Serologic Evidence of Previous Campylobacter jejuni Infection in Patients with the Guillain-Barre Syndrome (original) (raw)
Guillain-Barre syndrome and Campylobacter jejuni: a serological study
BMJ, 1984
The association between Campylobacter jejuni infection and Guillain-Barr6 syndrome was investigated serologically in a retrospective study of 56 patients admitted to this hospital over four years. Evidence of preceding C jejuni infection was found in 21 (38%) of these patients, indicating that C jejuni was the most common single identifiable pathogen precipitating the disease. Among those patients who had presented with preceding diarrhoea the serum antibody response was similar to that in uncomplicated C jejuni enteritis. Patients with serological evidence of preceding C jejuni infection manifested a significantly more severe form of the disease. In cerebrospinal fluid the predominant specific antibody class was IgG, and this was closely related to the serum titres of specific IgG. IgA and IgM specific antibodies were found only in the cerebrospinal fluid of patients with recent C jejuni infection. These findings support the possibility that humoral immune factors are responsible for the neural damage and demyelination seen in Guillain-Barre syndrome.
Neurology India, 2011
Background: Guillain-Barré syndrome (GBS), is a common post-infectious polyradiculoneuropathy worldwide. The commonest implicated causative organism the world over is Campylobacter jejuni (C. jejuni). This study was carried out to determine the relationship between C. jejuni infection and GBS in an Indian setting. Materials and Methods: This prospective study was carried out on a cohort of 50 patients with GBS who were treated in a tertiary care hospital in India. Based on electrophysiological findings the patients were divided into various subtypes. Serology for C. jejuni (Immunoglogulin G, IgG and Immunoglogulin, IgM) using an enzyme-linked immunosorbent assay method (ELISA) was done both in patients and 40 age, sex and geographically matched controls. Results: Evidence of recent C. jejuni infection was present in 30% of GBS patients compared to 8% of controls (15/50 vs. 3/40 P<0.005). Eight (47%) C. jejuni-positive patients reported symptoms of gastroenteritis 4-30 days (mean 13 days) prior to onset of GBS. Of the 15 patients with evidence of C. jejuni infection, 10 (67%) patients had axonal type of GBS. Axonal variety of GBS presented in a younger age group compared to acute inflammatory demyelinating polyradiculoneuropathy (AIDP) patients (mean age: axonal vs. AIDP: 30.11 + 13.73 vs. 40.2 + 18.77). C. jejuni-positive patients presented mainly in spring and winter and had a similar age and sex incidence as compared to the rest of the GBS patients. Conclusions: Preceding C. jejuni infection is common among GBS patients and is often associated with the axonal variety of GBS. Axonal variety of GBS generally presents in a younger age group as compared to AIDP.
Clinical and Vaccine Immunology, 2006
Guillain-Barré syndrome (GBS) is a postinfectious autoimmune polyradiculoneuropathy. The most frequent antecedent pathogen is Campylobacter jejuni, followed by cytomegalovirus. However, more than 40% of GBS cases currently cannot be attributed to triggering events. This might be due to the shortcomings of the serological assays used for diagnosing infections, in particular for C. jejuni. In our study investigating 36 patients with acute GBS, standard serological methods identified the triggering viral or bacterial etiology in only 25% of cases. However, using a highly specific enzyme-linked immunosorbent assay based on two recombinant outer antigens encoded by C. jejuni genes Cj0017 (P39) and Cj0113 (P18), we found serological evidence of a preceding C. jejuni infection in 80.6% of the patients but in only 3.5% of the controls. We conclude that the role of C. jejuni in triggering GBS has been greatly underestimated.
The risk of Guillain–Barré syndrome following infection with Campylobacter jejuni
Epidemiology and Infection, 1999
To estimate the incidence of Guillain-Barré syndrome (GBS) following Campylobacter jejuni infection (CI) we studied three populations where outbreaks of CI had occurred involving an estimated 8000 cases. No case of GBS was detected in the 6 months following the outbreaks in the local populations. The point estimate for the risk of GBS following CI estimated in this study was 0 in 8000 (95% confidence interval 0–3).
Guillain-Barré Syndrome and Campylobacter jejuni Infection: A Review
Delta Medical College Journal, 2014
Guillain-Barre´ syndrome (GBS), a neurologic disease that produces ascending paralysis, affects people all over the world. Acute infectious illness precedes 50%-75% of the GBS cases. Although many infectious agents have been associated with GBS, the strongest documented association is with Campylobacter infection. The first line of evidence supporting Campylobacter infection as a trigger of GBS is anecdotal reports. The second line of evidence is serological surveys, which have demonstrated that sera from GBS patients contain anti Campylobacter jejuni antibodies, consistent with recent infection. Finally, culture studies have proven that a high proportion of GBS patients have C. jejuni in their stools at the time of onset of neurological symptoms. One of every 1058 Campylobacter infections results in GBS. Sialic acid containing lipooligosaccharides (LOS) biosynthesis gene locus are associated with GBS and the expression of ganglioside mimicking structures. GM 1a was the most prevalent ganglioside mimic in GBS associated strains. Molecular mimicry between C. jejuni LOS and gangliosides in human peripheral nerves, and cross-reactive serum antibody precipitate the majority of GBS cases in Bangladesh, like worldwide.
Guillain‐Barre Syndrome Associated with Campylobacter jejuni Infection in England, 2000–2001
Clinical Infectious Diseases, 2003
To date, estimates of the burden of C. jejuniassociated GBS have been based on limited data regarding the proportion of GBS attributable to this pathogen. In this paper, we combine data obtained from Sweden and a large study of infectious intestinal disease with routine and surveillance data from England to estimate the number and proportion of GBS cases attributable to C. jejuni. We estimate that, between 1 April 2000 and 31 March 2001, symptomatic C. jejuni infection was responsible for 157 cases of GBS, constituting approximately 15% of all GBS cases in England.
Campylobacter infections and Guillain Barré syndrome
Journal of Gastrointestinal Infections
Guillain Barré syndrome (GBS) is a serious disorder of the peripheral nerves preceded by a recognized acute infectious illness. Campylobacter jejuni has been recognized as an important pathogen precipitating GBS and the structure of C. jejuni lipooligosaccharide (LOS) might have a role in the outcome of infection. The development of GBS and Miller Fisher syndrome has been reported to be due to expression of a GM1 like LOS in class A strains and GQ1b like LOS in class B strains of C. jejuni respectively. Virulence of C. jejuni, subtle differences in the interaction between different strains with the host T lymphocyte receptor and MHC class II and host susceptibility may have a role to play in the development of GBS. A humoral immunopathogenic mechanism for GBS has been envisaged as the disease develops 1 to 3 weeks after C. jejuni infection. Antibodies to C. jejuni may remain elevated for several weeks after acute infection. Host susceptibility factors are also important in the pathogenesis of GBS as this disease occurs within families. Association between the occurrence of GBS and a particular HLA type has been envisaged, but studies to prove it are inconclusive. Despite our increasing understanding of the pathophysiology of GBS, the triggering event leading to the disease is still indeed a great puzzle. This review describes the in-depth association of Campylobacter infections with GBS.
Guillain-Barre syndrome subtypes related to Campylobacter infection
Journal of Neurology, Neurosurgery & Psychiatry, 2011
Background: In Guillain-Barré syndrome (GBS) the diversity in electrophysiological subtypes is unexplained, but may be determined by geographical factors and preceding infections. Acute motor axonal neuropathy (AMAN) is a frequent GBS variant in Japan and one study proposed that in Japan Campylobacter jejuni infections exclusively elicit AMAN. In the Netherlands C. jejuni is the predominant type of preceding infection, yet AMAN is rare. This may indicate that not all Dutch GBS patients with C. jejuni infections have AMAN. Objective: To determine if GBS patients with a preceding C. jejuni infection in the Netherlands exclusively have AMAN. Methods: Retrospective analysis of preceding infections in relation to serial electrophysiology and clinical data from 123 GBS patients. C. jejuni-related cases were defined as having preceding diarrhea and positive C. jejuni serology. Electrophysiological characteristics in C. jejuni-related cases were compared with those in viral-related GBS patients. In addition, eight GBS patients from another cohort with positive stool cultures for C. jejuni were analysed. Results: Seventeen (14%) of 123 patients had C. jejuni-related GBS. C. jejuni patients had lower motor and higher sensory action potentials compared to viral-related cases. Nine (53%) C. jejuni patients had either AMAN or inexcitable nerves. However, three (18%) patients fulfilled the criteria for acute inflammatory demyelinating polyneuropathy (AIDP). Also, two (25%) of eight additional patients with a C. jejuni-positive stool sample had AIDP. Conclusion: In the Netherlands C. jejuni infections are strongly, but not exclusively associated with axonal GBS. Some patients with these infections fulfil current criteria for demyelination.
Clinical Microbiology and Infection, 2003
We present a case of Guillain-Barré syndrome (GBS) following Campylobacter jejuni HS serotype O:19 infection in a child. Antibodies against C. jejuni and autoantibodies to the peripheral nerve gangliosides GM1 were positive, a pattern correlating well with the existence of an inflammatory neuropathy like GBS. The patient shared the HLA-B35 and HLA-DR8 antigens, which have been found to be increased in GBS patients with previous C. jejuni infection. As this is the first diagnosed C. jejuni-associated GBS case reported from Greece, further clinical and epidemiologic investigations are warranted.
Guillain-Barré Syndrome Induced by Campylobacter jejuni
British Microbiology Research Journal, 2015
Purpose of Review: Guillain-Barré syndrome (GBS) is a neurologic disease that produces ascending paralysis that affects people all over the world. Several infectious agents have been associated with GBS and many reports suggest that infection with Campylobacter jejuni, a common enteric pathogen, may cause GBS by triggering demyelination of peripheral nerves. This review provides an update on the C. jejuni infections engaged in the developing of GBS. Summary and Results: Guillain-Barré syndrome is the most common cause of acute neuromuscular paralysis, yet its cause and pathogenesis are unknown. In approximately two thirds of patients, neuropathic symptoms follow an infection-often a mild, undiagnosed respiratory or gastrointestinal illness. The organism that has most frequently been described in association with GBS is C. jejuni, a gram-negative rod that is now the most common cause of bacterial gastroenteritis in developed countries. Although there has been a plethora of case reports and studies documenting the association, the specific clinical and epidemiologic features are not well Review Article Honarmand and Moghadam; BMRJ, 6(2): 71-83, 2015; Article no.BMRJ.2015.060 72 known. In addition, there is controversy about whether those with preceding C. jejuni infection have a more severe form of the GBS. C. jejuni can cause the disease by a mechanism called molecular mimicry. C. jejuni contains ganglioside-like epitopes in the lipopolysaccharide (LPS) moiety that elicit autoantibodies which can react with peripheral nerve targets. It seems that heterogeneity in the LPS structure determines the specificity of the antiglycolipid response and thereby the clinical features in patients with a post-campylobacter infection neuropathy.
Guillain-Barre syndrome and Campylobacter infection
PubMed, 2001
Campylobacter infection of the gastrointestinal tract has been observed as an antecedent illness in some patients with Guillain-Barre syndrome (GBS); these patients have been reported to have poor prognosis. We investigated 29 patients with GBS, admitted to our hospital from January 1996 to December 1999 for recent Campylobacter enteritis by culture of their stool specimens. Campylobacter upsaliensis and C. jejuni were isolated from stools of one patient each with acute motor axonal neuropathy (AMAN) and acute inflammatory demyelinating polyradiculoneuropathy (AIDP) respectively. The patient with C. upsaliensis infection was a 7 year-old male child who developed features of AMAN, 7 days after onset of diarrhea. He recovered gradually within 24 days with residual deficit in the form of foot drop. This deficit has persisted for last three and half years. The other patient with C. jejuni infection was a 9 year-old boy, who developed AIDP after 9 days of acute diarrhea. This patient recovered completely within 28 days of illness without any deficit. None of the patients had relapse of GBS. The present findings indicate the need of planned systematic studies to explore the role of C. upsaliensis and other campylobacters as agents of antecedent diarrhea in patients of GBS with different clinical presentations and prognosis.
Does Campylobacter jejuni infection elicit "demyelinating" Guillain-Barre syndrome?
Neurology, 2004
Background: Campylobacter jejuni enteritis is the most common antecedent infection in Guillain-Barré syndrome (GBS). C. jejuni-related GBS is usually acute motor axonal neuropathy (AMAN), but previous reports described many cases of the demyelinating subtype of GBS (acute inflammatory demyelinating polyneuropathy [AIDP]) after C. jejuni infection. Objective: To investigate whether C. jejuni infection elicits AIDP. Methods: In 159 consecutive patients with GBS, antibodies against C. jejuni were measured using ELISA. Antecedent C. jejuni infection was determined by the strict criteria of positive C. jejuni serology and a history of a diarrheal illness within the previous 3 weeks. Electrodiagnostic studies were performed weekly for the first 4 weeks, and sequential findings were analyzed. Results: There was evidence of recent C. jejuni infection in 22 (14%) patients. By electrodiagnostic criteria, these patients were classified with AMAN (n ϭ 16; 73%) or AIDP (n ϭ 5; 23%) or as unclassified (n ϭ 1) in the first studies. The five C. jejuni-positive patients with the AIDP pattern showed prolonged motor distal latencies in two or more nerves and had their rapid normalization within 2 weeks, eventually all showing the AMAN pattern. In contrast, patients with cytomegalovirus-or Epstein-Barr virus-related AIDP (n ϭ 13) showed progressive increases in distal latencies in the 8 weeks after onset. Conclusion: Patients with C. jejuni-related Guillain-Barré syndrome can show transient slowing of nerve conduction, mimicking demyelination, but C. jejuni infection does not appear to elicit acute inflammatory demyelinating polyneuropathy.
The American journal of tropical medicine and hygiene, 2018
In countries where poliomyelitis has been eradicated, Guillain-Barré syndrome (GBS) is the leading cause of acute flaccid paralysis. The range of infections that precede GBS in Brazil is unknown. Campylobacter jejuni infection is the most frequent trigger of GBS worldwide. Given the lack of systematic surveillance of diarrheal diseases, particularly in adults, the incidence of enteritis caused by C. jejuni in developing countries is unknown. From 2014 to 2016, pretreatment serum samples from 63 GBS patients were tested by immunoglobulin M (IgM) enzyme-linked immunosorbent assay for C. jejuni. Campylobacter jejuni IgM antibodies were detected in 17% (11/63) of the samples. There was no association between serological positivity (IgM) for C. jejuni and the occurrence of diarrhea among the investigated cases (P = 0.36). Hygiene measures, basic sanitation, and precautions during handling and preparation of food of animal origin may help prevent acute flaccid paralysis.
The Turkish journal of pediatrics
Recent studies have suggested that Campylobacter jejuni is a common pathogen causing Guillain-Barré syndrome (GBS). This study aimed to determine the frequency and clinical and electrophysiological features of C. jejuni infection in children with GBS. We carried out a prospective study on a cohort of 48 children with GBS admitted to Tabriz Children's Hospital in the northwest of Iran from January 2003 to March 2005. Serologic investigations were used to diagnose preceding C. jejuni infection. Evidence of a recent C. jejuni infection was found in 23 (47.9%) of the patients. C. jejuni-associated GBS patients were younger than others (p = 0.010), and they had a rapid progression to reach peak disability (p = 0.018). Neither the peak disability nor the residual one-year disability was different between the C. jejuni- positive and C. jejuni-negative patients. The patients with preceding C. jejuni infection were more likely to have axonal neuropathy (p = 0.021).
Journal of Infectious Diseases, 2006
The association between Campylobacter infection and subsequent Guillain-Barré syndrome (GBS) has been well documented. To date, however, there exists no direct estimate of the incidence of GBS among patients with Campylobacter infection. Using the General Practice Research Database, we estimate the incidence of GBS in a cohort of patients presenting with Campylobacter enteritis to be 1.17/1000 personyears, a rate 77 times greater than that in the general population. The probability that an individual who develops Campylobacter enteritis will also develop GBS during the subsequent 2-month period is !2/10,000.
Axonal variant of Guillain-Barre syndrome associated with Campylobacter infection in Bangladesh
Neurology, 2010
Background: Campylobacter jejuni enteritis is the predominant bacterial infection preceding Guillain-Barré syndrome (GBS), an acute postinfectious immune-mediated polyradiculoneuropathy. The purpose of this study was to define the clinical phenotype of GBS and the relation with preceding C jejuni infections in Bangladesh. Methods: We performed a prospective matched case-control hospital surveillance including 100 patients fulfilling the National Institute of Neurological Disorders and Stroke criteria for GBS from 2006 to 2007 in the Dhaka area of Bangladesh. Detailed clinical, electrophysiologic, serologic, and microbiologic data were obtained with a follow-up of 6 months. Results: GBS affected predominantly young adult males living in rural areas. Sixty-nine percent of the patients had clinical evidence of a preceding infection. The most frequent symptom was diarrhea (36%). The majority of patients had a pure motor variant of GBS (92%) with relatively infrequent cranial nerve involvement (30%). Twenty-five percent of patients required respiratory support. Electrophysiologic studies showed that 67% of patients had an axonal variant of GBS. Eleven patients (14%) died, and 23 (29%) remained severely disabled during the follow-up. Positive C jejuni serology was found in an unprecedented high frequency of 57% as compared with 8% in family controls and 3% in control patients with other neurologic diseases (p Ͻ 0.001). C jejuni infection was significantly associated with serum antibodies to the gangliosides GM1 and GD1a, axonal neuropathy, and greater disability. Conclusions: We report an unusually high frequency of the axonal variant of Guillain-Barré syndrome in Bangladesh, associated with preceding Campylobacter jejuni infection, severe residual disability, and high mortality. Neurology ® 2010;74:581-587 GLOSSARY AFP ϭ acute flaccid paralysis; AIDP ϭ acute inflammatory demyelinating polyneuropathy; AMAN ϭ acute motor axonal neuropathy; AMSAN ϭ acute motor sensory axonal neuropathy; BSMMU ϭ Bangabandhu Sheikh Mujib Medical University; DCH ϭ Dhaka Central Hospital; DMCH ϭ Dhaka Medical College Hospital; FC ϭ family control; GBS ϭ Guillain-Barré syndrome; Ig ϭ immunoglobulin; IVIg ϭ IV immunoglobulin; MRC ϭ Medical Research Council; OND ϭ other neurologic diseases. Guillain-Barré syndrome (GBS) is an acute polyradiculoneuropathy and worldwide the most frequent cause of acute flaccid paralysis (AFP), with an incidence of 1.2 to 2.3 per 100,000 persons per year. 1 The pathologic spectrum of GBS includes acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN). 1 GBS is a postinfectious disease, and approximately two-thirds of patients report symptoms suggestive for a preceding infectious illnesses. GBS consists of various phenotypes that are associated with specific types of preceding infection. Campylobacter jejuni has been identified as the predominant type of antecedent infections. 2-9 C jejuni infections are associated with a severe, 10,11 pure motor, 12,13 axonal variant of GBS 14 and with poor From the
Campylobacter Species and Guillain-Barré Syndrome
Clinical Microbiology Reviews, 1998
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 w...
Campylobacter 0:41 isolation in Guillain-Barre syndrome
Archives of Disease in Childhood, 1997
Over a period of 15 months, 17 children were admitted to the Red Cross War Memorial Children's Hospital (RCW-MCH) in Cape Town with Guillain-Barré syndrome. Stool specimens were collected from 14 children and campylobacter was isolated from nine. Six of the nine isolates of Campylobacter jejuni were further identified as C jejuni biotype 2, serotype 0:41. This biotype 2, serotype 0:41 has been identified in only 12 of the 7119 campylobacter isolates at the RCWMCH over a 19 year period. Eight of the nine patients with campylobacter isolates and one of five with negative stool cultures required ventilation. Patients with C jejuni biotype 2, serotype 0:41 were ventilated for a mean (SD) of 33.5 (19.4) days, whereas patients with other campylobacter isolates were ventilated for 17.3 (3.8) days. This is the first report of campylobacters of serotype 0:41 in Guillain-Barré syndrome and could reflect a geographical isolation of this strain. (Arch Dis Child 1997;76:526-528)
Guillain‐Barré Syndrome in South Africa Associated with Campylobacter jejuni O:41 Strains
The Journal of Infectious Diseases, 1997
Over a 20-month period, 3 adult and 6 pediatric patients were diagnosed with Guillain-Barré syndrome (GBS) at Groote Schuur and Red Cross Hospitals in Cape Town. All 9 GBS patients had Campylobacter jejuni biotype 2, serotype O:41 in their stools. C. jejuni infection was confirmed by ELISA testing of patient sera. Strains of this sero-biotype are rare: Only 12 such strains, including the GBS-associated strains, were recognized among 776 Campylobacter strains isolated and identified at Red Cross Hospital from March 1994 to October 1995. This is the first known association of C. jejuni biotype 2, serotype O:41 with GBS. Patients infected with this Campylobacter strain had a particularly severe form of the infection, requiring hospitalization and ventilation much longer than GBS patients infected with other Campylobacter species and patients with Campylobacter-negative stools. The O:41 Campylobacter isolates from the GBS patients are identical by phenotypic, serologic, and molecular criteria, and they are clonal. under microaerophilic growth conditions (12% CO 2 , 88% air, 95% Guillain-Barré syndrome (GBS) has been associated with a humidity). variety of preceding infections. However, enteric infections Biotyping and serotyping. Bacteria were identified by use of with Campylobacter appear to be the most common antecedent established procedures, and isolates were biotyped according to event, with evidence of infection rates up to 42% in adults [1] the scheme of Skirrow and Benjamin [4]. Serotyping on the basis and up to 88% in children [2]. We sought to determine the of thermostable somatic (O) antigens was done using the 66 antifrequency of Campylobacter infections among GBS patients sera of Penner's scheme [5] plus an additional 30 antisera to new in Cape Town and to characterize the Campylobacter isolates serotypes not included in Penner's scheme. with regard to biotype and serotype.