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16 mars 2011 3 16 /03 /mars /2011 15:13

WALL, N.J.March 15, 2011 /PRNewswire/ --

 

Researchers recently developed novel diagnostic tools able to distinguish between the various strains of bacteria responsible for causing Lyme disease.

For more than a decade, only one strain of B. burgdorferi (Lyme bacteria) had been sequenced (mapped), and although that helped research efforts, it was not sufficient to understand the relationship between geographic variations in strains and disease characteristics.

Scientists have suspected different strains may infect different parts of the body, causing different symptoms.

The recent completion of the genome sequencing of 13 additional isolates will greatly contribute to the improved understanding of the origins and effects of Lyme disease.

Described as a "superb discovery tool," Journal of Bacteriology 2-2011, sequencing will also provide a more solid foundation for detection, diagnostic, and prevention strategies.


The study was led by Dr. Steven Schutzer, Dr. Claire Fraser-Liggett, and Dr. Sherwood Casjens. (Click link for all authors & affiliations:http://jb.asm.org/cgi/content/full/193/4/1018)


Lyme Disease Association (LDA) is encouraged that this latest accomplishment will provide a more in-depth understanding of Lyme disease, which in turn will lead to improved patient care.

LDA funding often helps to start a project or complements federal funding such as that from the National Institutes of Health (NIH), which was the case here. LDA continues on its mission, having raised over $5 million to date for Lyme-related research and education, with 100% of incoming funds slated for research going directly to projects such as this latest genome sequencing effort and the groundbreaking study below.

In a separate new study -- by examining proteins in cerebrospinal fluid of Lyme and chronic fatigue patients and normal controls -- researchers led by Dr. Steven SchutzerUniversity of Medicine & Dentistry of New Jersey-New Jersey Medical School, and other scientists, discovered that chronic fatigue syndrome and neurologic Lyme disease are distinct disease entities.

Currently, Lyme patients may be misdiagnosed with chronic fatigue syndrome, so this finding will help scientists develop more accurate diagnostic tools and appropriate therapies.


The Columbia Lyme & Tick-Borne Diseases Research Center, Dr. Brian Fallon, Director, provided samples for the above Lyme-chronic fatigue study published in PLoS One 2-23-11(http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0017287). The Center was established in part through funding from the LDA. http://www.LymeDiseaseAssociation.org

 


ABOUT THE LYME DISEASE ASSOCIATION: 

The New Jersey-based national Lyme Disease Association has dedicated itself to providing funding for projects which can help prevent and cure Lyme disease.

To date, LDA funded studies have resulted in acknowledgement in 22 scientific peer review journal articles, including the two above.

The LDA is an all-volunteer national nonprofit, 501(c)(3), dedicated to Lyme disease education, prevention, raising monies for research, and patient support. It's a part of the 2010 Combined Federal Campaign and an Environmental Protection Agency PESP Partner and offers LymeAid 4 Kids program for children without insurance coverage.

LDA is associated with 43 Lyme organizations nationwide, working together to make a difference for Lyme patients.  

CONTACT:

 

Pat Smith
LYME DISEASE ASSOCIATION
888 366 6611
Lymeliter@aol.com

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16 mars 2011 3 16 /03 /mars /2011 12:47

Les perturbateurs endocriniens sont partout! Plastiques danger (Phtalates)

 

Un colloque sur les perturbateurs endocriniens s’est tenu le 14 septembre 2010 sous les auspices du Groupe Santé Environnementale de l’Assemblée Nationale, présidé par Gérard Bapt. Nous en rapportons ici les informations essentielles, mais aussi, malheureusement, les inquiétudes…  

 

Les perturbateurs endocriniens font, semble-t-il, que des ours polaires deviennent hermaphrodites, que le pénis des alligators se raccourcit, que des tortues se féminisent…

 

Les phtalates (ou phthalates), pris ici comme paradigme des molécules toxiques synthétisées par l’industrie chimique, ainsi qu’environ 100 000 autres substances – et il en arrive sur le marché à peu près 300 tous les ans – sont devenus le grand ennemi des espèces vivantes et tout particulièrement de l’espèce humaine.

 

Parmi les substances souvent citées, le tributyléthane et surtout les PCB (ou polycholorobiphényles) sont des polluants bioaccumulables trouvés dans les cellules graisseuses ayant une durée de vie variable qui peut dépasser les 100 ans !

 

Et ils peuvent avoir un effet nocif à des taux où ils ne sont pas dosables dans le plasma.  Plus personne n’ignore que les polluants chimiques pourraient être à l’origine de l’accroissement majeur des cancers hormonodépendants, en particulier des cancers du sein et de la prostate.

 

Mais ceux-ci sont loin d’être la seule conséquence de la présence de ces perturbateurs endocriniens dans notre environnement.

 

Quand ils sont présents en abondance chez une femme enceinte, ils vont parvenir à l’intestin du foetus et affecter la division des cellules, d’où chez l’adulte un nombre total réduit et un intestin moins fonctionnel.

 

En outre, par une série de mécanismes complexes, les cellules intestinales à vocation immunitaire seront moins nombreuses, ce qui diminuera les défenses du sujet.

 

L’obésité et le diabète sont généralement attribués à la sédentarité et aux excès alimentaires. Ces affections conduisent aux maladies cardiovasculaires et à leur complication parfois létales.

 Or, les perturbateurs endocriniens fixés sur les cellules adipeuses, dont on connaît maintenant les fonctions endocriniennes majeures, joueraient dans leur augmentation continue un rôle qui semble loin d’être négligeable.

Agriculture et baisse de fertilité

Parmi tous ces perturbateurs, le distilbène a été largement cité.

Or, il n’est pas exclu (et pas du tout prouvé non plus selon un orateur qui a fait preuve d’une très grande prudence) que les comportements des sujets ayant été exposés à cette substance puissent en être perturbés ou qu’ils aient une tendance à la dépression.

Et il n’y a aucune raison de penser que certaines autres substances toxiques ne puissent pas avoir de tels effets, elles aussi.

De nombreux perturbateurs sont très probablement, selon certains travaux, à l’origine de la multiplication par 4 du nombre d’enfants hypospades au Danemark, pays agricole utilisant de grandes quantités de substances toxiques.

Parallèlement, dans ce pays, les cancers du testicule sont devenus plus nombreux, ce qui n’est pas du tout le cas en Finlande, pays non agricole…, mais à forte in-dustrialisation.

Et d’un autre côté, la diminution observée par certains laboratoires et non par d’autres, de la concentration des spermatozoïdes dans les éjaculats pourrait annoncer une baisse de la fertilité.

Dans certaines publications, on peut en effet lire que le nombre de couples infertiles a été multiplié par 2 depuis quelques années.

Ainsi cancers, maladies cardiovasculaires, troubles digestifs, diminution de la fertilité, affectent les hommes, comme leur environnement animal.

 

Une situation plus grave qu’on ne l’imagine

Les phtalates sont présents dans une telle quantité de matériels médicaux qu’on ne voit pas par quoi on pourra les remplacer.

Le verre pourrait être utilisé certes, mais outre son coût, il est d’emploi bien moins commode.

Et les phtalates ne sont pas les seuls dangereux.

Le sont également les substances toxiques qui servent (ou ont servi) à la désinfection des biberons.

L’extermination des microbes a donc été la source d’autres nuisances.

Mais il y a plus terrifiant.

L’adulte qui souffre d’une maladie assez grave ou encore le prématuré très fragile sont souvent perfusés.

Or, les tuyaux de perfusion en plastique envoient des phtalates dans l’organisme malade.

Et le sac même qui contient les globules rouges les contamine par le même perturbateur endocrinien.

Le geste salvateur est également à longue échéance un geste dangereux.

Dans la vie des humains sains que se passe-t-il ?

Le fait même de boire nous met au contact de substances toxiques de toute nature, même dans les eaux qui sortent de l’épurateur le plus moderne et dans les gobelets où ils la consomment (et les boues sortant des épurateurs sont répandues sur les champs agricoles !).

Mangent-ils du poisson gras pour avoir leur ration d’oméga 3, ils seront plus riches alors de toutes les substances toxiques ayant fonction de perturbateurs endocriniens (disruptor, en anglais).

Et la poêle dans laquelle ils sont cuits peut en être recouverte. Même les fruits et légumes choisis avec soin par la ménagère risquent de leur en apporter.

 

Gare aux effluents

Les eaux superficielles et profondes sont infiltrées de toutes les hormones, y compris et surtout par l’éthinyl estradiol des pilules : aussi bien de celles qui ont été ingurgitées que des molécules qui ont été rejetées par les usines qui les fabriquent.

 

Et, ce qui est moins su, beaucoup plus encore, la contamination concerne également les patchs contraceptifs après usage.

 

Quant aux centres de soin dans lesquels toutes sortes de médicaments sont utilisés, ils deviennent de terribles pollueurs, parce que l’État ne leur a pas donné de moyens suffisants pour éviter la diffusion des médicaments urinés ou jetés…

Plus préoccupant, les cancers hormono- dépendants sont de plus en plus nombreux dans le monde entier.

Certes, ils tuent un peu moins qu’auparavant grâce aux progrès thérapeutiques.

Malheureusement, les antimitotiques sont eux aussi éliminés sans précautions particulières et ils viennent augmenter le stock de ces produits toxiques qui ne manquent pas de faire partie plus ou moins rapidement des 60 % d’eau de notre corps.

Les preuves de la nocivité de ces toxiques sont données par quelques catastrophes :

hécatombe de chiens tués par les neurotoxines sécrétées par les cyanobactéries ; 30 000 canards exterminés par la toxine botulique…

Les inquiétudes ne s’arrêtent pas là.

Les produits toxiques fabriqués dans un pays risquent, poussés par les vents et portés par les eaux, d’être envoyés dans les pays voisins ou lointains, par exemple au pôle Nord. Les efforts faits par un gouvernement risquent d’être annulés par des phénomènes climatiques inopinés.

 

Toxique dès la période foetale

Le ton d’une communication s’est distingué des autres.

Elle venait de Belgique. Avec une notion rassurante : depuis 1980, le taux de dioxine dans le corps des sujets testés a diminué de 8 % par an.

Et dans trois secteurs, en Belgique, les enfants ayant présenté le moins d’effets susceptibles d’être attribués aux perturbateurs endocriniens avaient été ceux nourris au sein !

Fait très important : il existe une fenêtre d’activité de ces perturbateurs.

En effet, ils sont surtout nocifs à la période foetale et durant la petite enfance.

En d’autres termes, le mal est fait dès l’arrivée à l’adolescence.

Et les pesticides et autres substances toxiques qui s’y surajouteront n’auront vraisemblablement d’effets que s’ils sont absorbés en quantité très excessive.

Le sort est donc jeté dès l’âge de 10 ans, et souvent plus tôt !

Est-ce que le taux de phtalates (parmi les autres substances chimiques nocives) présents dans un sujet à son entrée dans l’adolescence est prédictif de pathologies ultérieures ?

En fait, un taux élevé serait l’annonce d’un destin noirci : maladies et dépression.

 

Conclusion

Le danger est réel, mais il est très difficile à cerner car les paradigmes en cours pour juger de la toxicité d’une substance sont obsolètes et ne s’appliquent pas à la toxicité chronique.

 

De plus, on ne dispose, d’après les scientifiques réunis, d’aucun moyen de juger des risques de l’association de ces substances, et l’on est encore incapable de mesurer l’ensemble d’entre eux.

 

La nécessité de réagir vite est donc manifeste et indéniable. On peut cependant en toute quiétude regretter l’absence presque totale, dans l’ensemble des conférences, de réflexions globales sur le versant opposé : les effets bénéfiques apportés à l’humanité par les substances citées.

 

Il était dit le surlendemain de ce colloque, sur France Culture, que grâce à ces « progrès », l’agriculture avait permis de nourrir un nombre infiniment plus grand d’humains que par le passé.

 

Il faut donc prendre en compte l’urgence des décisions, mais aussi s’abstenir d’attribuer à la chimie une culpabilité excessive.

 

Heureusement, nos députés se sont vigoureusement investis dans l’affaire, comptons sur eux sans que nous médecins cessions d’être vigilants.

 

J. BELAISCH, Paris

 

 

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15 mars 2011 2 15 /03 /mars /2011 19:03

Le réseau EpiSouth, de contrôle des maladies transmissibles dans les pays d’Europe du Sud et du Bassin méditerranéen, auquel participent 27 pays, fait le point sur les épidémies d’infection à virus West Nile (WN) survenues d’août à novembre 2010.

 

L’analyse, au 15 novembre 2010, des données fournies par 17 pays du réseau recensait 375 cas humains rapportés par 5 pays (Grèce, Israël, Italie, Roumanie, Turquie), dont 34 fatals.

 

À ces cas humains, s’ajoutaient ceux équins rapportés par 5 pays (Bulgarie, Grèce, Italie, Maroc, Espagne). P. Barboza et coll. identifient des foyers actifs non seulement sur les principales routes de migration aviaire traversant la Région Méditerranée, mais aussi sur les sites de  nidification des oiseaux, dans le Bassin de la Volga, en Russie, et qualifient de sans précédent l’intensité de circulation du virus West Nile, à l’automne 2010, dans le Bassin méditerranéen et les régions avoisinantes.

 

Ces auteurs (de France, d’Italie et de Grèce) insistent sur l’importance des échanges rapides des informations et des alertes, l’accès aux dispositifs de surveillance, de veille permanente ou saisonnière, aux examens de laboratoires, variant considérablement entre les différents pays d’Episouth.

 

 

Dr Julie Perrot

 

Barboza P et coll. : West Nile outbreak in the Mediterranean Region, August-November 2010. International Meeting on Emerging Diseases and Surveillance – IMED (Vienne) : 4-7 février 2011. 
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13 mars 2011 7 13 /03 /mars /2011 11:04

ILADS Lyme Disease Treatment Guidelines Summary

by ILADS

 

In early 2004, The International Lyme and Associated Diseases Society (ILADS) released the first evidence-based comprehensive set of Lyme Disease Treatment Guidelines to assist physicians, public health officials and organizations involved in the evaluation and treatment of Lyme disease. The Lyme Disease Association (national) and the California Lyme Disease Association endorsed the Guidelines which were then peer-reviewed and made available to professionals and to the public.

Lyme is the number one tick-borne illness in the US. The CDC reports there are 24,000 new cases of Lyme disease in the US but the CDC says that figure could be under reported by tenfold. ILADS believes newly diagnosed cases of Lyme may occur at a rate five times higher than the number of new AIDS cases. Chronic Lyme is reported in up to half of patients treated for Lyme.

ILADS Lyme Treatment Guidelines suggest more aggressive treatment for people at risk.

A short summary of ILADS’ recommendations includes:

Treatment for symptomatic presentations

Treatment should not be withheld based on laboratory testing

Early use of antibiotics

Longer courses of antibiotics treatment

Repeat antibiotics for recurrence

Symptomatic Presentations of Lyme Disease include:

Fatigue

Low grade fevers, “hot flashes” or chills

Night sweats

Sore throat

Swollen glands

Stiff neck

Migrating arthralgias, stiffness and frank arthritis

Myalgia

Chest pain and palpitations

Abdominal pain, nausea

Diarrhea

Sleep disturbance

Poor concentration and memory loss

Irritability and mood swings

Depression

Back pain

Blurred vision and eye pain

Jaw pain

Testicular/pelvic pain

Tinnitus

Vertigo

Cranial nerve disturbance ( facial numbness, pain, tingling, palsy or optic neuritis)

Headaches

Lightheadedness

Dizziness

ILADS’ Lyme Treatment Guidelines address 45 subjects:

1.            ILADS defined

2.            Chronic Lyme disease: A growing epidemic

3.            The need for new guidelines

4.            A problem of definitions

5.            Competency and training

6.            The increasing role of primary care

7.            Highlights of guidelines

8.            Symptomatic presentations

9.            symptoms of Lyme disease

10.       Increasing evidence of persistent infection

11.       Disappointing results of symptomatic treatment

12.       Severity of chronic Lyme disease

13.       Atypical early presentations

14.       New chronic Lyme disease presentations

15.       The limitations of physical findings

16.       Sensitivity limitations of testing

17.       Seronegative Lyme disease

18.       Continued importance of differential diagnosis

19.       Clinical judgment

20.       Testing for coinfection

21.       Prompt use of antibiotics

22.       Choosing an antibiotic

23.       Oral antibiotic options

24.       Intravenous antibiotic options

25.       Intramuscular antibiotic options

26.       Combination antibiotic treatment

27.       Sequential treatment

28.       Dosage

29.       Duration of therapy

30.       Empiric treatment

31.       Persistent Lyme disease

32.       Recurrent Lyme disease

33.       Refractory Lyme disease

34.       Treatment failure

35.       Symptomatic treatment

36.       Fibromyalgia

37.       Decision to stop antibiotics

38.       Alternative antibiotics

39.       Therapy for coinfection

40.       Ongoing development of treatment guidelines

41.       Validation of guidelines

42.       Comparative studies

43.       Grading system for evidence-based guidelines

44.       Comparison of key IDSA and ILADS guidelines

45.       Criteria for evidence-based guidelines

Adapted from Cameron DJ, Gaito A, Harris N, Bach G, Bellovin S, Bock K, Bock S, Burrascano J, Dickey C, Horowitz R, Phillips S, Meer-Sheerer L, Raxlen B, Sherr V, Smith H, Smith P, Stricker R. Evidence-based guidelines for the management of Lyme disease. Expert Rev. Anti-infect. Ther. 2(1), 2004.

ILADS thanks Turn the Corner Foundation and the Lyme Disease Association for their financial support of the guideline development process.

 

 

South Med J. 2009 Jun;102(6):626-30.

In the lymelight: law and clinical practice guidelines.

Ronn S.

Almost from the beginning, the Ixodes scapularis and I pacificus, adult deer ticks, have been a breeding ground not only for Lyme disease, but also for political dissent.

Most recently, the battleground moved into the arena of clinical practice guidelines.

Both camps in the "Lyme Wars"-the Infectious Diseases Society of America (IDSA) and the International Lyme and Associated Diseases Society (ILADS)-have published Lyme disease practice guidelines.

The guidelines conflict regarding diagnosis and treatment.

The state of Connecticut's Attorney General's office conducted an investigation, under antitrust laws, into the development and promulgation of IDSA's 2006 guidelines.

In an unprecedented move, IDSA and the AG have entered into a legal agreement that necessitates a rethinking of the guidelines, requiring a new review panel reflecting balanced, conflict-of-interest-free perspectives on Lyme disease.

PMID: 19434013 [PubMed - in process]

 


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13 mars 2011 7 13 /03 /mars /2011 10:49

Med Hypotheses. 2009 Feb;72(2):153-6. Epub 2008 Nov 13.

 

Clinical trials validate the severity of persistent Lyme disease symptoms.


Cameron DJ.


First Medical Associates, Mt. Kisco, New York 10549, USA. Cameron@Lymeproject.com

BACKGROUND: 

 Persistent Lyme Disease Symptoms (PLDS) have included fatigue, headaches, poor concentration and memory, lightheadedness, joint pain, and mood disturbances.

Evidence-based guidelines committees disagree over the severity of PLDS.

 

The 2004 International Lyme and Associated Diseases Society (ILADS) concluded that PLDS are severe.

The 2006 Infectious Disease Society of America (IDSA) guidelines committee concluded that PLDS are nothing more than the "aches and pains of daily living" and an ad hoc International Lyme group concluded that PLDS are "symptoms common in persons who have never had Lyme disease."


HYPOTHESIS: 

 Clinical trials validate the severity of persistent Lyme disease symptoms.

 

EVALUATION OF THE HYPOTHESIS: There are 22 standardized instruments used to measure the severity of PLDS among the four published National Institutes of Health (NIH) sponsored double-blind randomized placebo-controlled trials (RCTs).

VALIDATING THE HYPOTHESIS: All four NIH sponsored RCTs validate the severity of PLDS.

PLDS are as severe as symptoms seen in other serious chronic illnesses, and result in a quality of life lower than for the general population as determined by 22 standardized measures of QOL, including fatigue, pain, role function, psychopathology, and cognition.

None of the four RCTs support the IDSA hypothesis that PLDS are nothing more than "the aches and pains of daily living" nor the ad hoc International Lyme group conclusion that PLDS are "symptoms common in persons who have never had Lyme disease."


IMPLICATIONS OF THE HYPOTHESIS: 

 If the QOL of life for these patients is as poor as for patients with other serious chronic diseases, their symptoms need to be addressed by their doctors.

Studies differ as to the precise cause of PLDS, the most effective treatments, and whether a cure is possible.

But the fact that there is disagreement is not a license for physicians to ignore or turn away patients complaining of PLDS, or to dismiss their symptoms as purely psychosomatic.

For physicians, the goal or purpose of treating PLDS should be the same as their purpose in treating other chronic illnesses that result in a poor QOL: vigorous pursuit of a cure, and where a cure proves impossible, amelioration of patients' symptoms and suffering.

Even if this hypothesis fails to be apply to more than a fraction of the total Lyme disease population, this still represents a significant number of patients, and these findings could address a neglected aspect of caring for patients with Lyme disease.

PMID: 19013025 [PubMed - indexed for MEDLINE]

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13 mars 2011 7 13 /03 /mars /2011 10:45

Vector Borne Zoonotic Dis. 2002 Winter;2(4):255-63.

Controlled trials of antibiotic treatment in patients with post-treatment chronic Lyme disease.


Klempner MS.


Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts 02118, USA. klempner@bu.edu

Some patients have persistence of profound fatigue, myalgias, arthralgias without arthritis, dysesthesia/paresthesia, and mood and memory disturbances after standard courses of antibiotic treatment for Lyme disease.

This constellation of symptoms has been variously referred to as "chronic Lyme disease," "post-Lyme disease syndrome," and "post-treatment chronic Lyme disease."

Persistent symptoms have been reported in patients who are seropositive for IgG antibodies against Borrelia burgdorferi as well as in patients who are seronegative.

The cause or causes of persistent symptoms in these patients have not been clearly defined and are controversial.

Because of the temporal association of these symptoms with infection with B. burgdorferi, some patients have been treated with prolonged courses of antibiotics.

Case reports and uncontrolled trials have reported the efficacy of prolonged antibiotic therapy, often with relapse of the symptoms after discontinuation of therapy.

To date, only one randomized, placebo-controlled, double-blind trial of antibiotic therapy for these patients has been published.

An abstract of a second placebo-controlled trial of antibiotic therapy in a smaller cohort has also been presented.

This paper will describe this patient population in detail and will review the clinical, microbiological, and selected biochemical and immunologic parameters and their responses to antibiotic treatment in the setting of a controlled trial.

PMID: 12804167 [PubMed - indexed for MEDLINE]

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13 mars 2011 7 13 /03 /mars /2011 10:42

Neurology. 2008 Mar 25;70(13):992-1003. Epub 2007 Oct 10.

A randomized, placebo-controlled trial of repeated IV antibiotic therapy for Lyme encephalopathy.

Fallon BAKeilp JGCorbera KMPetkova EBritton CBDwyer ESlavov ICheng JDobkin JNelson DRSackeim HA.

Columbia University, 1051 Riverside Drive, Unit 69, New York, NY 10032, USA. baf1@columbia.edu

Comment in:

 

BACKGROUND: Optimal treatment remains uncertain for patients with cognitive impairment that persists or returns after standard IV antibiotic therapy for Lyme disease.


METHODS: Patients had well-documented Lyme disease, with at least 3 weeks of prior IV antibiotics, current positive IgG Western blot, and objective memory impairment. Healthy individuals served as controls for practice effects. Patients were randomly assigned to 10 weeks of double-masked treatment with IV ceftriaxone or IV placebo and then no antibiotic therapy. The primary outcome was neurocognitive performance at week 12-specifically, memory. Durability of benefit was evaluated at week 24. Group differences were estimated according to longitudinal mixed-effects models.


RESULTS: After screening 3368 patients and 305 volunteers, 37 patients and 20 healthy individuals enrolled. Enrolled patients had mild to moderate cognitive impairment and marked levels of fatigue, pain, and impaired physical functioning. Across six cognitive domains, a significant treatment-by-time interaction favored the antibiotic-treated group at week 12. The improvement was generalized (not specific to domain) and moderate in magnitude, but it was not sustained to week 24. On secondary outcome, patients with more severe fatigue, pain, and impaired physical functioning who received antibiotics were improved at week 12, and this was sustained to week 24 for pain and physical functioning. Adverse events from either the study medication or the PICC line were noted among 6 of 23 (26.1%) patients given IV ceftriaxone and among 1 of 14 (7.1%) patients given IV placebo; these resolved without permanent injury.


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.

PMID: 17928580 [PubMed - indexed for MEDLINE]

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13 mars 2011 7 13 /03 /mars /2011 10:24

Proof that chronic Lyme disease exist

 

The evidence continues to mount that Chronic Lyme Disease (CLD) exists and must be addressed by the medical community if solutions are to be found.

Four National Institutes of Health (NIH) trials validated the existence and severity of CLD.

Despite the evidence, there are physicians who continue to deny the existence and severity of CLD, which can hinder efforts to find a solution.

Recognizing CLD could facilitate efforts to avoid diagnostic delays of two years and durations of illness of 4.7 to 9 years described in the NIH trials.

The risk to society of emerging antibiotic-resistant organisms should be weighed against the societal risks associated with failing to treat an emerging population saddled with CLD.

The mixed long-term outcome in children could also be examined.

Once we accept the evidence that CLD exists, the medical community should be able to find solutions.

Medical professionals should be encouraged to examine whether:

(1) innovative treatments for early LD might prevent CLD,

(2) early diagnosis of CLD might result in better treatment outcomes, and

(3) more effective treatment regimens can be developed for CLD patients who have had prolonged illness and an associated poor quality of life.


The evidence continues to mount that Chronic Lyme Disease (CLD) exists and must be addressed by the medical community if solutions are to be found.

Thirty-four percent (34%) of a population-based, retrospective cohort study in Massachusetts were found to have arthritis or recurrent arthralgias, neurocognitive impairment, and neuropathy or myelopathy, a mean of 6 years after treatment for Lyme disease (LD) [1].
Sixty-two percent (62%) of a cohort of 215 consecutively treated LD patients in Westchester County were found to have arthralgias, arthritis, and cardiac or neurologic involvement with or without fatigue a mean of 3.2 years after treatment [2].
Klempner trials' subjects presenting with “well-documented, previously treated Lyme disease…had persistent musculoskeletal pain, neurocognitive symptoms, or dysesthesia, often associated with fatigue” and were ill during a mean of 4.7 years after onset [3].
Fallon trial subjects presenting with “well-documented Lyme disease, with at least 3 weeks of prior IV antibiotics, current positive IgG Western blot, and objective memory impairment,” were ill during a mean of 9 years after onset [4].
Krupp LD subjects presented with “persistent severe fatigue at least 6 or more months after antibiotic therapy” [5].

There is also evidence that symptoms of CLD can be severe [48].
The Klempner trials described the quality of life for patients with posTttreatment chronic Lyme disease (PTLD) as being equivalent to that of patients with congestive heart failure or osteoarthritis, and their physical impairment was “more than 0.5 SD greater than the impairment observed in patients with type 2 diabetes or a recent myocardial infarction” [3].
Fallon et al. described pain reported by patients with Lyme encephalopathy as being “…similar to those of postsurgery patients”, and their fatigue “was similar to that of patients with multiple sclerosis.” Limitations in physical functioning on a quality of life scale were “comparable with those of patients with congestive heart failure” [4].

Despite the above documented evidence, the 2006 Infectious Diseases Society of America (IDSA) LD treatment guideline panel questioned the existence of CLD [9].
The IDSA panel concluded, “Considerable confusion and controversy exist over the frequency and cause of this process and even over its existence” [9].
The IDSA panel referred to chronic manifestations of LD as Post-Lyme disease syndrome (PLDS), PTLD and CLD. There are shortcomings for each term.
The PLDS nomenclature implies that an active LD has been successfully treated, that any remaining symptoms are merely harmless vestiges of previous illness, and that the patient has been cured.
The term PTLD merely implies that LD has been treated with antibiotics for 10 to 30 days. The CLD nomenclature implies that chronic manifestations of LD are present with or without evidence of active infection that cannot be reasonably explained by another illness.

There is no objective way to rule out an active infection.
Lab tests that can be very helpful in confirming a clinical diagnosis of Lyme disease (such as the ELISA and Western blot tests) are not useful in determining whether the infection has been adequately treated.
Common LD symptoms such as Bell's palsy, erythema migrans rash, meningitis, arthritis, or heart block, which are included in the current surveillance definitions, can be useful in “ruling in” Lyme disease, but the absence or disappearance of these symptoms cannot “rule out” an ongoing infection.
A population-based, retrospective cohort study of individuals with a history of LD revealed that they were significantly more likely to have joint pain, memory impairment, and poor functional status due to pain than persons without a history of LD, even though there were no signs of objective findings on physical examination or neurocognitive testing [10].
Two recent mouse studies revealed that spirochetes persist despite antibiotic therapy and that standard diagnostic tests are not able to detect their presence [1112].
In sum, there are no clinical or laboratory markers that identify the eradication of the pathogen.

The IDSA panel also questioned the severity of CLD symptoms.
The panel dismissed LD symptoms that persisted or recurred after their recommended, short-term course of treatment, stating that they were: “more related to the aches and pains of daily living rather than to either Lyme disease or a tickborne coinfection” [13].
The panel came to this conclusion despite four NIH retreatment trials that validated the severity of symptoms on 22 standardized measures of fatigue, pain, role function, psychopathology, cognition, and quality of life (QOL) [9].

Denying the existence and severity of CLD will continue to hinder the efforts to find a solution.
Even in a prospective trial of LD, 10 to 16% of patients treated at the time of an erythema migrans rash remained symptomatic a mean of 30 months after treatment; the results varied depending on the duration of antibiotics treatment [14].
The actual failure rate in this prospective at 30 months is uncertain, given that 38% of the subjects were not evaluable due to poor adherence, receipt of intercurrent antibiotics, or development of a second episode of erythema migrans [14].
Patients infected with many other kinds of common bacteria—such as those that cause tuberculosis, bronchitis, or UTIs—can experience relapses after an initial course of antibiotic treatment fails or proves inadequate.

Doctors routinely retreat patients who relapse in order to achieve a cure and prevent chronic symptoms. Why should patients with Lyme disease be treated differently?

The treatment failure rates could be exacerbated by diagnostic delays.
Feder described treatment delays of six weeks in LD patients initially misdiagnosed with cellulitis [15].
In his trial, Fallon noted treatment delays averaging 2 years [4] without examining the causes of the delay.
In my own practice, 32% of a consecutive case series of LD cases (confirmed by an ELISA and 5 or more positive bands on a IgG Western blot) had an average treatment delay of 1.8 years. [16]
Of these, 60% conformed to Centers for Disease Control and Prevention (CDC) epidemiological criteria, presenting with a rash, Bell's palsy, or arthritis, yet, still had a diagnostic delay [16].
Patients in this case series were significantly more likely to fail their initial antibiotic treatment if they had delayed treatment [16].
Vrethem et al. concluded that patients treated because of neurological symptoms of LD were much more likely to present with persistent neuropsychiatric symptoms (headache, attention problems, memory difficulties, and depression) three years after treatment than a control group with erythema migrans (50% versus 16%, P < .0001) [17].
The diagnostic delays could reflect the failure to consider CLD in the differential diagnosis of chronic manifestations of LD.
Steere did not include CLD in the differential diagnosis of patients seen in his university-based clinic. Instead, Steere diagnosed three-quarters of patients with “fibromyalgia” or “chronic fatigue syndrome” [18].
Similarly, Reid et al. did not include CLD as a diagnosis in their university LD clinic.
Instead, he diagnosed these patients with “arthralgia-myalgia syndrome,” primary depression, asymptomatic deer tick bites, osteoarthritis, and bursitis [16].
Hassett et al. diagnosed PTLD in patients with a history of objective evidence of LD, but withheld it from patients who lacked such a history. Instead, this group was diagnosed with “Chronic Multisymptom Illness (MUI) [19].
Their case definition for Chronic Multisymptom Illness was: “ [having] at least one or more chronic symptoms from at least 2 of 3 categories of symptoms including musculoskeletal, fatigue, and mood cognition” that includes fibromyalgia, chronic fatigue syndrome, and Gulf War syndrome [19].

The risks to the individual and society of CLD have not been adequately considered [20].
As a group, CLD subjects in the four NIH trials had a 4% risk of a serious adverse event in the antibiotic treatment arms [46].
Yet, this risk has not been weighed against the risk CLD patients face if burdened with a long-term debilitating illness. The risk to society of emerging resistant organisms also has not been weighed against the societal risks associated with an emerging population saddled with CLD [8].

The economic burden of CLD has yet to be addressed.
The mean cost estimate of CLD per patient in the US, of $16,199 per annum in 2002 dollars [8], reflects the toll on human health and cost to society.
The annual per-patient cost of CLD is substantially higher than the cost for other common chronic illnesses: $10,911 for fibromyalgia [21],
$ 10,716 for rheumatoid arthritis [21],
and $13,094 for lupus [22].
Eighty-eight percent (88%) of the cost ($14,327) of Lyme disease consisted of indirect medical cost, nonmedical cost, and productivity losses.
Cutting medical cost would save, at most, only 12% or $1,872 per annum. In 2002, the annual economic cost of LD in the US, based on the 23,000 cases reported to the CDC that year, was estimated to be $203 million [8].
Considering that the actual number of LD cases is believed to be 10 times higher than the number of cases reported to the CDC, the actual annual cost could be $2 billion [2324].

The burden of CLD is also reflected in testimony given by Connecticut's chief epidemiologist before the state's Public Health Department in 2004: “…roughly one percent of the entire population or probably 34,000 people are getting a diagnosis of Lyme Disease in Connecticut each year…20 to 25 percent of all families [in Connecticut] have had at least one person diagnosed with Lyme Disease ever and…three to five percent of all families have had someone diagnosed with Lyme Disease in the past year” [24].

No additional antibiotic trials have been planned for CLD patients despite the limitations of the Klempner and Fallon trials. Klempners' trials were limited by:
(1) uncertainty over whether the initial antibiotic treatment was effective,
(2) ongoing illness despite a mean of three previous treatments,
(3) long onsets of illness averaging 4.7 years,
(4) the poor quality of life of the subjects, and
(5) small, underpowered sample sizes of 51 and 78 subjects [25].
The Fallon trial had similar limitations including:
(1) uncertainty over whether the initial antibiotic treatment was effective,
(2) treatment delays averaging two years,
(3) onsets of illness averaging 9 years,
(4) the severe pain, fatigue, psychopathology, and poor QOL of subjects, and
(5) a small underpowered sample size of 37 subjects.
The IDSA panel did not suggest any further clinical trials to address these limitations. In an editorial titled “Enough is Enough”, which was published as a commentary on Fallon's trial, Halperin, an IDSA panel member, actually advised against further trials [26].

There is also an urgent need to address the mixed long-term outcome in children. Eleven percent of children with facial nerve palsy had persistent facial nerve palsy causing dysfunctional and cosmetic problems at 6-month followup [27].

Fourteen percent of 86 children had neurocognitive symptoms associated with or after classic manifestations of Lyme disease on followup [28].

Five of these children developed “behavioral changes, forgetfulness, declining school performance, headache or fatigue and in two cases a partial complex seizure disorder” [28].
Children with prior cranial nerve palsy have significantly more behavioral changes (16% vs. 2%), arthralgias and myalgias (21% vs. 5%), and memory problems (8% vs. 1%) an average of 4 years after treatment compared to controls [29].

Once we accept the evidence that CLD exists, the medical community should be able to find solutions. Professionals should be encouraged to examine whether:
(1) innovative treatments for early LD might prevent CLD,
(2) early diagnosis of CLD might result in better treatment outcomes, and
(3) more effective regimens can be developed for CLD patients who have had prolonged illness and an associated poor quality of life.

References

1. Shadick NA, Phillips CB, Logigian EL, et al. The long-term clinical outcomes of Lyme disease. A population-based retrospective cohort study. Annals of Internal Medicine1994;121(8):560–567.[PubMed]
2. Asch ES, Bujak DI, Weiss M, Peterson MGE, Weinstein A. Lyme disease: an infectious and postinfectious syndrome. Journal of Rheumatology1994;21(3):454–461. [PubMed]
3. Klempner MS, Hu LT, Evans J, et al. Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. New England Journal of Medicine.2001;345(2):85–92. [PubMed]
4. Fallon BA, Keilp JG, Corbera KM, et al. A randomized, placebo-controlled trial of repeated IV antibiotic therapy for Lyme encephalopathy. Neurology2008;70(13):992–1003. [PubMed]
5. Krupp LB, Hyman LG, Grimson R, et al. Study and treatment of post Lyme disease (STOP-LD): a randomized double masked clinical trial. Neurology2003;60(12):1923–1930. [PubMed]
6. Klempner MS. Controlled trials of antibiotic treatment in patients with post-treatment chronic Lyme disease. Vector Borne and Zoonotic Diseases2002;2(4):255–263. [PubMed]
7. Cameron DJ. Clinical trials validate the severity of persistent Lyme disease symptoms. Medical Hypotheses2009;72(2):153–156. [PubMed]
8. Zhang X, Meltzer MI, Pena CA, Hopkins AB, Wroth L, Fix AD. Economic impact of Lyme disease.Emerging Infectious Diseases2006;12(4):653–660. [PubMed]
9. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessments treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clinical Infectious Diseases2006;43(9):1089–1134.[PubMed]
10. Shadick NA, Phillips CB, Sangha O, et al. Musculoskeletal and neurologic outcomes in patients with previously treated Lyme disease. Annals of Internal Medicine1999;131(12):919–926. [PubMed]
11. Hodzic E, Feng S, Holden K, Freet KJ, Barthold SW. Persistence of Borrelia burgdorferi following antibiotic treatment in mice. Antimicrobial Agents and Chemotherapy2008;52(5):1728–1736.[PMC free article] [PubMed]
12. Yrjänäinen H, Hytönen J, Söderström K-O, Oksi J, Hartiala K, Viljanen MK. Persistent joint swelling and borrelia-specific antibodies in Borrelia garinii-infected mice after eradication of vegetative spirochetes with antibiotic treatment. Microbes and Infection2006;8(8):2044–2051.[PubMed]
13. Halperin JJ, Shapiro ED, Logigian E, et al. Practice parameter: treatment of nervous system Lyme disease (an evidence-based review): report of the quality standards subcommittee of the American Academy of Neurology. Neurology2007;69(1):91–102. [PubMed]
14. Wormser GP, Ramanathan R, Nowakowski J, et al. Duration of antibiotic therapy for early Lyme disease: a randomized, double-blind, placebo-controlled trial. Annals of Internal Medicine.2003;138(9):697–704. [PubMed]
15. Feder HM, Jr., Whitaker DL. Misdiagnosis of erythema migrans. American Journal of Medicine.1995;99(4):412–419. [PubMed]
16. Reid MC, Schoen RT, Evans J, Rosenberg JC, Horwitz RI. The consequences of overdiagnosis and overtreatment of Lyme disease: an observational study. Annals of Internal Medicine.1998;128(5):354–362. [PubMed]
17. Vrethem M, Hellblom L, Widlund M, et al. Chronic symptoms are common in patients with neuroborreliosis—a questionnaire follow-up study. Acta Neurologica Scandinavica.2002;106(4):205–208. [PubMed]
18. Steere AC, Taylor E, McHugh GL, Logigian EL. The overdiagnosis of Lyme disease. Journal of the American Medical Association1993;269(14):1812–1816. [PubMed]
19. Hassett AL, Radvanski DC, Buyske S, Savage SV, Sigal LH. Psychiatric comorbidity and other psychological factors in patients with “chronic Lyme disease” American Journal of Medicine.2009;122(9):843–850. [PubMed]
20. Cameron DJ. Insufficient evidence to deny antibiotic treatment to chronic Lyme disease patients.Medical Hypotheses2009;72(6):688–691. [PubMed]
21. Silverman S, Dukes EM, Johnston SS, Brandenburg NA, Sadosky A, Huse DM. The economic burden of fibromyalgia: comparative analysis with rheumatoid arthritis. Current Medical Research and Opinion2009;25(4):829–840. [PubMed]
22. Clarke AE, Esdaile JM, Bloch DA, Lacaille D, Danoff DS, Fries JF. A Canadian study of the total medical costs for patients with systemic lupus erythematosus and the predictors of costs. Arthritis and Rheumatism1993;36(11):1548–1559. [PubMed]
23. Ebel GD, Campbell EN, Goethert HK, Spielman A, Telford SR., III Enzootic transmission of deer tick virus in new England and Wisconsin sites. American Journal of Tropical Medicine and Hygiene.2000;63(1-2):36–42. [PubMed]
25. Cameron DJ. Generalizability in two clinical trials of Lyme disease. Epidemiologic Perspectives and Innovations2006;3, article 12
26. Halperin JJ. Prolonged Lyme disease treatment: enough is enough. Neurology.2008;70(13):986–987. [PubMed]
27. Skogman BH, Croner S, Nordwall M, Eknefelt M, Ernerudh J, Forsberg P. Lyme neuroborreliosis in children: a prospective study of clinical features, prognosis, and outcome. Pediatric Infectious Disease Journal2008;27(12):1089–1094. [PubMed]
28. Bloom BJ, Wyckoff PM, Meissner HC, Steere AC. Neurocognitive abnormalities in children after classic manifestations of Lyme disease. Pediatric Infectious Disease Journal1998;17(3):189–196.[PubMed]
29. Vázquez M, Sparrow SS, Shapiro ED. Long-term neuropsychologic and health outcomes of children with facial nerve palsy attributable to Lyme disease. Pediatrics2003;112(2):e93–e97.[PubMed]

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12 mars 2011 6 12 /03 /mars /2011 10:04

Acta Neurol Scand. 2011 Feb 15. doi: 10.1111/j.1600-0404.2010.01477.x. 


CXCL13 chemokine in pediatric and adult neuroborreliosis.

Wutte NBerghold ALöffler SZenz WDaghofer EKrainberger IKleinert GAberer E.


Department of Dermatology Institute for Medical Informatics, Statistics and Documentation Department of General Pediatrics Institute for Hygiene and Microbiology Department of Neurology, Medical University of Graz, Graz, Austria.


Wutte N, Berghold A, Löffler S, Zenz W, Daghofer E, Krainberger I, Kleinert G, Aberer E. CXCL13 chemokine in pediatric and adult neuroborreliosis. Acta Neurol Scand: DOI: 10.1111/j.1600-0404.2010.01477.x. © 2011 John Wiley & Sons A/S. Objectives - 

 

Diagnosis of Lyme neuroborreliosis (NB) depends on the proof of intrathecal antibody production against Borrelia burgdorferi.

 

CXCL13 has been seen to be elevated early in NB, before antibody production has started.

In this study, we determined the diagnostic role of the CXCL13 chemokine in cerebrospinal fluid (CSF) and serum for the first time in pediatric NB patients as well as in adults, compared to controls and blood donors (BD). Material and methods -  CXCL13 levels were measured in CSF and serum of 33 children and 42 adult patients. Serum CXCL13 was measured in 300 BD. Results -  CSF CXCL13 levels were significantly elevated in definite and probable acute NB in children and adults compared to seropositive and seronegative neurological controls (P < 0.001).

Serum CXCL13 levels showed great fluctuations and were not significantly elevated in NB patients. Conclusions -  Our study suggests that CSF CXCL13 can be used as a diagnostic marker for NB in children as well. In contrast, CXCL13 serum levels show great variance even in the healthy population and are not indicative of active NB.

© 2011 John Wiley & Sons A/S.

PMID: 21320077 [PubMed - as supplied by publisher]

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12 mars 2011 6 12 /03 /mars /2011 09:59

Clin Vaccine Immunol. 2011 Mar 2.


Multiplex immunoassay for Lyme disease using VlsE1-IgG and pepC10-IgM antibodies: improving test performance through bioinformatics.


Porwancher RBHagerty CGFan JLandsberg LJohnson BJKopnitsky MSteere ACKulas KWong SJ.


Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, New Jersey; Infectious Disease Consultants, PC, Mercerville, New Jersey; Department of Operations Research and Financial Engineering, Princeton University, Princeton, New Jersey; Division of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado; Zeus Scientific, Inc., Branchburg, New Jersey; Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Wadsworth Center, New York State Department of Health, Albany, New York.

The Centers for Disease Control and Prevention currently recommends a 2-tier serologic approach to Lyme disease laboratory diagnosis, comprised of an initial serum enzyme immunoassay (EIA) for antibody to Borrelia burgdorferi followed by supplementary IgG and IgM Western blotting of EIA-positive or -equivocal samples.


Western blot accuracy is limited by subjective interpretation of weak-positive bands, false-positive IgM immunoblots, and low sensitivity for early disease.


We developed an objective alternative second-tier immunoassay using a multiplex microsphere system that measures VlsE1-IgG and pepC10-IgM antibodies simultaneously from the same sample.

 

Our study population was comprised of 79 patients with early acute Lyme disease, 82 with early convalescent, 47 with stages II or III disease, 34 post-antibiotic treatment patients, and 794 controls.

 

A bioinformatic technique called partial receiver-operating characteristic (ROC) regression was used to combine individual antibody levels into a single diagnostic score with a single cutoff; this technique enhances test performance when high specificity is required (e.g. ≥95%).

 

Compared to the Western blot, the multiplex assay was equally specific (95.6%), but 20.7% more sensitive for early convalescent disease (89.0% versus 68.3%, respectively; 95% CI of difference: 12.1% to 30.9%) and 12.5% more sensitive overall (75.0% versus 62.5%, respectively; 95% CI of difference: 8.1% to 17.1%).

 

When used as a second-tier test, a multiplex assay for VlsE1-IgG and pepC10-IgM antibodies performed as well as or better than the Western blot for Lyme disease diagnosis. Prospective validation studies appear to be warranted.


PMID: 21367982 [PubMed - as supplied by publisher]

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