2011 ◽  
Vol 31 (2) ◽  
pp. 93-97 ◽  
Author(s):  
Krishna Sagar Sharma ◽  
Rupa Singh ◽  
Gauri Shankar Shah
Keyword(s):  
Acute Flaccid Paralysis ◽  
Axonal Neuropathy ◽  
Demyelinating Polyneuropathy ◽  
Flaccid Paralysis ◽  
Guillain Barre Syndrome ◽  
Supportive Treatment ◽  
Acute Motor Axonal Neuropathy ◽  
Ventilator Support ◽  
Acute Inflammatory Demyelinating Polyneuropathy ◽  
Inflammatory Demyelinating Polyneuropathy

Introduction. Guillain Barre Syndrome (GBS) is a post infectious polyneuropathy involving mainly motor but sometimes sensory and autonomic nerves. It is an acquired disease of the peripheral nerves that is characterized by rapidly progressing paralysis, areflexia and albumino-cytological dissociation in CSF. Methodology: Prospective, descriptive, observational, hospital based study was carried out to find out the clinico-epidemiological features of GBS including existing treatment modalities and its outcome. All cases fulfilled the criteria for AFP (Acute flaccid Paralysis) surveillance was included. Cases were reviewed for full medical history and examinations. To confirm the diagnosis, necessary investigations were carried out and combined with clinical symptoms. Results: Thirty patients were included in the study during study period. Among them 90% were diagnosed as GBS, 7.4% patients of GBS were associated with hypokalemic paralysis, 7.4% diagnosed as transverse myelitis and 3.7% diagnosed as idiopathic neuropathy. Different types of GBS were classified as AIDP (Acute inflammatory demyelinating polyneuropathy) 62.96%, AMAN (Acute motor axonal neuropathy) - 25.52%, AMASAN (Acute motor and sensory axonal neuropathy) - 3.3% and MFS (Miller fisher's syndrome) - 6.6% according to NCV result. Male female ratio is 1.7:1.0. There was 14.8% patients had relapse within 5 year. Associated diseases were URTI, pneumonia, sore throat and diarrhea. Facial Nerve palsy was commonest cranial nerve involvement.Sixty percentage of patients presented with sensory symptoms. There was transient bowel and bladder involvement in 20% of the cases. 69.2% patients became bed ridden at the nadir. There was albumin-cytological dissociation in 80% case. Majority of patients improved with supportive treatment alone, 19.5% patient required ventilator support among them 40% died. 7.4% of cases expired during treatment. Half of the patients fully recovered within 3 months. Conclusion: GBS is the commonest cause of AFP, AIDP being commonest subtype in our setting. We have to improve our existing treatment facilities and extend to different centers to detect and treat GBS. Most of the patients improve with supportive treatment alone. Ventilator support indicates grave prognosis. Key words: GBS (Gullein Barre Syndrome); AFP (Acute flaccid Paralysis); AIDP (Acute inflammatory demyelinating polyneuropathy; AMAN (Acute motor axonal neuropathy); AMASAN (Acute motor and sensory axonal neuropathy); MFS (Miller fisher's syndrome). DOI: 10.3126/jnps.v31i2.4065 J Nep Paedtr Soc 2010;31(2):93-97

Acute motor axonal neuropathy after Mycoplasma infection: Evidence of molecular mimicry

Neurology ◽  
2004 ◽  
Vol 62 (6) ◽  
pp. 949-956 ◽  
Author(s):  
K. Susuki ◽  
M. Odaka ◽  
M. Mori ◽  
K. Hirata ◽  
N. Yuki
Keyword(s):  
Molecular Mimicry ◽  
Axonal Neuropathy ◽  
Mycoplasma Infection ◽  
Acute Motor Axonal Neuropathy

Campylobacter jejuni lipopolysaccharides in Guillain-Barré syndrome

Neurology ◽  
1998 ◽  
Vol 51 (2) ◽  
pp. 371-378 ◽  
Author(s):  
K. A. Sheikh ◽  
I. Nachamkin ◽  
T. W. Ho ◽  
H. J. Willison ◽  
J. Veitch ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Normal Control ◽  
Axonal Neuropathy ◽  
Host Susceptibility ◽  
Guillain Barre Syndrome ◽  
Acute Motor Axonal Neuropathy ◽  
Acute Inflammatory Demyelinating Polyneuropathy ◽  
Guillain Barré Syndrome ◽  
Inflammatory Demyelinating Polyneuropathy ◽  
Guillain Barré

Objective: This study was designed to determine if the presence of specific ganglioside-like moieties in Campylobacter lipopolysaccharides(LPSs) is related to the development of Guillain-Barré syndrome (GBS), and to discover how frequently such moieties, including GM1, are present in these LPSs.Methods: We studied Campylobacter isolates and sera from seven patients with GBS (five acute motor axonal neuropathy, one acute inflammatory demyelinating polyneuropathy, and one Fisher's syndrome), and compared them with similar specimens from patients with Campylobacter enteritis alone.Results: All GBS patients had antiganglioside antibodies. Anti-GM1 and anti-GD1a titers were significantly elevated in post-Campylobacter GBS, both axonal and demyelinating, compared with normal control subjects or those with uncomplicated Campylobacter diarrhea. Campylobacter isolated from patients with GBS and with enteritis alone had similar ganglioside-like moieties.Conclusions: These results indicate that patients who develop GBS respond differently to the ganglioside-like epitopes on Campylobacter than do non-GBS diarrhea patients. Our findings support a role for host susceptibility as a determinant for the outcome following Campylobacter infection. These findings have important implications for the development of vaccines against Campylobacter jejuni.

scholarly journals A rare case of Acute Motor and Sensory Axonal Neuropathy (AMSAN) and Immune Thrombocytopenic Purpura (ITP) related to Hemophilus influenzae

2021 ◽  
Vol 2 (5) ◽  
Author(s):  
Vivek Satyasi ◽  
Aiesha Ahmed ◽  
Amtul Farheen
Keyword(s):  
Immune Thrombocytopenic Purpura ◽  
Rare Case ◽  
Molecular Mimicry ◽  
Case Reports ◽  
Axonal Neuropathy ◽  
Autoimmune Disorder ◽  
Severe Thrombocytopenia ◽  
Thrombocytopenic Purpura ◽  
Upper Respiratory Infection ◽  
Hemophilus Influenzae

We describe a rare case presenting with both signs of acute motor and sensory axonal neuropathy (AMSAN) and immune thrombocytopenic purpura (ITP) possibly triggered by Hemophilus influenzae. Guillain-Barre is an autoimmune disorder purported to be due to molecular mimicry, often with a preceding infection, leading to myelin sheath or even axonal damage, AMSAN, in the peripheral nervous system (PNS). Rarely, there have been case reports of concurrent acute autoimmune disorders leading to a more complex presentation and additional comorbidities. A 42-year-old man presented with 2 days of progressive lower and upper extremity paresthesia’s, ataxia preceded by an upper respiratory infection. Examination showed areflexia and purpura, recent oral mucosal hemorrhage. Lab results showed severe thrombocytopenia suspicious for ITP. Over the ensuing weeks while inpatient, his condition quickly deteriorated to requiring an intubation for respiratory failure and not immediately responsive to IVIG. Recovery, both for AMSAN confirmed by EMG and ITP, was eventually achieved with time and five treatments of plasmapheresis and eventually was discharged to a rehabilitation facility. A thorough infectious workup revealed a possible trigger being Haemophilus influenzae. There have been rare occasions of concurrent GBS and ITP, but even more rare is the presence of both AMSAN and ITP which requires quick recognition and evaluation. This case highlights the need for a thorough initial history taking and a general physical exam, in addition to unique management decisions and strategies in patients with suspected GBS as there may be signs of other associated disorders that require immediate attention.

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