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Enteritis caused by Campylobacter jejuni followed by acute motor axonal neuropathy: a case report

Biljana Miljković-Selimović1*, Dragana Lavrnić2, Olga Morić3, Lai-King Ng4, Lawrence Price4, Ljubica Šuturkova5, Branislava Kocic1, Tatjana Babić6, Ljiljana Ristić6 and Slobodan Apostolski2

Author Affiliations

1 Department of Microbiology and Immunology, School of Medicine, University of Niš, Bul Dr Z Ɖinđića, 81, 18000 Niš, Serbia

2 Institute of Neurology, School of Medicine, University of Belgrade, Dr Subotića 8, 11000 Belgrade, Serbia

3 Republic Institute of Public Health, Dr Subotića 5, 11000 Belgrade, Serbia

4 National Laboratory for Enteric Pathogens, National Microbiology Laboratory, The Canadian Science Centre for Human and Animal Health, 1015 Arlington Street, Winnipeg, Manitoba, R3E 2R2, Canada

5 School of Pharmacy, University of Skopje, Bul Krste Misirkov bb 91000 Skopje, Former Yugoslav Republic of Macedonia

6 Institute of Public Health in Niš, Center for Microbiology, Bul Dr Z Ɖinđića, 50, 18000, Niš, Serbia

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Journal of Medical Case Reports 2010, 4:101  doi:10.1186/1752-1947-4-101

Published: 31 March 2010

Abstract

Introduction

Campylobacter species represent the main cause of bacterial diarrhea in developed countries and one of the most frequent causes of enterocolitis in developing ones. In some patients, Campylobacter jejuni infection of the gastrointestinal tract has been observed as an antecedent illness of acute motor axonal neuropathy, a variant of Guillain-Barré syndrome.

Case presentation

We present a case of acute motor axonal neuropathy following infection with Campylobacter jejuni subspecies jejuni, biotype II, heat stable serotype O:19. A 46-year-old Caucasian man developed acute motor neuropathy 10 days after mild intestinal infection. The proximal and distal muscle weakness of his upper and lower extremities was associated with serum antibodies to Campylobacter jejuni and antibodies to ganglioside GM1. The electromyographic signs of neuropathic muscle action potentials with almost normal nerve conduction velocities indicated axonal neuropathy. Our patient's clinical and electrophysiological features fulfilled criteria for the diagnosis of an acute motor axonal neuropathy, a subtype of Guillain-Barré syndrome.

Conclusion

As this is the first case of acute motor axonal neuropathy following infection with Campylobacter jejuni subspecies jejuni reported from the Balkan area, the present findings indicate the need for systematic studies and further clinical, epidemiological and microbiological investigations on the prevalence of Campylobacter jejuni and its heat stable serotypes in the etiology of Guillain-Barré syndrome and other post-infectious sequelae.