Guillain-Barre Syndrome - Association with Campylobacter jejuni

12/16/02 (Hewitt)

Question: What is known about the association between Campylobacter jenuni infection and Guillain-Barre syndrome?

<1>

Unique Identifier:11274311

Authors: Hadden RD. Karch H. Hartung HP. Zielasek J. Weissbrich B. Schubert J. Weishaupt A. Cornblath DR. Swan AV. Hughes RA. Toyka KV. Plasma Exchange/Sandoglobulin Guillain-Barre Syndrome Trial Group.

Institution: Department of Neuroimmunology, Guy's, King's and St. Thomas' School of Medicine, Swan), London, UK. rob.hadden@doctors.org.uk

Title: Preceding infections, immune factors, and outcome in Guillain-Barre syndrome.

Source: Neurology. 56(6):758-65, 2001 Mar 27.

Abstract: OBJECTIVE: To test the hypothesis that different preceding infections influence the neurophysiologic classification and clinical features of Guillain-Barre syndrome (GBS). METHODS: We tested pretreatment sera, 7 +/- 3 (mean +/- SD) days from onset, from 229 patients with GBS in a multicenter trial of plasma exchange and immunoglobulin, for serological markers of infection, adhesion molecules, and cytokine receptors, and compared these with neurophysiologic and clinical features. RESULTS: Recent infection by Campylobacter jejuni was found in 53 patients (23%), cytomegalovirus in 19 (8%), and Epstein-Barr virus in four (2%). Patients with C. jejuni infection were more likely than others to have neurophysiologic criteria of axonal neuropathy or inexcitable nerves, antiganglioside GM(1) antibodies, pure motor GBS, lower CSF protein, and worse outcome. Patients with cytomegalovirus infection were younger and more likely than others to have raised serum concentrations of molecules important in T lymphocyte activation and migration, soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble leukocyte selectin, and soluble interleukin-2 receptor (sIL-2R). Concentrations of sICAM-1 and soluble tumor necrosis factor receptor were higher in patients with inexcitable nerves than those with demyelinating neurophysiology. Logistic regression analysis showed death or inability to walk unaided at 48 weeks were associated with diarrhea, inexcitable nerves, severe arm weakness, age over 50, raised sIL-2R concentration and absence of immunoglobulin (Ig) M antiganglioside GM(1) antibodies. CONCLUSIONS: Subtypes of GBS defined by preceding infections were only approximately associated with different patterns of clinical, neurophysiologic, and immunologic features. A single infectious agent caused more than one type of pathology in GBS, implying interaction with additional host factors. Most patients had no identified infection. CAS Registry/EC Number 0 (Antibodies). 0 (Cell Adhesion Molecules). 0 (Receptors, Cytokine). 37758-47-7 (G(M1) Ganglioside).

<2>

Unique Identifier:9780289

Authors: Moran AP. Prendergast MM.

Title: Molecular mimicry in Campylobacter jejuni lipopolysaccharides and the development of Guillain-Barre syndrome.[comment].

Source: Journal of Infectious Diseases. 178(5):1549-51, 1998 Nov.

<3>

Unique Identifier:9781538

Authors: Jacobs BC. Rothbarth PH. van der Meche FG. Herbrink P. Schmitz PI. de Klerk MA. van Doorn PA.

Institution: Department of Neurology, Erasmus University, Rotterdam, The Netherlands.

Title: The spectrum of antecedent infections in Guillain-Barre syndrome: a case-control study.

Source: Neurology. 51(4):1110-5, 1998 Oct.

Abstract: OBJECTIVE: To determine which antecedent infections are specifically associated with the Guillain-Barre syndrome (GBS). BACKGROUND: Infections with many agents have been reported preceding GBS. Some infections are related to specific clinical and immunologic subgroups in GBS. Most agents were reported in case reports and uncontrolled small series of GBS patients only, and their relation to GBS and its subgroups remains unclear. METHOD: A serologic study for 16 infectious agents in 154 GBS patients and 154 sex- and age-matched controls with other neurologic diseases. Acute phase, pretreatment samples were used from clinically well-defined GBS patients. The seasonal distribution of serum sampling in the GBS and control group was the same. RESULTS: Multivariate analysis showed that in GBS patients, infections with Campylobacter jejuni (32%), cytomegalovirus (13%), and Epstein-Barr virus (10%) were significantly more frequent than in controls. Mycoplasma pneumoniae infections occurred more often in GBS patients (5%) than in controls in univariate analysis. Infections with Haemophilus influenzae (1%), parainfluenza 1 virus (1%), influenza A virus (1%), influenza B virus (1%), adenovirus (1%), herpes simplex virus (1%), and varicella zoster virus (1%) were also demonstrated in GBS patients, but not more frequently than in controls. C. jejuni infections were associated with antibodies to the gangliosides GM1 and GD1b and with a severe pure motor form of GBS. Cytomegalovirus infections were associated with antibodies to the ganglioside GM2 and with severe motor sensory deficits. Other infections were not related to specific antiganglioside antibodies and neurologic patterns. CONCLUSIONS: Recent infections with C. jejuni, cytomegalovirus, Epstein-Barr virus, and M. pneumoniae are specifically related to GBS. The variety of infections may contribute to the clinical and immunologic heterogeneity of GBS. CAS Registry/EC Number 0 (Antibodies, Bacterial). 0 (Antibodies, Viral). 0 (Gangliosides).

<4>

Unique Identifier:9746040

Authors: Hahn AF.

Institution: Clinical Neurological Sciences, University of Western Ontario, London Health Sciences Centre, Canada. angelika.hahn@lhsc.on.ca

Title: Guillain-Barre syndrome. [Review] [74 refs]

Source: Lancet. 352(9128):635-41, 1998 Aug 22.

Abstract: Guillain-Barre syndrome (GBS) is viewed as a reactive, self-limited, autoimmune disease triggered by a preceding bacterial or viral infection. Campylobacter jejuni, a major cause of bacterial gastroenteritis worldwide, is the most frequent antecedent pathogen. It is likely that immune responses directed towards the infecting organisms are involved in the pathogenesis of GBS by cross-reaction with neural tissues. The infecting organism induces humoral and cellular immune responses that, because of the sharing of homologous epitopes (molecular mimicry), cross-react with ganglioside surface components of peripheral nerves. Immune reactions against target epitopes in Schwann-cell surface membrane or myelin result in acute inflammatory demyelinating neuropathy (85% of cases); reactions against epitopes contained in the axonal membrane cause the acute axonal forms of GBS (15% of cases). Care for such patients may be challenging, yet the prognosis overall is favourable. Optimal supportive care and anticipation and prevention of complications are the mainstay of therapy. Admission to the intensive-care unit is necessary in 33% of patients who require intubation and assisted ventilation. Immunomodulation with infusions of IgG or plasma exchange treatments foreshorten the disease course. [References: 74] CAS Registry/EC Number 0 (Epitopes).

<5>

Unique Identifier:9710005

Authors: Sheikh KA. Nachamkin I. Ho TW. Willison HJ. Veitch J. Ung H. Nicholson M. Li CY. Wu HS. Shen BQ. Cornblath DR. Asbury AK. McKhann GM. Griffin JW.

Institution: Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.

Title: Campylobacter jejuni lipopolysaccharides in Guillain-Barre syndrome: molecular mimicry and host susceptibility.

Source: Neurology. 51(2):371-8, 1998 Aug.

Abstract: 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-Barre 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. CAS Registry/EC Number 0 (Antibodies, Bacterial). 0 (Epitopes). 0 (Lipopolysaccharides). 0 (Polysaccharides, Bacterial).

<6>

Unique Identifier:9432521

Authors: Anonymous.

Title: Development of Guillain-Barre Syndrome following Campylobacter Infection. Proceedings of a workshop. Bethesda, Maryland, 26-27 August 1996.

Source: Journal of Infectious Diseases. 176 Suppl 2:S91-200, 1997 Dec.

<7>

Unique Identifier:9396700

Authors: Yuki N.

Institution: Department of Neurology, Dokkyo University School of Medicine, Tochigi, Japan.

Title: Molecular mimicry between gangliosides and lipopolysaccharides of Campylobacter jejuni isolated from patients with Guillain-Barre syndrome and Miller Fisher syndrome.[comment]. [Review] [27 refs]

Source: Journal of Infectious Diseases. 176 Suppl 2:S150-3, 1997 Dec.

Abstract: Some patients developed Guillain-Barre syndrome (GBS) after being given bovine gangliosides. Patients with GBS subsequent to Campylobacter jejuni enteritis frequently have IgG antibody to GM1 ganglioside. Miller Fisher syndrome (MFS), a variant of GBS, is associated with IgG antibody to GQ1b ganglioside. The existence of molecular mimicry between GM1 and lipopolysaccharide of C. jejuni isolated from a GBS patient and that between GQ1b and C. jejuni lipopolysaccharides from patients with MFS are shown herein. The molecular mimicry between infectious agents and gangliosides may function in the production of anti-ganglioside antibodies and the development of GBS and MFS. [References: 27] CAS Registry/EC Number 0 (Antibodies, Bacterial). 0 (Autoantibodies). 0 (Epitopes). 0 (Gangliosides). 0 (Immunoglobulin G). 0 (Lipopolysaccharides). 0 (O Antigens).

<8>

Unique Identifier:9396695

Authors: Allos BM.

Institution: Division of Infectious Diseases, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Title: Association between Campylobacter infection and Guillain-Barre syndrome. [Review] [30 refs]

Source: Journal of Infectious Diseases. 176 Suppl 2:S125-8, 1997 Dec.

Abstract: Guillain-Barre syndrome (GBS), a neurologic disease that produces ascending paralysis, affects people all over the world. Acute infectious illnesses precede 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 serologic 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 neurologic symptoms. Neurologic symptoms are more severe and more likely to be irreversible when GBS is preceded by C. jejuni infection. One of every 1058 Campylobacter infections results in GBS, and 1 of 158 Campylobacter type O:19 infections results in GBS. [References: 30] CAS Registry/EC Number 0 (Antibodies, Bacterial). 0 (O Antigens).

<9>

Unique Identifier:9396692

Authors: Nachamkin I.

Institution: Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104-4283, USA.

Title: Microbiologic approaches for studying Campylobacter species in patients with Guillain-Barre syndrome. [Review] [117 refs]

Source: Journal of Infectious Diseases. 176 Suppl 2:S106-14, 1997 Dec.

Abstract: Campylobacter jejuni is now considered to be the most common cause of bacterial diarrheal disease in the United States. Sufficient evidence exists to support the hypothesis that C. jejuni induces Guillain-Barre syndrome (GBS); however, many questions about the biology of the organism and host factors need to be answered. In order to study the role of C. jejuni and other Campylobacter species as a cause of GBS, isolates from patients with different forms of GBS and appropriate control populations must be obtained. To continue to study this association, research teams must have laboratory support for isolating and characterizing Campylobacter strains. This review summarizes current knowledge about the laboratory aspects of Campylobacter infection that may be pertinent to studies on GBS. [References: 117] CAS Registry/EC Number 0 (O Antigens).

<10>

Unique Identifier:9396691

Authors: Blaser MJ.

Institution: Department of Medicine, Vanderbilt University School of Medicine, Department of Veterans Affairs Medical Center, Nashville, Tennessee 37232-2605, USA.

Title: Epidemiologic and clinical features of Campylobacter jejuni infections. [Review] [25 refs]

Source: Journal of Infectious Diseases. 176 Suppl 2:S103-5, 1997 Dec.

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. [References: 25] CAS Registry/EC Number 0 (Antibiotics).

<11>

Unique Identifier:7477117

Authors: Rees JH. Soudain SE. Gregson NA. Hughes RA.

Institution: Department of Neurology, United Medical School, Guy's Hospital, London, United Kingdom.

Title: Campylobacter jejuni infection and Guillain-Barre syndrome.[comment].

Source: New England Journal of Medicine. 333(21):1374-9, 1995 Nov 23.

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 syndrome. C. jejuni infection was slightly more common in men (P = 0.14) and was more likely to be associated with a pure motor syndrome and a slower recovery (P = 0.03). The patients with preceding C. jejuni infection were more likely to have acute axonal neuropathy or axonal degeneration in association with acute inflammatory demyelinating polyradiculoneuropathy, and they had greater disability after one year (P = 0.02). C. jejuni infection was significantly associated with a poor outcome even after correction for other factors associated with a poor prognosis. CONCLUSIONS. Infection with C. jejuni often precedes the Guillain-Barre syndrome and is associated with axonal degeneration, slow recovery, and severe residual disability.

<12>

Unique Identifier:7941533

Authors: Peterson MC.

Institution: Department of Medicine, LDS Hospital, Salt Lake City, Utah.

Title: Clinical aspects of Campylobacter jejuni infections in adults.[comment]. [Review] [71 refs]

Source: Western Journal of Medicine. 161(2):148-52, 1994 Aug.

Abstract: Campylobacter jejuni is an almost ubiquitous, microaerophilic, gram-negative rod. Outbreaks have been associated with drinking raw milk or contaminated water and eating poultry. Campylobacter jejuni accounts for 3.2% to 6.1% of cases of diarrheal illness in the general population of the United States, and infected patients frequently present with abdominal pain and fever. Less frequently, C jejuni is responsible for bacteremia, septic arthritis, septic abortion, and other extraintestinal infections. Reactive arthritis, Reiter's syndrome, the Guillain-Barre syndrome, and pancreatitis may accompany or follow C jejuni enterocolitis. Campylobacter jejuni is an important cause of diarrheal illness and is a more commonly identified stool organism than Salmonella or Shigella species. Recurrent and chronic infection is generally reported in immunocompromised hosts. [References: 71] CAS Registry/EC Number 0 (Antibiotics).

<13>

Unique Identifier:1929902

Authors: Gruenewald R. Ropper AH. Lior H. Chan J. Lee R. Molinaro VS.

Institution: Enteric Bacteriology Laboratory, St Elizabeth's Hospital, Boston, MA 02135.

Title: Serologic evidence of Campylobacter jejuni/coli enteritis in patients with Guillain-Barre syndrome.

Source: Archives of Neurology. 48(10):1080-2, 1991 Oct.

Abstract: We performed serologic testing for Campylobacter jejuni in 17 consecutive patients with acute Guillain-Barre syndrome from the Boston, Mass area to compare the frequency of this preceding infection with the high rates reported from other areas of the world. The rate of seropositivity, 18%, was considerable, but it was lower than that reported in Australia. Moreover, all of our patients with definite serologic evidence of infection had severe enteritis before Guillain-Barre syndrome, usually with the organism cultured from stool samples. Campylobacter enteritis is an important antecedent illness for Guillain-Barre syndrome but did not precipitate the disease without enteritis. CAS Registry/EC Number 0 (Antibodies, Bacterial). 0 (Immunoglobulins).

<14>

Unique Identifier:3369973

Authors: Ropper AH.

Institution: Neurological/Neurosurgical Intensive Care Unit, Massachusetts General Hospital, Boston 02114.

Title: Campylobacter diarrhea and Guillain-Barre syndrome.

Source: Archives of Neurology. 45(6):655-6, 1988 Jun.

Abstract: Four of 106 consecutive patients with acute Guillain-Barre syndrome had preceding bacterial enteritis caused by Campylobacter jejuni. One had a severe illness with axonal damage and poor outcome; three had typical courses with good recovery. Preceding illnesses in the other 102 patients were the following: diarrhea in nine (with negative stool cultures in five), upper respiratory tract infections in 46, hepatitis in six, other infectious illnesses in eight, and none in 33. Eight patients previously reported with Campylobacter associated with Guillain-Barre syndrome, and the serologic and clinical diagnosis of Campylobacter enteritis in this context, are reviewed.

<15>

Unique Identifier:3277576

Authors: Sovilla JY. Regli F. Francioli PB.

Institution: Service of Neurology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.

Title: Guillain-Barre syndrome following Campylobacter jejuni enteritis. Report of three cases and review of the literature. [Review] [25 refs]

Source: Archives of Internal Medicine. 148(3):739-41, 1988 Mar.

Abstract: We describe three cases of Guillain-Barre syndrome (GBS) associated with Campylobacter jejuni enteritis and review the data from eight other cases described in detail in the literature. The recent recognition of this association is probably due to improved stool culture technique. In comparison with GBS associated with respiratory infections, the delay between the first symptoms of infection and the development of GBS is somewhat longer, an observation in accordance with GBS associated with gastrointestinal symptoms of unidentified etiology. The clinical picture and the outcome do not seem to differ from those of GBS associated with other disorders. Campylobacter jejuni appears to be a pathogen capable of triggering GBS and will probably become increasingly recognized if appropriate culture and serologic tests are performed. [References: 25]

<16>

Unique Identifier:6428580

Authors: Kaldor J. Speed BR.

Title: Guillain-Barre syndrome and Campylobacter jejuni: a serological study.

Source: British Medical Journal Clinical Research Ed.. 288(6434):1867-70, 1984 Jun 23.

Abstract: The association between Campylobacter jejuni infection and Guillain-Barre 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. CAS Registry/EC Number 0 (Antibodies, Bacterial). 0 (Immunoglobulin G).

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