http://www.infectiologie.com/site/_congres_conf_org_spilf.php

• EUCALB (European Union Concerted Action on Lyme Borreliosis)

http://meduni09.edis.at/eucalb/disease_overview_index.html

http://meduni09.edis.at/eucalb/diagnosis_serology-tests.html

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=85128&blobtype=pdf

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• Des infections bactériennes et virales systémiques ou du système nerveux central (Chlamydia pneumoniae, Borrelia burgdorferi, Mycoplasma species, human herpesvirus-1 et -6) pourraient être à la base des maladies d'Alzheimer et de Parkinson, de l'autisme, de la sclérose en plaques etc.   

Chronic Bacterial and Viral Infections in Neurodegenerative and Neurobehavioral Diseases Garth Nicolson

pdf du texte complet:

http://www.theoneclickgroup.co.uk/documents/ME-CFS_docs/Chronic%20Bacterial%20&%20Viral%20Infections,%20Neurodegenearative,%20Neurobehavioral%20Diseases.pdf

 

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• Thèse sur la persistance de Bb malgré les traitements antibiotiques. Proposition d'un traitement combinant Filgrastim (granulocyte colony-stimulating factor, G-CSF) pour soutenir le système immunitaire et antibiothérapie.

 

Dissertation de Diterich, Isabel  sous la direction du Dr Thomas Hartung, PD Dr, Université de Konstanz, Allemagne.

Date de publication: 27.03.2003  Texte complet pdf : Dokument 1.pdf (680 KB)  

Immunomodulation and new therapeutic strategies in Lyme borreliosis

If infection with Borrelia burgdorferi is not treated adequately with antibiotics in an early stage, it may lead to Lyme borreliosis (LB), a chronic multisystemic disorder which is difficult to cure. In some cases the pathogen survives in spite of antibiotic treatments. It is challenging to understand why Borrelia are often not eradicated, although being recognized by the host’s immune defense and occasionally inducing a strong inflammatory reaction. Thus, it remains an area of debate how this pathogen persists in human tissues. This question was addressed in the present thesis, examining possible immune evasion mechanisms of Borrelia. We propose that Borrelia modulate the host’s immune system in order to evade clearance in the immunologically competent host. Tolerance could represent the mechanism inhibiting host response thereby enabling survival and persistence of the pathogen. Promising results were obtained testing a novel treatment strategy for late stage LB, a combination of Filgrastim as an immunosupportive therapy with antibiotics. The respective clinical trial based on these findings was recently started.

http://www.ub.uni-konstanz.de/kops/volltexte/2003/981/

 

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• cette équipe Finlandaise a évolué ds le sens de la persistance de l'infection comme on peut le voir ds cette dernière étude, alors que ds leurs études passées ils étaient plutôt contre l'idée qu'un re-traitement pouvait être utile.
   
  Si vous voulez les voir en photo, cliquez sur le lien

Turku Immunology Centre

http://www.med.utu.fi/mikrobiologia/tutkimus/viljanen.pdf

Lyme borreliosis is a tick-transmitted disease caused by
the spirochete Borrelia burgdorferi.

During the early infection the spirochete spreads in the skin leading within a few days to a typical ring-like erythema migrans

lesion. In some individuals, the infection is limited to the skin and subsides even without treatment. However,

in some cases the spirochete invades into the blood and disseminates into various organs, where it may

survive and persist for months or even years. The main aim of this project is to understand the mechanisms

how borrelia manages to evade the first line immune response and spreads into a multi-organ infection. We

further aim to elucidate the mechanisms of persistent and treatment resistant Lyme borreliosis, since these

disease manifestations can lead to complicated and expensive investigations, delayed diagnosis and

longstanding disability of the patients.

 

The histological picture of erythema migrans lesion is mainly lymphocytic with very few neutrophils, which

is in striking contrast with other bacterial infections of the skin. Our hypothesis is that borrelia interferes with

the function of dendritic cells and thus prevents the recruitment of neutrophils to the site of infection. Using

large-scale gene expression studies we want to find out whether borrelia somehow manipulates neutrophils

and dendritic cells to its benefit. The phagocytosis of borrelia takes place through “tube-phagocytosis”.

We want to elucidate the cellular mechanisms of this interesting phenomenon by studying the receptors and

signalling pathways involved in the process.

 

One of the most debated questions in Lyme borreliosis research is pathogenesis of antibiotic

treatment resistant disease manifestations. Two main hypotheses presented to explain this phenomenon

are persistent infection and infection-induced autoimmunity.

 

We have succeeded in establishing a much-needed animal model for this disease

entity (Yrjänäinen et al., submitted). Our results show that the presence of vegetative spirochetes is no

prerequisite for the persisting symptoms. However, using this model we have found out that when the

mice receive immunosuppressive treatment with anti-TNF-α after a latent period of several weeks,

borreliae are activated from a dormant state and the animals develop spirochetemia (Yrjänäinen et al.,

manuscript in preparation). Thus, our results support the persistent infection hypothesis. 

Our mouse model makes possible to investigate where the microbe is hiding during latency, how it is adapted to latency,

how the microbe can be evicted from its hiding places, and how the immune response of the host

behaves during latency. In this investigation, we use, among other methods, both mouse and borrelia

gene arrays and modern imaging methods (e.g. livecell confocal microscopy, molecular PET etc.).

 

These studies should provide novel information concerning the pathogenesis and possible therapeutic approaches

of antibiotic treatment resistant Lyme arthritis and Lyme borreliosis in general. The results may have an

impact also on the understanding of other persistent infections like tuberculosis, chlamydia infections and

certain viral diseases.

• Conclusion: IV ceftriaxone therapy results in short-term cognitive improvement for patients with

  posttreatment Lyme encephalopathy, but relapse in cognition occurs after the antibiotic is discontinued.

  Treatment strategies that result in sustained cognitive improvement are needed .

   

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  Article de Daniel J. Cameron (mars 2009 - PDF) :

  Insufficient evidence to deny antibiotic treatment to chronic Lyme disease patients

   

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  L'étude de Brian Fallon :

  http://www.borelioza.org/materialy_lyme/Fallon's_Study_Oct_2007_Neurology.pdf

  The primary limitations of this study were its restrictive inclusion

  criteria (only 1% of screened patients were enrolled), the relatively small sample size, and the

  lack of posttreatment lumbar puncture or neurologic exam. Therefore, generalizability is uncertain

  to posttreatment Lyme patients without cognitive impairment or to seronegative patients

  with persistent symptoms.

   

  Conclusions from this study are mixed.

   

  At the primary efficacy end point of week 12, IV ceftriaxone

  treatment resulted in greater improvement in cognition and, among the more impaired, in

  physical functioning, pain, and fatigue. Clinical significance, however, depends on long-term effects.

  Notable were the long-term benefits for the ceftriaxone group on physical functioning and

  pain among the more severely affected patients at baseline, because these are among the most troubling

  aspects of posttreatment Lyme disease. However, our primary interest in this study was

  on cognition, for which the improvement was not sustained to week 24. Further, adverse effects attributed

  to IV ceftriaxone occurred in 26% of patients.

   

  Therefore, considering both the limited duration of cognitive improvement and the risks,

  10 weeks of IV ceftriaxone and then 14 weeks of no antibiotic is not an effective strategy for sustained

  cognitive improvement. Although certain subgroups (patients with more joint or neurologic

  abnormalities) may experience long-term benefit from ceftriaxone, the predictor analyses were exploratory

  rather than hypothesis driven, and they require independent confirmation. Pending such

  confirmation, treatment strategies that are safer and more durable are needed.

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Babesia

Babesiosis. Hunfeld et al 2008 review.pdf

(à suivre)