Haemophilus Influenzae Associated Guillain Barre Syndrome with Thrombocytopenic Purpura and Hyperthermia

Condon, Elizabeth; Tobin, Antony

doi:10.1177/0310057x0803600516

Cited by 3 publications

(2 citation statements)

References 17 publications

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“…Infection by Mycoplasma pneumoniae is also considered a potential cause for the development of GBS. In rare cases of GBS, infective endocarditis, rubella virus infection, Haemophlus influenzae, and Legionnella infection may be associated (Akyildiz et al 2008;Baravelli et al 2008;Condon and Tobin 2008;Figueiredo et al 2008). Vaccinations, including flu vaccine, immunization against group A streptococcus, rabies, and swine flu, may also trigger GBS (Ropper et al 1991;Yuki and Hirata 1998;Nachamkin et al 2008;Sivadon-Tardy et al 2009).…”

Section: Other Risk Factors In the Pathogenesis Of Gbsmentioning

confidence: 99%

Antiganglioside antibodies and their pathophysiological effects on Guillain-Barre syndrome and related disorders--A review

2009

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Guillain-Barré syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy which can cause acute quadriplegia. Infection with micro-organisms, including Campylobacter jejuni (C. jejuni), Haemophilus influenzae, and Cytomegalovirus (CMV), is recognized as a main triggering event for the disease. Lipooligosaccharide (LOS) genes are responsible for the formation of human ganglioside-like LOS structures in infectious micro-organisms that can induce GBS. Molecular mimicry of LOSs on the surface of infectious agents and of ganglioside antigens on neural cells is thought to induce cross-reactive humoral and cellular immune responses. Patients with GBS develop antibodies against those gangliosides, resulting in autoimmune targeting of peripheral nerve sites, leading to neural damage. Heterogeneity of ganglioside expression in the peripheral nervous system (PNS) may underlie the differential clinical manifestation of the GBS variants. Recent studies demonstrate that some GBS sera react with ganglioside complexes consisting of two different gangliosides, such as GD1a and GD1b, or GM1 and GD1a, but not with each constituent ganglioside alone. The discovery of antiganglioside complex antibodies not only improves the detection rate of autoantibodies in GBS, but also provides a new concept in the antibody-antigen interaction through clustered carbohydrate epitopes. Although ganglioside mimicry is one of the possible etiological causes of GBS, unidentified factors may also contribute to the pathogenesis of GBS. While GBS is not considered a genetic disease, host factors, particularly human lymphocyte antigen type, appear to have a role in the pathogenesis of GBS following C. jejuni infection.

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Section: Other Risk Factors In the Pathogenesis Of Gbsmentioning

confidence: 99%

Antiganglioside antibodies and their pathophysiological effects on Guillain-Barre syndrome and related disorders--A review

2009

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“…In our patient, Haemophilus influenzae was detected. There have been cases of both GBS and ITP associated with this bacteria, as well as a case reported with both GBS and ITP 5 . Mori et al investigated the link between H. influenzae and GBS and suspected that recovery was actually improved if GBS was associated with antecedent respiratory infection with this bacterium, and that EMG in these cases actually showed increased rate of axonal variants 6 , such as was observed in our case.…”

Section: Discussionmentioning

confidence: 93%

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

Satyasi¹,

Ahmed²,

Farheen

2021

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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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Triggers of Guillain–Barré Syndrome: Campylobacter jejuni Predominates

Finsterer¹

2022

IJMS

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Guillain–Barré syndrome (GBS) is a rare immune-mediated acute polyradiculo-neuropathy that typically develops after a previous gastrointestinal or respiratory infection. This narrative overview aims to summarise and discuss current knowledge and previous evidence regarding triggers and pathophysiology of GBS. A systematic search of the literature was carried out using suitable search terms. The most common subtypes of GBS are acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). The most common triggers of GBS, in three quarters of cases, are previous infections. The most common infectious agents that cause GBS include Campylobacter jejuni (C. jejuni), Mycoplasma pneumoniae, and cytomegalovirus. C. jejuni is responsible for about a third of GBS cases. GBS due to C. jejuni is usually more severe than that due to other causes. Clinical presentation of GBS is highly dependent on the structure of pathogenic lipo-oligosaccharides (LOS) that trigger the innate immune system via Toll-like-receptor (TLR)-4 signalling. AIDP is due to demyelination, whereas in AMAN, structures of the axolemma are affected in the nodal or inter-nodal space. In conclusion, GBS is a neuro-immunological disorder caused by autoantibodies against components of the myelin sheath or axolemma. Molecular mimicry between surface structures of pathogens and components of myelin or the axon is one scenario that may explain the pathophysiology of GBS.

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Haemophilus Influenzae Associated Guillain Barre Syndrome with Thrombocytopenic Purpura and Hyperthermia

Cited by 3 publications

References 17 publications

Antiganglioside antibodies and their pathophysiological effects on Guillain-Barre syndrome and related disorders--A review

Antiganglioside antibodies and their pathophysiological effects on Guillain-Barre syndrome and related disorders--A review

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

Triggers of Guillain–Barré Syndrome: Campylobacter jejuni Predominates

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