Campylobacter 0:41 isolation in Guillain-Barre syndrome (original) (raw)
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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.
Journal of clinical microbiology, 2000
Campylobacter jejuni O:41 strains are found in association with Guillain-Barré syndrome in South Africa. Strains of this serotype collected over 17 years were characterized by amplified fragment length polymorphism and flagellin typing to determine their clonal nature. Despite minor variation in GM1 expression, all of the strains were genetically indistinguishable, indicating that they are representative of a genetically stable clone.
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.
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...
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.
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).
The Journal of Infectious Diseases, 2001
Penner serotypes, such as HS:19, are linked particularly to GBS in some parts of the world, and there is good evidence for restricted genetic diversity in these isolates. However, GBS also occurs after Campylobacter infection due to other serotypes. Therefore, we asked whether Campylobacter jejuni non-HS:19 serotypes associated with GBS have a clonal structure and differ from strains isolated from patients with Campylobacter gastroenteritis. A worldwide selected population of C. jejuni non-HS:19 strains associated with GBS and gastroenteritis was analyzed by use of multilocus enzyme electrophoresis, automated ribotyping, pulsed-field gel electrophoresis, and flagellin gene typing. The results show that these isolates represent a heterogenic population and do not constitute a unique population across serotypes. No epidemiologic marker for GBS-associated strains was identified.
The Journal of Infectious Diseases, 1997
On the basis of the work presented and discussed at the • Serologic assays for diagnosis of C. jejuni infections need to be standardized and validated. workshop, a number of key points can be summarized, and from these, a series of recommendations can be made. These • All patients with acute flaccid paralysis should have their stools cultured for Campylobacter, and all isolated strains points are divided into the following categories: diagnostic aspects, epidemiology and surveillance, microbiology and should be serotyped. • Antibiotic resistance among Campylobacter species needs pathogenesis studies, and information management. to be monitored worldwide. Diagnostic Aspects Epidemiology and Surveillance Although there is substantial immunologic evidence linking the development of Guillain-Barré syndrome (GBS) with a The medical costs associated with Campylobacter-induced preceding infection with Campylobacter jejuni, microbiologic GBS have been estimated by the US Department of Agriculture evidence is less complete. This is likely due to the brief period to be 57−57-57−420 million per year in the United States. Total of excretion of C. jejuni in stools (median, 16 days) after an costs, which include days of lost productivity, are estimated to acute infection. Symptoms of GBS typically occur 10 days to be between 247millionand247 million and 247millionand1.8 billion per year. Clearly, 3 weeks after C. jejuni infection, when many patients have Campylobacter-induced GBS is a disease with a significant already cleared their stools. As such, studies of C. jejuni seroeconomic impact in this country. types associated with GBS are limited to a small number of Although GBS can probably result following a number of strains. If diarrheal cases were more frequently screened for bacterial and viral infections, infection with C. jejuni is the C. jejuni, and if more and better typing reagents were available, most often recognized preceding event. However, the epidemithe epidemiologic link between preceding infection with particology of infection with the campylobacters associated with ular strains and the development of GBS would become better GBS is not well understood. In particular, the specific reservoirs established. In addition, antibiotic resistance is emerging for GBS-related strains have not been identified. Although there among Campylobacter species in both developing and develis a marked seasonal pattern of C. jejuni infection (summer) oped countries. This could lead to difficulties in the treatment of in some countries, there is no clear seasonal variation in the human disease, and resistance enhances the need for protective incidence of GBS. An exception has been observed in northern vaccination of animals raised for food or of humans (or both). China, where outbreaks of GBS occur among children every The following recommendations can be made: summer and fall. • Diagnostic tests sensitive for detection of a variety of With the inclusion of C. jejuni and Campylobacter coli in the Campylobacter species are needed. It is likely that a large Centers for Disease Control and Prevention's (CDC) FoodNet number of Campylobacter infections go unrecognized. surveillance efforts, an opportunity exists to delineate the con-• Standardized microbiologic laboratory procedures are nection between prior infection with Campylobacter species needed to insure isolation of Campylobacter strains assoand the development of GBS. It is important that strains isolated ciated with GBS. In particular, C. jejuni and Campyloas a result of such surveillance efforts be archived, and that an bacter upsaliensis should be looked for, but other species analysis of the bacterial antigens related to GBS be conducted. also may play a role. The concept of viable but noncultura-The following recommendations are made: ble Campylobacter should be examined. • GBS (or more broadly defined acute flaccid paralysis cases) should be reportable by state health departments to the CDC (current estimates of the number of US GBS cases are 1 to 2/100,000 population per year).
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.
Journal of Clinical Microbiology, 2001
Guillain-Barré syndrome (GBS) and Miller-Fisher syndrome (MFS) are correlated with prior infection by Campylobacter jejuni in up to 40% of cases. Nucleotide sequence-based typing of 25 C. jejuni isolates associated with neuropathy permitted robust comparisons with equivalent data from approximately 800 C. jejuni isolates not associated with neuropathy. A total of 13 genetic lineages and 20 flaA short variable region nucleotide sequences were present among the 25 isolates. A minority of isolates (4 of 25) had the flaA short variable region nucleotide sequences that were previously proposed as a marker for GBS-associated isolates. These 4 isolates probably represented the Penner serotype 19 lineage, which has been proposed to have an association with GBS.