BORRELIOOSIN OIREET

Asiantuntijana Soile Juvonen TTT

Valvojat: Bb, Sailairina, maranoma, Tiina

BORRELIOOSIN OIREET

ViestiKirjoittaja soijuv » To Tammi 22, 2009 20:12

Matti K. Viljasen Duodecim-artikkelissa mainitaan borrelioosin oireita mm:

Iho-oireet. Yksittäisiä tai useampiakin metastaattisia EM- läiskiä voi ilmaantua myös primaarivaiheen jälkeen, eivätkä ne välttämättä sijaitse alkuperäisessä infektiokohdassa. Sekundaariset eryteemat ovat yleensä pienempiä kuin primaariset ja migroivat vähemmän. Niiden yhteydessä esiintyy usein neurologisia oireita.

Myöhäisoireet voivat ilmetä viikkoja tai vuosia primaarioireiden jälkeen.

Myöhäisoireita esiintyy ihon, nivelten, hermokudoksen tai sydämen taholta.

Bakteeri voi ACA-alueelta levitä suoraan alla tai lähellä oleviin luihin ja niveliin

Borrelia voi myös aiheuttaa kroonisen pannikuliitin eli ihonalaisen rasvakudoksen infektion.

Nivel- ja lihasoireet. Vaihtelevan ajan kuluttua primaarivaiheen jälkeen potilaille voi ilmaantua oligoartriitteja. Ne esiintyvät tavallisimmin suurissa nivelissä, erityisesti polvissa, ja yleensä niitä edeltävät uusiutuvat artralgia- ja myalgiavaiheet

Joskus artriittioireet esiintyvät jo EM-vaiheen lopussa. Artriiteille on tyypillistä oireettomien ja oireellisten kausien vuorottelu. Tauti kroonistuu noin 10 %:lla potilaista ja saattaa kestää vuosia. Vaikeissa tapauksissa tauti voi johtaa rustoeroosioiden syntymiseen.

myalgia ja artralgia ovat ainakin suomalaisessa myöhäisborrelioosissa hyvin yleisiä

Neurologiset oireet. Lymen taudissa neurologiset oireet ilmenevät pääasiassa aivokalvojen ja aivohermojen alueella eli erilaisina meningoradikuliitteina.

borrelioosille on tyypillistä esiintyminen Bannwarthin syndroomana tunnetussa muodossa

Särkyjen esiintyminen hartioissa ja lapaluiden seudussa on myös tavallista. Kivut voivat vaihdella samallakin potilaalla sekä paikaltaan että vaikeudeltaan

aivohermojen halvauksia, tavallisimpana kasvohermojen halvaus, tai radikulaarisia halvauksia ja tuntohäiriöitä

Päänsärkyä, niskajäykkyyttä, kroonista väsymystä, erilaisia parestesioita, muistihäiriöitä ja anoreksiaa voi esiintyä borrelioosin yhteydessä.

Sydänoireet. voi kehittyä eriasteisia eteis- kammiokatkoksia, myoperikardiitteja tai lievää vasemman kammion toiminnanvajausta

Disseminaatiovaiheen jälkeen borrelia voi aiheuttaa infektion lähes missä elimessä tahansa. Yksittäistapauksina on kuvattu esimerkiksi hepatiitteja, erilaisia silmänsisäisiä ja -ulkoisia infektioita

Borrelia voi myös levitä sikiöön ja johtaa sikiön kuolemaan


http://www.duodecimlehti.fi/web/guest/e ... ku_p_auth=


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http://www.hus.fi/ammattilaiselle/koulu ... alossa.pdf

Yleisoireet:
• Väsymys, uupumus
• Paikkaa vaihtavat lihas- tai nivelkivut, jäsensäryt, kuin ”flunssa” ilman
nuhaa, yskää tai kurkkukipua
• Päänsärky
• Lämpöily

Muut tuki –ja liikuntaelinoireet
• Artralgia
• Myalgia
• Niveltulehdus eli artriitti: synoviitti ja hydrops (harvoin)
• Jännetuppitulehdus (tendiniitti, daktyliitti) ja luutulehdus (harvoin)

Ääreishermoston oireet ja meningiitti
• Facialis-, abducens-, oculomotoriuspareesi, tinnitus
• Polttavat kivut, tuntomuutokset, kävelyvaikeudet, raajahalvaukset, rakon tai
sulkijalihaksen toiminnanhäiriöt. Huom lihas-, nivel- ja joskus rinta- ja vatsakivut
(meningoradikuliitti, Bannwarthin syndrooma)
• Plexusneuriitti, mononeuritis multiplex
• Lymfosytäärinen meningiitti (voi olla toistuvia episodeja, ei välttämättä
niskajäykkyyttä)

Keskushermoston oireet
• Huimaus
• Muistihäiriöt, kognition häiriöt (potilas huomaa), sekavuus,
persoonallisuusmuutos (ympäristö huomaa)
• Enkefaliitti
• Pikkuaivoataksia, myoclonus, apraksia, hemipareesi, Parkinson-oireet
• Akuutti halvausoireisto (vaskuliitti)

Sydänoireet
• Rytmihäiriötuntemukset (tarv. EKG, holter, ECHO)
• Rintakipu
• Perikardiitti, myokardiitti, eteiskammiokatkos, sydämen
vajaatoiminta

Silmäoireet
• Diplopia, kaksoiskuvat (aivohermotulehdukseen viittaava oire)
• Silmien punoitus
• Silmän takainen kipu (voi liittyä meningiittiin)
• Diagnosoitu silmän sidekalvon, värikalvon, näköhermon tai
verkkokalvon tulehdus

• Lymfosytooma, paikallinen
disseminaatio
– tummanpunainen pahkura
puremapaikan lähellä, esim
korvanlehdessä tai nännipihassa



_____________________________________

Mitä on elämä borrelioosin kanssa?

Tri John Sterngold 4.11.2009 The Willits News

Suom. S.Juvonen TTT

Borrelioosi on äärimmäisen monimuotoinen tauti.
?Mitkä ovat Borrelioosin oireet? Käytän niistä termiä "monimuotoiset" sillä oireiden aiheuttajana voi olla useita eri taudinaiheuttajia/lisäinfektioita joita ihminen on saanut esim. punkinpureman välityksellä. Tällaisia ovat esim. mykoplasma, Bartonella, babesia, anaplasma jne. Mikäli immuunipuolustus ei selviä kaikista taudinaiheuttajista, ne pääsevät leviämään eri puolille elimistöä aiheuttaen tulehduksia. Mikrobien erittämät toksiinit aiheuttavat sen lisäksi vaurioita soluille ja kudoksille. Siksi sairastuneiden oireiden voimakkuus ja kirjo voivat vaihdella suuresti.

Yhdellä voi olla ajoittain esiintyviä nivelkipuja, toisella täydellisen työkyvyttömyyden aiheuttava neuropatia jonka seurauksena hän ei kykene esim. kävelemään tai seisomaan, kolmannella voi olla hyytymiä silmissä ja niistä johtuva sokeus, joillakin voi olla niin voimakas uupumus etteivät he pysty nousemaan sängystä. Monilla on voimakkaita kipuja jaloissa tai selässä tai muualla elimistössä, jotkut menettävät kuulon, toiset kyvyn tuntea kylmää tai kuumaa, useimmilla on unettomuutta, kuivaa yskää, hikoilua, vilutusta, "aivosumua", joillakin on masennusta tai muita psykiatrisia oireita kuten ns. kaksisuuntainen mielialahäiriö. Borrelia-bakteeri voi aiheuttaa myös henkeä uhkaavia sydänoireita.

Kaikki edellä mainitut potilaat tarvitsevat antibioottihoitoa eivätkä yksinomaan oireiden mukaista lääkitystä.

Joillakin sairastuneilla on vain jokin oire, toisilla voi sen sijaan olla useita erilaisia oireita. Ei siis ole ihme, että tavalliset lääkärit joko pyörittelevät silmiään tai yksinkertaisesti kieltäytyvät uskomasta potilaan oireisiin ja siihen, että kyseessä on hoitoa vaativa infektiotauti. On paljon helpompaa luokitella potilaat psykiatrisiksi tapauksiksi - "oireet ovat vain mielikuvituksen tuotetta", "turhasta valittava - tyyppi" jne. Lääkärin elämä on paljon helpompaa, kun hän kieltää potilaan oireiden todellisuuden. "Kuten jo sanoin, oireesi eivät johdu Borrelioosista."

Oireiden moninaisuuden lisäksi diagnostiikkaa vaikeuttaa bakteerin/-ien geneettinen monimuotoisuus. Valitettavasti näiden taudinaiheuttajien laboratoriodiagnostiikka on pahasti "eksyksissä". On olemassa vain harvoja Borrelioosi/lisäinfektio -testejä ja nekin jättävät huomioimatta suurimman osan bakteerien geneettisistä muutoksista. Testituloksella on merkitystä mikäli se on positiivinen, mutta se on merkityksetön, mikäli tulos on negatiivinen. Emme yksinkertaisesti voi sulkea pois taudin olemassaoloa negatiivisen testituloksen pohjalta. Lääkärit jotka tekevät näin, ovat väärässä tai haluavat kieltää tosiasiat.

Bakteerit eivät ole yksinään syyllisiä taudin kulkuun. Jokaisella ihmisellä on yksilöllinen immuunipuolustus ja sen rooli on merkittävä. On huomattu, että genetiikaltaan tietyntyyppiset ihmiset saavat helpommin vakavamman taudinkuvan kuin muut. Joidenkin elimistö muodostaa helpommin vasta-aineita jotka hyökkäävät elimistön omia kudoksia vastaan (autoimmuunireaktio), toisilla immuunipuolustuksen kyky hajottaa ja poistaa toksiineja on heikentynyt. Tässä on joitakin syitä siihen, miksi tauti on jokaisen kohdalla yksilöllinen ja miksi tarvitsemme Borrelioosiin laajasti perehtyneitä asiantuntijoita.?


The Willits News 4.11.2009: Tri John Sterngold
http://www.willitsnews.com/ci_13712962
LIVING WITH LYME: A phenomenally complex disease
By Dr. Jon Sterngold/Special for The Willits News
Posted: 11/04/2009 01:56:27 PM PST

What are the symptoms of late-stage Lyme disease complex? I use the term 'complex' because the spectrum of symptoms are most often caused by the Lyme germ, Borrelia burgdorferi, and other co-infecting pathogenic organisms the ticks carry and transmit. With names such as Babesia, Bartonella, Mycoplasma, and Anaplasma, these pathogens can dramatically contribute to the degree of disease and complexity of diagnosis and treatment in infected individuals. So, as the immune system loses control of these bugs, they spread and cause inflammation, as well as release toxic molecules that cause symptoms and injury to cells and organs.

With so many different possible combinations of infecting organisms and degrees of immune system compromise, the list of potential symptoms is very long. While one person might just have waxing and waning joint pains, another could be totally disabled with neuropathies that interfere with the ability to walk or even to stand. Some become blind from blood clots in the eyes and some are so fatigued that getting out of bed each day might not be possible. Many are plagued with the dreaded "brain fog" and some develop what appear to be well-known psychiatric diseases, such as bipolar disorder and severe depression. But, these patients need antibiotic treatment as much or more than anti-depressants and other psych meds.
Many patients develop severe pain syndromes involving the back and legs, though involvement can be anywhere in the body. Some patients
lose intellectual ability, hearing, the ability to sense heat from cold, and coordinated movements. Most develop insomnia, and many get disabling pain in their feet. Fevers, chills, sweats, dry cough, and body aches can make it seem that some sort of "chronic flu" is going on.
Lyme disease can cause life-threatening cardiac abnormalities. And the list goes on.
Some patients have only several symptoms and some have scores. It is no wonder non-Lyme literate physicians either roll their eyes at the prospect of taking care of a Lyme patient or simply refuse to believe this constellation of symptoms is an active and treatable infectious disease. It is so much easier to believe these patients have psychiatric disease ("it's all in your head"-type illness) or suffer the aches and pains of aging and a low pain threshold (whiners). It makes the doctor's life so much easier. Just say no. And believe me, as I said before, I would not relish the notion of taking care of a patient with as complex a disease as my own.
And it's not even that simple. We now know that in addition to the major germ types listed above, there are dozens to hundreds of genetic variations of these organisms. This introduces a mind-boggling level of diagnostic complexity. Physicians faced with a bad disease, and complex long-term, sometimes dangerous treatment, need as much diagnostic data as possible to justify a treatment plan. But testing for these pathogens is almost a lost cause to date.
There are only a few tests for these bugs, and they miss most of the genetic variants. The tests are very meaningful and helpful when positive, but meaningless when negative. We simply cannot "rule out" an infection with a negative test. Physicians who believe otherwise are wrong, if not downright negligent.
But wait, there's more!
It's not just the bugs that determine our illness. Our unique immune system genetics and dysfunction play a large part creating the spectrum of symptoms we develop. It has been found that some genetic types tend to develop more severe disease than others, including subtypes that cannot get well. Some are more prone to creating antibodies that make us ill by attacking our own tissue and some have impaired ability to break down and excrete bacterial toxins. These are some of the reasons that one person's Lyme disease doesn't look another's and why we need Lyme experts to manage sick patients.
ABOUT THE AUTHOR: Jon Sterngold, MD, is a Willits resident and physician
Viimeksi muokannut soijuv päivämäärä Ke Huhti 18, 2012 20:17, muokattu yhteensä 6 kertaa
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » To Tammi 22, 2009 20:17

66:sta kroonista neuroborrelioosia sairastavasta henkilöstä 20 % ilmoitti kärsivänsä levottomat jalat -syndroomasta. Oire ilmenee levossa.

Restless Leg Syndrome As A Marker For Unsuspected Chronic Lyme Disease

By Virginia T. Sherr, MD (2002)

http://www.thehumansideoflyme.net/viewa ... php?aid=40

Objectives: Restless Legs Syndrome is characterized by a torturous sense of needing to move the reclining leg--a feeling that can not be denied by the sufferer. As it was more clearly understood that RLS is mediated by many neurologically related abnormalities, it was thought RLS might be provoked by the presence of known or unsuspected neuroborreliosis. A study was undertaken in and from an eastern Pennsylvania private psychiatric office to ascertain the likelihood of a Lyme/RLS connection in that area, highly endemic for infected deer ticks.

Method: Psychiatric patients who had been found to have previously unsuspected tick-borne diseases, primarily Lyme disease, were interviewed to ascertain the possibility of co-existent RLS. At the same time, a survey of the membership of an unrelated, local support group for known RLS sufferers was undertaken with the goal of locating people who were previously diagnosed or as yet possibly undiagnosed victims of chronic Lyme disease.

Results: Of the 66 chronically Lyme-infected psychiatric office outpatients, 20% described typical symptoms of Restless Legs Syndrome. They acknowledged RLS symptoms as causing excruciating distress to them. Some of these patients also had a related condition, Periodic Limb Movement Disorder, which is characterized by a jerking of the legs (or arms) during sleep. None was receiving usual dopamine agonist medications for treatment of RLS.

The situation in the totally unrelated RLS support group was different but also suggestive. In a survey of 150 members, approximately one third of whom responded, 50% described chronic non-RLS multi-system physical symptoms for which they could get no diagnosis after consulting multiple specialists. Of the 7 people who so far have allowed Western Blot and PCR testing, 5 tested positive for Lyme and, to some degree, other associated tick-borne infections. One other person apparently has lupus. There were 3 others who had past histories of treated LD.

The 5 RLS support group members who tested positive were relieved at the new diagnoses of chronic Lyme disease. Of the four of them to date who have allowed treatment for their infections, all have experienced reduction in their RLS, two no longer needing therapy other than iron supplements and antimicrobial medications.

In the psychiatric outpatient group, all the patients who underwent treatment for chronic Lyme disease lost their RLS and PLMD symptoms with the advent of appropriate antimicrobial medications and sans dopaminergics.

Conclusions: Experience with two unrelated sets of people--Lyme victims in treatment for emotional/cognitive problems and a cluster within a RLS support group indicates a likely role for Lyme disease as a causation of RLS.
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » To Tammi 22, 2009 20:18

ISKIAS.

"Iskias/lonkkahermosärky/ristiselkäkipu on eri puolilla maailmaa yksi yleisimmistä syistä hakeutua lääkärin vastaanotolle. Siitä huolimatta oireen patogeneesiä ei tunneta. Koska välilevyihin kohdistuva mekaaninen paine ei ole osoittautunut riittäväksi selitysmalliksi kivuille on viimeaikaisissa tutkimuksissa kiinnitetty huomiota hermojuurien tulehdusprosessiin. Tämän seurauksena on noussut esiin kysymys mikrobien osuudesta tulehdusten aiheuttajina. Tutkimuksessa huomattiin erilaisten mikrobien kuten Propionibacterium acnes ja tiettyjen stafylokokkien aiheuttavan ristiselän heromjuurien tulehduksia."

Myös borreliabakteerin on useiden lähteiden mukaan huomattu aiheuttavan hermojuuritulehduksia. Lukuisat Borrelioosiin sairastuneet ovat kertoneet kärsivänsä toistuvista ristiselkäkivuista. useimmiten hoidoksi on annettu fysioterapiaa, liikuntaa, kipulääkkeitä jne.

Muutama borrelioosia sairastava henkilö kertoi oireistaan seuraavasti:

1. "Perheenjäsenemme saivat lukuisia punkinpuremia 30 vuoden aikana edellisessä asuinpaikassamme. Borrelioosi vahvistettiin seerumin vasta-aine- ja virtsatesteillä. Omalla kohdallani krooninen väsymysoireyhtymä on pääoireena, miehelläni esiintyy prostatulehduksia ja iskiasta, pojallamme on neurologisia oireita. Meidän kaikkien oireet alkoivat vasta vuosien kuluttua puremista."

2. "Mieheni sairastaa borrelioosia. Hän saa toistuvasti voimakkaita ristiselkäkipukohtauksia. Antibioottihoidoilla kivut ovat hävinneet."


An association between sciatica and microorganisms

Investigators:

Professor TSJ Elliott(a), Consultant Microbiologist
Dr A Stirling(b), Consultant Spinal Surgeon
Dr P Lambert(c), Reader in Microbiology
Dr T Worthington(a), Clinical Research Scientist
Dr M Jiggins(b), Research Fellow

(a) University Hospital Birmingham NHS Trust, Edgbaston, Birmingham, UK
(b) Royal Orthopaedic Hospital, Northfield, Birmingham, UK
(c) Aston University, Aston Triangle, Birmingham, UK 28th February 2002

Introduction

The pathogenesis of low back pain and sciatica remains poorly understood despite being one of the commonest causes for consultation in primary care.(1) Since mechanical compression involving the spinal disc space is insufficient alone to account for the pain associated with sciatica, attention has focused on inflammation of the nerve root resulting from exposure to the disc during herniation. The inflammation that is associated with sciatica has raised the question of a microbial aetiology, possibly with low virulent microorganisms, as found for example, with prosthetic hip infections. Over the last two decades the skin commensals, coagulase-negative staphylococci and propionibacteria, considered primarily as contaminants when isolated from patients, are being increasingly recognised as aetiological agents of infection. Tunney and colleagues(2), for example, have demonstrated the presence of Propionibacterium acnes and coagulase-negative staphylococci in situ on prosthetic joints studied at revision arthoplasty.

The results of our recent research part funded by BackCare, also suggest that these microorganisms, particularly in P.acnes, may be associated with chronic low grade infection in the lower vertebral discs of patients with severe sciatica.(3) Indeed, 53% of patients with severe sciatica who were recruited into the study and underwent microdiscectomy, had positive cultures within 7 days of incubation. P.acnes was recovered in pure culture from 84% of the tissue samples. Furthermore, this preliminary study also demonstrated that significant elevations of a specific serum antibody to a novel exocellular bacterial cell wall component termed lipid S, a glycerophospholipid, was present in those patients yielding positive cultures. These results were significantly different from those obtained from control patients. Our preliminary results suggest that there is an association between P.acnes and sciatica, the diagnosis of which could be aided by the use of the novel lipid S antigen.

The aim of our research is to further investigate the role of Gram-positive microrganisms, particularly coryneforms such as P.acnes in the inflammatory reactions around the nerve root which can result in sciatica. If a link between those low virulent skin microorganisms and sciatica can be confirmed, early diagnosis may indeed lead to improved treatment strategies. Early intervention with appropriate antibiotics in selected patients may modify the subsequent clinical progression of this association between microorganisms and sciatica are presented in this progress report. In addition, a detailed plan of our future research extending over a 30-month period and associated costs is also given.

Methods
Microbiological assessment of tissue samples and estimation of serum levels of anti-lipid S IgG

Two-hundred and seven patients diagnosed as having discogenic radiculitis have been recruited into the study to date. The patients underwent microdiscectomy to relieve the unremitting pain associated with their sciatica. Disc and tissue samples were removed during surgery and sent for microbiological investigation. Disc and tissue samples were also taken from 27 control patients including those presenting with scoliosis, trauma and myelomas. All clinical samples were cultured by standard microbiological techniques, and microorganisms were identified by conventional methods. Ten-ml of blood was also taken from all patients for anti-lipid S IgG estimation by ELISA.(4)

Analysis of P.acnes isolates
10 strains of P.acnes isolated from disc material have been investigated for their antigenic composition by western blotting. Strains were grown in brain heart infusion broth (BHI) for 3 days under static, microaerophilic conditions. The culture medium was recovered by centrifugation and precipitated with 2 volumes of ethanol at -20û C. Preticipated material (i.e. potential exocellular antigen) was then subjected to electrophoresis (SDS-PAGE, 12% acrylamide gels) and either stained with coomassie blue to visualise proteins, or western blotted onto mitrocellulose membrane. Antigen profiles on the nitrocellulose were revealed by reacting with patient serum followed by protein A-peroxidase and chromogenic substrate. To investigate antibody response by a number of patients, ethanol-precipotated material from one strain on P.acnes was run in a single perparative lane, the nitrocellulose blot was cut into strips and each reacted with a different patient serum (strip blots).

Results
Patients with Sciatica
Spinal tissue was obtained from 207 patients undergoing microdiscectomy for severe unremitting sciatica. This tissue was examined for the presence of microorganisms. Seventy-six (37%) out of 207 patients yielded positive cultures. The microorganisms recovered from the microdiscectomy samples are shown in Table 1. Of these patients, 26 (34%) had elevated serum levels of anti-lipid S IgG.

One hundred and thirty one out of 207 patients had negative cultures and of these 111 (85%) had corresponding negative lipid S titres.


Table 1

Microorganisms recovered from microdiscectomy samples taken from patients presenting with sciatica

Microorganisms Number
(% of isolates)
bacterium acnes (pure growth) 49 (64%)
Propionibecterium granulosum 1 ( 1%)
Propionibacterium acnes/coagulase negative staphylococci 8 (11%)
Coagulase negative staphylococci 11 (14%)
Corynebacterium propinquum 1 ( 1%)
Micrococcus species 1 ( 1%)
Heavily mixed cultures 4 ( 5%)

Control patients
Microdiscectomy samples from 25 out of 27 (93%) of control patients yielded negative cultures. Propionibacterium acnes was recovered from the tissue samples of 2 out of 27 (7%) patients. Out of the control patients, 21 out of 27 (78%) had negative lipid S serology whilst 6 out of 27 (22%) had raised levels.

Statistical analysis of data
Statistical analysis of the data demonstrated the following:

There is an extremely significant difference in positive serology between patients with positive culture and those with negative culture (p=0.019, Table 2).
There is a significant difference between the positive cultures of patients with sciatica and controls (p=0.001, Table 3).
There is a significant difference between the pure cultures of P.acnes from patients with sciatica and controls (p=0.029 Table 4).

Table 2
Positive serology between patients with positive culture and those with negative culture
Positive
serology Negative
serology Total
Positive culture 26 50 76
Negative culture 20 111 131



--------------------------------------------------------------------------------



Table 3
Patients with sciatica versus controls: total positive cultures
Patients with sciatica Controls
Positive cultures 76 2
Negative cultures 131 25

--------------------------------------------------------------------------------



Table 4
Patients with sciatica versus controls: pure growth of P.acnes
Patients with sciatica Controls
Pure P.acnes 49 2
Negative culture 118 25
(not inclusive of other microorganisms) (190-47 25)

Antigenic analysis of P.acnes isolates
Protein profiles (a Coomassie blue stained SDS-PAGE gel) and a representative western blot developed with a patient serum are shown in figure 1 (not reproduced in here) for 10 isolates of P.acnes. Figure 2 (not reproduced here) shows a strip blot for a single strain developed with serum samples from 15 sciatica patients. A prominent cluster of antigens of molecular weight around 29-36kDal is present in all the strains and detected by all patients studied to date. This antigenic material does not appear to contain protein since it does not stain with Coomassie blue. We are currently investigating its composition and properties as a potential market of P.acnes infection and its possible role as a mediator of inflammation and nerve root pain.

Conclusions
These results suggest that low virulent microorganisms, in particular, P.acnes may be associated with infection in the vertebral discs of patients with severe sciatica. This has been confirmed by direct culture of the disc material, the application of a novel serologiacal assay and by comparison to the results obtained for control patients. Results of preliminary western blotting investigations have identified a novel exocellular antigen of P.acnes, which may serve as a further potential serological marker of infection due to the microorganism.


Further work
We propose to follow several lines of investigation.

We will confirm the association between the presence of P.acnes and related microorganisms in disc tissues from sciatica patients using more fully characterised patient groups.

We will investigate the role of the microorganisms in this condition. This will include genotyping and phenotyping of the microorganisms recovered from clinical samples, and studying the potential pro-inflammatory factors and cell-matrix degrading enzymes produced by the bacteria.

The response of the disc to the presence of the microorganisms including host production of inflammatory mediators from disc cells will be investigated. An in vitro model to study the release of inflammatory mediators from disc cells will also be utilised to study local tissue responses to microorganisms.

Patient groups and clinical, microbiological and host-response investigations
The study will be a double blinded, case controlled, randomised investigation.

The groups of patients will be as follows:

100 further patients with sciatica
30 patients undergoing surgery for back pain without radiculitis
50 control patients undergoing surgery for other reasons
50 patients with severe acne without radiculitis
Pre-operative and operative findings (where applicable) will be recorded.

Microbiological investigations including culture of clinical material and estimations of serum levels of anti-lipid S IgG will be undertaken on all patient groups.

Microorganisms recovered from clinical samples will be characterised by phenotypic and genotypic methods.

Tissue samples will be subjected to PCR analysis, in situ hybridisation and immunohistochemistry to reveal microorganisms, which cannot be cultured directly, and to reveal their precise location within the disc.

An investigation to assess the vascularisation of the disc tissue will be undertaken to determine whether or not macrophages infiltrate and dominate the cellular response to microbial mediators.

An investigation to assess the association between microorganisms and levels of metalloproteinases, cytokines and prostaglandins will be undertaken. Furthermore, the ability of microorganisms to stimulate the release of inflammatory mediators will be determined.

Results of the study will be presented at national and international orthopaedic, microbiology and cell biology meetings. Results will be published in medical and scientific journals.


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References 1. Office of Population Census and Surveys (OPCS). Morbidity statistics from general practice, 4th national study. Royal College of General Practitioners, OPCS, Department of Health, London. HMSO, 1995.
2. Tunney MM, Patrick S, Gorman SP, Nixon JR, Anderson N, Davis RI, Hnna D, Ramage G. Improved detection of infection in hip replacements. Journal of Bone and Joint Surgery [BR] 1998;80(4): 568-572
3. Stirling A, Worthington T, Rafiq M, Lambert PA, Elliott TSJ. Association between sciatica and Propionibacterium acnes. Lancet 2001;357:2024-2025
4. Worthington T, Lambert PA, Traube A, Elliott TSJ. A rapid ELISA for the diagnosis of intravascular catheter-related sepsis due to coagulase negative staphylococci. Accepted for publication Journal of Clinical Pathology 2001.
Viimeksi muokannut soijuv päivämäärä La Huhti 18, 2009 11:07, muokattu yhteensä 2 kertaa
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » To Tammi 22, 2009 20:27

Erilaiset pakko-oireet kuten jatkuva käsien peseminen voivat olla borreliabakteerin aiheuttamia. Seuraavassa kaksi tapausselostusta; nainen jolla oli jatkuvia seksifantasioita miehestä josta hän ei pitänyt ja nuori lääketieteen opiskelija joka pesi käsiään yhtämittaa. Kummankin tilanne parani huomattavasti antibioottihoidoilla. Nainen sai useita erilaisia antibioottihoitoja, mutta tilanne parani vasta lihakseen pistettävän antibioottihoidon jälkeen (Bicilliini 2,4 miljoonaa yksikköä).

Two Cases Of Lyme Disease-Associated Obsessive Compulsive Disorder (OCD)

Lyme Disease Foundation's XV International Conference
on Lyme disease and other Tick-borne Disorders
Farmington CT
April 6-7, 2002

TWO CASES OF LYME DISEASE-ASSOCIATED OBSESSIVE COMPULSIVE DISORDER (OCD) ARE DESCRIBED. OBSESSIONS MAY BE TERMINATED SUDDENLY AND PERMANENTLY BY THE FIRST INJECTION OF IM PENICILLIN

Abstract by Virginia T. Sherr, M.D.

Known, but more often unsuspected, streptococcal infections have been revealed to be capable of creating obsessive compulsive symptoms that are in perfect agreement with the criteria of the Diagnostic and Statistical Manual, Edition IV--American Psychiatric Association. (1) In addition, these symptoms have cleared up following aggressive treatment by appropriate antibiotics. In relationship to another infection, chronic neuroborreliosis (chronic neuro-Lyme disease), the author finds there is much evidence that the spirochetal microbe, Borrelia burgdorferi, the cause of Lyme disease (LD), may likewise negatively affect parts of the brain that control OCD. In the case of the streptococcal and now spirochetal infections, it has been shown that antibiotics can be effective treatments of the psychiatric disorder. The disorder itself is one of the few wherein treatment improvements can be monitored and actually visualized by PET and more recently devised scans following therapy. Disordered dopamine and serotonin chemistry at the neuron level may create a kind of circular effect of thoughts or behavioral rituals. Some areas of the brain that are affected are the orbital frontal cortex, the caudate nuclei and the anterior cingulate regions. The following cases represent 2 patients who experienced the onset of severe obsessive and/or compulsive symptoms with onset of LD and how their treatment with antibiotics led to the defeat or the amelioration of those symptoms.

Patient 1--Obsessions. A circumspect 50 y-o woman developed constant, intrusive, sexual fantasies about a man whom she actively disliked. She felt helpless in the face of this unwanted, total preoccupation and was contemplating suicide when her LD was diagnosed and treated. Obsessions continued to torture her despite use of a variety of antibiotics and psychotropics until she received IM Bicillin 2.4 million units. Within 24 hours of the first dose her mind was cleared of the ideation. She was grateful that this burden had been lifted from her. The obsessions have not returned in the past 5 months. Now it takes great mental effort for her to think of the man at all.

Patient 2--Compulsive hand washing. A medical student had such a severe hand-washing ritual that he confined himself to his own room. He feared vague but horrific contaminations that might, through him, somehow harm his family. He described himself as having "magical thinking" that led to washing his hands raw. Debilitated, he thought that he was doomed. "When diagnosed and treated with antibiotics for LD, I felt much better and lost the magical thinking but the hand-washing continued." Luvox was added to his medications. This controlled the ritual washing enough to allow him to enroll in a different graduate program, living independently. In similar cases, usual OCD treatments such as high dose SSRI medications do not work well until treatment with antibiotics is undertaken.

1. Perlmutter SJ, Garvey MA, Castellanos X, et al.
A case of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections.
Am J Psychiatry 155:11, November 1998. (Re: PANDAS)
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » To Tammi 22, 2009 21:14

Borreliabakteerin eri muodot saattavat olla syynä jatkuvaan vasta-ainereaktioon, kroonisiin oireisiin ja ne ovat todennäköisesti yhteydessä MS- ja Alzheimerin tauteihin. (Puolalainen tutkimus 2002)

Borreliabakteeri voi aiheuttaa mitä moninaisimpia keskushermostotulehduksia esim. ALS-taudille tyypillisiä oireita (Belgia 2009)


Przegl Epidemiol. 2002;56 Suppl 1:57-67.
New aspects of the pathogenesis of lyme disease
[Article in Polish]

* Zajkowska JM,
* Hermanowska-Szpakowicz T.

Klinika Chorob Zakaznych i Neuroinfekcji AM w Bialymstoku.

Morphological changes of B. burgdorferi as well as changes in expression of surface proteins caused by environmental determinants are essential in pathogenesis of Lyme disease. Cysts, spherical form (spheroplasts, L-form) and "blebs" (gemmae) can be responsible for long lasting antigenic stimulation, signs of chronic borreliosis, and even probably connected with MS and Alzheimer disease. Mechanisms to avoid elimination and persistence in the host include: expression of low heterogenic Osp A, B replaced by polymorphic in sequence and antigenic reactivity OspC, the hindrance of access to some membrane proteins by other proteins on the spirochete's surface, effects of tick saliva proteins action. Hiding of spirochetes is possible by invagination into fibrocytes membrane as well as, coating by antigens derived from lymphocytes B. Distribution of spirochetes is facilitated by binding to platelets through integrin aIIb b3, and to the endothelial cells through integrins av b3 i a5b1, recognition of decorin by lipoproteins DbpA i DbpB, receptor for NAG (N-acetyl glucosamina). Endothelial cells, toxic products of granulocytes, monocytes, macrophages as well as phagocytosis counterpart in pathogenesis. Induced cytokines are connected with activation subsets of T lymphocytes involved in inflammatory response. Cytokines produced by Th1 as cytotoxic CD8 accompany the disease. Important are also dendritic cells regarded as initiators of Th1 response with participation of IL-12. In pathogenesis of Lyme disease participation of autoimmunity is notified, especially molecular similarities between OspA and human lymphocytic antigen (hLFA-1).
Neurotoxin, produced by B. burgdorferi Bbtox1 was identified. Encephalopathy signs in Lyme borreliosis could be result of releasing toxico-metabolic products, ability of spirochetes to pass the blood-brain barrier as well as, effect of lymphocytes migration. Active invasion of brain endothelium as ability to adherence to endothelial wall could be the source of focused or disseminated inflammation of brain vessels. Antiaxonal antibodies could disturb axon conduction without damaging. But damage of white matter could be connected with damage of myelin production cells, probably by antibodies, induced in cross reaction.

PMID: 12194230 [PubMed - indexed for MEDLINE]


Acta Clin Belg. 2009 May-Jun;64(3):225-7. Motor neuron disease features in a patient with neuroborreliosis and a cervicalanterior horn lesion.

De Cauwer H, Declerck S, De Smet J, Matthyssen P, Pelzers E, Eykens L, Lagrou K. Department of Neurology, Klina Regional Hospital, Brasschaat, Belgium.harald.de.cauwer@klina.be

A variety of neurological syndromes has been described in neuroborreliosis:cranial nerve palsies, radiculopathy, axonal neuropathy, stroke, parkinsonism,transverse myelitis, supranuclear palsy, Guillain-Barre syndrome, ... We reporta case of neuroborreliosis with cervical myelitis presenting clinically as alower motor neuron syndrome of the upper and lower limbs with proximal anddistal pareses and atrophies as well as bulbar dysarthria and dysphagia. Duringthe course of the disease the patient developed the clinical picture of ameningoencephalitis. After initiating ceftriaxone treatment the patient showed acomplete recovery. In endemic regions for Lyme disease, in all neurologicalsyndromes neuroborreliosis has to be excluded. http://eutils.ncbi.nlm.nih.gov/entrez/e ... rlinksPMID: 19670562 [PubMed - in process]

----------------------------------------------------------------------------
Borreliabakteeri aiheuttaa toisinaan esim. aivokalvon-tai aivokudoksen tulehduksia. Seuraavassa artikkelissa kerrotaan keskushermostoinfektioiden oireista ja hoidosta.

INFEKTIOT

http://www.neurologiasaatio.fi/index.php?id=14


Määritelmä

Infektio tarkoittaa elimistön ulkopuolelta saatua tautitartuntaa, mutta myös taudinaiheuttajan siirtymistä elimistössä esimerkiksi nenän sivuontelosta aivoihin. Infektioon liittyy tulehdus eli inflammaatio, jonka tunnusmerkkejä ovat mm. kipu ja turvotus. Toisaalta inflammaatio voi kehittyä autoimmuuni-ilmiön pohjalta, jolloin syntyy toisin sanoen reaktio jotakin elimistön ainesosaa tai komponenttia kohtaan. Infektiot luokitetaan käytännön tarpeita varten kovakalvon eli duuran, pehmeiden aivokalvojen eli leptomeningien, aivokudoksen itsensä eli aivoparenkyymin ja selkäytimen infektioihin. Puhutaan myös äkillisistä eli akuuteista ja pitkällisistä eli kroonisista infektioista, joskaan niiden välille ei voida asettaa tarkkaa aikarajaa. Tavallisimmat hermoston infektiot ovat pehmeitä aivokalvoja infektoiva aivokalvotulehdus eli meningiitti ja aivokudosta infektoiva enkefaliitti.

Syyt

Aivokalvotulehduksista yleisimmän, aseptisen meningiitin, aiheuttaa virus. Sairaus liittyykin usein virusinfektioon, esimerkiksi adenoviruksen aiheuttamaan flunssaan. Viruksen laatu jää kuitenkin tutkimuksista huolimatta usein tuntemattomaksi. Toiseksi yleisimmän aivokalvotulehduksen, bakteerimeningiitin, aiheuttaa sairauden nimen mukaisesti bakteeri, Suomessa useimmiten meningokokki tai pneumokokki. Tärkeimmät enkefaliitin aiheuttajat ovat yskänrokko- eli herpes simplex -virus ja vesirokkovirus. Suomelle ominainen on varsinkin Ahvenanmaalla esiintyvä puutiaisenkefaliittivirus, joka aiheuttaa ns. Kumlingen taudin. Harvinaisempia infektioita aiheuttavat jotkut sienet ja alkueläimet.

Tutkimukset

Hermoston infektioiden tavallisia alkuoireita ovat kuume, lihassäryt ja ylähengitystieoireet, joiden perusteella harvoin osataan epäillä aivokalvo- tai aivotulehdusta. Niiden jäljille johtavat yleensä
päänsärky ja niskajäykkyys; jälkimmäinen oire johtuu tulehtuneiden aivokalvojen venyttymisen aiheuttamasta kivusta, miltä potilas pyrkii refleksinomaisesti suojautumaan. Muita infektioon viittaavia oireita ovat valonarkuus ja ääniherkkyys, bakteerimeningiitissä myös pienet
ihoverenvuodot ja toisinaan tajunnan heikentyminen. Aseptinen meningiitti on yleensä bakteerimeningiittiä lievempi ja toipuminen nopeampi. Lannepistolla otetun selkäydinnesteen bakteerivärjäys antaa edellisessä negatiivisen ja jälkimmäisessä positiivisen tuloksen, ja myös selkäydinnesteen solukuva on niissä erilainen. Taudinaiheuttajan tunnistamisessa käytetään lisäksi
vasta-aine- ja viljelytutkimuksia. Tietokonetomografia tai magneettikuvaus tehdään tarvittaessa, kuitenkin vasta lannepiston jälkeen. Kuvantaminen on usein tarpeen muiden sairauksien poissulkemiseksi. Elektroenkefalografiaa käytetään paljon enkefaliittidiagnostiikassa.

Hoito

Toisin kuin bakteerimeningiittiä aseptista meningiittiä hoidetaan vain harvoin sairaalassa, eikä hoidossa tarvita yleensä kuin tulehduskipu- ja pahoinvointilääkkeitä. Bakteerimeningiittiä hoidetaan aina joko penisilliinillä tai muulla antibiootilla taudinaiheuttajan mukaan. Ennuste riippuukin paljon siitä, kuinka nopeasti hoito saadaan alkuun; pahimmassa tapauksessa potilas ehtii kuolla. Enkefaliitin hoidon kulmakivi on asikloviiri-niminen antiviraalinen lääke tai sen johdos. Kaikissa infektioissa hoidetaan tarpeen mukaan mm. lisääntynyttä aivopainetta, epileptisiä kohtauksia ja psyykkisiä häiriöitä.

Esiintyvyys

Aseptiseen meningiittiin sairastuu vuosittain 20-40 ja bakteerimeningiittiin 5-10 henkeä 100 000 asukasta kohti. Enkefaliitteja arvioidaan ilmaantuvan 2,5-5 tapausta 100 000 asukasta kohti vuodessa. Julkisuudessa paljon esillä olleita prionitauteja esiintyy hyvin vähän, niistä tunnetuinta eli Creutzfeldt-Jakobin tautia vain yksi tapaus miljoonaa asukasta kohti vuodessa.

Tätä tutkitaan

Miksi tietyt mikrobit, kuten meningokokki, hakeutuvat juuri aivokalvoihin? Bakteerin seinämässä on sokeripitoisia kemiallisia sivuketjuja, joiden rakenne sattuu sopimaan aivokalvon pintasolujen rakenteisiin. Meningokokkibakteerin saapuessa verenkierron mukana aivokalvolle, se tarttuu tähän. Tällöin aktivoituu entsyymikoneisto, minkä avulla bakteeri pääsee tunkeutumaan aivokudokseen. Tutkimuksen kohteena on mm. se, miten borreliabakteeri hakeutuu aivokudokseen. Herpesvirus puolestaan tunkeutuu tuntohermosolun päätehaaraan vaikkapa iholla ja kulkeutuu solun sisällä selkäytimeen ja edelleen aivoihin. Mikrobin pintarakenteen tarkka tuntemus antaa mahdollisuuden kehittää rokote kyseiselle taudinaiheuttajalle. Lapset rokotetaan useita hermokudosta vaurioittavia mikrobeja, kuten meningokokkia, polio- ja vihurirokkovirusta vastaan. Borreliarokote on tutkimuksen kohteena. Prionitaudeissa on todettu ainutlaatuinen tarttumistapa. Tarttuva prioniproteiini on nimittäin muuttunut poikkeavaksi: se pystyy tunkeutumaan keskushermostoon ja muuttamaan kaikkialla aivoissa olevan normaalin prioniproteiinin kaltaisekseen. Seurauksena on aivokudoksen haurastuminen sienimäiseksi.

Elokuu 2003
Jorma Palo & Seppo Soinila
Viimeksi muokannut soijuv päivämäärä Ma Elo 31, 2009 15:19, muokattu yhteensä 2 kertaa
soijuv
 
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Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » To Tammi 22, 2009 21:29

Ruotsalaisen tutkimuksen mukaan henkilöillä (118 henkilöä), jotka olivat sairastuneet B.gariniin aiheuttamaan infektioon, oireet olivat voimakkaammat kuin B. afzeliin aiheuttamissa infektioissa. Heillä esiintyi ei-rengasmainen ihomuutos, kuumetta, kohonnut C-reaktiivinen proteiini ja seroreaktiivisuutta toipumisvaiheessa.

74 %:lla oli B.afzeliin aiheuttama infektio, 26 %:lla B.gariniin. 45 % ihomuutoksista oli rengasmaisia, 46 % ei-rengasmaisia ja 9,4 % epätyypillisiä.



http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed

Wien Klin Wochenschr. 2006 Sep;118(17-18 ):531-537.

Clinical appearance of erythema migrans caused by Borrelia afzelii and Borrelia garinii - effect of the patient's sex.

* Bennet L,
* Fraenkel CJ,
* Garpmo U,
* Halling A,
* Ingman M,
* Ornstein K,
* Stjernberg L,
* Berglund J.

Department of Clinical Sciences, University Hospital of Malmo, Lund University, Malmo, Sweden.

AIM: The aim in this survey was to study the clinical characteristics of infections caused by Borrelia genospecies in patients with erythema migrans where borrelial origin was confirmed by polymerase chain reaction. The aim was also to study factors influencing the clinical appearance of erythema migrans.

METHODS: The study was conducted in southern Sweden from May 2001 to December 2003 on patients 18 years and older attending with erythema migrans at outpatient clinics. All erythema migrans were verified by polymerase chain reaction, photographed and categorized as "annular" or "non-annular" lesions. A logistic regression model was used to analyze relations between the appearance of the erythema migrans (i.e. annular or non-annular) and factors that influenced its clinical appearance.

RESULTS: A total of 118 patients, 54 women (45.8%) and 64 men (54.2%), fulfilled the inclusion criteria. Of these patients, 74% were infected by B. afzelii and 26% by B. garinii (p < 0.001).
A total of 45% (38/85) of the erythema migrans were annular, 46% (39/85) were nonannular and 9.4% (8/85) were atypical. For men infected by B. afzelii, the odds ratio of developing non-annular erythema migrans was 0.09 (95% CI: 0.03-0.33) in comparison with women with the same infection.

CONCLUSIONS: In this prospective study of a large series of erythema migrans, where infecting genospecies were confirmed by polymerase chain reaction, the sex of patients infected with B. afzelii had a strong influence on the appearance of the rash.

Patients infected by B. garinii more often had non-annular erythema migrans and a more virulent infection with more individuals presenting with fever, raised levels of C-reactive protein and seroreactivity in the convalescence sera. PMID: 17009065 [PubMed - as supplied by publisher]
soijuv
 
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ViestiKirjoittaja soijuv » To Tammi 22, 2009 22:10

Tutkimuksen mukaan 75 %:lla borrelioosia sairastavista esiintyy epänormaali EEG-löydös. "Neurofeedback"-terapialla aivokäyrät saatiin useissa tapauksissa paranemaan. (Suom. huom. Olisi mielenkiintoista tietää kuinka monelle on tehty EEG tutkimus ja kuinka monelta on löytynyt poikkeavuuksia.)


http://www.allheadlinenews.com/articles/7005156955

Neurofeedback Training May Help Normalize Some Abnormal Brain Wave Patterns

October 12, 2006 1:47 p.m. EST


Linda Young - All Headline News Staff Writer
Salt Lake City, Utah (AHN) - A new study reveals that neurofeedback training may help normalize abnormal brain waves caused by some medical conditions.

The study was published in the latest edition of Biofeedback a journal published by the Association for Applied Psychophysiology and Biofeedback.

According to Newswise, individuals with Lyme disease, systematic lupus, erythematosus, migraines, irritable bowel syndrome, and cardiopulmonary bypass surgery patients typically have disturbed electroencephalography patterns.

Other conditions that may produce abnormal EEG patterns are fibromyalgia, chronic fatigue and exposure to toxic substances or large doses of radiation.

The study found that 75 percent of patients with Lyme disease had abnormal EEG patterns. After neurofeedback treatment that declined to 54 percent of those treated.

The report stated that these results could be used as baseline to help therapists treat patients with abnormal brain wave patterns.

The study focused on children with migraines. The study was done by D. Corydon Hammond, Ph.D., University of Utah School of Medicine.
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 14:08

1. Borreliabakteeri aiheutti aiemmin terveelle miehelle täydellisen eteiskammiokatkoksen joka vaati väliaikaisen tahdistimen asentamisen.

http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed


2. Borreliabakteeri saattaa aiheuttaa dilatoivan kardiomyopatian: "Dilatoiva kardiomyopatia saa aikaan verta pumppaavan sydänlihaksen asteittaisen hiipumisen ja kammion laajenemisen. Oireina on usein pitempään jatkunut väsymys ja hengästyminen yhä kevyemmissä rasituksissa.

Dilatoiva kardiomyopatia on Suomessa tärkeimpiä sydämensiirron syitä.

http://www.sydanliitto.fi/sydanpiirit_j ... omyopatia/ "


Prague Med Rep. 2006;107(2):213-26.
Lyme borreliosis infection as a cause of dilated cardiomyopathy.

* Bartunek P,
* Gorican K,
* Mrazek V,
* Varejka P,
* Veiser T,
* Hercogova J,
* Hulinska D,
* Janovska D.

Fourth Department of Medicine of the First Faculty of Medicine, Charles University in Prague, Czech Republic. petr.bartunek@lf1.cuni.cz

The relatively low percent of patients affected with the cardiac form of Lyme borreliosis is difficult to diagnose, especially if the disease
manifests itself in ways other than atrio-ventricular blockade. The advanced stage of Lyme carditis manifesting as dilated cardiomyopathy is a special case of this affliction. The authors of this report present clinical experience with an attempt to support the working hypothesis about involvement of Lyme borreliosis infection in the development of dilated cardiomyopathy. The patients were clinically examined thoroughly with special attention to the cardiovascular system. In addition to the basic clinical methods, the following procedures have been employed: dynamic Holter's electrocardiography, exercise ECG test, coronarography, and myocardial biopsy. From laboratory methods pertaining to the detection of Borrelia, ELISA method, Western blot, PCR, electron microscopy and histopathological analysis were used. In all three cases, clinical and laboratory findings provided the evidence of the borreliosis infection involvement in the development of dilated cardiomyopathy.

PMID: 17066741 [PubMed - in process]


Borreliabakteeri aiheutti aiemmin terveelle miehelle täydellisen eteis-kammiokatkoksen joka vaati väliaikaisen tahdistimen asentamisen.

http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed

Hellenic J Cardiol. 2006 Sep-Oct;47(5):313-6.

Lyme carditis: complete atrioventricular dissociation with need for temporary pacing.

* Xanthos T,
* Lelovas P,
* Kantsos H,
* Dontas I,
* Perrea D,
* Kouskouni E.

Department of Experimental Surgery and Surgical Research, Aretaieion Hospital, University of Athens Medical School, Greece. theodorosxanthos@yahoo.com

Lyme borreliosis is a tick-borne disease. Cardiac manifestations of the disease are extremely rare. We report a case of Lyme carditis in an otherwise healthy male, who presented to the Accident & Emergency Department with chest pain, dizziness and generally symptoms indicating ischaemic heart disease. This patient, without documented history of Lyme disease, acutely developed third-degree atrioventricular block, which required placement of a transvenous pacemaker and resolved when the patient was administered doxycycline.

PMID: 17134068 [PubMed - in process]
soijuv
 
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Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 14:10

Saksalaisen tutkimuksen mukaan toistuva antibioottihoito on joidenkin borrelioosiin sairastuneiden kohdalla välttämätöntä ja joidenkin kohdalla niveltulehdus tms. jää krooniseksi hoidoista huolimatta.

http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed


: Best Pract Res Clin Rheumatol. 2006 Dec;20(6):1099-118.

Lyme borreliosis.

* Schnarr S,
* Franz JK,
* Krause A,
* Zeidler H.

Rheumaklinik Ostbayern, Bad Fuessing, Germany.

Lyme borreliosis is a tick-borne infectious disease caused by the spirochaetes Borrelia burgdorferi, B. garinii and B. afzelii. It comprises a wide spectrum of symptoms affecting skin, musculoskeletal system, heart, eyes, central and peripheral nervous system. The diagnosis is based on clinical findings in combination with detection of specific IgM and/or IgG antibodies. Diagnostic problems arise from patients with non-specific symptoms and positive IgG antibody detection. Adequate antibiotic therapy cures more than 90% of the patients. However, in some patients repeated therapy is necessary and a small number of patients develop chronic arthritis or other features. While there is currently no vaccine available, prevention of tick bite is the most effective prophylaxis.

PMID: 17127199 [PubMed - in process]
soijuv
 
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ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 14:11

9-vuotiaalla pojalla ilmeni äkillisesti kuulon alenemista alemmissa rekistereissä. Dg: borrelioosi. Hoito: 2 vk antibiootteja. Kuulo parani normaaliksi. Tällaisissa oireissa antibioottihoito saattaa joillakin osoittautua tehokkaaksi hoitomuodoksi.


http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed

HNO. 2006 Nov 14; [Epub ahead of print]

Sensorineural loss of hearing in lower registers as the main symptom of Lyme disease.
[Article in German]

* Mehler K,
* Emmel M,
* Petereit HF,
* Spruth A,
* Droge A,
* Brockmeier K.

Klinik und Poliklinik fur Kinderkardiologie, Klinikum der Universitat zu Koln, Joseph-Stelzmann-Str. 9, 50924, Koln, Deutschland, katrin.mehler@gmx.de.

In a 9-year-old boy with sudden sensorineural loss of hearing in the lower registers in both ears, serology showed elevated levels of antibodies against Borrelia burgdorferi and examination of the CSF revealed a positive antibody index against Borrelia burgdorferi. The boy was treated with antibiotics for 2 weeks. Audiometry performed 4 weeks after treatment was completely normal. Inner ear involvement in Lyme disease has often been discussed. Treating these patients with antibiotics may lead to an improvement in some.

PMID: 17103202 [PubMed - as supplied by publisher]
Related Links
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 14:14

43-vuotiaalla naisella oli ollut aiemmin kuumeilua ja ihomuutos, mutta ei muita oireita. Myöhemmin testeissä ilmeni borrelioosi ja alaraajojen lihastulehdus.


Arthritis and Rheumatism Volume 54, Issue 8, Pages 2697-2700
Published online: 26 July 2006
Copyright © 2006 by the American College of Rheumatology

Research Article
Lyme myositis
Aaron R. Holmgren *, Eric L. Matteson
Mayo Clinic, Rochester, Minnesota

email: Aaron R. Holmgren (holmgren.aaron@mayo.edu)

*Correspondence to Aaron R. Holmgren, Division of Rheumatology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905

Abstract
Myositis has been reported as a rare manifestation of Lyme disease, and Lyme myositis can be an important consideration in the differential diagnosis of unusual cases, especially in patients who live in or travel to endemic areas. We report the case of a 43-year-old man who presented with focal myositis of the proximal lower extremity and was subsequently diagnosed as having Lyme myositis. The patient had previously experienced a febrile illness and rash, but had no ongoing symptoms of Lyme disease. Myositis was confirmed by magnetic resonance imaging and muscle biopsy; Borrelia burgdorferi infection was confirmed by Lyme serology and polymerase chain reaction testing of synovial fluid and biopsy material. The current case is reviewed in the context of findings from previous case descriptions.
soijuv
 
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Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 14:14

Borreliabakteeri aiheuttaa joillekin silmien tahattomia liikkeitä ja nykimistä. Seuraavan tutkimuksen mukaan bakteeri saattaa aiheuttaa silmiin mm. ns. OMS-syndrooman.

http://jnnp.bmjjournals.com/cgi/content ... /77/9/1090

Journal of Neurology, Neurosurgery, and Psychiatry 2006;77:1090-1091; doi:10.1136/jnnp.2006.091728
© 2006 by BMJ Publishing Group Ltd

SHORT REPORT

Opsoclonus?myoclonus as a manifestation of Lyme disease

L Peter1, J Jung1, C Tilikete2, P Ryvlin1 and F Mauguiere1

1 Service de Neurologie et d?épileptologie, Hôpital Neurologique, Lyon, France
2 Service de Neuro-ophtalmologie, Hôpital Neurologique

Correspondence to:
L Peter
Service de Neurologie et d?Epileptologie, Hôpital Neurologique, 59 Boulevard Pinel, 69003 Lyon, France;laure.peter@wanadoo.fr


ABSTRACT
Opsoclonus?myoclonus syndrome (OMS) is a rare condition that includes chaotic multidirectional saccadic eye movements associated with myoclonus and ataxia. In adults, it is usually considered to be an autoimmune disease occurring either in a paraneoplastic context or after central nervous system infection. We report the case of a patient who presented with the classic features of OMS as a manifestation of acute Borrelia burgdorferi infection that was shown both on serum and cerebrospinal fluid examination. The outcome was favourable after prolonged antibiotic treatment. Lyme disease could be added to the list of aetiologies to be screened in OMS, as it would allow effective treatment and avoidance of unnecessary investigations.

Abbreviations: CNS, central nervous system; CSF, cerebrospinal fluid; OMS, opsoclonus?myoclonus syndrome
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Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 14:31

Miklossyn tutkimus v. 1993: Alzheimerin tauti ? spirokeettojen aiheuttama sairaus? Alzheimerin taudin etiologia on tuntematon eikä siihen ole vielä syyn mukaista hoitoa. Tutkimuksessa selvitettiin ruumiinavauksessa 14 Alzheimerin tautiin kuolleen taudin etiologiaa. Kontrolliryhmänä toimi 13 samanikäistä henkilöä joilla ei ollut todettu sairautta. Kaikilta 14:ltä Alzheimerin tautiin kuolleelta löydettiin spirokeettoja verestä, selkäydinnesteestä ja aivoista. Yhdeltäkään vertailuryhmän henkilöltä niitä ei löytynyt. Tutkijoiden mukaan spirokeetat saattavat näin ollen olla yksi Alzheimerin taudin aiheuttajista.Myös neuroborrelioosissa tavataan aivokuoren surkastumista ja mikroglioosia (hermotukikudoksen lisäkasvua) (tutkimukset 6 ja 7). "Syfiliksen tavoin spirokeetat pääsevät keskushermostoon jo sairauden varhaisvaiheessa. Joillakin infektio jää latentiksi vuosikausiksi, jopa vuosikymmeniksi. Dementia voi alkaa ilmetä vasta 43 vuoden kuluttua infektiosta."

Alzheimer's disease--a spirochetosis?

Miklossy J,
Neuroreport 1993 Jul;4(7):841-848 Alzheimer's disease--a spirochetosis?
Judit Miklossy University Institute of Pathology, Division of Neuropathology, University of Lausanne, Rue du Bugnon 27, 1005 Lausanne, Switzerland

The aetiology of Alzheimer's disease (AD), which affects a large proportion of the aged population is unknown and the treatment unresolved. The role of beta amyloid protein (ßA4), derived from a larger amyloid precursor protein (APP) in AD is the subject of intense research. Here I report observations that in 14 autopsy cases, with histopathologically confirmed AD, spirochetes were found in blood and cerebrospinal fluid and, moreover, could be isolated from brain tissue. Thirteen age-matched control cases were without spirochetes.

Reference

Strains of spirochetes and those isolated from brains of AD patients, showed positive immunoreaction with monoclonal antibody against the ß amyloid precursor protein. These observations suggest that spirochetes may be one of the causes of AD and that they may be the source of the ß amyloid deposited in the AD brain.

Discussion

There is evidence suggesting an infectious aetiology for AD. Cases of familial AD can be transmitted to the chimpanzee in the form of spongiform encephalopathy, resembling Creutzfeldt-Jakob disease (CJ).[16] In addition, the inoculation of experimental animals by the scrapie agent may induce the formation of senile plaques, morphologically similar to, but biochemically distinct from, AD plaques.[17] Masters et al[18] suggested that there are sufficient similarities between the amyloid filaments and proteins in AD and in scrapie to suspect that they are derived by mechanisms which have in common the generation of self aggregating polypeptides of low molecular weight. The authors' comment that if the scrapie filaments and proteins in CJ are an integral part or a direct effect of the infectious agent, it follows that AD is also an infectious process similar to scrapie. The present finding that reference strains of Treponema pallidum and Borrelia burgdorferi as well as the spirochetes found in the AD cases showed positive immunoreaction with a monoclonal antibody against APP, suggests that the APP may be an integral part of the infectious agent and thus may be the source of the excess of ßA4 deposited in the AD brain. The fact that spirochetes of the Borrelia burgdorferi reference strain, cultured in a synthetic medium also exhibit a positive immunoreaction with the APP antibody may suggest that spirochetes synthesize their own APP

In AD, ßA4 is often deposited in the leptomeningeal and cortical vessel walls. In addition ßA4 deposits were detected in tissues other than brain[19] suggesting that AD is a systemic disorder. This would be in agreement with spirochetal invasion of the brain via the vascular
system.

Probably, as in syphilis, spirochetes may invade the CNS during the early stage of the disease. In a small proportion of patients infection takes place but may remain latent for periods of varying length. In general paresis, dementia may appear as long as 43 years after the primary infection.[20] Subsequently, the accumulation of the microorganisms in small clusters in the cortex may cause the formation of 'argyrophylic', 'senile' or 'neuritic' plaques while damage to the neurones may lead to neurofibrillary changes The clinical reports made no mention of signs or symptoms of meningitis, encephalitis or polyradiculoneuritis, nor were histological signs of meningitis or encephalitis in the 14 AD cases investigated here. Spirochetes may invade the parenchyma of several organs including the brain without the challenge of an inflammatory reaction.[14] However, we cannot exclude the possibility that the amyloid-bearing plaques may be the sites of a chronic inflammatory process.[21

There were no Alzheimer-like changes in the 13 age matched control cases investigated in this study. It is well known that in the older population there are cases demonstrating a small number of plaques and neurofibrillary tangles. These cases where the number of plaques and tangles with respect to the age of the patients[22] are not sufficient for the neuropathological diagnosis of AD, are said to reflect 'normal ageing'. In the cortex of these cases one may expect to find spirochetes in a small or moderate number. This was not seen in any of the 13 control cases (with use of the silver techniques for AD, or with the immunohistochemical technique for the demonstration of ßA4), probably because of the restricted number of cases investigated. When a larger, particularly an aged, population without AD is tested, one may well find spirochetes in the blood in a number of cases but not in the CSF and in cerebral cortex. In a number of AD cases spirochetes may well be present in the CSF and in the cerebral cortex but not in the blood.

Recently the microorganism, Actinomyces, has been reported to be present in the brain of patients with an incidence that was four times higher than in other pathological or normal conditions.[23] Gram Actinomyces in the AD cases presented here.

It was demonstrated that the messenger RNAs encoding the three major APPs, are present in many tissues besides brain in both control and AD cases, suggesting that APP is a natural constituent of a variety of cells.[24,25] The finding that the APP gene resides also on chromosome 21,[26] suggested the possibility that the APP gene, as the site of mutations, may cause AD. This hypothesis was subsequently challenged, when further studies revealed that the AD locus and the APP gene are not linked and not coinherited in familial cases of AD.[27,28]

Few familial AD cases, representing only a very small proportion of all AD cases (familial and sporadic cases together) are caused by a genetic defect.[29-31] The similar localization and distribution of the ßA4 deposited in the brain in both forms--familial and sporadic--are difficult to explain. An alternative reconciliation of the genetic and infectious aetiology of AD lies in the supposition that the genetic defects associated with AD may lead to a predisposition for pirochetal infection, or may favour its progress.

Conclusion

In conclusion, the isolation of spirochetes from all the 14 AD cases investigated suggests that AD may correspond to a tertiary stage of neurospirochetosis. The fact that spirochetes isolated from AD brains, as well as reference strains of Treponema pallidum and Borrelia burgdorferi, express positive immunoreactivity with a specific antibody against APP would seem to indicate that several types of spirochetes may contribute to the aetiology of AD. An immunochistochemical [sic] and ultrastructural analysis that demonstrated a similar localization of APP, of ßA4 and of spirochetes in the brain of a patient with concurrent AD and Lyme disease, would appear to support this hypothesis.

The characterization of the spirochetes found in AD is now needed. Knowing the genus and species of these spirochetes would indicate the source, the mode of transmission, and the site of the primary infection. It would enable one to develop serological tests for early detection of the infection. The pathological process is thought to begin long before the diagnosis of 'dementia' is made; and thus, appropriate antibiotic treatment should start early in order to prevent the development of dementia.

The presence of histological signs of AD in the brain, even in small numbers, would signify that the illness is in progress. At all times the late latent stage may turn into tertiary clinical. manifestations.[20] In this light, the use of quantitative criteria for the neuropathological diagnosis of AD is unjustified.
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Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 14:34

1. Tutkimuksessa 7:ltä Alzheimerin tautia sairastaneelta löytyi spirokeettoja aivoista. Tutkijan mukaan löydös ei voi olla pelkkää sattumaa.

2. Alzheimerin tauti etenee vaiheittain aiheuttaen ajoittain vaurioita "tsunamin lailla". Uutena mahdollisena aiheuttajana mainitaan borreliabakteeri - taudista käyetään artikkelissa nimitystä "Alzheimerin neuroborrelioosi".



St. Catherine of Siena Medical Center ? An Incubator For Research

November is Alzheimer?s awareness month in the United States in acknowledgment of the 4 million people who suffer from Alzheimer?s disease (AD), a progressive, degenerative disorder that damages the brain cells responsible for intellectual functioning in the brain, including memory, intelligence, judgment, and speech. Alzheimer?s disease also leads to the loss of physical functions.

While most people diagnosed with AD are over 65 years of age, a rare and aggressive form of Alzheimer's does affect a small percentage of people in their 40s and 50s. The average course of the disease from the time it is diagnosed to death is about 6 to 8 years.

Alzheimer's is characterized by a loss of brain cells, as well as changes in the cerebral cortex (the outer layer of the brain). An accumulation of diseased nerves with tangled fibers, plaques with amyloid centers, and nerves with peculiar round granular forms inside their cytoplasm (GVB) are hallmarks under the microscope. After more than a decade and the expense of 2 billion dollars in research, the ?amyloid hypothesis? of causation of Alzheimer?s has been abandoned; with the acceptance that amyloid is an occurrence event in the disease, but is not its root cause. Researchers are divided as to whether or not there is a genetic cause for this debilitating disease.

St Catherine of Siena Medical Center through its Institutional Review Board and the support of a research grant from the Turn the Corner Foundation in New York City, has approved a Molecular study of Alzheimer?s disease brain tissues obtained from the world renowned Harvard Medical School Brain tissue bank, under the direction of Dr. Alan MacDonald. Dr. MacDonald believes that a paradigm shift in the direction of a non-genetic cause might be in order. His hypothesis is derived from the model of another potentially brain-wasting disease: spirochetal infection (syphilis) which shows many parallels with Borrelia infections, ?which are highly endemic in Long Island and around the world.

?With a small grant I was able to conduct research on brain tissue from 10 unrelated individuals, from different geographic regions, who had lived and died with AD. Of these 10 samples 7 yielded ?sharp? bands of DNA. To my surprise these 7 samples produced identical fusion DNA sequences to each other, but do not match any DNA sequences in the National Gene Data Bank,? explained Dr. MacDonald. ?The DNA sequence that all the samples shared was not human but spirochetal?a bacteria that appears to have inserted itself ( by transfection) into the brain cells of the individuals who died with Alzheimer?s disease. Of course this is a small study with a small sample, but what would the probability of this occurring by chance be? Colleagues in statistics have offered a one chance in 100 billion scenario, based on length and structure of the DNA sequences deposited into the National Gene Bank. These results are unlikely to have come from ?accident? or ?dumb luck?. Only time and more research will tell us whether the antibiotic treatment of dementia of the Alzheimer type in its very early stages might offer stabilization, or even improvement in brain function , based on the known benefits of Penicillin therapy in the General paresis dementias of the last century.?

For more information please call the Office of Community Relations at 631.862.3523.


2. http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed

Med Hypotheses. 2006 Nov 16; [Epub ahead of print]

Alzheimer's disease Braak Stage progressions: Reexamined and redefined as Borrelia infection transmission through neural circuits.

* Macdonald AB.

St. Catherine of Siena Medical Center, Department of Pathology, 50 Rte 25 A, Smithtown, NY 11787, USA.

Brain structure in health is a dynamic energized equation incorporating chemistry, neuronal structure, and circuitry components. The chemistry "piece" is represented by multiple neurotransmitters such as Acetylcholine, Serotonin, and Dopamine. The neuronal structure "piece" incorporates synapses and their connections. And finally circuits of neurons establish "architectural blueprints" of anatomic wiring diagrams of the higher order of brain neuron organizations. In Alzheimer's disease, there are progressive losses in all of these components. Brain structure crumbles. The deterioration in Alzheimer's is ordered, reproducible, and stepwise. Drs. Braak and Braak have described stages in the Alzheimer disease continuum. "Progressions" through Braak Stages benchmark "Regressions" in Cognitive function. Under the microscope, the Stages of Braak commence in brain regions near to the hippocampus, and over time, like a tsunami wave of destruction, overturn healthy brain regions, with neurofibrillary tangle damaged neurons "marching" through the temporal lobe, neocortex and occipital cortex. In effect the destruction ascends from the limbic regions to progressively destroy the higher brain centers. Rabies infection also "begins low and finishes high" in its wave of destruction of brain tissue. Herpes Zoster infections offer the paradigm of clinical latency of infection inside of nerves before the "marching commences". Varicella Zoster virus enters neurons in the pediatric years. Dormant virus remains inside the neurons for 50-80years, tissue damage late in life (shingles) demonstrates the "march of the infection" down neural pathways (dermatomes) as linear areas of painful blisters loaded with virus from a childhood infection. Amalgamation of Zoster with Rabies models produces a hybrid model to explain all of the Braak Stages of Alzheimer's disease under a new paradigm, namely "Alzheimer's neuroborreliosis" in which latent Borrelia infections ascend neural circuits through the hippocampus to the higher brain centers, creating a trail of neurofibrillary tangle injured neurons in neural circuits of cholinergic neurons by transsynaptic transmission of infection from nerve to nerve.

PMID: 17113237 [PubMed - as supplied by publisher]
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 14:35

HIV-positiivisella 38-vuotiaalla naisella esintyi toistuvaa kuumeilua. Syyksi paljastui borreliabakteeri.

http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed

Niger J Med. 2006 Oct-Dec;15(4):455-6.

Spirochaetemia in a HIV positive patient.

* Okwori EE.

BACKGROUND: Borreliosis, caused by Borrelia recurrentis and several other Borrelia species is not a commonly reported case in our environment, but the search for the cause of recurrent pyrexia in this patient made it possible to discover the spirochete as the cause of the disease.

METHOD: A 38 year old married HIV positive woman presented with recurrent fever in a private clinic. Six thin smears were made out of the patient serum and dried in the air. Three slides each were stained with 0.12% Leishman and 20% Giemsa stains and examined under the light microscope.

RESULT: Three of the Giemsa slides were positive for spirochetes (4-5 spirals), which were constituents with Borrelia species. The patient responded very well to tetracycline and serum became negative for the organism after ten days of treatment.

CONCLUSION: Borrelia was discovered to be the cause of the recurrent pyrexia in this patient who responded very well to tetracycline. Borrelia should be looked for in cases of pyrexia of unknown origin

PMID: 17111740 [PubMed - in process]
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 14:36

Kroonista borrelioosia sairastavilla ilmeni tutkimuksen
mukaan ongelmia muistin ja puheentuottamisen alueilla.


J Int Neuropsychol Soc. 2006 Jan;12(1):119-29.

WAIS-III and WMS-III performance in chronic Lyme disease.

* Keilp JG,
* Corbera K,
* Slavov I,
* Taylor MJ,
* Sackeim HA,
* Fallon BA.

Columbia University College of Physicians and Surgeons, Department of
Psychiatry, New York, New York 10032, USA. jgk13@columbia.edu

There is controversy regarding the nature and degree of intellectual and
memory deficits in chronic Lyme disease. In this study, 81 participants with
rigorously diagnosed chronic Lyme disease were administered the newest
revisions of the Wechsler Adult Intelligence Scale (WAIS-III) and Wechsler
Memory Scale (WMS-III), and compared to 39 nonpatients. On the WAIS-III,
Lyme disease participants had poorer Full Scale and Performance IQ's. At the
subtest level, differences were restricted to Information and the Processing
Speed subtests. On the WMS-III, Lyme disease participants performed more
poorly on Auditory Immediate, Immediate, Auditory Delayed, Auditory
Recognition Delayed, and General Memory indices. Among WMS-III subtests,
however, differences were restricted to Logical Memory (immediate and
delayed) and Family Pictures (delayed only), a Visual Memory subtest.
Discriminant analyses suggest deficits in chronic Lyme are best
characterized as a combination of memory difficulty and diminished
processing speed. Deficits were modest, between one-third and two-thirds of
a standard deviation, consistent with earlier studies. Depression severity
had a weak relationship to processing speed, but little other association to
test performance. Deficits in chronic Lyme disease are consistent with a
subtle neuropathological process affecting multiple performance tasks,
although further work is needed to definitively rule out nonspecific illness
effects.

PMID: 16433951 [PubMed - indexed for MEDLINE]
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja borrelioosi » Pe Tammi 23, 2009 21:59

Borreliabakteeri saattaa aiheuttaa kystan polven takaosaan kuten seuraavan tutkimuksen lasten kohdalla havaittiin.

http://www.genou.com/anglais/poplitealc ... alcyst.htm )



J Pediatr Orthop. 2006 November/December;26(6):725-727.

Lyme Disease Presenting as Popliteal Cyst in Children.

* Magee TH,
* Segal LS,
* Ostrov B,
* Groh B,
* Vanderhave KL.

From the *Department of Orthopaedics and Rehabilitation, daggerDivesion of Pediatric Orthopaedics, double daggerPediatric Rheumatology and Rheumatology, Milton S. Hershey Medical Center, The Pennsylvania State University College of Medicine, Hershey, PA.

Lyme disease is the most common tick-borne disease in North America. Our review of the literature found few reports of Lyme disease presented in the orthopaedic literature. However, Lyme disease presenting as a popliteal cyst, with or without rupture, is rarely reported. We present 4 cases of Lyme disease that initially presented to our pediatric orthopaedic clinic for treatment of a popliteal cyst. The early diagnosis and treatment of Lyme disease may help prevent the often-devastating long-term sequelae of Lyme disease. The goal of this article is to increase the awareness of Lyme disease presenting in children as a popliteal cyst.

PMID: 17065933 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
borrelioosi
 

ViestiKirjoittaja borrelioosi » Pe Tammi 23, 2009 22:00

Borreliabakteeri aiheuttaa toisinaan erilaisia sydänsairauksia esim ns. dilatoivan kardiomyopatian josta seuraa vähitellen paheneva sydämen vajaatoiminta.


http://www.sydanliitto.fi/sydanpiirit_j ... omyopatia/
Dilatoiva kardiomyopatia saa aikaan verta pumppaavan sydänlihaksen asteittaisen hiipumisen ja kammion laajenemisen. Oireina on usein pitempään jatkunut väsymys ja hengästyminen yhä kevyemmissä rasituksissa. Dilatoiva kardiomyopatia on Suomessa tärkeimpiä sydämensiirron syitä.


http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed

Prague Med Rep. 2006;107(2):213-26.

Lyme borreliosis infection as a cause of dilated cardiomyopathy.

* Bartunek P,
* Gorican K,
* Mrazek V,
* Varejka P,
* Veiser T,
* Hercogova J,
* Hulinska D,
* Janovska D.

Fourth Department of Medicine of the First Faculty of Medicine, Charles University in Prague, Czech Republic. petr.bartunek@lf1.cuni.cz

The relatively low percent of patients affected with the cardiac form of Lyme borreliosis is difficult to diagnose, especially if the disease manifests itself in ways other than atrio-ventricular blockade. The advanced stage of Lyme carditis manifesting as dilated cardiomyopathy is a special case of this affliction. The authors of this report present clinical experience with an attempt to support the working hypothesis about involvement of Lyme borreliosis infection in the development of dilated cardiomyopathy. The patients were clinically examined thoroughly with special attention to the cardiovascular system. In addition to the basic clinical methods, the following procedures have been employed: dynamic Holter's electrocardiography, exercise ECG test, coronarography, and myocardial biopsy. From laboratory methods pertaining to the detection of Borrelia, ELISA method, Western blot, PCR, electron microscopy and histopathological analysis were used. In all three cases, clinical and laboratory findings provided the evidence of the borreliosis infection involvement in the development of dilated cardiomyopathy.

PMID: 17066741 [PubMed - in process]
borrelioosi
 

ViestiKirjoittaja borrelioosi » Pe Tammi 23, 2009 22:17

Tutkimuksen mukaan borrelioosi voi ilmetä kroonisen väsymysoireyhtymän kaltaisina oireina. Asia tulee huomioida diagnostiikassa ja hoidoissa. 33-vuotiasta naista oli hoidettu kahden vuoden ajan väsymysoireyhtymän mukaisesti. Hoidot eivät olleet tuottaneet tulosta. Viimein hänellä alettiin epäillä borrelioosia.

http://www.immunesupport.com/library/sh ... text/lyme/>lyme/

Lyme Disease Presenting as Chronic Fatigue Syndrome

by Samuel Shor
ImmuneSupport.com

11-01-2006

Journal: Journal of Chronic Fatigue Syndrome. Vol. 13(4) 2006 pp. 73-82.
[Published online ahead of print. Article copies are available for a fee
from The Haworth Document Delivery Service: 1-800-HAWORTH. E-mail
docdelivery@haworthpress.com


Author and affiliation: Samuel Shor. George Washington University Health Care Sciences, Reston, VA.
E-mail: sshor@intmednova

DOI: 10.1300/J092v13n04_06

Objective: Chronic Fatigue Syndrome (CFS) by definition represents a diagnosis of exclusion. Late stage or "Chronic lyme" infection with or without "co-infections" is a difficult diagnosis to establish. The symptom complex of both conditions can be very similar. This case study represents an attempt to support serious consideration for a subpopulation of patients otherwise diagnosed with "CFS," as actually representing chronic lyme disease.

Method: A case study is presented of a 33-year-old man, who for two years, was being managed as having CFS. However, after ~2 years of utilizing multiple modalities of management with limited success, the diagnosis of lyme was reconsidered. Historical exposure risks to lyme in this individual were high. He had prolonged exposure in the highly tick-infested mountains of North Carolina for 18 months, several years prior to becoming ill. More aggressive investigation confirmed the diagnosis of lyme. Appropriate changes in management were associated with an improved level of functioning that was far in excess of what maximal management of CFS was able to achieve. The features of CFS and chronic lyme can be very similar and include the following: Profound fatigue often associated with cognitive impairment. Other common symptoms related to both of these conditions include sleep disturbances, fibromyalgia, and dysautonomias.In pursuing clarification of this diagnosis, the author was exposed to a contrast in medical opinion regarding diagnostic tools and criteria that were perceived as creating potential barriers to the management of patients presenting with these symptoms.

Conclusion: Acceptance and awareness of the possibility that lyme disease can present as CFS has important therapeutic and prognostic implications.

Keywords: lyme disease, chronic lyme, chronic fatigue syndrome, CFS, fatigue.
borrelioosi
 

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 22:42

Borrelioosia sairastavilla esiintyy erilaisia neuro-kognitiivisia oireita esim. tarkaavaisuushäiriö, lyhytkestoisen muistin häiriöitä, masennus, paniikkikohtaus, persoonallisuuden muutos, mieleialanvaihtelu, oppimisvaikeudet, kaksisuuntainen mielialahäiriö jne. Alla on useita asiaa käsitteleviä tutkimuksia.


NEURO-COGNITIVE LYME DISEASE
Lyme disease patients can experience symptoms such attention problems, short-term memory loss, depression, panic attacks, personality changes, mood swings, and/or learning disabilities. Literature on these manifestations is found below.

http://www.lymeinfo.net/neuropsych.html


--------------------------------------------------------------------------------

LymeInfo's Recommendations:

Distinct pattern of cognitive impairment noted in study of Lyme patients by Marian Rissenberg, Ph.D. & Susan Chambers, M.D. The Lyme Times, Vol. 20, January-March 1998, pp. 29 -32

SUMMARY: The following items are covered: Cognitive Characteristics of Chronic Lyme Encephalopathy, Neuropsychological deficits, Possible Pathophysiologic Mechanisms of Cognitive Impairment in Lyme Disease, Clinical Impressions and Implications for Diagnosis and Treatment in Chronic Lyme Disease, Cognitive impairment in Lyme disease: specific functions and the impact or deficits.

Brochure: What Psychiatrists Should Know About Lyme Disease (pdf file) by ILADS

SUMMARY: This printable brochure outlines information that psychiatrists need to be aware of, such as when to suspect Lyme disease and how to treat it.

The Role of Neuropsychological Testing in Children with Lyme Disease (pdf file) by Leo Shea, Ph.D. and Judith Leventhal, Ph.D.

SUMMARY: Provides a comprehensive review of neuropsych testing and its benefits for Lyme patients, particularly children.

The Neuropsychiatric Assessment of Lyme Disease by Robert Bransfield, M.D.

SUMMARY: "From a combination of clinical experience, journal review, and discussion with colleagues, a structured interview was developed" to assist in the overall clinical assessment when late state Lyme disease is suspected. Additional material is available at the same website.

SEE: Mental Health and Illness .Com
Overview of Neuropsychiatric Lyme Disease
Columbia University Lyme Website

SUMMARY: The following items are covered: Typical time course, symptoms, cognitive and psychiatric aspects for both children and adults.

Bibliography of Neuropsychiatric Lyme

A collection of references to medical/scientific literature on psychiatry and Lyme/tick-borne disease. One item worth obtaining the full-text of is "The Neuropsychiatric Manifestations of Lyme Borreliosis".

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Full Text Peer-Reviewed Articles

The following articles, listed alphabetically, are available online at no charge. Additional peer-reviewed articles are listed in the bibliography above, and some of those may be worth obtaining through your medical library.

A Controlled Study of Cognitive Deficits in Children With Chronic Lyme Disease (pdf file)
Tager, Fallon, et. al.
J Neuropsychiatry Clin Neurosci 13:500-507, November 2001
Functional Brain Imaging and Neuropsychological Testing in Lyme Disease (pdf file) by Fallon, Das, Plutchok, Tager, Liegner, Van Heertum
CID 1997; 25:S57-63
(Requires Adobe Acrobat)
Higher Prevalence of Antibodies to Borrelia Burgdorferi in Psychiatric Patients Than in Healthy Subjects by Hajek, et. el.
Am J Psychiatry 159:297-301, February 2002
Late-Stage Neuropsychiatric Lyme Borreliosis: Differential Diagnosis and Treatment by Fallon, et. al.
Psychosomatics 1995;36:295-300
Lyme Disease: A Neuropsychiatric Illness by Fallon, Nields
Am J Psychiatry 151:11, November 1994 pp.1571-1580
Musical Hallucinations in Patients with Lyme Disease by Stricker, Winger
Southern Medical Journal 2003; 96(7):711-715
The neuropsychiatric manifestations of Lyme borreliosis by Fallon, Nields, Burrascano, Liegner, DelBene, Liebowitz
Psychiatr Q 1992 Spring;63(1):95-117

**RECOMMENDED ITEM
The Physician as a Patient: Lyme Disease, Ehrlichiosis, and Babesiosis: A Recounting of a Personal Experience with Tick-Borne Diseases by Sherr
Practical Gastroenterology, January 2000
Potential uses of Modafinil in Psychiatric Disorders (pdf file) by Bransfield
Journal of Applied Research, 2004 Spring; 4(2): 198-208
(Requires Adobe Acrobat)
For insurance, see: Forms 1 and Forms 2
Seasonal correlation of sporadic schizophrenia to Ixodes ticks and Lyme borreliosis by Fritzsche
International Journal of Health Geographics 2002 1:2
The Underdiagnosis of Neuropsychiatric Lyme Disease in Children and Adults
by Fallon, Kochevar, Gaito, Nields
Psychiatric Clinics of North America, 1998; 21: 693-703

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Misc. Articles (News, Newsletters, Websites, etc.)

Articles By Robert Bransfield, M.D.
Lyme Alliance Newsletter

The following articles are available: "All in Your Head?", "Microbes and Mental Illness", "Spirochetes On the Brain", "Lyme Disease and Cognitive Impairments", "Lyme, Depression, and Suicide", "Agression and Lyme Disease", "A Tale of Two Spirochetes" and "Sex and Lyme Disease". The following are the most recently added: "Gettysburg Times Article", "The Klempner Study", "Posttraumatic Stress Disorder and Infectious Encephalopathies", "The Psychotropic Management of Late-Stage Lyme and Associated Diseases" and "What Causes Illness and Mental Illness?".

Understanding the Puzzle of Chronic Lyme
Columbia University Medical Center News, August 2004
Brain Scans Distinguish Lyme Disease From Primary Psychiatric Disorders
Doctor's Guide to the Internet, October 24, 1997
Can Lyme Disease Cause Psychiatric Disorders? by Joan Arehart-Treichel
Psychiatric News: March 15, 2002
Teen Angst or Depression?
Seattle Post-Intelligencer: October 2002
Neurological Impairment Seen in Patients Given Lymerix
DG News: October, 2002
I Refused to Give Up on My Daughter
Good Housekeeping: October 2003
Lyme Signs Missed by James Schaller, MD
Psychological and Neurological Basic Findings of Active Lyme Disease by James Schaller, MD
Actress with Migraines and ADD Reports Both Due to Lyme
by James Schaller, MD
Cognition Problems Fuel Lyme Disease Debate by Nancy Walsh
Clinical Psychiatry News: October 2002
Free Registration Required
Lyme disease victims find new hope in study on Cape
Cape Cod Times: November 2002
Free Registration Required
Amy Tan, Ticked Off About Lyme
Washington Post, August 2003
A Disease in Disguise
Newsweek: August, 2004
Diseases of the Mind
Newsweek International: December 2003
Brain Imaging
Columbia University Lyme Website
Treatment of Lyme Disease
Columbia University Lyme Website
Lyme Disease and Psychiatric Disorders
P&S Journal: Winter 1998, Vol.18, No.1

--------------------------------------------------------------------------------

Presentations

Psychiatric and neuropsychological aspects of Lyme Disease by Felice A. Tager, Ph.D. and Brian A. Fallon, M.D.
Meeting of the American Psychiatric Association, May 2002
Testimonies of Brian Fallon, M.D. and Carolyn Britton, M.D.
NY Assembly Health Committee Hearing on Lyme Disease
November, 2001 (Scroll down)
Testimony of Robert Bransfield, M.D.
NY Assembly Health Committee Hearing on Lyme Disease November, 2001
Spirochetes may "love the brain to death" by Dr. Diego Cadavid
101st General Meeting of the American Society for Microbiology, May, 2001.
Neurologic Lyme Disease: Defining and Treating an Elusive Target by Brian A. Fallon, M.D., and Harry Goldhagen, MS
14th International Scientific Conference on Lyme Disease & Other ick-Borne Disorders, April, 2001.
(Free Registration Required)
Review of Lyme Neuroborreliosis
13th International Scientific Conference on Lyme Disease and other Tick-borne Disorders, March, 2000.
Lyme Neuroborreliosis: Recognition, Treatment, and Retreatment of Relapse
13th International Scientific Conference on Lyme Disease and other Tick-borne Disorders, March, 2000.
Cognitive Remediation by Leo Shea, PhD
12th International Conference on Lyme Disease and Other Spirochetal and Tick-Borne Disorders, April 1999.

Also See: presentation abstract
Summary of Neurologic Lyme Disease Presentations by Brain A. Fallon, M.D.
12th International Conference on Lyme Disease and Other Spirochetal and Tick-Borne Disorders, April 1999.
Lyme Disease vs. Somatoform Disorders by Brian A. Fallon, M.D.
10th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, April 1997.
Psychiatric Aspects of LD & the Use of SPECT Imaging by Brian A. Fallon, M.D.
10th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, April 1997.
Seronegative Chronic Meningoencephalomyelitis in LD by Kenneth B. Liegner, M.D.
10th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, April, 1997.
Lyme Disease and the Clinical Spectrum of Antibiotic-Responsive Chronic Meningoencephalomyelitides by Kenneth B. Liegner, M.D.
9th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, April, 1996.
Lyme Disease vs. Depression vs. Somatization: Cognitive Tests & Functional Imaging by Brian A. Fallon, M.D.
9th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, April 1996
Neurofeedback and Lyme Disease: A Clinical Application of the Five Phase Model of CNS Functional Transformation by Valdeane Brown, Ph.D.
Annual Conference of the Society for the Study of Neuronal Regulation, May 1995

--------------------------------------------------------------------------------

Books & Videos:

Bipolar Odyssey
By David Moyer, CSW, Lt Col
Too Good to be True? Nutrients Quiet the Unquiet Brain - A Four Generation Bipolar Odyssey
Neuropsychiatric Aspects of Other Infectious Diseases. By Brian A. Fallon, M.D.
Comprehensive Textbook of Psychiatry., Ed. Kaplan and Sadock. Williams & Wilkins, 2002.
Lyme & Other Tick-borne Diseases: A 21st Century View, 2001
Neuropsychiatric Lyme Disease Update by Brian A. Fallon, M.D.
Neurological Manifestations of Lyme Disease by Richard S. Rhee, MD
Neuropsychiatric Manifestations of Lyme Borreliosis by Brian A. Fallon, M.D.
Columbia University Lyme Website

--------------------------------------------------------------------------------

Additional Resources:

The Human Side of Lyme
Dr. Virginia Sherr's website on neuroborreliosis.
Lyme Research in Adolescents
Patrick McAuliffe's Doctoral Dissertation
Medical Literature Summaries
In particular, the symptoms file has information pertaining to neuropsychiatric Lyme. The Neurologic system begins on page 17 of the symptoms file.

Journal Articles

A Selection of Free Journal Articles Available Online on the subject of Lyme and Other Tick-Borne Diseases.
Lyme slide show
SPECT perfusion images
The Whole Brain Atlas
SPECT Scans
Neurological Testing Procedures
Not Lyme-specific
Neuropsychological Testing
Not Lyme-specific
Neuropsychiatric Lyme Page
By Kay
Annotated Bibliographies
Art Doherty's "Annotated Bibliographies of Medical and Scientific Articles on Lyme Disease Issues".
Other Diseases/Conditions and Lyme Disease
by Art Doherty
Lyme Disease and Bipolar Disorder
by Art Doherty
Lyme Disease and Neurological Manifestations
by Art Doherty
Lyme Disease and Sleep Disorders
by Art Doherty
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 22:43

Tutkimuksen mukaan skitsofreniaan sairastumisen yksi suurimmista riskitekijöistä on mikäli on syntynyt talvella tai keväällä. Syyksi arvellaan borreliabakteeria. Äiti on saanut borreliatartunnan keväällä/kesällä ja hänen kauttaan se välittyy lapseen.


Int J Health Geogr. 2002 Nov 1;1:2 12453316
Seasonal correlation of sporadic schizophrenia to Ixodes ticks and Lyme borreliosis.
Markus Fritzsche

BACKGROUND: Being born in winter and spring is considered one of the most robust epidemiological risk factors for schizophrenia. The
aetiology and exact timing of this birth excess, however, has remained elusive so far. Since during phylogeny, Borrelia DNA has led to multiple germ-line mutations within the CB1 candidate gene for schizophrenia, a meta analysis has been performed of all papers on schizophrenic birth excesses with no less than 3000 cases each. All published numerical data were then plotted against the seasonal distributions of Ixodes ticks worldwide.

RESULTS: In the United States, Europe and Japan the birth excesses of those individuals who later in life develop schizophrenia mirror the seasonal distribution of Ixodes ticks nine months earlier at the time of conception. South of the Wallace Line, which limits the spread of Ixodes ticks and Borrelia burgdorferi into Australia, seasonal trends are less significant, and in Singapore, being non-endemic for Ixodes ticks and Lyme disease, schizophrenic birth excesses are absent.

CONCLUSION: At present, it cannot be excluded that prenatal infection by B.burgdorferi is harmful to the implanting human blastocyst. The epidemiological clustering of sporadic schizophrenia by season and locality rather emphasises the risk to the unborn of developing a congenital, yet preventable brain disorder later in life.

Latest citations:
Int J Health Geogr. 2002 Dec 20;1:5 12537588 [Pubmed] [Scholar]

Geographical and seasonal correlation of multiple sclerosis to sporadic schizophrenia.
Fritzsche

Muita tutkimuksia:
Ann Agric Environ Med. 2004 ;11:105-8 15236506 [Pubmed] [Scholar]

The prevalence of spirochete Borrelia burgdorferi sensu lato in ticks Ixodes ricinus and mosquitoes Aedes spp. within a selected recreational area in the city of Szczecin.
Danuta Kosik-Bogacka , Wanda Kuźna-Grygiel , Katarzyna Bukowska
Ann Agric Environ Med. 2004 ;11:109-14 15236507 [Pubmed] [Scholar]

Ixodes ricinus as a vector of Borrelia burgdorferi sensu lato, Anaplasma phagocytophilum and Babesia microti in urban and suburban forests.
Joanna Stańczak , Refaat Mohammed Gabre , Wiesława Kruminis-
Łozowska , Maria Racewicz , Beata Kubica-Biernat
Eur J Clin Microbiol Infect Dis. 2004 Aug ;23:603-8 15278727 [Pubmed]
[Scholar]

Risk of Borrelia burgdorferi infection in western Switzerland following a tick bite.
I Nahimana , L Gern , D S Blanc , G Praz , P Francioli , O Péter Parassitologia. 2004 Jun ;46:119-22 15305699 [Pubmed] [Scholar]

[Ixodes ricinus, transmitted diseases and reservoirs]
A Rizzoli , R Rosà , B Mantelli , E Pecchioli , H Hauffe , V Tagliapietra, T Beninati , M Neteler , C Genchi, J Med Entomol. 2004 Jul ;41:768-73 15311473 [Pubmed] [Scholar]

Life stage-related differences in density of questing ticks and infection with Borrelia burgdorferi sensu lato within a single cohort of Ixodes pacificus (Acari: Ixodidae).
Rebecca J Eisen , Jeomhee Mun , Lars Eisen , Robert S Lane J Med Entomol. 2004 Jul ;41:779-84 15311475 [Pubmed] [Scholar]

Abundance of Ixodes scapularis (Acari: Ixodidae) after the complete removal of deer from an isolated offshore island, endemic for Lyme Disease.
Peter W Rand , Charles Lubelczyk , Mary S Holman , Eleanor H Lacombe , Robert P Smith Jr
Med Vet Entomol. 2004 Sep ;18:228-31 15347389 [Pubmed] [Scholar]

Borreliae in Ixodes ricinus ticks feeding on humans.
Z Hubálek , J Halouzka , Z Juricová
Med Hypotheses. 2005 ;64:438-48 15617845 [Pubmed] [Scholar]

Chronic Lyme borreliosis at the root of multiple sclerosis--is a cure with antibiotics attainable?
Markus Fritzsche
Psychiatry Clin Neurosci. 2006 Apr ;60:249-52 16594951 [Pubmed] Scholar]

Seasonality of birth in patients with schizophrenia in Japan.
Yoshio Mino , Iwao Oshima
Eur Psychiatry. 2006 Nov 24;: 17129712 [Pubmed] [Scholar]

Schizophrenic subtype, seasonality of birth and social class: A preliminary analysis.
Bernard J Gallagher 3rd , Brian J Jones , Joseph A McFalls Jr , Anthony M Pis
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 22:46

"Viimeaikaisissa artikkeleissa on yhä useammin esitetty näkemyksiä borrelioosin ja autismin yhteydestä toisiinsa. Borrelioosin oireet saattavat olla samanlaisia kuin autismissa. Asiaan liittyen on perustettu omat sivut http://www.lymeinducedautism.com/ . Asiaa tutkitaan parhaillaan USA:ssa."


Is There a Connection Between Lyme Disease and Autism?
http://autism.about.com/b/a/257714.htm

Recent articles in the media suggest that there may be a connection between Lyme disease and autism. Lyme disease, which is caused by tick bites, does indeed manifest itself with symptoms that, in some cases, are similar to those of autism. In addition, Lyme disease can lower the immune threshold, making bodies more susceptible to immune system insults (a possible cause of autism).

Lyme disease is treated with antibiotics. If indeed it were the case that at least some cases of autism are triggered by Lyme disease, then perhaps these cases of autism could be treated. This would, of course, be an enormous benefit to the autism community.


How likely is it that Lyme disease may cause some cases of autism? While an organization called Lyme Induced Autism http://www.lymeinducedautism.com/ suggests that it's very likely, no serious research has been conducted to date. The group has been raising money to conduct research, and is hoping to find the proof they seek.


Meanwhile, Columbia University researcher Brian A. Fallon is now in the process of conducting an epidemiological study which compares rates of Lyme disease to rates of autism. If that study suggests a connection, then further research may be warranted.


Given the extremely preliminary nature of this idea, it's interesting to compare the views of the two organizations involved in research. The press release from the Lyme Induced Autism Foundation http://tinyurl.com/yzzpmw states:


New reports indicate up to 90% of children with autism are infected with Lyme disease. With autism at a staggering 1 out of 166 children, parents are questioning this new finding.

Meanwhile, however, Columbia University's research description http://www.columbia-lyme.org/flatp/childstud-n.html states:
In our work with children who have developed Lyme disease, we have encountered a few children who had developed autistic-like disorders which were eventually also diagnosed as having Lyme disease due to other concomitant symptoms; when the child received intensive antibiotic therapy, the autistic syndromes dramatically improved and, in some cases, resolved. We hypothesize: a) that a small subpopulation of children with autism in Lyme endemic areas may have an antibiotic responsive disorder due to a spirochete-induced autistic syndrome...

Obviously, these two perspectives are very much at odds. Given that no true research has taken place to date, it's hard to know where the "new reports" cited in the press release could be coming from. In short, it looks to me like yet another opportunity for the media to get very excited about very little. Until an epidemiological study shows a probable connection between Lyme and autism, and until double-blind, placebo-based studies actually show that antibiotics can improve autistic symptoms -- I'd recommend that parents sit tight.


Meanwhile, however, it's a great idea to protect yourself and your children from Lyme disease, which does indeed have the potential to cause serious harm.


Wednesday January 10, 2007 |
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 22:47

Alla olevissa lääketieteellisissä tutkimuksissa käsitellään pseudotuumorin esiintymistä neuroborrelioosissa:

1: Steenhoff AP, Smith MJ, Shah SS, Coffin SE. Neuroborreliosis with progression from pseudotumor cerebri to aseptic meningitis.
Pediatr Infect Dis J. 2006 Jan;25(1):91-2.
PMID: 16395117 [PubMed - indexed for MEDLINE]

2: Nord JA, Karter D.
Lyme disease complicated with pseudotumor cerebri.
Clin Infect Dis. 2003 Jul 15;37(2):e25-6. Epub 2003 Jul 9.
PMID: 12856231 [PubMed - indexed for MEDLINE]

3: Garcia-Moreno JM, Borobio-Enciso MV, Angulo-Fraile S, Izquierdo G.
[Pseudotumour cerebri in a patient with Lyme disease and hypothyroidism]
Rev Neurol. 2003 Apr 16-30;36(8 ):727-9. Spanish.
PMID: 12717650 [PubMed - indexed for MEDLINE]

4: Hartel C, Schilling S, Neppert B, Tiemer B, Sperner J. Intracranial hypertension in neuroborreliosis.
Dev Med Child Neurol. 2002 Sep;44(9):641-2.
PMID: 12227619 [PubMed - indexed for MEDLINE]

5: Ansari I, Crichlow B, Gunton KB, Diamond GR, Melvin J. A child with venous sinus thrombosis with initial examination findings of
pseudotumor syndrome.
Arch Ophthalmol. 2002 Jun;120(6):867-9. No abstract available.
PMID: 12049606 [PubMed - indexed for MEDLINE]

6: Zemel L. Related Articles, Links
Lyme disease and pseudotumor.
Mayo Clin Proc. 2000 Mar;75(3):315. No abstract available.
PMID: 10725963 [PubMed - indexed for MEDLINE]

7: Bachman DT, Srivastava G. Related Articles, Links
Emergency department presentations of Lyme disease in children.
Pediatr Emerg Care. 1998 Oct;14(5):356-61. Review.
PMID: 9814407 [PubMed - indexed for MEDLINE]

8: Kan L, Sood SK, Maytal J.
Pseudotumor cerebri in Lyme disease: a case report and literature review.
Pediatr Neurol. 1998 May;18(5):439-41. Review.
PMID: 9650688 [PubMed - indexed for MEDLINE]

9: Awad A.
Case 1-1998: a boy with a seizure.
N Engl J Med. 1998 May 21;338(21):1549-50. No abstract available.
PMID: 9599118 [PubMed - indexed for MEDLINE]

10: Jonsell G.
[Pseudotumor cerebri in children. Neuroborreliosis may be the cause]
Lakartidningen. 1996 Apr 17;93(16):1557-8. Swedish. No abstract available.
PMID: 8667759 [PubMed - indexed for MEDLINE]

11: Ellermann A, Hjelt K.
[Pseudotumor cerebri caused by Lyme borreliosis]
Ugeskr Laeger. 1995 Feb 13;157(7):901. Danish.
PMID: 7701654 [PubMed - indexed for MEDLINE]

12: Belman AL, Iyer M, Coyle PK, Dattwyler R. Neurologic manifestations in children with North American Lyme disease.
Neurology. 1993 Dec;43(12):2609-14.
PMID: 8255465 [PubMed - indexed for MEDLINE]

13: Jacobson DM, Frens DB.
Pseudotumor cerebri syndrome associated with Lyme disease.
Am J Ophthalmol. 1989 Jan 15;107(1):81-2. No abstract available.
PMID: 2912122 [PubMed - indexed for MEDLINE]

14: Bourke SJ.
Lyme disease.
Biomed Pharmacother. 1989;43(6):397-400. Review.
PMID: 2686764 [PubMed - indexed for MEDLINE]

15: Raucher HS, Kaufman DM, Goldfarb J, Jacobson RI, Roseman B, Wolff RR.
Pseudotumor cerebri and Lyme disease: a new association.
J Pediatr. 1985 Dec;107(6):931-3. No abstract available.
PMID: 4067752 [PubMed - indexed for MEDLINE]
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 22:49

Myöhäisvaiheen borrelioosissa esiintyy usein mitä moninaisimpia oireita jotka vaikeuttavat diagnostiikkaa. Tutkimuksessa esitetään tapaus, jossa borrelioosia sairastavalla henkilöllä oli useita imukudostiivistymiä luuytimessä ja imusolmukkeissa. Diagnoosiin päädytiin luuydinpunktion ja PET-kuvauksen avulla.


Journal of Infection
Volume 51, Issue 4 , November 2005, Pages e203-e206

doi:10.1016/j.jinf.2005.02.014
Copyright © 2005 The British Infection Society Published by Elsevier Ltd.
Case Report

Successful antibiotic treatment of Borreliosis associated pseudolymphomatous systemic infiltrates

A. Aigelsreiter ym.Department of Pathology, Medical University Graz, Auenbruggerplatz 25, A-8036 Graz, Austria
Accepted 15 February 2005. Available online 23 March 2005.

Abstract
The clinical management of late stage Borreliosis can be difficult due to various associated symptoms and signs and cumbersome microbiological tests. We report a case of successful antibiotic treatment of Borreliosis-associated pseudolymphomatous infiltrates in bone marrow and lymph nodes, which were diagnosed by bone marrow trephine biopsy and positron emission tomography.

Keywords: Lyme; Borreliosis; Fever of unknown origin; Lymphoma-like; Pseudolymphoma
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 22:50

Borreliabakteereita löytyi 7 %:lla tutkituista eläimistä. Bakteereita oli useimmin virtsarakon seinämässä ja vain yhdeltä jyrsijältä löydettiin bakteereita aivoista. (Itävalta)

http://www.ncbi.nlm.nih.gov/entrez/quer ... h&DB=pubme

Wien Klin Wochenschr. 2006 Dec;118(23-24):754-758.

Seasonal variations in detecting Borrelia burgdorferi sensu lato in rodents from north eastern Austria.

* Khanakah G,
* Kocianova E,
* Vyrostekova V,
* Rehacek J,
* Kundi M,
* Stanek G.

Institute of Hygiene and Medical Microbiology, Medical University of Vienna, Vienna, Austria, gelas.khanakah@meduniwien.ac.at.

Austria is well known as an endemic area of Lyme borreliosis. To assess the annual variation of rodent populations that may host agents of Lyme borreliosis we collected rodents in northeastern Austria. Life traps were set out every six weeks during a year consecutively in one each of the three different zones (Hohenau, Ernstbrunn, Vienna Woods) that cover the main habitat characteristics of small mammals in northeastern Austria. Rodents were collected and identified.

Samples of heart, urine bladder and brain were removed under aseptic conditions for cultivation of borrelia. Samples of heart muscle were additionally used for molecular detection of borrelia by Real-Time polymerase chain reaction. PCR was performed with borrelia universal primers and with species-specific primers. 938 mice were caught, most frequently Apodemus flavicollis (44%), followed by Clethrionomys glareolus (35%), Microtus arvalis (9%), A. sylvaticus (7%) and Mus musculus (6%).

Significant differences were seen in the total number of catch per area (Hohenau, Ernstbrunn, Vienna Woods equal 10:9:2) and in the distribution of the various rodent species in the respective areas. Borrelia strains were grown from only 65 (7%) animals, and more frequently isolated from bladder wall than from heart muscle, and only once from brain. Heart specimens of 223 animals were positive by borrelia PCR (24%), most frequently of the rodent species A. flavicollis (43%) and C. glareolus (38%). Borrelia afzelii was most frequently identified, followed by B. burgdorferi sensu stricto, B. garinii and by mixed infection of B. afzelii with B. burgdorferi sensu stricto. B. garinii was most frequently detected in heart samples of A. sylvaticus (about 20%). In about 3% of PCR positive samples the identification of one of the three mentioned genospecies of borrelia could not be ascertained with the test panel used. The results confirm the rodent species A. flavicollis, A. sylvaticus, M. arvalis and C. glareolus as reservoir animals for B. afzelii, B. garinii and B. burgdorferi sensu stricto, agents of Lyme borreliosis. Notable is the salient presence of B. garinii in heart specimens of A. sylvaticus.

PMID: 17186171 [PubMed - as supplied by publisher]
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 22:54

1. Uuden tutkimuksen mukaan borreliabakteerin aiheuttaman infektion seurauksena immuunijärjestelmä aktivoituu. Sen seurauksena seerumin IFN-gamma -pitoisuus nousee. Tästä on seurauksena eriasteisia kroonisia tulehduksellisia kudosvaurioita jotka korreloivat taudin vakavuuteen.

2. "Kaikki krooniset sairaudet ? masennuksesta syöpään ? ovat pohjimmiltaan tulehdustauteja. Se voidaan käytännössä osoittaa mittaamalla potilaan veren ja syljen tulehdussytokiineja, jotka ovat koholla. Tuumorinekroosititekijä alfa (TNF-) tuottaa kudoksissa tulehdusta ja syöpää aiheuttavaa interleukiini 8:aa (IL8). IL6 puolestaan tuottaa maksassa C-reaktiivista proteiinia (CRP), joka vaurioittaa valtimoiden sisäpintaa, endoteelia. IL18 lisää astman, insuliiniresistenssin ja diabeteksen riskiä. Onneksi sytokiineja voidaan vaimentaa monin ravintolisin. Tämä "uusi" ravintolisien vaikutusmekanismi selittää niistä saatavaa hyötyä kaikissa akuuteissa ja kroonisissa taudeissa. Niistä on tässä artikkelissa muutamia esimerkkejä."

....Interferoni gamma (IFN-) ja MS-tauti
Interferonit ovat polypeptidejä, joilla on antiviraalisia, solujen kasvua estäviä ja immuunijärjestelmää sääteleviä vaikutuksia elimistössä. Interferoneja on kahta päätyyppiä: interferoni-alfa/beta sekä interferoni-gamma. Interferoneja käytetään lääkkeinä, joilla pyritään estämään vaikeita infektioita sekä lievittämään niiden vaikeusastetta.

Ihmisen T-valkosolut tuottavat luonnostaan interferoneja virusinfektion aikana ja niillä on tärkeä rooli monien virusten lisääntymisen estäjinä infektion alkuvaiheessa. Interferonit sitoutuvat kohdesolujen pinnalla oleviin spesifisiin reseptoreihin, mikä saa aikaan antiviraalisten geenien aktivoitumisen tumassa. Näiden geenien koodittamat proteiinit estävät virusten kasvua.

Naiset tuottavat luonnostaan enemmän interferoni gammaa kuin miehet. Sen arvellaan selittäävän sitä, että naiset sairastuvat miehiä useammin esimerkiksi MS-tautiin. Tauti puhkeaa yleensä juuri virusinfektion jälkeen. Uuden kansainvälisen tutkimuksen mukaan suuri IFG-pitoisuus voi pahentaa multippeliskleroosia (MS-tautia). IFG ja TNF-alfa ovat syypäitä MS-potilaiden krooniseen väsymykseen ja masentuneisuuteen (Multiple Sclerosis. 2004;10(2):165-9). Nämä havainnot selittävät sitä, miksi IFG:tä ja TNF-alfaa vaimentavia ravintolisiä käyttävät potilaat ovat parammassa kunnossa kuin ne, jotka eivät niitä käytä. MS-tautiin sopii sama ravinnehoito kuin masennukseen, josta tulee lisää puhetta tuonnempana.

Myös lykopeeni estää interferoni-gammaa, jolloin se vähentää eturauhassyövän vaaraa ja jarruttaa taudin etenemistä (lue lisää). Interleukiini 12 (IL12) puolestaan vuorovaikuttaa interferoni gamman kanssa; IL12 tehostaa tiettyjen interferoni gammaan ja angiogeneesiin liittyvien syöpätautien (mm. melanoman ja munuaissyövän) hoitoa (Journal of Clinical Oncology 2005).

Toisaalta lehmänmaidolle allergisisten vauvojen IFN:n eritys on tavallista vähäisempää.. Kun heille on annettu maitohappobakteereja (LGG), on IFN.n ja Th1-solujen eritys lisääntynyt ja allergian oireet ovat samalla lieventyneet. Havainto selittää LGG-hoidon myönteistä vaikutusta pikkulasten atooppisessa ihottumassa, kirjoittavat suomalaiset allergiatutkijat Emma Marschan ja Mirva Viljanen (Allergiasäätiön Allergiakoulu 2005; 70?71; 104?105).

Koko artikkeli: http://www.biovita.fi/suomi/terveyssivut/tnf.html Tuumorinekroositekijä (TNF)-alfa, ja muut tulehdus- ja syöpäsytokiinit



1. J Immunol. 2007 Jan 15;178(2):1172-9.
IFN-{gamma} Alters the Response of Borrelia burgdorferi-Activated
Endothelium to Favor Chronic Inflammation.

* Dame TM,
* Orenzoff BL,
* Palmer LE,
* Furie MB.

Graduate Program in Genetics.

Borrelia burgdorferi, the agent of Lyme disease, promotes proinflammatory changes in the endothelium that lead to the recruitment of leukocytes. The host immune response to infection results in increased levels of IFN-gamma in the serum and lesions of Lyme disease patients that correlate with greater severity of disease. Therefore, the effect of IFN-gamma on the gene expression profile of primary human endothelial cells exposed to B. burgdorferi was determined. B. burgdorferi and IFN-gamma synergistically augmented the expression of 34 genes, 7 of which encode chemokines. Six of these (CCL7, CCL8, CX3CL1, CXCL9, CXCL10, and CXCL11) attract T lymphocytes, and one (CXCL2) is specific for neutrophils. Synergistic production of the attractants for T cells was confirmed at the protein level. IL-1beta, TNF-alpha, and LPS also cooperated with IFN-gamma to induce synergistic production of CXCL10 by the endothelium, indicating that IFN-gamma potentiates inflammation in concert with a variety of mediators. An in vitro model of the blood vessel wall revealed that an increased number of human T lymphocytes traversed the endothelium exposed to B. burgdorferi and IFN-gamma, as compared with unstimulated endothelial monolayers. In contrast, addition of IFN-gamma diminished the migration of neutrophils across the B. burgdorferi-activated endothelium. IFN-gamma thus alters gene expression by endothelia exposed to B. burgdorferi in a manner that promotes recruitment of T cells and suppresses that of neutrophils. This modulation may facilitate the development of chronic inflammatory lesions in Lyme disease.

PMID: 17202382 [PubMed - in process]
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Tammi 23, 2009 23:00

Jackie Rouse sai kaksi sydäninfarktia, joiden syyksi osoittautui BORRELIABAKTEERI. Hänellä ei ollut aiemmin minkäänlaisia sydänongelmia. Infarktien jälkeen hänelle jouduttiin tekemään sydämensiirto marraskuun 27. päivä 2006.

January 03, 2007

Man, 29, learns mystery illness means he needs new heart

By SANDRA FREDERICK
Staff Writer

NEW SMYRNA BEACH -- When Kenny St. George arrived at Bert Fish Medical Center the day after Christmas, he had no idea an inflated stomach and 30-pound weight gain meant he needed a new heart.

"I didn't know why I was gaining all this weight all of sudden. I knew something was wrong," the 29-year-old New Smyrna Beach man said from his bedside.

After several cardiac tests, Dan St. George was told by doctors at the hospital his son was suffering from congestive heart failure and had stored the body fluids instead of pumping them out of his system. But the message that followed floored the father.

"They said he needs a heart real soon or he will die," Dan St. George said with tears swelling in his eyes.

Six months earlier, he had similar -- but milder -- symptoms and was told he might have a valve problem and more tests were needed. But, Kenny St. George was working as a part-time produce clerk at a grocery store and didn't have insurance. Not realizing the severity of the problem, he said time slipped away and he didn't get the needed test.

Kenny St. George is the second area patient to be seen at the hospital in recent months urgently needing a transplant. Jackie Rouse received a heart on Nov. 27 at Mayo Clinic at St. Luke's Hospital in Jacksonville after being transferred in critical condition after suffering two heart attacks, one nearly fatal. Rouse said she had no inkling the heart disease, in her case caused by Lyme Disease, was so advanced, with a new organ being the only way to survive.

......

sandra.frederick@news-jrnl.com
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 18:23

ALS/neuroborrelioosi
runsaasti tutkimuksia, linkkejä jne.

http://home.goulburn.net.au/~shack/lyme.htm
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 18:28

Tutkimuksia joiden mukaan borreliabakteeri viihtyy hyvin esim. sydämessä ja virtsateissä. Viimeisen tutkimuksen mukaan edes negatiivinen PCR-testitulos ei poissulje aktiivisen infektion mahdollisuutta.


1.. ...marked tropism of the spirochete for myocardial and urinary tract tissues. Fifty-six of 57 hearts (98%) and 52 of 58 bladders (90%) were culture positive. The cardiac infection was persistent and could be documented in 21 of 22 hearts (96%) cultured from days 28 to 84 postinfection. The urinary tract was also a site of persistent infection in most animals, with 18 of 23 bladders (78%) being culture positive from days 28 to 84. The persistence of spirochetes was specific for the heart and bladder, as indicated by negative cultures of specimens from the liver and spleen, in which only 1 of 23 cultures was positive from days 28 to 84...
http://jcm.asm.org/cgi/content/abstract/29/5/89

2. http://www.pubmedcentral.nih.gov/articl ... tid=257737
We could detect 10 fg (less than 10 molecules) of B. burgdorferi or less than five spirochetes added to human urine. Finally, we were able to use the PCR to detect B. burgdorferi DNA in the urine of four of eight patients with suspected active LD (three with arthritis and one with neurologic manifestations)

3. B. burgdorferi DNA was detected in urine samples from nine patients;..
http://jcm.asm.org/cgi/content/abstract/30/7/1646

4. B. burgdorferi DNA was detected in 25 urine samples of 17 patients with active disease, whereas 26 samples from this group of patients were negative. Only one asymptomatic case with previous infection showed a positive result, and the urine samples of the patients without Lyme disease were uniformly negative. Two of four patients from whom samples before and directly after onset of therapy were available converted from negative to positive PCR results after initiation of therapy, accompanied by the symptoms of a Jarisch-Herxheimer reaction. It can be concluded from these results that a positive PCR from urine is with high probability an indicator of active Lyme disease. On the other hand, as only 17 of the 26 patients with active infection were positive, a negative PCR result does not exclude active infection... http://www.springerlink.com/(zom2d255rittdcrrpjd3zm2s)/app/home/contribution.asp?referrer=parent&backto=issue,10,16;journal,56,237;linkingpublicationresults,1:103905,1
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 18:29

33-vuotiaalle miehelle annettiin diagnoosiksi krooninen väsymysoireyhtymä. Kahden vuoden kuluttua oireiden aiheuttajaksi todettiin borreliabakteeri. Asia tulee ottaa huomioon, koska sillä on sekä hoidollista että prognostista merkitystä.


Lyme Disease Presenting as Chronic Fatigue Syndrome

Page Range: 67 - 75
DOI: 10.1300/J092v13n04_06
Copyright Year: 2006


Contributors:
Samuel Shor MD, FACP, Associate Clinical Professor, George Washington University Health Care Sciences, Reston, VA, 20190, sshor@intmednova.com

Abstract:

Objective: Chronic Fatigue Syndrome (CFS) by definition represents a diagnosis of exclusion. Late stage or "Chronic Lyme" infection with or without "co-infections" is a difficult diagnosis to establish. The symptom complex of both conditions can be very similar. This case study represents an attempt to support serious consideration for a subpopulation of patients otherwise diagnosed with "CFS," as actually representing chronic Lyme disease.

Method: A case study is presented of a 33-year-old man, who for two years, was being managed as having CFS. However, after ~2 years of utilizing multiple modalities of management with limited success, the diagnosis of Lyme was reconsidered. Historical exposure risks to Lyme in this individual were high. He had prolonged exposure in the highly tick-infested mountains of North Carolina for 18 months, several years prior to becoming ill. More aggressive investigation confirmed the diagnosis of Lyme. Appropriate changes in management were associated with an improved level of functioning that was far in excess of what maximal management of CFS was able to achieve. The features of CFS and chronic Lyme can be very similar and include the following: Profound fatigue often associated with cognitive impairment. Other common symptoms related to both of these conditions include sleep disturbances, fibromyalgia, and dysautonomias. In pursuing clarification of this diagnosis, the author was exposed to a contrast in medical opinion regarding diagnostic tools and criteria that were perceived as creating potential barriers to the management of patients presenting with these symptoms.

Conclusion: Acceptance and awareness of the possibility that Lyme disease can present as CFS has important therapeutic and prognostic implications. doi:10.1300/J092v13n04_06

Journal Title:

Journal of Chronic Fatigue Syndrome:
Multidisciplinary Innovations in Research, Theory, and Clinical Practice
Volume: 13 Issue: 4
ISSN: 1057-3321 Pub Date: 4/5/2007
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 18:58

Borrelioosidiagnoosi saattaa jäädä virheellisesti tekemättä esim. silloin kun henkilöllä on kilpirauhasen vajaatoiminnasta johtuvia oireita.


J Am Osteopath Assoc. 1995 Jul;95(7):435-7.
Hypothyroidism with concurrent Lyme disease.
Paparone PW.
Lyme Disease Center for South Jersey, Absecon 08201, USA.

Lyme disease can be seen as localized, disseminated, acute, or chronic and can mimic other, more serious diseases. Even though it is a multisystemic illness, very few spirochetes are present; yet, once established in the host, it can persist for years. The antibody response is slow and variable, and the spirochete is difficult to isolate from clinical specimens, even those obtained from the pathognomonic skin lesion. These variables, together with nonspecific symptoms, make the diagnosis of Lyme disease difficult. The author describes an unusual case of Lyme disease superimposed on severe primary hypothyroidism in which the thyroid disorder was so advanced and pronounced that the diagnosis of Borrelia infection could easily have been missed.

PMID: 7642407 [PubMed - indexed for MEDLINE]
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 19:03

1. "Borrelioosissa esiintyvät neurologiset ja psyykkiset oireet ovat niin moninaiset että sitä kutsutaan 'suureksi matkijaksi'. Lääkäreiden on välttämätöntä tuntea borrelioosin aiheuttama laaja oireiden kirjo. Neurologisia oireita voi esiintyä missä tahansa; keskushermostosta ääreishermostoon ja lihaksiin." (Ranskalainen tutkimus 2007)

Med Mal Infect. 2007 Mar 8; [Epub ahead of print]

[Neurologic and psychiatric manifestations of Lyme disease.]
[Article in French]

* Blanc F;
* GEBLY.

Departement de neurologie, hopitaux universitaires de Strasbourg, 1, place de l'Hopital, 67091 Strasbourg, France.

The neurological and psychiatric manifestations of Borrelia burgdorferi sensu lato are so numerous that Borrelia is also called the "new great imitator". Thus knowing about the multiple clinical aspects of neuroborreliosis is necessary for the clinician. We reviewed literature for "classical" neuroborreliosis such as acute meningoradiculitis or chronicle encephalomyelitis, but also for encephalitis, myelitis, polyneuritis, radiculitis and more controversial disorders such as chronic neurological disorders, ischemic and hemorrhagic stroke, and motor neuron disease. We specified every time on which basis each disorder was attributed to Lyme disease, particularly if European or American criteria were met. Every part of the nervous system can be involved: from central to peripheral nervous system, and even muscles.In endemic areas, Lyme serology must be assessed in case of unexplained neurological or psychiatric disorder. In case of positive serology, CSF assessment with intrathecal anti-Borrelia antibody index will be more efficient to prove the diagnosis.

PMID: 17350199 [PubMed - as supplied by publisher]


2. Borrelioosissa esiintyy mitä erilaisimpia systeemisiä ja neurologisia oireita. Neurologiset ja psyykkiset oireet esiintyvät usein sairauden toisessa vaiheessa esim. masennus, meningoradikuliitti, enkefaliitti jne. Kolmannessa vaiheessa esiintyy kroonista esim. enkefalopatiaa, polyneuropatiaa jne. (Ranska 2007)

Med Mal Infect. 2007 Mar 15; [Epub ahead of print] Links
[Clinical manifestations and epidemiological aspects leading to a diagnosis of Lyme borreliosis: neurological and psychiatric manifestations in the course of Lyme borreliosis.]
[Article in French]
Creange A.
Service de neurologie, centre hospitalier universitaire Henri-Mondor, APHP, universite Paris-XII, 94000 Creteil, France.

Lyme disease is associated with various systemic and neurological manifestations. The neurological and psychiatric manifestations of Lyme disease are more frequently observed during its secondary phase (stage 2) than during its late tertiary phase (stage 3). In stage 2, cerebrospinal fluid and bacterial tests are consistent with the ongoing infection. Painful meningoradiculitis, encephalomyelitis and encephalitis, and symptoms of depression are the most characteristic at this stage. The diagnosis should be based on the association of clinical, epidemiological, and biological features. Adequate treatment usually leads to recovery. In stage 3 of the disease, the link between neurological manifestations and initial infection is uncertain. Distal axonal polyneuropathy and chronic encephalopathy are the most frequently reported presentations.

PMID: 17368785 [PubMed - as supplied by publisher]
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 20:14

1. Erityisesti raajoissa esiintyvä ihotulehdus on tyypillinen Euroopassa esiintyvä Borrelia afzeliin aiheuttama oire. Nyt ihotulehdusta on todettu esiintyvän myös muualla kehossa:

http://www.ncbi.nlm.nih.gov/entrez/quer ... MD=search&
DB=pubmed

J Med. 1999;30(3-4):267-78.

Clinical features and specific immunological response to Borrelia afzelii in patients with acrodermatitis chronica atrophicans.

* Flisiak I,
* Schwartz RA,
* Chodynicka B.

Department of Dermatology and Venereology, Medical Academy of Bialystok, Sw. Rocha 3 15-879 Bialystok, Poland.

Acrodermatitis chronica atrophicans (ACA) occurs mostly in Europe. Borrelia afzelii is considered to be responsible for this manifestation of Lyme borreliosis. The aim of the study was to observe the clinical features of the ACA and evaluate the specific immunological response to Borrelia afzelii. Nine patients from an endemic Lyme borreliosis region in northeastern Poland were studied. The serum samples were tested routinely with IFA and EIA and, following testing, with immunoblots using Borrelia afzelii antigens. ACA was located mainly on the skin of the arms, forearms, thighs and chest. The only extracutaneal manifestation of Lyme borreliosis was paresis of the brachial plexus observed in one patient. Analysis of the immunoblot-banding pattern revealed positive reactions in all patients against flagellar antigen (41 kDa). Interpretation of the immunoblots revealed positive IgG results in all cases and IgM in five of them. Concluding, ACA develops not only on the extremities, but also on the trunk. The immunoblot technique using Borrelia afzelii antigens is of value in the diagnosis of ACA.

PMID: 17312680 [PubMed - in process]


2. Borrelibakteeri aiheuttaa toisinaan iho-/lihastulehduksen (dermatomyosiitti).

http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed


Rev Med Interne. 2007 Jan 26; [Epub ahead of print]

[Lyme disease could mimic dermatomyositis.]
[Article in French]

* Waton J,
* Pinault AL,
* Pouaha J,
* Truchetet F.

Service de dermatologie, CHR Metz-Thionville, Thionville, France.

We report a dermatomyositis associated with Lyme disease. OBSERVATION: A 73-years-old woman has developed for 5 months an asthenia, a periorbital oedema and a forearm's skin infiltration without other signs suggesting of dermatomyositis. Laboratory studies showed an elevation of muscular enzymes, and inflamation signs. The skin and the muscles biopsies were compatible with the diagnostic of dermatomyositis. The patient was seropositive for Lyme disease. The patient was efficiently treated with doxycycline.
DISCUSSION: Lyme disease could mimic a dermatomyositis. Indeed, Lyme disease should be considered as a differential diagnosis of dermatomyositis.

PMID: 17337098 [PubMed - as supplied by publisher]
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 20:16

1. Englantilainen 50-vuotias mies sairastui näköhermonystyn tulehdukseen. Borreliavasta-aineet olivat positiiviset. Mies ei ollut nähnyt itsessään punkkeja, mutta hänellä oli ollut ihomuutos puoli vuotta aiemmin. Miehen kissassa oli ollut punkkeja. Hän sai hoidoksi 2 vk iv keftriaksonia, mutta hoito ei tuottanut tulosta.

Riski saada borrelioosi lemmikkikissan välittämänä ei ole yleisesti tunnettu asia. Jo 1970-luvulla huomattiin, että borrelioosia sairastavilla oli usein lemmikkinään kissa. Heillä esiintyi borrelioosia useammin kuin naapureilla joilla ei ollut kissaa. Borrelioosi saattaa aiheuttaa erilaisia silmätulehduksia. Esim. näköhermotulehdukseen antibioottihoito ei silti välttämättä auta.


http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed

Eye. 2007 Jan 19; [Epub ahead of print]
Papillitis, Lyme disease, and cats.

* Mishra SK,
* Murjaneh S,
* Morgan MS,
* Simcock PR,
* Glover S.

Correspondence: PR Simcock, West of England
Eye Unit, Royal Devon and Exeter Hospital
(Wonford), Barrack Road, Exeter EX2 5DW, UK
Tel: + 44 139 240 6008;
Fax: + 44 139 240 6022.
E-mail: psimcock@hotmail.com
Sir
Papillitis, Lyme disease and cats

We present a case of papillitis caused by Lyme disease in the UK. We also highlight the increased risk of Lyme disease in cat owners.

Case report

A 50-yr-old man presented with a 10 day history of central blurring of vision in his left eye. He had noted a rash on his right forearm 6 months previously. There was no definite history of a tick bite or of visiting high-risk areas, but his cat had ticks. Unaided vision was 6/6-3 right and 6/4 left improving to 6/12 with pin hole. There was a mild left relative afferent pupillary defect, a paracentral scotoma inferior fixation, and mild impairment of colour vision, and a pink swollen optic disc on this side.

Lyme disease antibody titres were +ve for ELISA and Western blot methods, confirmed by a reference lab. The following investigations were normal or negative: FBC, ESR, Auto-antibody screen, coagulation screen, angiotensin converting enzyme anticoagulant. The patient was treated with a 2 week course of IV ceftriaxone. The visual acuity however did not change with treatment.

Comment

Lyme disease can mimic many ophthalmic conditions. It has been reported to cause eyelid oedema, conjunctivitis, keratitis, episcleritis, anterior uveitis, vitritis, choroiditis, endophthalmitis, neuroretinitis, exudative retinal detachment, retinal vasculitis, optic neuritis, optic atrophy, pseudomotor cerebri, paresis of cranial nerves and orbital myositis. Optic neuritis in Lyme disease may or may not respond to treatment with antibiotics.

In the mid-1970s, Dr Allen Steere and colleagues noted that a significant number of patients with Lyme disease had cats and had noted ticks on their pets, compared with their unaffected neighbours. Lyme disease is now known to occur in cats, and Borrelia burgdorferi has been isolated from the tissue of adult and nymphal ticks removed from domestic cats. The increased risk of Lyme disease in cat owners is not widely known. This case report may represent Lyme disease causing papillitis transmitted from the patient's cat.


2. Monet systeemisairaudet kuten borrelioosi, aiheuttavat esim. silmän keskikalvon tulehdusta.


An eye on inflammatory eye disease.
Kestelyn PG.
Afdeling Oogheelkunde, Universitair Ziekenhuis, Gent.
philippe.kestelyn@ugent.be

The purpose of this article is to outline the interaction between ophthalmologists and internists in the management of uveitis. Two issues will be addressed: 1) which strategies should the internist follow when asked to investigate a case of uveitis; and 2) in which systemic diseases should the internist order an ocular examination to rule out intraocular inflammation. The modern approach to the diagnosis of uveitis is based on the naming-meshing system popularized by Smith and Nozik. After a short history (ocular complaints, general health) an ophthalmic examination is carried out to determine the anatomic structures involved. Based on the results a uveitis is classified as anterior uveitis, intermediate uveitis, posterior uveitis, or panuveitis. Associated factors (eg, unilateral versus bilateral, acute versus chronic, granulomatous versus nongranulomatous, etc.) are also assessed. Based on this information the type of uveitis will be named (eg, acute, nongranulomatous, unilateral, anterior uveitis) and matched (meshing) to a potential list of etiologies (eg, viral iritis, HLA-B 27 associated iritis). Targeted questioning and selected medical and laboratory investigations based on the shortlist will then identify a possible cause for a particular patient's uveitis. In other words the ophthalmologist should never ask the internist to run the full battery of tests in a patient with uveitis. He rather should indicate which type of uveitis is present and what are the most likely diagnoses to be
excluded.

Many systemic diseases cause diffuse inflammation and are associated with uveitis. These include tuberculosis, spirochaetal diseases such as *Lyme disease* and syphilis, sarcoidosis, Behcet syndrome, juvenile idiopathic arthritis, and HIV infection amongst many others.

Routine ophthalmic examination in patients with systemic disease may be indicated for diverse reasons: to prevent profound damage due to asymptomatic uveitis in JIA; to detect diagnostic clues in patients with febris e causa ignota; or to rule out opportunistic infections in HIV positive patients. It is clear that the information gained from routine examination in systemic disease will be greatly dependent on the prevalence of ocular involvement in a particular disease.
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 20:27

Borrelioosin kliininen kuva vaihtelee. Kuitenkin kaikille borrelioositapauksille, sekä akuuteille että kroonisille, on tyypillistä voimakas tulehdus. Bb saa aikaan useiden tulehdussytokiinien erittymisen.


http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed

APMIS. 2007 Feb;115(2):134-41.

Propensity to excessive proinflammatory response in chronic Lyme borreliosis.

* Kisand KE,
* Prukk T,
* Kisand KV,
* Luus SM,
* Kalbe I,
* Uibo R.

Department of Immunology, Institute of General and Molecular Pathology, Centre of Molecular and Clinical Medicine, Tartu, Estonia.

The clinical course of Lyme borreliosis is extremely variable. However, all the clinical manifestations, acute or chronic, are characterized by strong inflammation. Borrelia burgdorferi can induce the production of several proinflammatory and anti-inflammatory cytokines.

The aim of our study was to find out whether the balance between inflammatory and regulatory mechanisms is important in determining the course of Lyme borreliosis. 13 patients with early Lyme borreliosis, 8 patients with chronic Lyme disease with neurological or joint manifestations, and 15 age- and sex-matched healthy controls were studied. Chronic forms of Lyme borreliosis were characterized by stronger TNF-alpha response by monocytes to lipopolysaccharide as well as to borrelia antigen compared to early Lyme borreliosis and the healthy state. The percentage of IL-10-secreting monocytes in response to borrelia lysate was lower in the Lyme borreliosis patients than in healthy controls. The percentage of CD4(+) CTLA-4(+) regulatory T cells showed the highest values in early Lyme borreliosis. We conclude that chronic forms of Lyme borreliosis can evolve due to an aberrant innate proinflammatory response.

PMID: 17295680 [PubMed - in process]
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 20:47

Kahdella borrelioosia sairastavalla esiintyi tulehduksellinen selkäkipu johon tavanomaiset tulehduskipulääkkeet eivät auttaneet. Antibioottihoito auttoi kummankin oireisiin.


http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed

Presse Med. 2007 Jan;36(1):61-63. Epub 2006 Dec 11.

Back pain without radiculitis as an initial manifestation of Lyme disease.
[Article in French]

* Chanier S,
* Lauxerois M,
* Rieu V.

Service de medecine, Centre hospitalier, Thiers (63).

INTRODUCTION: The most frequent neurological expression of Lyme disease (borreliosis) during its secondary phase is meningoradiculitis, but atypical presentations occur. Lyme disease must be considered especially in endemic areas and during the summer (May-October).

CASES: We report cases of two patients with unusual clinical presentations of neuroborreliosis. Both had acute inflammatory back pain, resistant to the usual analgesic treatment. Both patients responded negatively to questions about tick bites and erythema migrans. Laboratory tests revealed an inflammatory process in only one patient. Lyme disease was confirmed by lymphocytic meningitis and serological tests positive for Borrelia in blood (both cases) and cerebrospinal fluid (one case). Antibiotic treatment led to the disappearance of pain and the normalization of laboratory tests. DISCUSSION: Inflammatory back pain, even without radiculitis, may be related to Lyme disease in endemic areas.

PMID: 17261450 [PubMed - as supplied by publisher]
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 20:57

Puolalaisen tutkimuksen mukaan krooninen väsymysoireyhtymä on erittäin yleinen borrelioosia sairastavilla. Tutkimuksessa 75 % borrelioosia sairastavista kärsi mm. kroonisesta väsymyksestä kuitenkin vain 24 %:lla se oli diagnosoitu.


Neurol Neurochir Pol. 2003 Nov-Dec;37(6):1211-21.
[Chronic fatigue syndrome following tick-borne diseases]

[Article in Polish]

Gustaw K.

Pracownia Diagnostyki i Terapii Chorób Naczyniowych Instytutu Medycyny Wsi w Lublinie.

The chronic fatigue syndrome (CFS) is characterized by a feeling of tiredness persisting for over 6 months, associated with a number of other symptoms including headaches, myalgia and arthralgia, memory and concentration impairment. Its cause is unknown, there are neither objective diagnostic methods, nor causal treatment of the condition. In view of hypotheses suggesting a relationship between CFS and infections, 86 patients with a history of borreliosis or tick-borne encephalitis were examined. In 50% of these cases CFS could be identified. This clinical pattern was found in as many as 71% of the borreliosis patients, while only 24% of those with history of tick-borne encephalitis were diagnosed with CFS. Moreover, in the patients with a history of borreliosis afte! r symptomatic treatment recommended for CFS, an amelioration was noted in as many as 61% of the cases. The findings suggest that the chronic fatigue syndrome is frequent among patients with a history of borreliosis.

PMID: 15174234 [PubMed - indexed for MEDLINE]
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 20:58

Borreliabakteerin ja reuman aiheuttamat niveltulehdukset ovat samanlaiset. Tutkimuksessa havaittiin myös niiden patogeneesissä olevan yhtäläisyyksiä.


http://tinyurl.com/39t4gy
Clin Vaccine Immunol. 2007 Sep 19; [Epub ahead of print] Links
Serum Reactivity against Borrelia burgdorferi OspA in Rheumatoid Arthritis.
Hsieh YF, Liu HW, Hsu TC, Wei JC, Shih CM, Krause PJ, Tsay GJ.
Institute of Immunology, Department of Medicine, Chung Shan Medical University, Taichung, Taiwan, and Department of Parasitology and Tropical Medicine, National Defense Medical Center, Taipei, Taiwan, and Department of Pediatrics, University of Connecticut School of Medicine, Farmington, Connecticut, USA.

Lyme arthritis and rheumatoid arthritis share common clinical features and synovial histology. It is unclear whether they also share a similar pathogenesis. Previous studies have shown that the severity and duration of Lyme arthritis correlates directly with serum concentrations of antibody against outer surface protein A (OspA) of the causative pathogen Borrelia burgdorferi. We tested the sera of 68 subjects with rheumatoid arthritis, 147 subjects with other autoimmune diseases, and 44 healthy subjects who had never had Lyme disease, as well as that of 16 patients who had Lyme disease, for reactivity against B. burgdorferi OspA protein. The sera of about a quarter of the rheumatoid arthritis patients and a tenth of the autoimmune disease and Lyme disease patients reacted against OspA antigen. Of 50 rheumatoid arthritis patients who could be evaluated for disease severity, a 28 joint count Disease Activity Score of >2.6 was noted in 11 of 15 (73%) patients whose sera reacted against OspA antigen and 13 of 35 (37%, p<0.05) whose sera was non-reactive. Serum reactivity against OspA antigen is associated with the pathogenesis of rheumatoid arthritis.

PMID: 17881508 [PubMed - as supplied by publisher]
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 21:05

Useita tutkimuksia joissa todetaan borreliabakteerin aiheuttavan virtsatieinfektioita. Toistuvat infektiot saattavat olla merkkinä siitä että infektio ei ole koskaan parantunut kunnolla. Bb:n aiheuttamista virtsateiden oireista yleisimmät ovat virtsaamispakko, runsas yövirtsaaminen ja pakkoinkontinenssi.


USA Today--Friday, Nov. 20, 1998---pg. 3A

"BLADDER INRECTION STUDY: Recurring urinary tract infections actually might be one long infection that's never cured, rather than a series of new ones, research out today suggests. The finding could have implications for how such infections, which strike a million Americans a year, are treated. The research was done at Washington University in St. Louis abd published in the journal Science."
_________________________________

TITLE: Molecular detection of persistent Borrelia burgdorferi in the urine of patients with active Lyme disease.


AUTHORS: Goodman JL; Jurkovich P; Kramber JM; Johnson RC
AUTHOR AFFILIATION:
Department of Medicine, University of Minnesota School of Medicine, Minneapolis 55455.
SOURCE: Infect Immun 1991 Jan;59(1):269-78
CITATION IDS: PMID: 1987041 UI: 91099973

ABSTRACT: Current diagnostic tests for Lyme disease (LD) are dependent upon the host serologic response and are insensitive early in infection and, possibly, following antibiotic therapy. We cloned a library of Borrelia burgdorferi 297 DNA and studied one clone, Ly-1, for its potential in diagnostic and pathogenic studies. Using pulsed-field electrophoresis, we demonstrated that Ly-1 is of chromosomal origin and estimated that the B. burgdorferi chromosome is approximately 1,100 kb in size. The 3.7-kb Ly-1 clone hybridizes with geographically diverse strains of B. burgdorferi. No cross hybridization occurs with DNA from human cells, Escherichia coli, Staphylococcus aureus, Clostridium difficile, or the closely related B. hermsii. We used a dot blot assay to detect 100 pg of B. burgdorferi DNA. We partially determined the nucleotide sequence of Ly-1 and used it to select and synthesize oligonucleotides for use in the polymerase chain reaction (PCR). Two different primer pairs were found to amplify DNA from nine geographically diverse isolates. We could detect 10 fg (less than 10 molecules) of B. burgdorferi or less than five spirochetes added to human urine. Finally, we were able to use the PCR to detect B. burgdorferi DNA in the urine of four of eight patients with suspected active LD (three with arthritis and one with neurologic manifestations), all of whom responded to antibiotic treatment. In contrast, those patients who were PCR negative either had inactive disease or had been appropriately treated and did not respond to additional antibiotics, and all four control urine specimens were PCR negative. We conclude that B. burgdorferi DNA can be sensitively detected by the PCR with the primers and methods we describe and that the urinary tract is a site of persistent infection in some cases of human LD, an observation of potential diagnostic and pathogenic importance.
__________________________

"......Because of the high isolation rates, tropism, and persistence that we found for B. burgdorferi in the hamster heart and bladder, these sites will be useful and important for the cultivation of spirochetes..."

Tropism for urinary bladders in hamsters


TITLE: Persistent cardiac and urinary tract infections with Borrelia burgdorferi in experimentally infected Syrian hamsters.

AUTHORS: Goodman JL; Jurkovich P; Kodner C; Johnson RC
AUTHOR AFFILIATION:
Department of Medicine, University of Minnesota School of Medicine, Minneapolis 55455.
SOURCE: J Clin Microbiol 1991 May;29(5):894-6
CITATION IDS: PMID: 2056054 UI: 91277193

ABSTRACT: The heart can be severely affected in humans with Lyme disease, causing conduction defects and, rarely, heart failure. Although immunodeficient and young mice may develop cardiac lesions, cultivation of Borrelia burgdorferi from cardiac tissues of experimentally infected animals has not been reported previously. We infected Syrian hamsters with B. burgdorferi 297 and found a marked tropism of the spirochete for myocardial and urinary tract tissues. Fifty-six of 57 hearts (98%) and 52 of 58 bladders (90%) were culture positive. The cardiac infection was persistent and could be documented in 21 of 22 hearts (96%) cultured from days 28 to 84 postinfection. The urinary tract was also a site of persistent infection in most animals, with 18 of 23 bladders (78%) being culture positive from days 28 to 84. The persistence of spirochetes was specific for the heart and bladder, as indicated by negative cultures of specimens from the liver and spleen, in which only 1 of 23 cultures was positive from days 28 to 84. Because of the high isolation rates,
tropism, and persistence that we found for B. burgdorferi in the hamster heart and bladder, these sites will be useful and important for the cultivation of spirochetes in experimental studies that evaluate the efficacies both of candidate vaccines in preventing infection and of antibiotics in eradicating organisms from privileged sites. In addition, the clear demonstration of persistent cardiac infection with B. burgdorferi may provide a useful model for studying the pathogenesis of cardiac Lyme disease.
___________________________

Title:Urinary dysfunction in Lyme disease.
Authors:Chancellor MB, McGinnis DE, Shenot PJ, Kiilholma P, Hirsch IH
Source:J Urol 1993 Jan;149(1):26-30
Organization:Department of Urology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania.

Abstract:
Lyme disease, which is caused by the spirochete Borrelia burgdorferi, is associated with a variety of neurological sequelae. We describe 7 patients with neuro-borreliosis who also had lower urinary tract dysfunction. Urodynamic evaluation revealed detrusor hyperreflexia in 5 patients and detrusor areflexia in 2. Detrusor external sphincter dyssynergia was not noted on electromyography in any patient. We observed that the urinary tract may be involved in 2 respects in the course of Lyme disease: 1) voiding dysfunction may be part of neuro-borreliosis and 2) the spirochete may directly invade the urinary tract. In 1 patient bladder infection by the Lyme spirochete was documented on biopsy. Neurological and urological symptoms in all patients were slow to resolve and convalescence was protracted. Relapses of active Lyme disease and residual neurological deficits were common. Urologists practicing in areas endemic for Lyme disease need to be aware of B. burgdorferi infection in the differential diagnosis of neurogenic bladder dysfunction. Conservative bladder management including clean intermittent catheterization guided by urodynamic evaluation is recommended.

Language: Eng
___________________________


Title:Lyme disease presenting as urinary retention.

Authors:Chancellor MB, Dato VM, Yang JY
Source:J Urol 1990 Jun;143(6):1223-4
Organization:Department of Urology, College of Physicians and Surgeons, Columbia University, New York, New York.

Abstract:
We report a case of Lyme disease that presented with urinary retention. The individual then experienced lower extremity paralysis. Paralysis and urinary retention resolved with intravenous ceftriaxone antibiotic. To our knowledge this is the first report of a urological manifestation as the initial clinical presentation of Lyme disease. Recognition of clinical symptoms and urological complications of Lyme disease also are discussed.

Language: Eng


Unique ID: 90258152
___________________________



Title:Cystitis induced by infection with the Lyme disease spirochete, Borrelia burgdorferi, in mice.Authors:Czub S, Duray PH, Thomas RE, Schwan TG
Source:Am J Pathol 1992 Nov;141(5):1173-9
Organization:Department of Health and Human Services National Institutes of Health National Institute of Allergy and Infectious Diseases Hamilton MT 59840.

Abstract:
Previous studies have demonstrated that the urinary bladder is a onsistent source for isolating the Lyme disease spirochete, Borrelia burgdorferi, from both experimentally infected and naturally exposed rodents. We examined histopathologic changes in the urinary bladder of different types of rodents experimentally infected with Lyme spirochetes, including BALB/c mice (Mus musculus), nude mice (M. musculus), white-footed mice (Peromyscus leucopus), and grasshopper mice (Onychomys leucogaster). Animals were inoculated intraperitoneally, subcutaneously, or intranasally with low-passaged spirochetes, high-passaged spirochetes, or phosphate-buffered saline. At various times after inoculation, animals were killed and approximately one-half of each urinary bladder and kidney were cultured separately in BSK-II medium while the other half of each organ was prepared for histologic examination. Spirochetes were cultured from the urinary bladder of all 35 mice inoculated with low- passaged spirochetes while we were unable to isolate spirochetes from any kidneys of the same mice. The pathologic changes observed most frequently in the urinary bladder of the infected mice were the presence of lymphoid aggregates, vascular changes, including an increase in the number of vessels and thickening of the vessel walls, and perivascular infiltrates. Our results demonstrate that nearly all individuals (93%) of the four types of mice examined had a cystitis associated with spirochetal infection.


Keywords:
Animal, Bladder, MI, PA, Borrelia burgdorferi, IP, Cystitis, MI, PA, Female, Kidney, MI, PA, Lyme Disease, Male, Mice, Mice, Inbred BALB C, Mice, Nude, Peromyscus, Medline File


Language: Eng


Unique ID: 93072249
___________________________


Title:Efficacy of the urinary bladder for isolation of Borrelia burgdorferi from naturally infected, wild Peromyscus leucopus.
Authors:Callister SM, Agger WA, Schell RF, Brand KM

Source:J Clin Microbiol 1989 Apr;27(4):773-4
Organization:Microbiology Research Laboratory, Gundersen Medical Foundation, La Crosse, Wisconsin.

Abstract:
The efficacy of culturing urinary bladder tissue for Borrelia burgdorferi from naturally infected, wild Peromyscus leucopus mice was determined. The urinary bladder cultures were as efficient as spleen, kidney, and blood tissue cultures. The rapid B. burgdorferi isolation (mean, 6 days) from mouse urinary bladders should aid in defining new Lyme disease foci.


Language: Eng
______________________________


Title:Lyme disease presenting as isolated acute urinary retention caused by transverse myelitis[as though the spinal cord has been severed]: an electrophysiological and urodynamical study.

Authors:Olivares JP, Pallas F, Ceccaldi M, Viton JM, Raoult D, Planche D, Delarque ASource:Arch Phys Med Rehabil 1995
Dec;76(12):1171-2Organization:Department of Rehabilitation, Timone Hospital, Marseille, France.

Abstract:
Several neurological manifestations of Lyme disease, both central and peripheral, have been described. Reported here is a case of acute transverse myelitis related to a Lyme neuroborreliosis that presented with isolated acute urinary retention and no lower-extremity impairment. This case, documented by urodynamic and electrophysiological investigations, partially resolved after 6 weeks of intravenous ceftriaxone, affording the removal of the indwelling catheter. Alpha blocker therapy was needed for 3 months, until the complete normalisation of urodynamic and electrophysiological records. This case study indicates that whenever urinary retention is encountered associated with acute transverse myelitis or alone, the patient should be investigated for Lyme disease.

Language: Eng


Unique ID: 96130000
___________________________


Title:The urinary bladder, a consistent source of Borrelia burgdorferi in experimentally infected white-footed mice (Peromyscus leucopus).

Authors:Schwan TG, Burgdorfer W, Schrumpf ME, Karstens RHSource: JClin Microbiol 1988 May;26(5):893-5
Organization:Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840.

Abstract:
White-footed mice, Peromyscus leucopus, were experimentally infected in the laboratory with Borrelia burgdorferi, the causative agent of Lyme disease. After mice were infected by intraperitoneal or subcutaneous inoculation or by tick bite, attempts were made to culture spirochetes from the urinary bladder, spleen, kidney, blood, and urine. Spirochetes were most frequently isolated from the bladder (94%), followed by the kidney (75%), spleen (61%), and blood (13%). No spirochetes were isolated from the urine. Tissue sectioning and immunofluorescence staining of the urinary bladder demonstrated spirochetes within the bladder wall. The results demonstrate that cultivation of the urinary bladder is very effective at isolating B. burgdorferi from experimentally infected white-footed mice and that culturing this organ may be productive when surveying wild rodents for infection with this spirochete.


Language: Eng


Unique ID: 88257349
__________________________

TITLE: Molecular detection of persistent Borrelia burgdorferi in the urine of patients with active Lyme disease.
AUTHORS: Goodman JL; Jurkovich P; Kramber JM; Johnson RC
AUTHOR AFFILIATION:
Department of Medicine, University of Minnesota School of Medicine, Minneapolis 55455.
SOURCE: Infect Immun 1991 Jan;59(1):269-78
CITATION IDS: PMID: 1987041 UI: 91099973

ABSTRACT: Current diagnostic tests for Lyme disease (LD) are dependent upon the host serologic response and are insensitive early in infection and, possibly, following antibiotic therapy. We cloned a library of Borrelia burgdorferi 297 DNA and studied one clone, Ly-1, for its potential in diagnostic and pathogenic studies. Using pulsed-field electrophoresis, we demonstrated that Ly-1 is of chromosomal origin and estimated that the B. burgdorferi chromosome is approximately 1,100 kb in size. The 3.7-kb Ly-1 clone hybridizes with geographically diverse strains of B. burgdorferi. No cross hybridization occurs with DNA from human cells, Escherichia coli, Staphylococcus aureus, Clostridium difficile, or the closely related B. hermsii. We used a dot blot assay to detect 100 pg of B. burgdorferi DNA. We partially determined the nucleotide sequence of Ly-1 and used it to select and synthesize oligonucleotides for use in the polymerase chain reaction (PCR). Two different primer pairs were found to amplify DNA from nine geographically diverse isolates. We could detect 10 fg (less than 10 molecules) of B. burgdorferi or less than five spirochetes added to human urine. Finally, we were able to use the PCR to detect B. burgdorferi DNA in the urine of four of eight patients with suspected active LD (three with arthritis and one with neurologic manifestations), all of whom responded to
antibiotic treatment. In contrast, those patients who were PCR negative either had inactive disease or had been appropriately treated and did not respond to additional antibiotics, and all four control urine specimens were PCR negative. We conclude that B. burgdorferi DNA can be sensitively detected by the PCR with the primers and methods we describe and that the urinary tract is a site of persistent infection in some cases of human LD, an observation of potential diagnostic and pathogenic importance.


http://www.pubmedcentral.nih.gov/articl ... id=1472851

Excerpt
Infectious neurologic processes. There are a number of infectious causes of incomplete emptying of the bladder:
? Acquired immune deficiency syndrome (AIDS): Neurologic complications, involving both the central and peripheral nervous systems, occur in as many as 40% of patients with AIDS.5 Urinary retention is the most common presenting symptom.
? Neurosyphilis (tabes dorsalis): Neurosyphilis has long been recognized as a cause of central and peripheral nerve abnormalities. Voiding dysfunction related to neurosyphilis was common in the era before penicillin use.
? Herpes zoster and herpes simplex: Herpes zoster is an acute, painful mononeuropathy associated with a vesicular eruption in the distribution of the affected nerve. The viral activity is predominantly located in the dorsal root ganglia of the cranial nerves. However, sacral nerve involvement may be associated with loss of bladder and anal sphincter control.
? Lyme disease: Caused by the spirochete Borrelia burgdorferi, Lyme disease is associated with a variety of neurologic sequelae. Urologic manifestations of Lyme disease can be primary or late manifestations of disease and affect both sexes and persons of all ages. Urinary urgency, nocturia, and urge incontinence are the most common urologic symptoms.6
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 21:09

Edenneessä borrelioosissa voi esiintyä useita erilaisia keskushermosto-oireita. Seuraavassa tapauselostuksessa borrelioosiin sairastuneen henkilön psyykessä ilmeni akuutisti selkeitä muutoksia.

J Med Case Reports. 2007 Aug 9;1(1):62 [Epub ahead of print] Links
Altered mental status, an unusual manifestation of early disseminated Lyme disease: A case report.
Chabria SB, Lawrason J.

ABSTRACT: Early disseminated Lyme disease can have a myriad of central nervous system manifestations. These run the gamut from meningitis to radiculopathy and cranial neuropathy. Here we present a case that manifested with only acute mental status change in the setting of central nervous system involvement with Lyme disease. A paucity of other central nervous system manifestations is rare, especially with positive serum and cerebrospinal fluid markers. This article underscores the importance of a high index of clinical suspicion in detection of Lyme disease related manifestations in endemic areas.

PMID: 17688693
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 21:29

Useiden tutkimusten mukaan borreliabakteeria löydetään erittäin usein virtsarakosta. Seuraavassa tutkimuksessa lähes jokaisella borrelioosiin sairastuneella hiirellä oli borrelibakteerin aiheuttama rakkotulehdus.

www.ncbi.nlm.nih.gov/entrez/query.fcgi? ... t=Abstract

ajp.amjpathol.org/cgi/content/abstract/141/5/1173

American Journal of Pathology, Vol 141, 1173-1179, Copyright © 1992 by American Society for Investigative Pathology
--------------------------------------------------------------------------------

REGULAR ARTICLES

Cystitis induced by infection with the Lyme disease spirochete, Borrelia burgdorferi, in mice

S Czub, PH Duray, RE Thomas and TG Schwan
Department of Health and Human Services, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Hamilton, MT 59840.

Previous studies have demonstrated that the urinary bladder is a consistent source for isolating the Lyme disease spirochete, Borrelia burgdorferi, from both experimentally infected and naturally exposed rodents. We examined histopathologic changes in the urinary bladder of different types of rodents experimentally infected with Lyme spirochetes, including BALB/c mice (Mus musculus), nude mice (M. musculus), white-footed mice (Peromyscus leucopus), and grasshopper mice (Onychomys leucogaster). Animals were inoculated intraperitoneally, subcutaneously, or intranasally with low-passaged spirochetes, high-passaged spirochetes, or phosphate-buffered saline. At various times after inoculation, animals were killed and approximately one-half of each urinary bladder and kidney were cultured separately in BSK-II medium while the other half of each organ was prepared for histologic examination. Spirochetes were cultured from the urinary bladder of all 35 mice inoculated with low-passaged spirochetes while we were unable to isolate spirochetes from any kidneys of the same mice. The pathologic changes observed most frequently in the urinary bladder of the infected mice were the presence of lymphoid aggregates, vascular changes, including an increase in the number of vessels and thickening of the vessel walls, and perivascular infiltrates.

Our results demonstrate that nearly all individuals (93%) of the four types of mice examined had a cystitis associated with spirochetal infection.
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ViestiKirjoittaja soijuv » La Tammi 24, 2009 21:34

Uuden tutkimuksen mukaan jopa kolmannnes autistisista tapauksista saattaa olla borreliabakteerin tai jonkin muun mikrobin aiheuttamia. Tutkija R. Brandsfieldien mukaan punkkien välittämät infektiot, kuten borrelioosi, heikentävät immuunipuolustusta ja tekevät henkilön alttiimmaksi autismin tyyppisille häiriöille. Hänen mukaansa 20 - 30 % autistisista lapsista on saanut punkkien välittämän infektion. Mikäli asia on näin koskettaa ongelma yksinomaan Yhdysvalloissa 140 000 lasta. Mikäli he saisivat ajoissa korkea-annoksista antibioottihoitoa, hoitoa jonka katsotaan tällä hetkellä olevan tehokkain hoitomuoto, saataisiin aikaiseksi huomattavia säästöjä terveydenhuollossa ja koulutuksessa.


WDDTY

14 February 2008

http://www.wddty.com/033638003722145685 ... sease.html

Up to a third of all cases of autism may be the result of Lyme disease and other chronic infections, new research suggests.
Researcher Robert Bransfield believes that tick-borne infections, such as Lyme disease, can weaken the immune system during infancy and make the sufferer more vulnerable to autistic-spectrum diseases.

He estimates that between 20 per cent and 30 per cent of all autistic children may be infected by Lyme disease or other similar infections.

If so, it means that 140,000 autistic children in the USA alone have the problem as a direct result of an infection. If they were treated with high-dose antibiotics ? considered to be the most effective therapy, especially in the early stages of infection ? the savings in healthcare and education costs would amount to around $358bn, he estimates.
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ViestiKirjoittaja soijuv » Su Tammi 25, 2009 10:37

Trombosytopeniaa eli verihiutaleiden niukkuutta esiintyy yleisesti kaikissa punkkien levittämissä taudeissa. Ne heikentävät taudin ennustetta. Trombosytopenian oireet: trombosytopenian tyyppioireita ovat ihovuodot, kuten purppura, petekiat ja mustelmat, sekä limakalvovuodot, kuten ien- ja nenäverenvuoto, runsas kuukautisvuoto, ruoansulatuskanavavuoto ja hematuria. DIC:iin ja TTP:hen liittyy vuotojen lisäksi intravaskulaaristen trombien aiheuttamia iskeemisiä oireita. Pistokohdat tihkuvat kauan.


Lisää tietoa esim sivulta: http://www.therapiafennica.fi/wiki/inde ... osytopenia)http://tinyurl.com/2vm9y4full text url

Mechanisms of Thrombocytopenia in Tick-Borne Diseases Liron Pantanowitz, MDDepartment of PathologyBeth Israel Deaconess Medical CenterHarvard Medical SchoolBoston Massachusetts USA

Abstract
Thrombocytopenia is a common manifestation of all tick-borne diseases.Low platelet numbers contribute significantly towards the morbidityand mortality of infection. However, the pathogenesis ofthrombocytopenia in many of the tick-borne diseases is poorlyunderstood. Quantitative changes in platelet counts associated withinfection may result from decreased marrow production, hypersplenism,consumption due to widespread endothelial damage or disseminatedintravascular coagulation, as well as immune-mediated plateletdestruction. Infection-induced thrombocytopenia may infrequently beassociated with serious thrombosis. Direct infection of platelets byselected tick-borne pathogens also facilitates their disseminationwithin the host. This article reviews the mechanisms ofthrombocytopenia associated with tick-borne infections, and discussesthe therapeutic options available for managing this potentially fatalcomplication.
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ViestiKirjoittaja soijuv » Su Tammi 25, 2009 10:38

33-vuotiaalla miehellä oli diagnoosina krooninen väsymysoireyhtymä. Erilaisista hoidoista ei ollut saatu merkittävää hyötyä. Kahden vuoden kuluttua oireen syyksi löydettiin borreliainfektio.


http://www.immunesupport.com/library/sh ... fm/ID/8398

Lyme Disease Presenting as Chronic Fatigue Syndrome ? Source: Journal of Chronic Fatigue Syndrome, Vol 3 #4, 2007
by Samuel Shor, MD, FACP
ImmuneSupport.com

10-10-2007

Objective: Chronic Fatigue Syndrome (CFS) by definition represents a diagnosis of exclusion. Late stage or "Chronic Lyme" infection with or without "co-infections" is a difficult diagnosis to establish. The symptom complex of both conditions can be very similar. This case study represents an attempt to support serious consideration for a subpopulation of patients otherwise diagnosed with "CFS," as actually representing chronic Lyme disease.

Method: A case study is presented of a 33-year-old man, who for two years was being managed as having CFS. However, after ~2 years of utilizing multiple modalities of management with limited success, the diagnosis of Lyme was reconsidered.


Historical exposure risks to Lyme in this individual were high. He had prolonged exposure in the highly tick-infested mountains of North Carolina for 18 months, several years prior to becoming ill. More aggressive investigation confirmed the diagnosis of Lyme.


Appropriate changes in management were associated with an improved level of functioning that was far in excess of what maximal management of CFS was able to achieve.


The features of CFS and chronic Lyme can be very similar and include the following: Profound fatigue often associated with cognitive impairment. Other common symptoms related to both of these conditions include sleep disturbances, Fibromyalgia, and dysautonomias.


In pursuing clarification of this diagnosis, the author was exposed to a contrast in medical opinion regarding diagnostic tools and criteria that were perceived as creating potential barriers to the management of patients presenting with these symptoms.


Conclusion: Acceptance and awareness of the possibility that Lyme disease can present as CFS has important therapeutic and prognostic implications.


Source: Journal of Chronic Fatigue Syndrome. 2007 Vol 13 Issue 4 pp: 67-75. DOI: 10.1300/J092v13n04_06, by Samuel Shor, MD, FACP, Associate Clinical Professor, George Washington University Health Care Sciences, Reston, Virginia, USA. [E-mail: sshor@intmednova.com]
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ViestiKirjoittaja soijuv » Su Tammi 25, 2009 10:39

Neuroborrelioosia sairastavalla todettiin EEG:ssä muutoksia aivoissa. Muutokset johtuivat aineenvaihdunnan häiriöistä. (Ruotsi)

Acta Neurol Scand. 2007 Aug;116(2):133-6.

EEG with triphasic waves in Borrelia burgdorferi meningoencephalitis.

Eriksson B, Wictor L.
Division of Clinical Neurology, Lund University Hospital, Lund, Sweden.
Bengt.B.Eriksson@skane.se

We describe a case of encephalopathy in which the clinical picture and triphasic waves in the EEG indicated a metabolic cause. However, the illness was caused by neuroborreliosis. The occurrence of triphasic waves in the EEG is a strong evidence of metabolic encephalopathy, but triphasic waves are not specific for metabolic encephalopathy. Triphasic waves have been described in a number of non-metabolic encephalopaties and structural brain lesions. To our knowledge, this is the first report of triphasic waves in Borrelia burgdorferi meningoencephalitis.

PMID: 17661801
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ViestiKirjoittaja soijuv » Su Tammi 25, 2009 11:45

Borreliabakteerin alalaji, Bb lusitaniae, aiheutti 13-vuotiaalle portugalilaiselle tytölle verisuonitulehduksen. Tutkijat huomauttavat että vasta-ainetestit voivat taudista huolimatta olla negatiiviset tai vain heikosti positiiviset.

Clin Rheumatol. 2008 Sep 16.

Vasculitis-like syndrome associated with Borrelia lusitaniae infection.

Lopes de Carvalho I, Fonseca JE, Marques JG, Ullmann A, Hojgaard A, Zeidner N, Núncio MS.
Center for Vector and Infectious Diseases Research, Instituto Nacional de Saúde Dr. Ricardo Jorge, Lisbon, Portugal.

We report the isolation of Borrelia lusitaniae from a 13-year-old female child presenting with a vasculitis syndrome. The patient was treated with doxycycline, 100 mg bid for 20 days, and is in remission after a follow-up of 2 years. These results should alert clinicians to the fact that B. lusitaniae may be pathogenic in humans, highlighting that patients may be seronegative or present with minimal positive antibody titres and clinical signs that are not specific for Lyme borreliosis. In order to prevent the occurrence of more serious disease manifestations via timely treatment, the analysis by molecular methods may be a useful approach when antibody titres are uninformative.
PMID: 18795392 [PubMed - as supplied by publisher
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ViestiKirjoittaja soijuv » Su Tammi 25, 2009 11:46

Seuraavalta keskustelusivulta löytyy useita tutkimuksia borrelioosin aiheuttamista erilaisista silmäsairauksista

http://www.lymeneteurope.org/forum/view ... ?f=6&t=246
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ViestiKirjoittaja soijuv » Su Tammi 25, 2009 11:47

Primaari effuusio lymfooma (suom.huom. kuuluu nopeakasvuisiin B-solu -lymfoomiin, non-Hodgkin lymfooma) ei muodosta selkeää kiinteää kasvainta. Artikkelissa esitetään olettamus, että kyseinen lymfooma on yhteydessä neuroborrelioosiin ja MS-tautiin. MS-taudin etiologiassa nimenomaan borreliabakteeri näyttää olevan merkittävässä osassa. Myös MS-taudin levinneisyysalueet vastaavat borreliabakteerin esiintymisalueita.

Lymfoomat saattavat olla yhteydessä myös herpes viruksiin kuten Epstein-Barr (HHV-4) ja HHV-8.


Lyme borreliosis and multiple sclerosis are associated with primary effusion lymphoma.
Med Hypotheses. 2007; 69(1):117-9 (ISSN: 0306-9877)
Batinac T; Petranovic D; Zamolo G; Petranovic D; Ruzic A
Department of Dermatovenerology, Rijeka University Hospital, Kresimirova 42, 51000 Rijeka, Croatia.

Multiple sclerosis (MS) is a chronic disease of the central nervous system characterized by chronic inflammation and demyelination. Studies suggested that the viral, especially Epstein-Barr virus infection, and bacterial infections, especially Borrelia burgdorferi infection, play a role in etiology of MS. MS prevalence parallels the distribution of the Lyme disease pathogen B. burgdorferi. Criteria used for diagnosis of MS can also be fulfilled in other conditions such as Lyme disease, a multisystem disorder resulting from infection by the tick-borne spirochete, B. burgdorferi. In the late period of Lyme disease demyelinating involvement of central nervous system can develop and MS can be erroneously diagnosed. A Lyme borreliosis can mimick central nervous system lymphoma. Also, B. burgdorferi has been implicated not only in etiology of MS, but also in etiology of lymphoma. Studies suggested that there is an increased risk of non-Hodgkin lymphoma in patients, who had a history of autoimmune diseases such as MS and that both non-Hodgkin's lymphomas and Hodgkin's disease were associated with Epstein-Barr virus infection.

A small group of lymphomas called primary effusion lymphomas (PEL) is a recently individualized form of non-Hodgkin's lymphoma (WHO classification) that exhibit exclusive or dominant involvement of serous cavities, without a detectable solid tumor mass. These lymphomas have also been linked to Epstein-Barr virus and human herpes virus type 8 infections but virus negative cases have been described. Therefore, we propose that MS and neuroborreliosis are linked to central nervous system primary effusion lymphomas. As a first step in confirming or refuting our hypotheses, we suggest a thorough study of CSF in the patients suspected for the diagnosis of MS and Lyme borreliosis.


PreMedline Identifier: 17197115
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ViestiKirjoittaja soijuv » Su Tammi 25, 2009 11:48

Keski-eurooppalaisilta löydettiiin borreliabakteerin aiheuttamaa kroonista ihotulehdusta:

Histopathology. 2008 May 6; [Epub ahead of print]

Detection of spirochaetal microorganisms by focus floating microscopy in necrobiosis lipoidica in patients from central Europe.

Eisendle K, Baltaci M, Kutzner H, Zelger B.

Department of Dermatology and Venerology, Innsbruck Medical University, Innsbruck, Austria. klaus.eisendle@i-med.ac.at

AIMS: Necrobiosis lipoidica (NL) is a chronic inflammatory skin disease with unknown aetiology. The aim was to determine the presence of spirochaetal microorganisms in NL.

METHODS AND RESULTS: Focus-floating microscopy (FFM) is a modified immunohistochemical technique that was developed to detect borrelial spirochaetes within tissue sections. It has proven to be more sensitive for the detection of spirochaetes than polymerase chain reaction (PCR). Fifty-six cases of NL as well as 44 negative and 33 positive controls were investigated for the presence of Borrelia within tissue specimens. Using FFM, Borrelia could be detected in 42 cases (75.0%) and were seen significantly more often in histologically active inflammatory-rich (38/41, 92.7%) than in inflammatory-poor (4/15, 26.7%) cases of NL (P < 0.001). Seven cases investigated with a Borrelia-specific PCR (23s-RNA) remained negative. In contrast, FFM was positive in 30 of 33 (90.9%) positive controls of acrodermatitis chronica atrophicans and 15 of the positive controls (45.5%) were also positive with PCR, whereas nonegative controls revealed any microorganisms.

CONCLUSIONS: Detection of spirochaetes in NL points to a specific involvement of B. burgdorferi or other similar strains in the development of or trigger for this disease.

PMID: 18462358 [PubMed - as supplied by publisher]
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Su Tammi 25, 2009 11:49

Miehellä oli neurologisia oireita. Hänellä ei ollut tietoa punkinpuremasta. Borrelioositesti oli positiivinen vasta useiden testauskertojen jälkeen. Tutkimuksessa otetaan kantaa hoitojen aloittamiseksi yksinomaan kliinisten löydösten perusteella.


Neurol Sci. 2008 Apr;29(2):109-112. Epub 2008 May 16.

Multiple cranial nerve involvement in Bannwarth's syndrome.

Vianello M, Marchiori G, Giometto B.

O.U. Neurology, "Ca' Foncello" Hospital, Piazza Ospedale 1, 31100, Treviso,
Italy.

Bannwarth's syndrome is a tick-transmitted neurological disease caused by spirochetes of the Borrelia burgdorferi group. Neurological manifestations of the disease occur after skin erythema and include: neuritic pain, lymphocytic pleocytosis without headache and sometimes cranial neuritis. We present the case of a man who complained of a neurological syndrome without evidence of tick biteand concurrent manifestation of the infection, for whom **serological analysis only revealed the infection after testing repetitive specimens**. We discuss the need to start early therapy when clinical manifestations are suggestive of the disease in endemic areas.

PMID: 18483708 [PubMed - as supplied by publisher]
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

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