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Bucurescu ST. J Neurol Neuromedicine (2018) 3(2): 8-10 Neuromedicine www.jneurology.com www.jneurology.com Journal of Neurology && NeuromedicineNeuromedicine

Case Report Open Access

Yersinia enterocolitica and Chlamydia pneumoniae possible triggering agents of Guillain-Barré syndrome: a case report Septimiu Tudor Bucurescu Neurology at Vital-Klinik, Bad Driburg, Germany

Article Info ABSTRACT

Article Notes In this paper we describe the case of a Guillain-Barré syndrome patient who Received: August 31, 2017 was diagnosed with an active and past chlamydiosis. We also discuss the Accepted: March 17, 2018 diagnosis, therapy and recovery prognosis of patients with Guillain-Barré syndrome. *Correspondence: Dr. Septimiu Bucurescu Neurology at Vital-Klinik, Bahnhofstr. 3, 33014 Bad Driburg, Germany, Email: [email protected] Introduction

© 2018 Bucurescu ST. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License demyelinating polyradiculoneuropathy usually preceded by a bacterial or viralGuillain-Barré infection. The syndrome disease is has an usually self-limited, three evolutionary acute inflammatory phases:

Keywords: Guillain-Barré syndrome triggering agent thirdin the phase, first phase, lasting lasting up to twoseveral to four months weeks, symptoms symptoms improve worsen,1. Overall in the enterocolitica second phase, lasting up to several weeks, symptoms stabilize and in the Chlamydia pneumoniae anti-ganglioside antibody induction incidence of the disease is low: 0.34-1.34/100,000/year in children2. The under 15 years of age, 1.1-1.8/100,000/year in adults under 50 years of$ 1.7 age billion and 1.7-3.3/100,000/year yearly in adults over 50 years of age economicagent of Guillain-Barré burden of3 disease syndrome in the isUnited Campylobacter States only jejuni, was estimated the disease at is considered to be. Although an idiopathic the most disease frequently. Diagnosis identified is triggeringbased on clinical history, neurological and laboratory4 examination5. Treatment 6 or intravenous immunoglobulin for 5 days7. Recovery can be calculated using a clinical recommendationsprognostic scoring are system plasma8 exchange for 6 to 10 days 9 acute care and 26 days in rehabilitation; mortality is .between 3-10% and disability after 6 months 20% . The average length10 of hospital stay is 34 days in Patient history

A 38-year-old man was admitted to the emergency department of an acute care hospital with severe tetraparesis and hypoesthesia. The symptoms occurred 2 days before hospital admission, 10 days after influenza infection. The anamnesis provided information about previous diseases, sinusitis 2 months ago with nasal congestion and pain, and gastroenteritis 10 months ago with abdominal pain and medication,, as onlywell asibuprofen vaccination on-demand. status, the The patient clinical was examination not vaccinated (i.e., against influenza. The patient was not taking any fixed-schedule

general, neurological and psychopathological) showed tetraparesis, gamma-glutamylhypoesthesia and transferase,absent tendon hemoglobin, reflexes. A standardhematocrit, laboratory international blood test was done. All investigated parameters (i.e., sodium, potassium, urea,

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mean corpuscular hemoglobin concentration, mean corpuscularnormalized ratio, volume, creatinine, activated mean partial corpuscular thromboplastin hemoglobin, time, induction due to molecular mimicry between bacterial membranecell wall glycolipids lipooligosaccharides12 and myelin sheath calcium, lactate dehydrogenase, glutamic oxaloacetic oligosaccharideoften acute and corechronic of gangliosides,gastroenteritis which are neuronal transaminase,thrombocytes, hemoglobin erythrocytes, A1c leucocytes, and thyroid creatine stimulating kinase, . Yersinia enterocolitica13 causes most . Chlamydia. Inpneumoniae the bacterial is cell wall of human strains lipopolysaccharides14 have been hormone) were normal. The cerebrospinal fluid analysis detectedinfections and15 characterized (i.e., proteins, glucose, red blood cells, white blood cells, a common cause of upper and lower16. A respiratory case report tract has Reiber nomograms) showed normal values. ECG showed . In the bacterial cell wall lipopolysaccharides no pathological findings. Electroneurographic examination havecould been trigger detected Guillain-Barré and characterized syndrome17. There are no motorof upper latency, and lowerand normal limbs (i.e., motor median, and sensory ulnar, tibial velocity and been published suggesting that Mycoplasma pneumoniae ofperoneal nerve nerve)conduction. showed normalAnother F-wave,electroneurographic normal distal preceding Guillain-Barré syndrome. There is no evidence published case reports on yersiniosis and/or chlamydiosis examination done 2 days after hospital admission showed lipopolysaccharidesin the biomedical literature are inducing that anti-ganglioside Yersinia enterocolitica antibody absence of F-wave, motor but not sensory conduction response.and/or Chlamydia pneumoniae bacterial cell wall syndromeblock, findings and receivedthat are typicalintravenous for an immunoglobulin acute demyelinating for 5 days.neuropathy. Symptoms The patientimproved was after diagnosed treatment. with Guillain-Barré Conclusions and future perspectives for neurological rehabilitation. The clinical examination In order to elucidate whether Yersinia enterocolitica After acute care the patient was transferred to our clinic Guillain-Barré syndrome or not, future studies on mice mustand/or to Chlamydiabe done. Anti-ganglioside pneumoniae are antibody triggering induction agents by of showed tetraparesis and hypoesthesia, tendon reflexes 18 were present. Barthel activities of daily living index was done. The values of glutamic oxaloacetic transaminase lipooligosaccharides was proven 70 points (0-100). A standard laboratory blood test was by immunization studies in mice . Mice were immunized with Campylobacter jejuni lipopolysaccharides isolated 69 U/L (<50), alanine aminotransferase 114 U/L (<50), of Guillain-Barré syndrome, and anti-ganglioside mice from patients with Miller-Fisher syndrome, a variant potassium 4.9 mmol/L (3.5-4.5), cholesterol 210 mg/dL (<200) were increased. The value of HDL-cholesterol 36 of binding to the nerve terminal and cause complement- laboratory blood test, microbiological blood and stool tests antibodies were cloned. Mice antibodies were capable mg/dL (>40) was decreased. In addition to the standard mediated paralysis in ex-vivo muscle nerve preparation. were done. Blood ELISA-tests were negative for Yersinia This approach could be used to investigate whether enterocolitica IgG 0,681 ratio (<0.8) and positive for IgA Yersinia enterocolitica and/or Chlamydia pneumoniae 1.181 ratio (<0.8) antibodies, results suggesting an active ganglioside antibody response or not. bacterial cell wall lipopolysaccharides are inducing anti- infection. Blood ELISA-tests were positive for Chlamydia Clinical studies must be done in order to clarify pneumoniae IgG 2.145 ratio (<0.8) and negative for IgA 0.6 ratio (<0.8) antibodies, results suggesting a previous and positive blood tests for above mentioned infection. Blood ELISA-tests were positive for Mycoplasma whether adult patients with Guillain-Barré syndrome acutepneumoniae infection. IgG Stool 1.538 antigen ratio (<0.8) detection and borderlineof Campylobacter, for IgA plasma exchange or intravenous immunoglobulin. There 0.863 ratio (0.8-1.1), results suggesting a questionable arecould no benefitpublished from studies antibiotic on antibiotics treatment use in additionin Guillain- to and stool culture of Salmonella, Shigella, Yersinia and for Campylobacter jejuni could receive erythromycin Campylobacter were negative. The patient received Barré syndrome. Patients with positive blood tests physiotherapy for 4 weeks which improved his condition. 19 During neurological rehabilitation no drug therapy was 500 mg twice daily for 5 days or azithromycin 500 mg necessary. Barthel activities of daily living index was 95 daily for 3 days . Patients with positive blood tests for physiotherapypoints (0-100). after Since discharge. the patient was not completely daysYersinia enterocolitica could receive trimethoprim/ recovered, he was supposed to continue ambulatory sulfamethoxazole20 160/800 mg twice daily for at least 7-10 Discussions . Patients with positive blood tests for Chlamydia Campylobacter jejuni is a leading cause of acute pneumoniae could receive tetracycline 500 mg four times gastroenteritis11. Campylobacter jejuni is triggering daysdaily21 for 14 days, 100 mg twice daily for 14 Guillain-Barré syndrome by anti-ganglioside antibody shoulddays or reduce erythromycin also the economic 500 mg fourburden times of disease. daily for 14 . Reduced mortality and/or length of hospital stay

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