Epidemiology ofCampylobacter jejuniIsolated from Patients with Guillain-Barré and Fisher Syndromes in Japan

Abstract

Campylobacter jejuni isolation is the standard for the diagnosis of this type of bacterial infection, but there have been no epidemiological studies of a large number of C. jejuni isolates from patients with Guillain-Barré syndrome (GBS) and Fisher syndrome (FS). For 13 years, stool specimens from GBS/FS patients have been sent from 378 hospitals throughout Japan to the Tokyo Metropolitan Institute of Public Health. A total of 113 strains (11%) were isolated from the stool specimens from 1,049 patients. The isolation rate did not differ by region. The rates were 22% for 449 patients with a history of diarrhea and 2% for the others. An additional 18 isolates were provided by various hospitals. There was no noticeable seasonal distribution in the onset of C. jejuni isolated from patients with GBS/FS. The male/female ratios were 1.7:1 for GBS and 2.2:1 for FS. The patient age range showed a peak in 10-to 30-year-old subjects who had GBS and in 10-to 20-year-old subjects who had FS. The predominance of young adults and male patients who had C. jejuni-associated GBS/FS may be related to the preponderance of young adults and male patients who had C. jejuni enteritis. The median interval from diarrhea onset to neurologic symptom onset was 10 days for GBS/FS. Penner's C. jejuni serotype HS:19 was more frequently present in GBS (67%) than in enteritis (6%) patients. HS:2 was more frequent in FS (41%) than in enteritis (14%) patients. These findings suggest that certain C. jejuni strains specifically trigger GBS and that others specifically trigger FS.

Isolated insular infarction eliminates contralateral cold, cold pain, and pinprick perception

“…Most of the strains used were included in our previous study. 19 Two, OH4384 and OH4382, were obtained from sibling GBS patients 6,20 ; the others were from sporadic cases with geographically equal distributions. A questionnaire was filled in by the primary physician as to whether diagnostic criteria for GBS or a clinical variant were fulfilled.…”

A case of Miller Fisher syndrome with progression and early relapse

“…Even though areflexia is amongst the classical triad of MFS, it might not always be present [1,6]. Other than these three symptoms, some other symptoms such as ptosis, dysesthesia, facial or bulbar paralysis, optic neuritis, headache, urinary retention, subclinical or clinical autonomic dysfunction have also been reported [1,6,13]. Our case has other symptoms such as paracetamol-responsive headache, dysphagia, papilledema, bradycardia, and hypotension.…”

“…The classic triad of the disease was defined by Charles Miller Fisher as ataxia, ophthalmoplegia and areflexia in 1956 [3]. The existence of systemic infections such as gastrointestinal system or upper respiratory tract infections before the appearance of the clinical picture is known [5,6]. The initial complaints of our patient were ataxia, ptosis and ophthalmoplegia, followed by a mild dysphagia.…”

“…It was reported that ataxia occurs as a result of the nonadherence of proprioceptive knowledge about muscle spindles, joints and other proprioceptors [8,9,11,12]. Even though areflexia is amongst the classical triad of MFS, it might not always be present [1,6]. Other than these three symptoms, some other symptoms such as ptosis, dysesthesia, facial or bulbar paralysis, optic neuritis, headache, urinary retention, subclinical or clinical autonomic dysfunction have also been reported [1,6,13].…”

Caracterização molecular de linhagens de Campylobacter coli isoladas de origens diversas

“…O desenvolvimento desta síndrome se dá através de um mecanismo de mimetismo antigênico entre os lipopolissacarídeos da parede celular bacteriana e os gangliosídeos da membrana dos nervos periféricos. Uma vez que a estrutura do gangliosídeo GM1 presente na membrana das células nervosas é semelhante aos glicolipídios do polissacarídeo de parede celular do Campylobacter, os anticorpos produzidos devido à infecção pela bactéria podem produzir uma reação cruzada e atacar os nervos, interferindo na condução dos estímulos nervosos, causando fraqueza muscular que pode evoluir para paralisia muscular aguda (Takahashi et al, 2005).…”