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R A C Hughes - One of the best experts on this subject based on the ideXlab platform.

  • Campylobacter Jejuni infection and guillain barre syndrome
    The New England Journal of Medicine, 1995
    Co-Authors: J H Rees, Sara Soudain, N A Gregson, R A C Hughes
    Abstract:

    Background Although infection with Campylobacter Jejuni is recognized as a common antecedent of the Guillain–Barre syndrome, the clinical and epidemiologic features of this association are not well understood. Methods We performed a prospective case–control study in a cohort of patients with Guillain–Barre syndrome (96 patients) or Miller Fisher syndrome (7 patients) who were admitted to hospitals throughout England and Wales between November 1992 and April 1994. Bacteriologic and serologic techniques were used to diagnose preceding C. Jejuni infection. Results There was evidence of recent C. Jejuni infection in 26 percent of the patients with Guillain–Barre or Miller Fisher syndrome, as compared with 2 percent of household controls and 1 percent of age-matched hospital controls (P<0.001). Of the 27 patients with C. Jejuni infection, 19 (70 percent) reported having had a diarrheal illness within 12 weeks before the onset of the neurologic illness. No specific serotypes were associated with Guillain–Barre ...

  • hla class ii alleles in guillain barre syndrome and miller fisher syndrome and their association with preceding Campylobacter Jejuni infection
    Journal of Neuroimmunology, 1995
    Co-Authors: J H Rees, Robert Vaughan, E Kondeatis, R A C Hughes
    Abstract:

    HLA typing for class II alleles was performed on 97 patients with Guillain-Barre syndrome or Miller Fisher syndrome and compared with 100 controls. There was a significant association between HLA-DQB1*03 and preceding Campylobacter Jejuni infection (Pc = 0.05).

J H Rees - One of the best experts on this subject based on the ideXlab platform.

  • Campylobacter Jejuni infection and guillain barre syndrome
    The New England Journal of Medicine, 1995
    Co-Authors: J H Rees, Sara Soudain, N A Gregson, R A C Hughes
    Abstract:

    Background Although infection with Campylobacter Jejuni is recognized as a common antecedent of the Guillain–Barre syndrome, the clinical and epidemiologic features of this association are not well understood. Methods We performed a prospective case–control study in a cohort of patients with Guillain–Barre syndrome (96 patients) or Miller Fisher syndrome (7 patients) who were admitted to hospitals throughout England and Wales between November 1992 and April 1994. Bacteriologic and serologic techniques were used to diagnose preceding C. Jejuni infection. Results There was evidence of recent C. Jejuni infection in 26 percent of the patients with Guillain–Barre or Miller Fisher syndrome, as compared with 2 percent of household controls and 1 percent of age-matched hospital controls (P<0.001). Of the 27 patients with C. Jejuni infection, 19 (70 percent) reported having had a diarrheal illness within 12 weeks before the onset of the neurologic illness. No specific serotypes were associated with Guillain–Barre ...

  • hla class ii alleles in guillain barre syndrome and miller fisher syndrome and their association with preceding Campylobacter Jejuni infection
    Journal of Neuroimmunology, 1995
    Co-Authors: J H Rees, Robert Vaughan, E Kondeatis, R A C Hughes
    Abstract:

    HLA typing for class II alleles was performed on 97 patients with Guillain-Barre syndrome or Miller Fisher syndrome and compared with 100 controls. There was a significant association between HLA-DQB1*03 and preceding Campylobacter Jejuni infection (Pc = 0.05).

Nobuhiro Yuki - One of the best experts on this subject based on the ideXlab platform.

  • guillain barre syndrome and Campylobacter Jejuni enteritis
    2016
    Co-Authors: Nortina Shahrizaila, Nobuhiro Yuki
    Abstract:

    Guillain–Barre syndrome is an immune-mediated neuropathy that accounts for one of the most common acute neuromuscular paralysis worldwide. Characteristic to its history is an antecedent illness and this includes Campylobacter Jejuni enteritis. The pathogenesis of C. Jejuni-related Guillain–Barre syndrome has been extensively studied, and there is good evidence to support molecular mimicry between self and microbial components as the mechanism of disease. Self-antigens in the form of gangliosides which are predominantly cell-surface glycolipids highly expressed in nervous tissue share similar characteristics as lipo-oligosaccharides of C. Jejuni outer membrane. Molecular mimicry has been demonstrated between GM1 ganglioside and lipo-oligosaccharide of C. Jejuni isolated from Guillain–Barre syndrome patients. This includes the establishment of disease models by sensitisation of rabbits with GM1 and C. Jejuni lipo-oligosaccharide. This chapter discusses the current understanding of Guillain–Barre syndrome following C. Jejuni enteritis.

  • bickerstaff s brainstem encephalitis after an outbreak of Campylobacter Jejuni enteritis
    Journal of Neuroimmunology, 2008
    Co-Authors: Masahiro Mori, Michiaki Koga, Takamichi Hattori, Nobuhiro Yuki, Satoshi Kuwabara
    Abstract:

    Twenty-eight patients suffered Campylobacter Jejuni enteritis after eating raw chicken. Among them, only one patient developed Bickerstaff's brainstem encephalitis, who carried anti-GQ1b IgG antibodies. In contrast, none of the others did the autoantibodies. C. Jejuni was cultured from all stool samples from five patients with enteritis alone. All the isolates had the same genotype, cst-II (Asn51), which are characteristic of strains isolated from Bickerstaff's brainstem encephalitis. These findings suggest that host susceptibility may play a role in inducing the production of anti-ganglioside antibodies and the development of Bickerstaff's brainstem encephalitis.

  • Acute isolated bulbar palsy with anti-GT1a IgG antibody subsequent to Campylobacter Jejuni enteritis.
    Journal of the Neurological Sciences, 2002
    Co-Authors: Masakazu Onodera, Toshio Fukutake, Michiaki Koga, Masahiro Mori, Takamichi Hattori, Nobuhiro Yuki, Ikuo Kamitsukasa, Satoshi Kuwabara
    Abstract:

    Abstract We describe a patient with acute isolated bulbar palsy following enteritis. A 29-year-old man developed dysphagia and nasal voice without limb weakness, ataxia, or areflexia. High titres of serum anti-GT1a and anti- Campylobacter Jejuni IgG antibodies were detected. He was treated with plasmapheresis, resulting in rapid clinical improvement. This case suggests that an acute isolated bulbar palsy may be caused by a pathology relating to Guillain–Barre syndrome (GBS), in which anti-GT1a IgG antibody may have a role.

  • fisher syndrome after Campylobacter Jejuni enteritis human leukocyte antigen and the bacterial serotype
    The Journal of Pediatrics, 1995
    Co-Authors: Nobuhiro Yuki, Hiroo Ichikawa, Ayumi Doi
    Abstract:

    Abstract We describe two children who had Fisher syndrome subsequent to Campylobacter Jejuni enteritis. The C. Jejuni isolates from both patients, who lived in different areas, belonged to PEN 2: LIO 4. One patient had the following human leukocyte antigens (HLAs): HLA-A24, 33; B44, 52; DQ1; and DR2, 6 antigens. Another had the HLA-A24, 33; B44, 54; Cw1; DQ1, 4; and DR4, 6. An effort should be made to isolate C. Jejuni from patients with Fisher syndrome and to perform HLA typing so that the pathogenesis of this syndrome can be clarified. (J P EDIATR 1995;126:55-7)

Bjorn Olsen - One of the best experts on this subject based on the ideXlab platform.

  • Campylobacter Jejuni actively invades the amoeba Acanthamoeba polyphaga and survives within non digestive vacuoles.
    PloS one, 2013
    Co-Authors: Jenny Olofsson, Bjorn Olsen, Diana Axelsson-olsson, Lars Brudin, Patrik Ellström
    Abstract:

    The Gram-negative bacterium Campylobacter Jejuni is able to enter, survive and multiply within the free living amoeba Acanthamoeba polyphaga, but the molecular mechanisms behind these events are st ...

  • multilocus sequence typing and flaa sequencing reveal the genetic stability of Campylobacter Jejuni enrichment during coculture with acanthamoeba polyphaga
    Applied and Environmental Microbiology, 2013
    Co-Authors: Petra Griekspoor, Bjorn Olsen, Jonas Waldenstrom, Jenny Olofsson, Diana Axelssonolsson
    Abstract:

    Low concentrations of Campylobacter Jejuni cells in environmental samples make them difficult to study with conventional culture methods. Here, we show that enrichment by amoeba cocultures works well with low-concentration samples and that this method can be combined with molecular techniques without loss of genetic specificity.

  • marked host specificity and lack of phylogeographic population structure of Campylobacter Jejuni in wild birds
    Molecular Ecology, 2013
    Co-Authors: Petra Griekspoor, Frances M Colles, Noel D Mccarthy, Philip M Hansbro, Chris Ashhurstsmith, Bjorn Olsen, Dennis Hasselquist, Martin C J Maiden, Jonas Waldenstrom
    Abstract:

    Zoonotic pathogens often infect several animal species, and gene flow among populations infecting different host species may affect the biological traits of the pathogen including host specificity, transmissibility and virulence. The bacterium Campylobacter Jejuni is a widespread zoonotic multihost pathogen, which frequently causes gastroenteritis in humans. Poultry products are important transmission vehicles to humans, but the bacterium is common in other domestic and wild animals, particularly birds, which are a potential infection source. Population genetic studies of C. Jejuni have mainly investigated isolates from humans and domestic animals, so to assess C. Jejuni population structure more broadly and investigate host adaptation, 928 wild bird isolates from Europe and Australia were genotyped by multilocus sequencing and compared to the genotypes recovered from 1366 domestic animal and human isolates. Campylobacter Jejuni populations from different wild bird species were distinct from each other and from those from domestic animals and humans, and the host species of wild bird was the major determinant of C. Jejuni genotype, while geographic origin was of little importance. By comparison, C. Jejuni differentiation was restricted between more phylogenetically diverse farm animals, indicating that domesticated animals may represent a novel niche for C. Jejuni and thereby driving the evolution of those bacteria as they exploit this niche. Human disease is dominated by isolates from this novel domesticated animal niche.

  • Protozoan Acanthamoeba polyphaga as a Potential Reservoir for Campylobacter Jejuni
    Applied and environmental microbiology, 2005
    Co-Authors: Diana Axelsson-olsson, Bjorn Olsen, Jonas Waldenstrom, Tina Broman, Martin Holmberg
    Abstract:

    We showed by a laboratory experiment that four different Campylobacter Jejuni strains are able to infect the protozoan Acanthamoeba polyphaga. C. Jejuni cells survived for longer periods when cocultured with amoebae than when grown in culture alone. The infecting C. Jejuni cells aggregated in amoebic vacuoles, in which they were seen to be actively moving. Furthermore, a resuscitation of bacterial cultures that were previously negative in culturability tests was observed after reinoculation into fresh amoeba cultures. After spontaneous rupture of the amoebae, C. Jejuni could be detected by microscopy and culturability tests. Our results indicate that amoebae may serve as a nonvertebrate reservoir for C. Jejuni in the environment.

Martin J Blaser - One of the best experts on this subject based on the ideXlab platform.

  • epidemiologic and clinical features of Campylobacter Jejuni infections
    The Journal of Infectious Diseases, 1997
    Co-Authors: Martin J Blaser
    Abstract:

    Gram-negative bacteria of the genus Campylobacter and of related genera frequently colonize the gastrointestinal tracts of humans, other mammals, and birds. One organism, Campylobacter Jejuni, has been recognized as an important human pathogen, usually causing a diarrheal illness. Infection is common throughout the world, but clinical and epidemiologic features differ in developed and developing countries. The high incidence of C. Jejuni infections and their propensity to invade tissue and to induce inflammation are compatible with a role in the causation of Guillain-Barre syndrome.