Zoonoze

Postez cateva link-uri importante :
http://www.sanatatea...ta-preturi.html
Aceasta firma medicala are centre in mai multe locatii din tara.

Prezentarea Lidei Mattman de la Chicago 2005
[ https://www.youtube-nocookie.com/embed/WozrCFW0mRM?feature=oembed - Pentru incarcare in pagina (embed) Click aici ]

http://jcm.asm.org/c.../2/319.full.pdf

In prezent , un alt centru medical mare , pune bazele unui alt laborator dedicat bolilor transmise de capuse . Dotarea acestui laborator va fi similara celui de la Augsburg.Voi scrie aici cand se va deschide.

Martz devoted the next two and a half years to a project that gave extended antibiotics to about 90 ALS patients, and demonstrated objective improvements in 15% of them. He has also treated more than 800 chronic Lyme patients, with good response and minimal side effects. That work is currently being written up for publication.

Restul il cititi in link-ul de mai jos :
http://lymedisease.o...bylyme/372.html

S-a facut o asociatie pentru bolnavii cu Lyme , in Constanta :
http://www.maladialyme.org/

Blogul lor este acesta :
http://maladialyme.blogspot.ro/

Pe facebook exista o pagina pentru participarea Romaniei la protestul international ( pagina are sustinerea necesara pentru participare si  a fost deja "reportata " dar fara succes )
Worldwide Lyme Protest _Romania

Sarbatori fericite tuturor !

Studiu publicat pe site-ul CDC :

In Romania, cases of Lyme disease and tick-borne encephalitis (caused by tick-borne encephalitis virus) have been identified (3)

http://wwwnc.cdc.gov..._article.htm#r2

Edited by ditaanca, 29 January 2013 - 09:00.

Buna ziua, sunt noua pe acest forum si va rog sa ma ajutati cu parerea dvs ref la situatia fetitei mele in varsta de 7 ani, care a fost muscata de o capusa in iunie 2012.

Capusa a fost descoperita in zona scalpului dupa aprox 30 ore, a fost extrasa la chirurgie, a primit tratament profilactic 10 zile de la V Babes si vaccin antitetanos. Sigurul simptom a fost inflamarea ganglionilor de dupa urechea din vecinatatea muscaturii. La terminarea curei de antibiotice inflamatia a disparut. Nu a apurut eritem migrator, locul intepaturii s-a vindecat repede si bine.

Dupa 4 saptamani am facut Western Blot si microscopia, descoperindu-se B. garinii si Haemobartonella (VIsE B garinii + 29; Flagellin +36, IgG +90, IgM negativ)

Am inceput un tratament cu Cefort (plus hepato-protectoare, si tot arsenalul de suplimente) ,dar nu a rezistat decat 2 sapt, dezvoltand o pseudolitiaza biliara care ne-a facut sa intrerupem tratamentul. Precipitatul din colecist a remis dupa 4 saptamani, ecografic perfect sanatoasa, analize de sange uzuale normale. Totul s-a facut sub supravegherea infectionistului.

Acum, in Ianuarie 2013, am repetat analizele ptr borellia si intensitatea anticorpilor este mai crescuta (VIsE B garinii + 52; Flagellin +64, IgG +113, IgM negativ). Microscopic aceeasi B garinii si haemobartonella.

Copilul nu prezinta simptome de boala, se simte bine, totul normal. Doar usoare troznituri la ambii genunchi, fara dureri, care au inceput din vara trecuta...

Ce ati face in locul meu? Ar trebui instituit tratament antibiotic (exclus cefort, desigur) pana la disparitia bacteriei din sange, chiar daca nu exista simptome de boala? Sau asteptam cu speranta ca NU vor aparea niciodata aceste simptome, eventual incercand doar intarirea sistemului imunitar? Poate disparea aceasta bacterie din sangele fetitei mele?

Va multumesc foarte mult pentru orice parere a dvs!

Rezultatele serologice pot rămâne pozitive timp de câțiva ani de la primul contract chiar dacă tratamentul s-a făcut corect și bacteria a fost ucisă complet.
Importantă e supravegherea pacientului în vedea apariției unei simptomatologii caracteristice bolii Lyme.
Dat fiind că s-a identificat B. garinii, aceasta este corelată de obicei cu problemele neurologice mai degrabă decât cu cele articulare. De asemenea, B. garinii nu prea dă eritem migrator.
În general, schema de tratament cu cefalosporine timp de 2 săptămâni la pacienții pediatrici cu semne neurolohice s-a dovedit eficientă și studiile indică faptul că apariția problemelor neurologice este puțin probabilă dar nu exclusă. De aceea se recomandă supravegherea.

P.S. Alte scheme terapeutice recomandă Doxiciclina numai pentru 10 zile așadar tipul prelungit de tratament nu e direct corelat cu succesul tratamentului.



Desigur, nu strică întărirea sistemului imun.

Am rasfoit cele 24 de pagini de discutii si am observat ca discutia este purtata de persoane avizate.
Ar fi bine sa se discute si despre solutiile de prevenire.
Cum putem sa prevenim aceste infectari, cum trebuie tratate animalele, care sunt animalele care transmit mai usor acesti paraziti.
Animalele cu care intra oamenii in contact sunt testate ?

terratec, on 11 februarie 2013 - 09:24, said:

B. Lyme nu prea se poate preveni decat evitand zonele rurale, mai ales cele impadurite. La origine Borellia prefera cerbii si alte rudenii care au in comun faptul ca sunt mamifere si se transmitea cu ajutorul capuselor (genul Ixodes). Omul a patruns prea mult in habitatul natural al acestor animale si cumva a devenit si el o victima. In Europa se cunosc 3 tipuri de Borelii care pot da Lyme (in SUA doar 2, B. garinii inca nu afecteaza acolo).

Iesi la munte>te imbraci bine, dai cu Autan. Cea mai buna metoda de preventie e totusi...abstinenta de a frecventa acele locuri.

@ anaeva ,
Sunteti intre opinii medicale care se bat cap in cap : unii medici considera ca trebuie eradicata bacteria , altii ca trebuie sa dispara simptomele, altii ca doua saptamani de tratament este suficient . Fiecare" tabara " are argumentele ei si punctul ei de vedere  pe care si-l sustine , mai mult sau mai putin vehement .
Din pacate pentru dumneavoastra , ca mama , nimeni nu va poate da un raspuns exact .

Dar acum , laboratoarele Synevo fac o analiza care se cheama : LTT borrelia si care indica daca aceasta infectie este activa sau nu .
Poate ca pe langa supravegherea atenta pe care trebuie sa o acordati copilului , ar fii bine sa faceti aceasta analiza . Ii doresc sanatate fetitei si dumneavoastra rabdare si liniste .

Mi-am adus aminte de un material pe care mi l-a trimis cineva, sper sa va ajute  :
http://www.lymepa.or...ricLymeTalk.pdf

A Report Issued by the Special Commissionto Conduct an Investigation and Study of the Incidence and Impacts of Lyme Disease  -28 februarie 2013

Regardless of whether this continued symptomatology is termed post-Lyme disease or chronic Lyme disease, the cause of the persisting symptoms has yet to be delineated, and there are currently no tests to determine that the causative organisms are still present or absent in a given individual; the currently available antibody-based tests cannot be used to determine that one no longer has, or does have Lyme disease, or toassess response to treatment. Clinical judgment and assessment of all available information remain the keys to appropriate management of all patients with Lyme disease.

Health care providers need to be aware that currently published recommendations and guidelines regarding treatment of Lyme disease are based on limited data

Until there are additional controlled treatment trials to prove or disprove other antibiotic regimens, healthcare providers should make themselves aware of available alternative regimens so that their patients can be provided the opportunity to resolve their persisting symptoms.

Physicians should also be reminded of the Physician Protection Act, which protects them from any disciplinary action should they choose to diagnose and treat according to clinical criteria, relying on history and symptoms even in the absence of positive lab results. This may include prescribing antibiotics over a prolonged period of time when warranted by the patient’s presentation.

si multe alte lucruri interesante  a stabilit aceasta comisie :

http://www.scribd.co...chusetts-Report

O intrebare: analizele facute la Infectioase Cluj arata Lyme IgM, IgG Non Reactiv, e de ajuns ptr a exclude borrelia ?
Pacientul cf RMN: "leziuni de demielinizare fronto-parietal stanga subcortical, respectiv periventricular dreapta, ce corespund criteriilor de distributie spatiala Mcdonald 2010 pentru scleroza multipla dar nu si celor de distributie temporala. Leziune activa de demielinizare cordon medular cervical."

Pentru excluderea borreliei , si pentru linistea dumneavoastra , faceti LTT-borrelia la Synevo .  Asta este parerea mea .
In privinta RMN-ului si a criteriilor pentru scleroza multipla , nu am nici cea mai mica idee .

Va dau un link  unde veti gasi urmatorul comentariu :
Multiple sclerosis (MS) is characterized by a loss of the myelin sheath surrounding axons in the CNS [201]. Demyelination is associated with elevated levels of CD4+ T cells specific for major myelin proteins, and the disease is generally thought to be autoimmune [202–204]. Although it is not known precisely what triggers the development of MS, it is well established that relapses or disease flares in patients diagnosed with the relapsing–remitting form of MS are often associated with exogenous infections, particular upper respiratory infections. In total, more than 24 viral agents have been linked to MS [205,206]. Most of the associations have been circumstantial, but some studies have found evidence of specific pathogens in human tissue. Antigens from herpesvirus type 6 were found in MS plaques but not from tissues from other neurological disorders [207]. Similarly, compared with CSF from patients with other neurological diseases, CSF from MS patients was shown to have higher levels of the bacteria Chlamydia pneumoniae[208]. In vitro studies have also provided evidence linking MS and infectious agents. MS patients have activated T cells specific for MBP [209–211]. Eight pathogen-derived peptides, including epitopes from HSV, adenovirus and human papillomavirus, were identified that are able to activate MBP-specific T cell clones derived from MS patients [212]. Significantly, these peptides were found to be presented most efficiently by subtypes of HLA-DR2 that are associated with susceptibility to MS. Despite the difficulty in linking MS to any one pathogen, the amount of epidemiological evidence reported over the years shows that environmental factors play a strong role in disease development, and suggests that a cumulative lifetime exposure to certain microorganisms can influence disease development [213–216]. In addition, a recent study showed that the degree of concordance for monozygotic twins (generally reported at 40% or less) was influenced by environmental factors [217].
There are numerous rodent models of demyelination which, although not identical to the human disease, are used to study MS. The major infectious models in mice are Theiler's murine encephalomyelitis virus (TMEV), murine hepatitis virus (MHV) and Semliki Forest virus (SFV). Each has distinct immunopathological mechanisms and illustrate the various potential ways pathogens may induce MS. There are two strains of TMEV (TMEV-DA and TMEV-BeAn) which cause an initial acute grey matter disease followed by a chronic progressive demyelination in the white matter of the spinal chord known as TMEV-induced demyelinating disease (TMEV-IDD) [205,218,219]. Although the two strains induce slightly different diseases, the key characteristics of TMEV-IDD (abnormal gait and spastic hindlimb paralysis) remain the same. Intracerebral (i.c.) injection of virus leads to persistent CNS infection; the level of infectious virus is low during the chronic phase, but abundant amounts of viral RNA and viral antigen can be detected throughout the lifetime of the mouse [220–222]. The immune response is initiated by the presentation of persistent viral antigens by CNS-resident APCs to Th1-type CD4+ T cells, but reactivity to myelin does not appear until after the onset of clinical symptoms (30–35 days post-infection) [223–226]. Thus, TMEV-IDD is caused by epitope spreading from viral determinants to self-myelin determinants. Interestingly, in SJL mice, reactivity appears to multiple myelin peptides starting with the immunodominant epitope and spreading at later time-points to other subdominant myelin determinants in a hierarchical manner [226,227]. In contrast to TMEV, mice inoculated with neurotropic strains of MHV will have a single major symptomatic episode (ataxia, hindlimb paresis, paralysis) from which the majority will recover [228]. CNS infection results in an influx of immune cells that for the most part will clear the virus, although virus does persist in low amounts [229]. Demyelination begins about 1 week post-infection and peaks at week 3, after which lesion repair and remyelination generally occurs [230–232]. The exact mechanism of demyelination in this model is somewhat controversial, but appears to be bystander myelin destruction by the immune response recruited initially to the CNS to control viral infection. There is no evidence of self-specific immunity in the CNS of MHV-infected mice [233]. T and B-cell deficient RAG1−/− mice, which were resistant to demyelination, developed histological disease after adoptive transfer with splenoctyes from MHV-inoculated mice, which involved the recruitment of activated macrophages/microglia to sites of demyelination in the spinal cord [234]. Chemokine receptor knock-out mice (CCR5−/−) showed reduced demyelination that correlated with reduced macrophage but not T cell infiltration into the CNS of MHV-infected mice [235]. CD4-deficient mice showed less severe disease than CD8-deficient mice [236,237]. Collectively, these studies suggest that macrophages are responsible primarily for myelin destruction in the MHV model, but that T cells are required to recruit macrophages into the CNS. Like MHV, SFV leads to a transient clinical disease [238,239]. The virus is, for the most part, cleared from the CNS by day 6 post-infection, while demyelination peaks at day 14 and then wanes [240,241]. Demyelination is not seen in nude or SCID mice, demonstrating that it is T cell-mediated [240,242]. In BALB/c mice it is thought that demyelination is due to cytolytic damage of virus-infected oligodendrocytes, although this has not been proved definitively. Depletion of CD8+ T cells virtually abolished lesions of demyelination, whereas depletion of CD4+ T cells did not have that effect [243]. Other studies in BALB/c mice have shown that Th1-type cytokines are involved in viral clearance but not demyelination [244,245]. In C57/Bl6 mice, molecular mimicry may also play a role in demyelination. Infected mice have MBP-reactive T cells [246], and antibodies reactive to MBP and myelin oligodendrocyte protein (MOG) [247]. Computer algorithms uncovered homology between an epitope in the SFV surface protein E2 and MOG18–32[248]. Mice primed with either peptide develop paralytic symptoms with histopathology resembling that of mice infected with SFV. The authors of that study concluded that the cross-reactive antibody response was mainly responsible for the demyelinating lesions.

http://onlinelibrary...08.03834.x/full

Am aflat cu bucurie ca in acest moment, in Bucuresti , prin intermediul clinicii Eco-Para-Diagnostic ,
http://www.ecoparadiagnostic.ro/
se pot face analize la Augsburg. Mai mult chiar, in functie de simptomele pe care le descrie pacientul , acesta va fi consiliat in privinta analizelor pe care sa le solicite . Apelati cu incredere la aceasta clinica.

http://www.ronos.ro/

Lucrarea prezentata de medici romani la conferinta de la Oxford din 2013 . ( raportare de caz , situatie unica )
http://www.ronos.ro/...Oxford-2013.pdf