Overblog Suivre ce blog
Administration Créer mon blog
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]

Repost 0
Published by chronimed - dans Infections froides
commenter cet article
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.


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]

Repost 0
Published by chronimed - dans Infections froides
commenter cet article
11 mars 2011 5 11 /03 /mars /2011 16:00

Le nombre de cas de dengue hospitalisés va croissant aux États-Unis.

Cette tendance à l’augmentation est mise en évidence par l’analyse rétrospective des données intéressant les patients sortis d’hospitalisation avec un diagnostic de dengue entre 2000 et 2007 dans la cohorte du National Inpatients Sample discharges.

L’accroissement observé est considérable : le nombre d’hospitalisations pour dengue dans le pays aurait été multiplié par plus de 3 au cours de la période d’étude, les taux régionaux d’incidence indiquant les voyages comme source la plus probable de cette augmentation.

Streit J et coll. : Increasing trends in hospitalizations for dengue in the United States. International Meeting on Emerging Diseases and Surveillance – IMED (Vienne) : 4-7 février 2011.

Repost 0
Published by chronimed - dans Infections froides
commenter cet article
10 mars 2011 4 10 /03 /mars /2011 13:14

Espagne : les tiques profitent du réchauffement pour passer à l’attaque


Un nouveau scénario catastrophe vient s¹ajouter à la longue liste des

fléaux que pourrait provoquer le changement climatique. Une

augmentation importante des populations de tiques est prévue,

accompagnée d¹une recrudescence des maladies graves que ces

arthropodes transmettent à l¹homme. Un phénomène déjà observé depuis

plusieurs années en Europe et en Amérique du Nord.


© Liane Nothaft


Les tiques verraient leur population s¹accroître avec le réchauffement climatique.


Selon Agustín Estrada Peña, professeur en parasitologie à la faculté

de médecine vétérinaire de Saragosse, le réchauffement climatique va

permettre l’expansion en altitude et en latitude des populations de

tiques. Si le scientifique estime qu¹il n’y a pas lieu de s¹alarmer

pour l’instant, il souligne néanmoins que le risque pour la santé

publique est avéré. Un seul degré d’augmentation de la température

moyenne pourrait entraîner une accélération notable de la reproduction

des tiques et étendre considérablement leurs zones d’habitat.


C¹est dans le sang des vertébrés, notamment de l’homme et du chien,

que la plupart des tiques puisent leur alimentation. Le cycle de vie

de ces parasites est très dépendant des conditions de température,

d¹humidité et de luminosité. C’est donc entre le printemps et

l’automne qu’ils sont les plus actifs.


Ces animaux minuscules sont présents sur l’ensemble du territoire

espagnol. On les rencontre le plus souvent dans les parcs publics, les

jardins et les piscines, voire même dans les maisons. Les femelles ont

la capacité de pondre entre 1 500 et 2 000 oeufs d’un coup. Ceux-ci

mettant entre 17 à 30 jours pour se développer. Cette fécondité élevée

peut conduire à un accroissement rapide et exponentiel de leur



Le Centre Européen pour la Prévention et le Contrôle des Maladies

(ECDC : European Centre of Disease Prevention and Control) vient de

rendre public un rapport qui établit un lien direct entre le

réchauffement climatique et l¹expansion de la distribution

géographique de certaines espèces de tiques. Elles seraient

responsables de la transmission de maladies graves au sein de la

population. Ces travaux affirment par ailleurs que l¹Europe sera

touchée par ce phénomène au cours des prochaines années et que des

zones jusque là épargnées verront apparaître des cas graves liés à ces



Les pathologies concernées sont très nombreuses et comprennent entre

autres la fièvre boutonneuse méditerranéenne, l’encéphalite à tique,

la fièvre hémorragique de Congo-Crimée et la maladie de Lyme, encore

appelée borréliose. Agustín Estrada Peña indique que cette dernière

touche actuellement plus de 85 000 personnes en Europe, dont 8 000 en



Même si les personnes souffrant de ces affections sont la plupart du

temps exposées directement à des animaux ou des végétaux du fait de

leur profession, l’augmentation importante du nombre de tiques rendra

vulnérable l¹ensemble de la population

Repost 0
Published by chronimed - dans Infections froides
commenter cet article
6 mars 2011 7 06 /03 /mars /2011 10:44




Le point en 71 pages bien présentées . 







Repost 0
Published by chronimed - dans Infections froides
commenter cet article
6 mars 2011 7 06 /03 /mars /2011 10:33


Summary: The possibility of a Rickettsial origin for symptoms of depression and psychotic disfunction has been suggested by French scientists (Ch. Nicolle, Giroud, Legag, Jadin, Bottero) in their published works. Hence 300 patients, diagnosed as suffering from depression, or other neuropsychiatric dysfunction have been treated with antibiotic where a positive indicaton of Rickettsial infection was revealed as follows:

1.Many symptoms of these patients were similar to those exhibited in chronic Rickettsial diseases. 2.The treatment followed the finding that their serum reacted positively to the Giroud micro-agglutination test.

Giroud Test - specific for testing antibodies to these 5 antigens (R36):

ß Rickettsia Prowazeki ß R. Mooseri ß R. Conori ß Coxiella Burnetti

ß Neo-R. Q18

Done by micro agglutination Depends on the quality of antigens Comparative studies with IFA test gave very similar result

ß Positive reaction = presence of antibodies; (does not necessarily mean illness)

ß Negative reaction does not suppress Rickettsial etiology (R1,25)

Done by micro agglutination Patients and Methods: Statistics of 300 patients (100% Caucasian)







Repost 0
Published by chronimed - dans Infections froides
commenter cet article
3 mars 2011 4 03 /03 /mars /2011 19:05
Evidence of direct cell-cell fusion in Borrelia by cryogenic electron tomography.


Parasitology, Department of Infectious Diseases, University of Heidelberg Medical School, Im Neuenheimer Feld 324, 69120 Heidelberg, Germany. Department of Molecular Structural Biology, Max Planck Institute for Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany. Institute for Immunology, University of Heidelberg Medical School, Im Neuenheimer Feld 305, 69120 Heidelberg, Germany.




Some Borrelia species are the causative agents of tick-borne Lyme disease responsible for different disabilities depending on species and hosts. Borrelia are highly motile bacterial cells, and light microscopy shows that these spirochetes can associate with each other during movement. Using cryo-electron tomography, we observed closely associated Borrelia cells. Some of these showed a single outer membrane surrounding two longitudinally arranged cytoplasmic cylinders. We also observed fusion of two cytoplasmic cylinders and differences in the surface layer density of fused spirochetes. These processes could play a role in the interaction of Borrelia species with the host's immune system

Repost 0
Published by chronimed - dans Infections froides
commenter cet article
3 mars 2011 4 03 /03 /mars /2011 19:03
CD14 signaling reciprocally controls collagen deposition and turnover to regulate the development of lyme arthritis.
Am J Pathol Feb 2011; 178(2) :724-34

Center for Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA.



CD14 is a glycosylphosphatidylinositol-anchored protein expressed primarily on myeloid cells (eg, neutrophils, macrophages, and dendritic cells). CD14(-/-) mice infected with Borrelia burgdorferi, the causative agent of Lyme disease, produce more proinflammatory cytokines and present with greater disease and bacterial burden in infected tissues. Recently, we uncovered a novel mechanism whereby CD14(-/-) macrophages mount a hyperinflammatory response, resulting from their inability to be tolerized by B. burgdorferi. Paradoxically, CD14 deficiency is associated with greater bacterial burden despite the presence of highly activated neutrophils and macrophages and elevated levels of cytokines with potent antimicrobial activities. Killing and clearance of Borrelia, especially in the joints, depend on the recruitment of neutrophils. Neutrophils can migrate in response to chemotactic gradients established through the action of gelatinases (eg, matrix metalloproteinase 9), which degrade collagen components of the extracellular matrix to generate tripeptide fragments of proline-glycine-proline. Using a mouse model of Lyme arthritis, we demonstrate that CD14 deficiency leads to decreased activation of matrix metalloproteinase 9, reduced degradation of collagen, and diminished recruitment of neutrophils. This reduction in neutrophil numbers is associated with greater numbers of Borrelia in infected tissues. Variation in the efficiency of neutrophil-mediated clearance of B. burgdorferi may underlie differences in the severity of Lyme arthritis observed in the patient population and suggests avenues for development of adjunctive therapy designed to augment host immunity.

Repost 0
Published by chronimed - dans Infections froides
commenter cet article
3 mars 2011 4 03 /03 /mars /2011 18:58
European neuroborreliosis: quality of life 30 months after treatment.
Acta Neurol Scand Feb 2011;

Department of Neurology, Sørlandet Hospital, Arendal, Norway Department of Neurology, Sørlandet Hospital, Kristiansand, Norway Department of Clinical Medicine, University of Bergen, Bergen, Norway Clinic of Rehabilitation, Sørlandet Hospital, Kristiansand, Norway.



Eikeland R, Mygland Å, Herlofson K, Ljøstad U. European neuroborreliosis: quality of life 30 months after treatment. Acta Neurol Scand: DOI: 10.1111/j.1600-0404.2010.01482.x. © 2011 John Wiley & Sons A/S. Objectives -  The prognosis after Lyme neuroborreliosis (LNB) is debated. The aim of this study was to assess health-related Quality of Life (QoL) and neurological symptoms 30 months after treatment in European patients with LNB. Materials and methods -  In a prospective case-control designed study, we investigated 50 well-characterized patients with LNB who had participated in a treatment trial for LNB 30 months earlier and 50 matched control persons with the health QoL questionnaire Short-Form 36 (SF-36), the Fatigue Severity Scale (FSS), the Montgomery and Åsberg Depression Rating Scale (MADRS), the Starkstein Apathy Scale (SAS), and the Mini Mental State (MMS). Clinical and demographic data were collected by semi-structured interviews and clinical neurological examination. Results -  Lyme neuroborreliosis-treated patients scored lower than control persons in the SF-36 domains physical component summary (PCS) (44 vs 51 P < 0.001) and mental component summary (MCS) (49 vs 54 P = 0.010). They also scored lower than control persons in all the SF-36 subscales, except for bodily pain, and on FSS (3.5 vs 2.1 P < 0.001), but not on MMS (28 vs 29 P = 0.106). There was a difference in MADRS (3.1 vs 0. 8 P = 0.003) and SAS (13 vs 11 P = 0.016), but the scores were low in both groups. Fatigue was the most frequently reported symptom among LNB-treated patients (50%). Patients who reported complete recovery (56%) after LNB had similar QoL scores as the controls. Conclusion -  European persons treated for LNB have poorer health-related QoL and have more fatigue than persons without LNB

Repost 0
Published by chronimed - dans Infections froides
commenter cet article
3 mars 2011 4 03 /03 /mars /2011 18:56
Postural orthostatic tachycardia syndrome following Lyme disease.

Cardiol J 2011; 18(1) :63-6



Background: A subgroup of patients suffering from Lyme disease (LD) may initially respond to antibiotics only to later develop a syndrome of fatigue, joint pain and cognitive dysfunction referred to as 'post treatment LD syndrome'. We report on a series of patients who developed autonomic dysfunction in the form of postural orthostatic tachycardia syndrome (POTS). Methods: All of the patients in this report had suffered from LD in the past and were successfully treated with antibiotics. All patients were apparently well, until years later when they presented with fatigue, cognitive dysfunction and orthostatic intolerance. These patients were diagnosed with POTS on the basis of clinical features and results of the tilt table (HUTT) testing. Results: Five patients (all women), aged 22-44 years, were identified for inclusion in this study. These patients developed symptoms of fatigue, cognitive dysfunction, orthostatic palpitations and either near syncope or frank syncope. The debilitating nature of these symptoms had resulted in lost of the employment or inability to attend school. Three patients were also suffering from migraine, two from anxiety and depression and one from hypertension. All patients demonstrated a good response to the employed treatment. Four of the five were able to engage in their activities of daily living and either resumed employment or returned to school. Conclusions: In an appropriate clinical setting, evaluation for POTS in patients suffering from post LD syndrome may lead to early recognition and treatment, with subsequent improvement in symptoms of orthostatic intolerance. (Cardiol J 2011; 18, 1: 63-66).

Repost 0
Published by chronimed - dans Infections froides
commenter cet article