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#1743 De: Fernando Almazán <fernandoalmazn@...>
Fecha: Do, 1 de Mayo, 2005 12:08 pm
Asunto: Hoy Documentos TV
fernandoalmazn
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 

Recuerdo que hoy en la 2 a las 23:00h, Documentos TV, “Carga Tóxica”.

No os lo perdáis.


#1742 De: "anapieraa" <anapieraa@...>
Fecha: Sáb, 30 de Abr, 2005 12:09 am
Asunto: RE: Para Anap y todos
anapieraa
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
vale Asun, preguntaré a ver, pero también tengo dos galgas para
cologar...

--- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
asuncion serrano gomez <roquebusqueros@y...> escribió:
> Ana, ya hablaremos por el messenger, ahora prefiero
> ponerte la historia de Lola. Sólo entro para
> pedirte/pediros que leáis esto y a ver si se puede
> echar un cable a la gente de la protectora de animales
> de Cádiz.
> La historia completa está en la web:
> http://www.refugiokimba.org/
> Pincháis en Urgente
>
> Muchas gracias a todos, especialmente a ti, Miguel,
> por dejarme poner estas cositas.
>
> El jueves 24 de febrero, a la altura de Facinas me
> pareció ver un perro en la cuneta con la cabeza
> levantada, di la vuelta para sacarlo de allí y evitar
> que lo atropellasen y al parar el coche a su lado la
> perrita se asustó y recorrió un metro arrastrando las
> patas traseras ¡¡ya la habían atropellado!!
> Llovía y se estaba haciendo de noche, y a pesar de
> poner el triángulo y llevar el chaleco refractante era
> peligroso estar allí mucho tiempo, pero no sabía qué
> hacer, y no iba a dejar a la perrita allí abandonada a
> su suerte…. Llovía y lo único que podía hacer yo era
> taparla con el paraguas y hablarle para que confiase
> un poco en mí mientras encontraba una solución, pues
> no me atrevía a cogerla por si intentaba morderme del
> mismo miedo o se iba a la carretera y causaba un
> accidente, siendo además ella rematada del todo...
>
> Casualmente un par de coches de trafico pasaron por
> allí y me preguntaron si me podían ayudar, la idea de
> cortar el trafico no les pareció muy buena pero se
> prestaron a ayudarme a coger a la perra, me
> preguntaron si tenía una manta y yo les di mi chal que
> era lo más parecido, así que se lo echaron encima y
> para mi sorpresa la perra ni se quejó, quedó
> totalmente inmóvil, era puro pellejo levantado por el
> cuello y el lomo, parecía casi muerta… y estaba peor
> de lo que me había parecido en un principio… La
> metieron en el coche y me la llevé al veterinario
> quien la atendió estupendamente y le hizo todas las
> pruebas que creyó oportuno, viendo de entrada que
> tenía las dos patas traseras rotas en la radiografía.
> Me recomendó llevarla a otro veterinario especializado
> en operar ese tipo de fracturas múltiples y allí que
> me fui yo, pues aunque ya era tarde, él lo había
> llamado por teléfono y me estaban esperando en la
> clínica…
> El veterinario dijo que HABÍA ESTADO EN LA CUNETA DE
> 10 A 15 DÍAS ¡¡Ya os podéis imaginar sus
> sufrimiento!!...
>
> Ahora busco familia que la quiera adoptar, eso sí,
> alguien que sea muy consciente del calvario que ha
> pasado la perra y que aún está pasando y que la quiera
> para siempre y le de el cariño y la seguridad que
> necesita, que nunca vuelva a encontrarse en la misma
> situación.
> La perrita se llamaba Facina pero ahora le llaman Lola
> que es más corto y tiene unos dos años o dos años y
> medio. Muy cariñosa.
> Estoy dispuesta a llevarla al extranjero si allí está
> esa familia ideal para ella.
> ¿Alguien me puede ayudar?
> Muchas gracias.
> Silvia
>
> Mail:  silviacalap@t...
>
>
>
>
>
>
>
>
>
>
>
>
> ______________________________________________
> Renovamos el Correo Yahoo!
> Nuevos servicios, más seguridad
> http://correo.yahoo.es

#1741 De: asuncion serrano gomez <roquebusqueros@...>
Fecha: Vie, 29 de Abr, 2005 7:11 pm
Asunto: Para Anap y todos
roquebusqueros
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
Ana, ya hablaremos por el messenger, ahora prefiero
ponerte la historia de Lola. Sólo entro para
pedirte/pediros que leáis esto y a ver si se puede
echar un cable a la gente de la protectora de animales
de Cádiz.
La historia completa está en la web:
http://www.refugiokimba.org/
Pincháis en Urgente

Muchas gracias a todos, especialmente a ti, Miguel,
por dejarme poner estas cositas.

El jueves 24 de febrero, a la altura de Facinas me
pareció ver un perro en la cuneta con la cabeza
levantada, di la vuelta para sacarlo de allí y evitar
que lo atropellasen y al parar el coche a su lado la
perrita se asustó y recorrió un metro arrastrando las
patas traseras ¡¡ya la habían atropellado!!
Llovía y se estaba haciendo de noche, y a pesar de
poner el triángulo y llevar el chaleco refractante era
peligroso estar allí mucho tiempo, pero no sabía qué
hacer, y no iba a dejar a la perrita allí abandonada a
su suerte…. Llovía y lo único que podía hacer yo era
taparla con el paraguas y hablarle para que confiase
un poco en mí mientras encontraba una solución, pues
no me atrevía a cogerla por si intentaba morderme del
mismo miedo o se iba a la carretera y causaba un
accidente, siendo además ella rematada del todo...

Casualmente un par de coches de trafico pasaron por
allí y me preguntaron si me podían ayudar, la idea de
cortar el trafico no les pareció muy buena pero se
prestaron a ayudarme a coger a la perra, me
preguntaron si tenía una manta y yo les di mi chal que
era lo más parecido, así que se lo echaron encima y
para mi sorpresa la perra ni se quejó, quedó
totalmente inmóvil, era puro pellejo levantado por el
cuello y el lomo, parecía casi muerta… y estaba peor
de lo que me había parecido en un principio… La
metieron en el coche y me la llevé al veterinario
quien la atendió estupendamente y le hizo todas las
pruebas que creyó oportuno, viendo de entrada que
tenía las dos patas traseras rotas en la radiografía.
Me recomendó llevarla a otro veterinario especializado
en operar ese tipo de fracturas múltiples y allí que
me fui yo, pues aunque ya era tarde, él lo había
llamado por teléfono y me estaban esperando en la
clínica…
El veterinario dijo que HABÍA ESTADO EN LA CUNETA DE
10 A 15 DÍAS ¡¡Ya os podéis imaginar sus
sufrimiento!!...

Ahora busco familia que la quiera adoptar, eso sí,
alguien que sea muy consciente del calvario que ha
pasado la perra y que aún está pasando y que la quiera
para siempre y le de el cariño y la seguridad que
necesita, que nunca vuelva a encontrarse en la misma
situación.
La perrita se llamaba Facina pero ahora le llaman Lola
que es más corto y tiene unos dos años o dos años y
medio. Muy cariñosa.
Estoy dispuesta a llevarla al extranjero si allí está
esa familia ideal para ella.
¿Alguien me puede ayudar?
Muchas gracias.
Silvia

Mail:  silviacalap@...












______________________________________________
Renovamos el Correo Yahoo!
Nuevos servicios, más seguridad
http://correo.yahoo.es

#1740 De: "anapieraa" <anapieraa@...>
Fecha: Vie, 29 de Abr, 2005 12:35 am
Asunto: RE: Preguntas, Miguel y los demás
anapieraa
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
Hola Asun,

No tengo yo mi cabeza para contestar correos pero la verdad que me
apetece. Aunque la verdad que yo no te hablo de conocimientos sino
de "ideas sueltas", como yo lo llamo.

De la Triple Reacción de Arthus no tengo ni idea. Pero cuando
preguntas que si tiene que ver con el síndrome de Raynaud, creo que
para tener síndrome de Raynaud hay primero que tener el fenómeno de
Raynaud ¿no? Y este asociado a algunas otras patologías propias del
síndrome de Raynaud. ¿Es a este síndrome al que te refieres? No
sabía que estaba relacionado con fm.
Yo tengo una urticaria colinergica, pero lo que dices no creo que me
pase tan exagerado como dices. ¿a ti también te pasa en otros
lugares como dice ferran?

En el muslo lo que me ha pasado muchas veces es que tenía dolor en
el músculo que me aliviaba dando golpes con el puño en él, no sé que
cosa tan rara será esta.

A mi el olor del oxido desde luego me daba asco y no lo soportaba,
yo creo que prefería no jugar en los columpios por luego no oler a
oxido, pero no tenía vómitos, quizás es que como si que me gustaban
las matemáticas... jeje
Pero si que me molestan mucho algunos olores desagradables.

Asun, yo también sospecho de la infección desde pequeñita o algo
relacionado y además me gustaría llegar a saber la relación con
nuestra herencia familiar.

¿Qué lees que te sorprende de sfc y fm?

Bueno, bien, llegué hasta aquí, buf, ha tenido que ser rapidito
porque sino me bloqueo y ya no puedo.

Besitos. Ana.


--- En
lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com, "roquebusquer
os" <roquebusqueros@y...> escribió:
>
> Hola a todos.
> Miguel, he preguntado algunas cosillas al Dr. Ferrán y os voy a
poner
> las preguntas y respuestas. Quisiera saber si os ocurre lo mismo,
> sobre todo cuando me habla de la triple reacción de Arthus. Intento
> buscar en Internet, pero hasta ahora todas las págs. que leo se
> refieren a la vacuna antitetánica. En las pruebas de alergia no me
> salió nada positivo, tampoco a la larga lista de alimentos que
> analizó. ¿Esta cosa me la podría provocar la bacteria?
>
> Muchas gracias, y besos a todos.
>
> Buenas tardes, Dr. Ferrán. Quisiera hacerle tres
> > preguntas.
> > 1ª Al rascarme, sobre todo en la parte del cuello
> > hasta el pecho, se queda la marca durante un buen
> > rato, debe ser alarmante ver los arañazos porque
> > siempre me preguntan "qué te has hecho". No me rasco
> > con un rastrillo ni tampoco con fruición, es algo de
> > picor y al rascarme se queda el arañazo. También se
> > queda enrojecida un rato si dejo mi mano sobre esta
> > zona. Soy blanquita de piel, pero me parece exagerado.
> > A los demás no les ocurre. ¿Esto tiene que ver con el
> > síndrome de Rinhaud? He leído que este síndrome es
> > normal en los pacientes de fm.
>
> No tiene nada que ver. Esto se conoce como Triple Reacción de
Arthus y
> es un
> fenómeno de hipersensibilidad de tipo alérgico. Pasa mucho en el
escote,
> pero puede pasar también en otros lugares del cuerpo. Queda el
rastro
> de la
> uña enrojecido y sobreelevado durante bastante tiempo. Esto un
alergólogo
> podría analizarlo.
>
> >
> > 2ª Muchas veces siento en los muslos mucho frío, pero
> > la frialdad parte de dentro afuera, es el músculo el
> > que siento frío, como si me hubiesen inyectado algún
> > líquido que lo enfriase, va acompañado de dolor hasta
> > las rodillas. Hace muchos años busqué información en
> > libros de medicina y leí que podía estar relacionado
> > con el estrés, de modo que decidí no ir a ningún
> > médico. ¿Tiene esto algún nombre? ¿Es normal también
> > en fm y sfc?
>
> Tendría que interrogarla y explorarla para poder orientarla. Sólo
con
> lo que
> me comenta y sin valorar el caso en su conjunto no tengo
suficiente.
> Pienso
> que podría tratarse se alguna sensación neurológica, pero habría
que hacer
> un estudio fino de sensibilidad del muslo. No veo relación con el
estrés.
>
> >
> > 3ª Leo mensajes sobre sensibilidad química múltiple,
> > pacientes de sfc que no toleran determinados olores.
> > De niña después de jugar en los columpios me olía las
> > manos y el olor del óxido, del hierro, me provocaba
> > mareos y vómitos. Esto me venía muy bien para librarme
> > de las matemáticas, antes de ir a clase me olía las
> > manos y como vomitaba, me las pasaba en la cocina
> > tomando manzanilla. Algo bueno tenía que tener esta
> > cosa. ¿Pudiera ser sospechosa de sensibilidad química
> > múltiple o es normal vomitar si se huele  hierro
> > oxidado? Si esto fuese así, con tantos puntos de
> > conexión lyme, sfc y fm, casi confirmaría mis
> > sospechas de tener la infección desde pequeñita.
>
> No es de las sustancias que producen habitualmente una SQM. Los
pacientes
> con SQM empeoran mucho de sus síntomas como el dolor, la fatiga o
el
> trastorno cognitivo ante la inhalación de sustancias. No es una
reacción
> gastrointestinal, sino un empeoramieento claro de los síntomas que
incluso
> produce alteraciones valorables en el PET ante la inhalación. No se
> trata de
> "no tolerar el olor".
>
> >
> > Espero no resultar una hipocondríaca, es que cada día
> > me sorprenden más las cosas que leo sobre sfc y fm.
> >
> > Siento la extensión del mensaje, y como siempre muchas
> > gracias.
> >
>
> No hay de qué. Un cordial saludo.

#1739 De: Miguel Angel Ramírez <ramirezortega@...>
Fecha: Jue, 28 de Abr, 2005 12:33 am
Asunto: Re: [Lyme-E] Preguntas, Miguel y los demás
miguelramire...
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
Hola Asun,
 
A Yoli lo de quedársele la piel del cuello marcada le pasa de toda la vida y ella no tiene Lyme que sepamos. A mí no me pasa, y debe ser de las pocas cosas que no me pasen. Hasta hoy nunca había oído relacionarlo con el Lyme.
 
Lo del frío si me ocurría algo parecido, pero con el tratamiento llevo ya mucho tiempo que no me pasa. Debe ser uno de los muchos problemas de neuropatía periférica que nos provocan las Borrelias.
 
En cuanto a las múltiples sensibilidades químicas si que es frecuente que lo comenten en los foros de Lyme, pero tampoco es exclusivo del Lyme, mi madre se pone malísima cuando huele pintura o algunos otros productos químicos, y ella tampoco tiene Lyme. 
 
Besos,
 
Miguel
 
----- Original Message -----
From: juanca
Sent: Wednesday, April 27, 2005 10:28 PM
Subject: Re: [Lyme-E] Preguntas, Miguel y los demás

Le pregunté al dr Jesus sala sobre esto que tb me pasa a mi y a el( lo de
rascarte y quedarse la marca )y me dijo que una especialista le había
dicho que era a causa de una alteración del sisteam nervioso central.
 
La sensibilidad a ciertos olores tb me ocurre a mi y es frecuente en lyme
 
Saludos,
 
J.C
----- Original Message -----
Sent: Wednesday, April 27, 2005 10:17 PM
Subject: [Lyme-E] Preguntas, Miguel y los demás


Hola a todos.
Miguel, he preguntado algunas cosillas al Dr. Ferrán y os voy a poner
las preguntas y respuestas. Quisiera saber si os ocurre lo mismo,
sobre todo cuando me habla de la triple reacción de Arthus. Intento
buscar en Internet, pero hasta ahora todas las págs. que leo se
refieren a la vacuna antitetánica. En las pruebas de alergia no me
salió nada positivo, tampoco a la larga lista de alimentos que
analizó. ¿Esta cosa me la podría provocar la bacteria?

Muchas gracias, y besos a todos.

Buenas tardes, Dr. Ferrán. Quisiera hacerle tres
> preguntas.
> 1ª Al rascarme, sobre todo en la parte del cuello
> hasta el pecho, se queda la marca durante un buen
> rato, debe ser alarmante ver los arañazos porque
> siempre me preguntan "qué te has hecho". No me rasco
> con un rastrillo ni tampoco con fruición, es algo de
> picor y al rascarme se queda el arañazo. También se
> queda enrojecida un rato si dejo mi mano sobre esta
> zona. Soy blanquita de piel, pero me parece exagerado.
> A los demás no les ocurre. ¿Esto tiene que ver con el
> síndrome de Rinhaud? He leído que este síndrome es
> normal en los pacientes de fm.

No tiene nada que ver. Esto se conoce como Triple Reacción de Arthus y
es un
fenómeno de hipersensibilidad de tipo alérgico. Pasa mucho en el escote,
pero puede pasar también en otros lugares del cuerpo. Queda el rastro
de la
uña enrojecido y sobreelevado durante bastante tiempo. Esto un alergólogo
podría analizarlo.

>
> 2ª Muchas veces siento en los muslos mucho frío, pero
> la frialdad parte de dentro afuera, es el músculo el
> que siento frío, como si me hubiesen inyectado algún
> líquido que lo enfriase, va acompañado de dolor hasta
> las rodillas. Hace muchos años busqué información en
> libros de medicina y leí que podía estar relacionado
> con el estrés, de modo que decidí no ir a ningún
> médico. ¿Tiene esto algún nombre? ¿Es normal también
> en fm y sfc?

Tendría que interrogarla y explorarla para poder orientarla. Sólo con
lo que
me comenta y sin valorar el caso en su conjunto no tengo suficiente.
Pienso
que podría tratarse se alguna sensación neurológica, pero habría que hacer
un estudio fino de sensibilidad del muslo. No veo relación con el estrés.

>
> 3ª Leo mensajes sobre sensibilidad química múltiple,
> pacientes de sfc que no toleran determinados olores.
> De niña después de jugar en los columpios me olía las
> manos y el olor del óxido, del hierro, me provocaba
> mareos y vómitos. Esto me venía muy bien para librarme
> de las matemáticas, antes de ir a clase me olía las
> manos y como vomitaba, me las pasaba en la cocina
> tomando manzanilla. Algo bueno tenía que tener esta
> cosa. ¿Pudiera ser sospechosa de sensibilidad química
> múltiple o es normal vomitar si se huele  hierro
> oxidado? Si esto fuese así, con tantos puntos de
> conexión lyme, sfc y fm, casi confirmaría mis
> sospechas de tener la infección desde pequeñita.

No es de las sustancias que producen habitualmente una SQM. Los pacientes
con SQM empeoran mucho de sus síntomas como el dolor, la fatiga o el
trastorno cognitivo ante la inhalación de sustancias. No es una reacción
gastrointestinal, sino un empeoramieento claro de los síntomas que incluso
produce alteraciones valorables en el PET ante la inhalación. No se
trata de
"no tolerar el olor".

>
> Espero no resultar una hipocondríaca, es que cada día
> me sorprenden más las cosas que leo sobre sfc y fm.
>
> Siento la extensión del mensaje, y como siempre muchas
> gracias.
>

No hay de qué. Un cordial saludo.

#1738 De: "juanca" <juancaqd@...>
Fecha: Mié, 27 de Abr, 2005 8:28 pm
Asunto: Re: [Lyme-E] Preguntas, Miguel y los demás
juancaqd
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
Le pregunté al dr Jesus sala sobre esto que tb me pasa a mi y a el( lo de
rascarte y quedarse la marca )y me dijo que una especialista le había
dicho que era a causa de una alteración del sisteam nervioso central.
 
La sensibilidad a ciertos olores tb me ocurre a mi y es frecuente en lyme
 
Saludos,
 
J.C
----- Original Message -----
Sent: Wednesday, April 27, 2005 10:17 PM
Subject: [Lyme-E] Preguntas, Miguel y los demás


Hola a todos.
Miguel, he preguntado algunas cosillas al Dr. Ferrán y os voy a poner
las preguntas y respuestas. Quisiera saber si os ocurre lo mismo,
sobre todo cuando me habla de la triple reacción de Arthus. Intento
buscar en Internet, pero hasta ahora todas las págs. que leo se
refieren a la vacuna antitetánica. En las pruebas de alergia no me
salió nada positivo, tampoco a la larga lista de alimentos que
analizó. ¿Esta cosa me la podría provocar la bacteria?

Muchas gracias, y besos a todos.

Buenas tardes, Dr. Ferrán. Quisiera hacerle tres
> preguntas.
> 1ª Al rascarme, sobre todo en la parte del cuello
> hasta el pecho, se queda la marca durante un buen
> rato, debe ser alarmante ver los arañazos porque
> siempre me preguntan "qué te has hecho". No me rasco
> con un rastrillo ni tampoco con fruición, es algo de
> picor y al rascarme se queda el arañazo. También se
> queda enrojecida un rato si dejo mi mano sobre esta
> zona. Soy blanquita de piel, pero me parece exagerado.
> A los demás no les ocurre. ¿Esto tiene que ver con el
> síndrome de Rinhaud? He leído que este síndrome es
> normal en los pacientes de fm.

No tiene nada que ver. Esto se conoce como Triple Reacción de Arthus y
es un
fenómeno de hipersensibilidad de tipo alérgico. Pasa mucho en el escote,
pero puede pasar también en otros lugares del cuerpo. Queda el rastro
de la
uña enrojecido y sobreelevado durante bastante tiempo. Esto un alergólogo
podría analizarlo.

>
> 2ª Muchas veces siento en los muslos mucho frío, pero
> la frialdad parte de dentro afuera, es el músculo el
> que siento frío, como si me hubiesen inyectado algún
> líquido que lo enfriase, va acompañado de dolor hasta
> las rodillas. Hace muchos años busqué información en
> libros de medicina y leí que podía estar relacionado
> con el estrés, de modo que decidí no ir a ningún
> médico. ¿Tiene esto algún nombre? ¿Es normal también
> en fm y sfc?

Tendría que interrogarla y explorarla para poder orientarla. Sólo con
lo que
me comenta y sin valorar el caso en su conjunto no tengo suficiente.
Pienso
que podría tratarse se alguna sensación neurológica, pero habría que hacer
un estudio fino de sensibilidad del muslo. No veo relación con el estrés.

>
> 3ª Leo mensajes sobre sensibilidad química múltiple,
> pacientes de sfc que no toleran determinados olores.
> De niña después de jugar en los columpios me olía las
> manos y el olor del óxido, del hierro, me provocaba
> mareos y vómitos. Esto me venía muy bien para librarme
> de las matemáticas, antes de ir a clase me olía las
> manos y como vomitaba, me las pasaba en la cocina
> tomando manzanilla. Algo bueno tenía que tener esta
> cosa. ¿Pudiera ser sospechosa de sensibilidad química
> múltiple o es normal vomitar si se huele  hierro
> oxidado? Si esto fuese así, con tantos puntos de
> conexión lyme, sfc y fm, casi confirmaría mis
> sospechas de tener la infección desde pequeñita.

No es de las sustancias que producen habitualmente una SQM. Los pacientes
con SQM empeoran mucho de sus síntomas como el dolor, la fatiga o el
trastorno cognitivo ante la inhalación de sustancias. No es una reacción
gastrointestinal, sino un empeoramieento claro de los síntomas que incluso
produce alteraciones valorables en el PET ante la inhalación. No se
trata de
"no tolerar el olor".

>
> Espero no resultar una hipocondríaca, es que cada día
> me sorprenden más las cosas que leo sobre sfc y fm.
>
> Siento la extensión del mensaje, y como siempre muchas
> gracias.
>

No hay de qué. Un cordial saludo.





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#1737 De: "roquebusqueros" <roquebusqueros@...>
Fecha: Mié, 27 de Abr, 2005 8:17 pm
Asunto: Preguntas, Miguel y los demás
roquebusqueros
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
Hola a todos.
Miguel, he preguntado algunas cosillas al Dr. Ferrán y os voy a poner
las preguntas y respuestas. Quisiera saber si os ocurre lo mismo,
sobre todo cuando me habla de la triple reacción de Arthus. Intento
buscar en Internet, pero hasta ahora todas las págs. que leo se
refieren a la vacuna antitetánica. En las pruebas de alergia no me
salió nada positivo, tampoco a la larga lista de alimentos que
analizó. ¿Esta cosa me la podría provocar la bacteria?

Muchas gracias, y besos a todos.

Buenas tardes, Dr. Ferrán. Quisiera hacerle tres
> preguntas.
> 1ª Al rascarme, sobre todo en la parte del cuello
> hasta el pecho, se queda la marca durante un buen
> rato, debe ser alarmante ver los arañazos porque
> siempre me preguntan "qué te has hecho". No me rasco
> con un rastrillo ni tampoco con fruición, es algo de
> picor y al rascarme se queda el arañazo. También se
> queda enrojecida un rato si dejo mi mano sobre esta
> zona. Soy blanquita de piel, pero me parece exagerado.
> A los demás no les ocurre. ¿Esto tiene que ver con el
> síndrome de Rinhaud? He leído que este síndrome es
> normal en los pacientes de fm.

No tiene nada que ver. Esto se conoce como Triple Reacción de Arthus y
es un
fenómeno de hipersensibilidad de tipo alérgico. Pasa mucho en el escote,
pero puede pasar también en otros lugares del cuerpo. Queda el rastro
de la
uña enrojecido y sobreelevado durante bastante tiempo. Esto un alergólogo
podría analizarlo.

>
> 2ª Muchas veces siento en los muslos mucho frío, pero
> la frialdad parte de dentro afuera, es el músculo el
> que siento frío, como si me hubiesen inyectado algún
> líquido que lo enfriase, va acompañado de dolor hasta
> las rodillas. Hace muchos años busqué información en
> libros de medicina y leí que podía estar relacionado
> con el estrés, de modo que decidí no ir a ningún
> médico. ¿Tiene esto algún nombre? ¿Es normal también
> en fm y sfc?

Tendría que interrogarla y explorarla para poder orientarla. Sólo con
lo que
me comenta y sin valorar el caso en su conjunto no tengo suficiente.
Pienso
que podría tratarse se alguna sensación neurológica, pero habría que hacer
un estudio fino de sensibilidad del muslo. No veo relación con el estrés.

>
> 3ª Leo mensajes sobre sensibilidad química múltiple,
> pacientes de sfc que no toleran determinados olores.
> De niña después de jugar en los columpios me olía las
> manos y el olor del óxido, del hierro, me provocaba
> mareos y vómitos. Esto me venía muy bien para librarme
> de las matemáticas, antes de ir a clase me olía las
> manos y como vomitaba, me las pasaba en la cocina
> tomando manzanilla. Algo bueno tenía que tener esta
> cosa. ¿Pudiera ser sospechosa de sensibilidad química
> múltiple o es normal vomitar si se huele  hierro
> oxidado? Si esto fuese así, con tantos puntos de
> conexión lyme, sfc y fm, casi confirmaría mis
> sospechas de tener la infección desde pequeñita.

No es de las sustancias que producen habitualmente una SQM. Los pacientes
con SQM empeoran mucho de sus síntomas como el dolor, la fatiga o el
trastorno cognitivo ante la inhalación de sustancias. No es una reacción
gastrointestinal, sino un empeoramieento claro de los síntomas que incluso
produce alteraciones valorables en el PET ante la inhalación. No se
trata de
"no tolerar el olor".

>
> Espero no resultar una hipocondríaca, es que cada día
> me sorprenden más las cosas que leo sobre sfc y fm.
>
> Siento la extensión del mensaje, y como siempre muchas
> gracias.
>

No hay de qué. Un cordial saludo.

#1736 De: virginia anez <virginia_anez@...>
Fecha: Mar, 26 de Abr, 2005 9:04 pm
Asunto: RE: [Lyme-E] virginia, como tienes el colesterol?
virginia_anez
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
sera verdad porque cada vez que tenia la oprtunidad de comer comidad del mar lo que siempre queria eran los mussels!

antsettler <sacorroto@...> wrote:

que curioso, yo tambien tengo alergia a esos alimentos (IgG, por
alcat), unos 20 en total; lo que peor llevo es haber dejado el
huevo, lo comia a diario; dicen que aquel alimento que uno come
mucho inconscientemente es por ser alergico, porque los peptidos
alergicos hacen de 'opioides' dando una sensacion de bienestar


--- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
virginia anez <virginia_anez@y...> escribió:
> No me ordenaron ningun examen para controlar el colesterol que yo
sepa.
> La dieta es la del Lyme más otra dieta mas detallada hecha en base
a unos analisis de sangre que ordeno burrascano donde por primera
vez supe que era alergica a ciertos alimentos.Como el huevo, las
mussels ,string beans, lentils,etc.
>
> antsettler <sacorroto@h...> wrote:
>
> virginia, como tienes los analisis de los colesteroles? te van a
> hacer seguimiento de ellos mientras estas con la colestiramina? te
> han puesto alguna dieta?
> pablo
>
> --- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
> virginia anez <virginia_anez@y...> escribió:
> > Gracias por el ofrecimiento de tus habilidades que en algun
> momento te pueda consultar con respecto al estudio de JOnes.
> > 
> > Tomo el colesteramine 2 veces al dia. Son sobresitos que
contienen
> un polvo parecido al metamucil.
> > Lo puedo hacer con las comidas, pero dos horas antes o despues
de
> abx y vitaminas.
> > 
> > Lo tengo que tomar por lo menos 4 meses.
> > 
> > Yo vi unprograma en The Learning Channel y Dicovery Channel
donde
> Shoemaker salia explicando su teoria junto con otros pacientes.
> Estos pacientes eran pescadores y parece que padecian de otro
tippo
> de toxina pero tambien muy mala.
> > 
> > Hablando del colon Burrascano ordeno que colectara por tres dias
> seguidos poops cada vez que fuera al baño .Esta muestra fue
> conservada en liquidos de alto riesgo (tenia que usar gloves para
> almacenar la muestra en estos tubos previamente llenados)......a
lo
> mejo querian examinar algo de lo que tu mencionas en cuanto a la
> absorcion de mis intestinos.
> > 
> > Yo, me siento super differente y lo unico que a cambiado en mi
> tratamiento es este cholesteramyne....sino son toxinas, no lo se
ni
> mi importa, pero de que me esta mejorando y me disminuye casi
> completo muchsimos symptomas es verdad y noes un painkiller o
> antinflmatorio.....
> > 
> > Espero que cuando lo pare no regresen los symptomas.!!!
> > 
> > Si he estado un poco estreñida pero la dieta ayuda.
> > 
> > Quiero que sepan que estoy a la orden para responder cualquier
> curiosidad y les dejare saber si esta mejoria tiene relapse.
> >
> > antsettler <sacorroto@h...> wrote:
> >
> > hola,
> >
> > todo ese conocimiento acumulado que mencionas es oro puro para
los
> > enfermos de lyme; si yo puedo aportar algo cuenta conmigo,
aunque
> > estoy limitado, estadisticas, sistemas expertos o analizar
> > dinamicas, en la medida que pueda
> >
> > sobre las neurotoxinas de la borrelia hay que decir que nadie ha
> > aislado nunca ninguna, y que no hace falta la teoria de las
> toxinas
> > para explicar daños en organos, la bacteria misma los ocasiona;
si
> > el herx es una respuesta inmune a bacterias muertas, tampoco
> tienen
> > nada que ver las toxinas; los ciclos se explican con variacion
de
> > antigenos, y la resistencia con la forma cistica; sobre la
> > inmunomodulacion hay estudios en alemania que muestran que se
debe
> > principalmente a saturacion de receptores toll-like para el
> > reclutamiento de macrofagos y neutrofilos, estimulando la il-10
> > (como hace tambien el ebv),no hace falta inventarse toxinas
> > misteriosas de la borrelia, y menos que lo haga un medico de
> familia
> > (shoemaker (zapatero?)), sin ningun estudio firmado;
> >
> > la colestiramina tampoco es trigo limpio del todo, intercambia
en
> el
> > colon iones cloro por bicarbonato organico, acidificando el
> > organismo; y arrastran todo antibiotico o vitamina liposoluble
> > orales; lo digo por ser excepticos mientras no haya un estudio
> > serio, como tantos otros remedios; ahora, si te va bien,
estupendo!
> >
> > cuanto tiempo vas a tomarlo? notaste mejoria en breve? lo tomas
> con
> > el estomago vacio o con las comidas? te provoca estreñimiento?
> >
> > encantado de oir tus mejorias, dan animos, un saludo a todos,
> > pablo
> >   
> >
> >
> > --- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
> > virginia anez <virginia_anez@y...> escribió:
> > > Fijate:
> > > 
> > > Empe'ze hace 10 dias el colesteramine+levaquin+omeprazole al
> mismo
> > tiempo.
> > > Tengo entendido (dime que opinas porfavor) de que la bart hay
> que
> > tratarla minimo 3 meses, pues como cualquier otra lyme-co-
> > infection ,pero menos severa, lo que quiere de cir que es
deficil
> > tener  tanta mejoria en este lapso de tiempo .Tambien de que el
> > levaquin es bueno contra el Lyme (me lo dijo JOnes)...ahora sino
> he
> > ni siquiera tenido herx ni del Lyme, ni bart  antes de sentirme
> > mejor (aunque burrascano dijo que el bart no causa herxes)....
Lo
> > que he tenido es mas bien como un lifting o disminucion de los
> > sintomas hasta cierto punto magico.... por eso pense que el
> > colesteramine me lo hizo excretar de mi organismo y ya.
> > > Tambien yo como he tenido muchas infecciones urinarias en el
> 2004
> > yo ya habia tomado incluso por 14 dias el leva y de 500mgs en
vez
> de
> > 250 como me mando burrascano.
> > > 
> > > Tambien pienso que como de alguna manera he usado buenos
> > antibioticos desde el principio y atacado casi todas las co-
> > infections (espero que burrascano no me diga que no encontro
algo
> > mas en los examenes que me practico) y nunca habia addressed las
> > neurotoxinas.
> > > 
> > > El medijo en la cita del 24 de marzo que a la tercera o cuarta
> > semana de tratamiento me hiba a sentir mejor. Las primeras dos
> > semanas fueron de puras vitaminas recetadas por el asi como b12
> > injections.
> > > Me dijo que el sospechaba de neurotoxinas de bart pero que el
> lyme
> > itself lo tenia en la minima expresion.
> > > 
> > > Me dijo que fortalezer el sistema inmunologico es clave para
> > seqguir recuperandose.
> > > 
> > > MIGUEL:dejame saber tu opinion por favor.
> > > 
> > > Tambien queria preguntarte si tubieras las historias medicas
de
> Dr
> > Jones en una base de datos que le pidirias al systema que te
> > arrojara..por ejemplo"Cual fue el antibiotico de mayor empleo en
> > niños de 5 a 8 anos que resolvio mas symptomas??? o Cuales eran
> los
> > cinco symptomas comunes en los ninos que llegaban al consultorio
> sin
> > saber que tenian lyme???
> > > 
> > > Te pregunto esto por que Jones quiere dejar su legado de
alguna
> > manera y para que le otorguen un grant o donacion para ese
estudio
> > de recolection de data, analisis, clasificacion necesita que la
> > investigacion tenga un objetivo specifico y claro. Jones tiene
una
> > mina de oro en su consultorio (todos las historias medicas paso
> por
> > paso) pero el esta muy ocupado tratando a sus pacientes..es
obvio
> > que el tiene la palabra final y el conocimiento supremo en
cuanto
> a
> > cual deberia de ser el mejor objetivo para su estudio, pero por
> > curiosisdad seria bueno saber que quisieras tu u otras personas
> que
> > ese estudio respondiera.
> > >
> > > Miguel Angel Ramírez <ramirezortega@t...> wrote:
> > > Virginia,
> > > 
> > > ¿Por qué estas tan segura de que es la colestiramina la
> > responsable de tu mejoría espectacular y no el levaquin? Según
> > entiendo has comenzado los dos tratamientos a la vez y los
> mantienes
> > ambos ¿No es así?¿Cuánto tiempo llevas tomándolos?
> > > 
> > > Miguel
> > > ----- Original Message -----
> > > From: virginia anez
> > > To: lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com
> > > Sent: Friday, April 22, 2005 3:32 AM
> > > Subject: Re: [Lyme-E] donde estas herx?
> > >
> > >
> > > Migue:
> > > 
> > > No tenia ni idea de esta reaccion.
> > > 
> > > Gracias por la informacion........pero es que yo no senti esa
> > molestia o  intensification the los symptomas..sera que esta por
> > venir en las siguientes semanas????
> > > 
> > > Pero queria contribuir con mi testimonio acerca del
> > cholesteramyne.Ya yo habia oido antes acerca de este medicamento
y
> > sus beneficios a los lyme sufferers pero nunca me imagine que de
> > verdad, por lo menos en mi caso ,eran las neurotoxins mi gran
> > molestia y que releasing them de mi cuerpo la mejoria hiba a ser
> tan
> > rapida y significativa.
> > >
> > >
> > >
> > >
> > > Para cancelar su suscripción a este grupo, envíe un mensaje de
> > correo-e a:
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> > >
> > >
> > >
> > >
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> > >
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> > >
> > >    Para visitar tu grupo en la web, accede a :
> > >
> >
>
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> > ol/
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#1735 De: "antsettler" <sacorroto@...>
Fecha: Mar, 26 de Abr, 2005 8:54 pm
Asunto: RE: [Lyme-E] virginia, como tienes el colesterol?
antsettler
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
que curioso, yo tambien tengo alergia a esos alimentos (IgG, por
alcat), unos 20 en total; lo que peor llevo es haber dejado el
huevo, lo comia a diario; dicen que aquel alimento que uno come
mucho inconscientemente es por ser alergico, porque los peptidos
alergicos hacen de 'opioides' dando una sensacion de bienestar


--- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
virginia anez <virginia_anez@y...> escribió:
> No me ordenaron ningun examen para controlar el colesterol que yo
sepa.
> La dieta es la del Lyme más otra dieta mas detallada hecha en base
a unos analisis de sangre que ordeno burrascano donde por primera
vez supe que era alergica a ciertos alimentos.Como el huevo, las
mussels ,string beans, lentils,etc.
>
> antsettler <sacorroto@h...> wrote:
>
> virginia, como tienes los analisis de los colesteroles? te van a
> hacer seguimiento de ellos mientras estas con la colestiramina? te
> han puesto alguna dieta?
> pablo
>
> --- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
> virginia anez <virginia_anez@y...> escribió:
> > Gracias por el ofrecimiento de tus habilidades que en algun
> momento te pueda consultar con respecto al estudio de JOnes.
> >
> > Tomo el colesteramine 2 veces al dia. Son sobresitos que
contienen
> un polvo parecido al metamucil.
> > Lo puedo hacer con las comidas, pero dos horas antes o despues
de
> abx y vitaminas.
> >
> > Lo tengo que tomar por lo menos 4 meses.
> >
> > Yo vi unprograma en The Learning Channel y Dicovery Channel
donde
> Shoemaker salia explicando su teoria junto con otros pacientes.
> Estos pacientes eran pescadores y parece que padecian de otro
tippo
> de toxina pero tambien muy mala.
> >
> > Hablando del colon Burrascano ordeno que colectara por tres dias
> seguidos poops cada vez que fuera al baño .Esta muestra fue
> conservada en liquidos de alto riesgo (tenia que usar gloves para
> almacenar la muestra en estos tubos previamente llenados)......a
lo
> mejo querian examinar algo de lo que tu mencionas en cuanto a la
> absorcion de mis intestinos.
> >
> > Yo, me siento super differente y lo unico que a cambiado en mi
> tratamiento es este cholesteramyne....sino son toxinas, no lo se
ni
> mi importa, pero de que me esta mejorando y me disminuye casi
> completo muchsimos symptomas es verdad y noes un painkiller o
> antinflmatorio.....
> >
> > Espero que cuando lo pare no regresen los symptomas.!!!
> >
> > Si he estado un poco estreñida pero la dieta ayuda.
> >
> > Quiero que sepan que estoy a la orden para responder cualquier
> curiosidad y les dejare saber si esta mejoria tiene relapse.
> >
> > antsettler <sacorroto@h...> wrote:
> >
> > hola,
> >
> > todo ese conocimiento acumulado que mencionas es oro puro para
los
> > enfermos de lyme; si yo puedo aportar algo cuenta conmigo,
aunque
> > estoy limitado, estadisticas, sistemas expertos o analizar
> > dinamicas, en la medida que pueda
> >
> > sobre las neurotoxinas de la borrelia hay que decir que nadie ha
> > aislado nunca ninguna, y que no hace falta la teoria de las
> toxinas
> > para explicar daños en organos, la bacteria misma los ocasiona;
si
> > el herx es una respuesta inmune a bacterias muertas, tampoco
> tienen
> > nada que ver las toxinas; los ciclos se explican con variacion
de
> > antigenos, y la resistencia con la forma cistica; sobre la
> > inmunomodulacion hay estudios en alemania que muestran que se
debe
> > principalmente a saturacion de receptores toll-like para el
> > reclutamiento de macrofagos y neutrofilos, estimulando la il-10
> > (como hace tambien el ebv),no hace falta inventarse toxinas
> > misteriosas de la borrelia, y menos que lo haga un medico de
> familia
> > (shoemaker (zapatero?)), sin ningun estudio firmado;
> >
> > la colestiramina tampoco es trigo limpio del todo, intercambia
en
> el
> > colon iones cloro por bicarbonato organico, acidificando el
> > organismo; y arrastran todo antibiotico o vitamina liposoluble
> > orales; lo digo por ser excepticos mientras no haya un estudio
> > serio, como tantos otros remedios; ahora, si te va bien,
estupendo!
> >
> > cuanto tiempo vas a tomarlo? notaste mejoria en breve? lo tomas
> con
> > el estomago vacio o con las comidas? te provoca estreñimiento?
> >
> > encantado de oir tus mejorias, dan animos, un saludo a todos,
> > pablo
> >
> >
> >
> > --- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
> > virginia anez <virginia_anez@y...> escribió:
> > > Fijate:
> > >
> > > Empe'ze hace 10 dias el colesteramine+levaquin+omeprazole al
> mismo
> > tiempo.
> > > Tengo entendido (dime que opinas porfavor) de que la bart hay
> que
> > tratarla minimo 3 meses, pues como cualquier otra lyme-co-
> > infection ,pero menos severa, lo que quiere de cir que es
deficil
> > tener  tanta mejoria en este lapso de tiempo .Tambien de que el
> > levaquin es bueno contra el Lyme (me lo dijo JOnes)...ahora sino
> he
> > ni siquiera tenido herx ni del Lyme, ni bart  antes de sentirme
> > mejor (aunque burrascano dijo que el bart no causa herxes)....
Lo
> > que he tenido es mas bien como un lifting o disminucion de los
> > sintomas hasta cierto punto magico.... por eso pense que el
> > colesteramine me lo hizo excretar de mi organismo y ya.
> > > Tambien yo como he tenido muchas infecciones urinarias en el
> 2004
> > yo ya habia tomado incluso por 14 dias el leva y de 500mgs en
vez
> de
> > 250 como me mando burrascano.
> > >
> > > Tambien pienso que como de alguna manera he usado buenos
> > antibioticos desde el principio y atacado casi todas las co-
> > infections (espero que burrascano no me diga que no encontro
algo
> > mas en los examenes que me practico) y nunca habia addressed las
> > neurotoxinas.
> > >
> > > El medijo en la cita del 24 de marzo que a la tercera o cuarta
> > semana de tratamiento me hiba a sentir mejor. Las primeras dos
> > semanas fueron de puras vitaminas recetadas por el asi como b12
> > injections.
> > > Me dijo que el sospechaba de neurotoxinas de bart pero que el
> lyme
> > itself lo tenia en la minima expresion.
> > >
> > > Me dijo que fortalezer el sistema inmunologico es clave para
> > seqguir recuperandose.
> > >
> > > MIGUEL:dejame saber tu opinion por favor.
> > >
> > > Tambien queria preguntarte si tubieras las historias medicas
de
> Dr
> > Jones en una base de datos que le pidirias al systema que te
> > arrojara..por ejemplo"Cual fue el antibiotico de mayor empleo en
> > niños de 5 a 8 anos que resolvio mas symptomas??? o Cuales eran
> los
> > cinco symptomas comunes en los ninos que llegaban al consultorio
> sin
> > saber que tenian lyme???
> > >
> > > Te pregunto esto por que Jones quiere dejar su legado de
alguna
> > manera y para que le otorguen un grant o donacion para ese
estudio
> > de recolection de data, analisis, clasificacion necesita que la
> > investigacion tenga un objetivo specifico y claro. Jones tiene
una
> > mina de oro en su consultorio (todos las historias medicas paso
> por
> > paso) pero el esta muy ocupado tratando a sus pacientes..es
obvio
> > que el tiene la palabra final y el conocimiento supremo en
cuanto
> a
> > cual deberia de ser el mejor objetivo para su estudio, pero por
> > curiosisdad seria bueno saber que quisieras tu u otras personas
> que
> > ese estudio respondiera.
> > >
> > > Miguel Angel Ramírez <ramirezortega@t...> wrote:
> > > Virginia,
> > >
> > > ¿Por qué estas tan segura de que es la colestiramina la
> > responsable de tu mejoría espectacular y no el levaquin? Según
> > entiendo has comenzado los dos tratamientos a la vez y los
> mantienes
> > ambos ¿No es así?¿Cuánto tiempo llevas tomándolos?
> > >
> > > Miguel
> > > ----- Original Message -----
> > > From: virginia anez
> > > To: lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com
> > > Sent: Friday, April 22, 2005 3:32 AM
> > > Subject: Re: [Lyme-E] donde estas herx?
> > >
> > >
> > > Migue:
> > >
> > > No tenia ni idea de esta reaccion.
> > >
> > > Gracias por la informacion........pero es que yo no senti esa
> > molestia o  intensification the los symptomas..sera que esta por
> > venir en las siguientes semanas????
> > >
> > > Pero queria contribuir con mi testimonio acerca del
> > cholesteramyne.Ya yo habia oido antes acerca de este medicamento
y
> > sus beneficios a los lyme sufferers pero nunca me imagine que de
> > verdad, por lo menos en mi caso ,eran las neurotoxins mi gran
> > molestia y que releasing them de mi cuerpo la mejoria hiba a ser
> tan
> > rapida y significativa.
> > >
> > >
> > >
> > >
> > > Para cancelar su suscripción a este grupo, envíe un mensaje de
> > correo-e a:
> > > lyme_y_otras_zoonosis_cronicas_espanol-
> unsubscribe@yahoogroups.com
> > >
> > >
> > >
> > >
> > > Patrocinio de Yahoo! Grupos
> > >
> > > ---------------------------------
> > > Enlaces a Yahoo! Grupos
> > >
> > >    Para visitar tu grupo en la web, accede a :
> > >
> >
>
http://es.groups.yahoo.com/group/lyme_y_otras_zoonosis_cronicas_espan
> > ol/
> > >
> > >    Para cancelar tu suscripción a este grupo, envía un mensaje
a:
> > > lyme_y_otras_zoonosis_cronicas_espanol-
> unsubscribe@yahoogroups.com
> > >
> > >    El uso que hagas de Yahoo! Grupos está sujeto a las
> Condiciones
> > del servicio de Yahoo!.
> > >
> > >
> > >
> > > ---------------------------------
> >
> >
> >
> >
> >
> > Para cancelar su suscripción a este grupo, envíe un mensaje de
> correo-e a:
> > lyme_y_otras_zoonosis_cronicas_espanol-
unsubscribe@yahoogroups.com
> >
> >
> >
> >
> > Patrocinio de Yahoo! Grupos
> >
> > ---------------------------------
> > Enlaces a Yahoo! Grupos
> >
> >    Para visitar tu grupo en la web, accede a :
> >
>
http://es.groups.yahoo.com/group/lyme_y_otras_zoonosis_cronicas_espan
> ol/
> >
> >    Para cancelar tu suscripción a este grupo, envía un mensaje a:
> > lyme_y_otras_zoonosis_cronicas_espanol-
unsubscribe@yahoogroups.com
> >
> >    El uso que hagas de Yahoo! Grupos está sujeto a las
Condiciones
> del servicio de Yahoo!.
> >
> >
> >
> > ---------------------------------
>
>
>
>
>
> Para cancelar su suscripción a este grupo, envíe un mensaje de
correo-e a:
> lyme_y_otras_zoonosis_cronicas_espanol-unsubscribe@yahoogroups.com
>
>
>
>
> Patrocinio de Yahoo! Grupos
>
> ---------------------------------
> Enlaces a Yahoo! Grupos
>
>    Para visitar tu grupo en la web, accede a :
>
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ol/
>
>    Para cancelar tu suscripción a este grupo, envía un mensaje a:
> lyme_y_otras_zoonosis_cronicas_espanol-unsubscribe@yahoogroups.com
>
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del servicio de Yahoo!.
>
>
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> ---------------------------------

#1734 De: "juanca" <juancaqd@...>
Fecha: Mar, 26 de Abr, 2005 4:24 pm
Asunto: Lyme disease bacteria need protein to live,BptA protein
juancaqd
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http://washingtontimes.com/upi-breaking/20050425-063029-8173r.htm

Lyme disease bacteria need protein to live


Dallas, TX, Apr. 25 (UPI) -- U.S. researchers Monday said a protein critical
for survival in the bacteria that causes Lyme disease may be a target for
therapies.

The Lyme-causing bacterium, known as Borrelia burgdorfei, lives in the gut
of ticks and is transmitted from the insect to animals and humans.

Researchers from the University of Texas Southwestern Medical Center
reported in the Proceedings of the National Academy of Sciences when
Borrelia burgdorfei lacks the protein BptA, it is unable to be transmitted
from the tick to a new animal host, suggesting the protein is essential for
the bacteria to survive in the tick's gut.

In the study, the researchers generated a strain of the bacteria that lacked
the gene for the BptA protein. Without the protein, the bacteria were unable
to metabolize nutrients found in the blood the tick usually feeds on and
ultimately died off.

Lyme disease can cause fever, fatigue, and muscle and joint aches in people.
If antibiotics are started soon after infection, the chronic complications
associated with the disorder can usually be prevented.


© 2005 News World Communications, Inc











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#1733 De: Miguel Angel Ramírez <ramirezortega@...>
Fecha: Lun, 25 de Abr, 2005 11:18 pm
Asunto: Prolonged Ab treatment of Lyme Borreliosis
miguelramire...
Sin conexión Sin conexión
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Orv Hetil. 2002 May 26;143(21):1223-4.

[Borrelia burgdorferi Group: in-vitro antibiotic sensitivity]

[Article in Hungarian]

Henneberg JP, Neubert U.

Department of Dermatology, Ludwig-Maximilians-University, Munchen,
Germany.

Failures in the antibiotic therapy of Lyme disease have repeatedly been
demonstrated by post-treatment isolations of the infecting borreliae.
Analyses of the antibiotic susceptibility patterns of borreliae may
help to understand the causes of such treatment failures and to develop
new therapeutic regimens. AIMS AND METHODS: The three subspecies of
Borrelia burgdorferi known to be pathogenic for humans and to differ in
their virulence and organ affinity possibly may also show divergent
susceptibilities to some common antibacterial agents. In order to get
real clues for such probable differences we compared the efficacy of
six antimicrobial agents against 24 borrelial tick and skin isolates
belonging to the three subspecies of B. burgdorferi sensu lato.
RESULTS: In five comparative evaluations, some significantly different
antibiotic sensitivity of the three borrelial species was found. The
Borrelia burgdorferi sensu stricto isolates showed lower sensitivity to
cephalosporin, tetracycline and ciprofloxacin as well as a higher
sensitivity to erythromycin compared to the B. afzelii and B. garinii
isolates. The B. garinii isolates proved to be more sensitive to
penicillin in comparison to the B. burgdorferi s.s. and B. afzelii
isolates. CONCLUSIONS: In the light of these data, treatment failures
may be interpreted by serum and tissue levels of the antibiotic too low
for an effective killing of the infecting Spirochetes. However,
prolonged treatment regimens applying higher dosages of antibiotics, in
order to get complete clearing of the infection, may be linked to
aggravated side effects. PROPOSAL: Therefore, the combination of
different antiborrelial agents with synergistic effect seems to be a
meaningful alternative and should be included in future studies in
vitro as well as in vivo.

PMID: 12073540 [PubMed - indexed for MEDLINE]
----------------------------------------------------------------------------------
 
 
Acta Clin Belg. 1998 Jun;53(3):178-83.

Lyme borreliosis--a review of the late stages and treatment of four cases.

Petrovic M, Vogelaers D, Van Renterghem L, Carton D, De Reuck J, Afschrift M.

Department of Internal Medicine, University Hospital Ghent, Belgium.

Difficulties in diagnosis of late stages of Lyme disease include low sensitivity of serological testing and late inclusion of Lyme disease in the differential diagnosis. Longer treatment modalities may have to be considered in order to improve clinical outcome of late disease stages. These difficulties clinical cases of Lyme borreliosis. The different clinical cases illustrate several aspects of late borreliosis: false negative serology due to narrow antigen composition of the used ELISA format, the need for prolonged antibiotic treatment in chronic or recurrent forms and typical presentations of late Lyme disease, such as lymphocytic meningo-encephalitis and polyradiculoneuritis.

Publication Types:
  • Case Reports
  • Review
  • Review of Reported Cases

PMID: 9701852 [PubMed - indexed for MEDLINE]
 
-------------------------------------------------------------------------------
 
J Neuropsychiatry Clin Neurosci. 1995 Summer;7(3):345-7.  

Rapidly progressive frontal-type dementia associated with Lyme disease.

Waniek C, Prohovnik I, Kaufman MA, Dwork AJ.

New York State Psychiatric Institute, NY 10032, USA.

The authors report a case of fatal neuropsychiatric Lyme disease (LD) that was expressed clinically by progressive frontal lobe dementia and pathologically by severe subcortical degeneration. Antibiotic treatment resulted in transient improvement, but the patient relapsed after the antibiotics were discontinued. LD must be considered even in cases with purely psychiatric presentation, and prolonged antibiotic therapy may be necessary.

Publication Types:
  • Case Reports

PMID: 7580195 [PubMed - indexed for MEDLINE]
 
-------------------------------------------------------------------------------
 
 
Expert Opin Investig Drugs. 2003 Oct;12(10):1609-14
 
The Lyme Wars: time to listen.

Stricker RB, Lautin A.


Department of Medicine, California Pacific Medical Center, 450 Sutter Street, Suite 1504, San Francisco, CA, USA. rstricker@...

Lyme disease represents a public health threat of major proportions. The murky science and acrimonious politics of Lyme disease have created barriers to reliable diagnosis and effective treatment of this protean illness. Two major clinical problems with the disease are the absence of a therapeutic end point in treating Borrelia burgdorferi, the spirochetal agent of Lyme disease, and the presence of tick-borne co-infections, such as babesiosis, anaplasmosis and bartonellosis, that may complicate the course of the illness. From a pathophysiological standpoint, the affinity of B. burgdorferi for multiple cell types and the presence of non-replicating forms of the spirochete have contributed to persistent infection and failure of simple antibiotic regimens. Newer approaches to the treatment of Lyme disease should take into account its clinical complexity in co-infected patients and the possible need for prolonged combination therapy in patients with persistent symptoms of this potentially debilitating illness. The risk and prevention of human transmission of Lyme disease merit further study.

PMID: 14519082 [PubMed - indexed for MEDLINE]
 
--------------------------------------------------------------------
 
 
Clin Infect Dis. 1997 Jul;25 Suppl 1:S52-6.  

Tetracycline therapy for chronic Lyme disease.

Donta ST.

Boston University Medical Center and Boston Veterans Affairs Medical Center, Massachusetts 02118, USA.

Two hundred seventy-seven patients with chronic Lyme disease were treated with tetracycline for 1 to 11 months (mean, 4 months); the outcomes for these patients were generally good. Overall, 20% of the patients were cured; 70% of the patients' conditions improved, and treatment failed for 10% of the patients. Improvement frequently did not take place for several weeks; after 2 months of treatment, 33% of the patients' conditions were significantly improved (degree of improvement, 75%-100%), and after 3 months of treatment, 61% of the patients' conditions were significantly improved. Treatment outcomes for seronegative patients (20% of all patients) were similar to those for seropositive patients. Western immunoblotting showed reactions to one or more Borrelia burgdorferi-specific proteins for 65% of the patients for whom enzyme-linked immunosorbent assays were negative. Whereas age, sex, and prior erythema migrans were not correlated with better or worse treatment outcomes, a history of longer duration of symptoms or antibiotic treatment was associated with longer treatment times to achieve improvement and cure. These results support the use of longer courses of treatment in the management of patients with chronic Lyme disease. Controlled trials need to be conducted to validate these observations.

Publication Types:
  • Clinical Trial

PMID: 9233665 [PubMed - indexed for MEDLINE]
 
------------------------------------------------------------------------------
 
 
Tex Med. 1991 Sep;87(9):62-6.  

Lyme borreliosis in Texas.

Goldings AS, Taylor JP, Rawlings J.

Department of Health, Austin, TX 78756.

Lyme borreliosis is a protean infection caused by B burgdorferi, a recently recognized arthropod-borne spirochete. The disease is generally acquired during warm weather, and its onset is characterized by a skin lesion, EM, and flulike symptoms. Neurologic, cardiac, and/or rheumatologic abnormalities may emerge weeks, months, or years later. In the absence of the pathognomonic skin lesion, determination of antibody response is currently the most practical laboratory aid in diagnosis. However, clinical judgement is necessary for the correct interpretation of laboratory results because false-positive and false-negative results are common. Antibiotics remain the mainstay of therapy. Longer courses of antibiotic therapy than those previously recommended may be needed to obtain a cure, particularly in later stages of the illness.

PMID: 1759253 [PubMed - indexed for MEDLINE]
 
----------------------------------------------------------------------------------
 
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15698718

  Diagn Microbiol Infect Dis. 2005 Feb;51(2):127-30.

  Severe neuroborreliosis: The benefit of prolonged high-dose combination
  of antimicrobial agents with steroids--an illustrative case.

  Massengo SA, Bonnet F, Braun C, Vital A, Beylot J, Bastard J.

  Department of Neurology, Centre Hospitalier de Mont de Marsan, 40000
  Mont de Marsan, France. massengoserge@...

  Neuroborreliosis frequently occurs in endemic areas, whereas
  encephalomyelitis is uncommon. Treatment consists classically of 2 to 4
  weeks of recommended antimicrobial agents with a generally good
  outcome. A severe case is reported combining an encephalomyelitis with
  an axonal polyneuropathy. Clinical improvement was observed only with
  the use of prolonged high dose of 2 antimicrobial agents combined with
  steroids.

  PMID: 15698718 [PubMed - in process]

----------------------------------------------------------------
 
 
J Clin Microbiol. 1993 Aug;31(8):1961-3.
 
Lyme disease: the sensible pursuit of answers.

Liegner KB.


Lyme Borreliosis and Related Disorders, Internal and Critical Care Medicine, Armonk, New York 10504.

PMID: 8370722 [PubMed - indexed for MEDLINE]
Full text :
 
------------------------------------------------------------------------------
 
 
Lancet. 1995 Jun 3;345(8962):1436-7.
 
Lyme borreliosis.
 
Ferris i Tortajada J, Lopez Andreu JA, Salcede Vivo J, Sala Lizarraga JV.

Publication Types:
  • Case Reports
  • Comment
  • Letter

PMID: 7760623 [PubMed - indexed for MEDLINE]
 

SIR- Vartiovaara (April 1, p 842) describes his experience of living with lyme disease. We wish to make the following comments.

 

One of us (JVSL) (hereinafter referred to as “the patient”) has been living with lyme since the spring of 1988, and has cronic neurological, cardiac, and osteomusculoarticular problems 1. Until the patient was diagnosed three and a half years after being bitten by an arthropod, he had been regarded as a depressive neurotic, despite his efforts to convince his doctor that his illness was organic and serious. Lyme borreliosis is diagnosed clinically 2, which underlines the importance of listening to the patient, investigating, understanding, and evaluating each one of the symptoms and signs, and searching for an organic cause. Like Vartiovaara, he had no erythema migrans, but had a lump near the site of the bite (back) and was seronegative. These findings delayed antibiotic treatment until his illness became life-threatening. We think that in seronegative patients the inmune system should be evaluated and antibiotics are needed.

 

Our patient received during 2 years seven short-term antibiotic treatments, achieving transitory improvements. Nonetheless, his condition greatly deteriored. In October, 1993, he started a different antibiotic regimen (ceftriaxone, 2 g per day intravenously for 12 months, and oral roxithromycin 150 mg per day for 2 months) After ceftriaxone  he has continued with oral minocycline, 100 mg per 12 hours for 7 months. His quality of life has greatly improved and the treatment is more tolerable than the borreliosis.

 

Perhaps Vartiovaara´s problems are caused by autoimmune events since his PCR for Borrelia burgdorferi was negative. There is controversy about the value of such techniques. 3,4 We agree with Vartiovaara´s comment that “When the whole picture leans towards Lyme borreliosis it is both ethically and medically right to treat” We add, however, in accord with the advice of others 3,5 that antibiotics should be continued in the long term, until achieve cure or delay the progression of the disease.

*Josep Ferris i Tortajada, Juan A López Andreu, José Salcede Vivó, Jesús V Sala Lizarraga.

Departament of Paediatrics and Clinical Biopathology, Hospital Infantil “La Fé”. Valencia 46009 Spain; and Rehabilitation Service, Hospital General Universitat Val

 

1  López Andreu JA, Ferris J, Canosa CA, Sala-Lizarraga JA, Treatm of late Lyme disease: a challenge to accept. J clin Microbiol 1994; 3 1415-16

2 Burrascano J Jr. Managing Lyme disease: late-stage Lyme disease: treatment options and guidelines. Int Med Sped 1989; 10: 102-07

3 Pachner AR, Delaney E The polymerase chain reaction in the diagnosis of Lyme neuroborreliosis. Ann Neurol 1993; 34: 544-49

4 Liegner KB. Lyme disease: the sensible pursuit of answers J Clin Microbiol 1993; 31: 1961-63


#1732 De: "juanca" <juancaqd@...>
Fecha: Lun, 25 de Abr, 2005 10:49 pm
Asunto: Comparative Genome Analysis of the Pathogenic Spirochetes Borrelia burgdorferi and Treponema pallidum
juancaqd
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Infect Immun. 2000 March; 68(3): 1633–1648.
Copyright notice
 
Comparative Genome Analysis of the Pathogenic Spirochetes Borrelia burgdorferi and Treponema pallidum
 
G. Subramanian,1 Eugene V. Koonin,2* and L. Aravind2
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases,1 and National Center for Biotechnology Information, National Library of Medicine,2 National Institutes of Health, Bethesda, Maryland 20894
 
Editor: A. D. O'Brien
 
*Corresponding author. Mailing address: National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894. Phone: (301) 435-5913. Fax: (301) 480-9241. E-mail: koonin@....
 
Received August 2, 1999; Revisions requested October 15, 1999; Accepted November 29, 1999.
 
This article has been cited by other articles in PMC.
Top
 Abstract
MATERIALS AND METHODS
RESULTS AND DISCUSSION
REFERENCES
Abstract
 
A comparative analysis of the predicted protein sequences encoded in the complete genomes of Borrelia burgdorferi and Treponema pallidum provides a number of insights into evolutionary trends and adaptive strategies of the two spirochetes. A measure of orthologous relationships between gene sets, termed the orthology coefficient (OC), was developed. The overall OC value for the gene sets of the two spirochetes is about 0.43, which means that less than one-half of the genes show readily detectable orthologous relationships. This emphasizes significant divergence between the two spirochetes, apparently driven by different biological niches. Different functional categories of proteins as well as different protein families show a broad distribution of OC values, from near 1 (a perfect, one-to-one correspondence) to near 0. The proteins involved in core biological functions, such as genome replication and expression, typically show high OC values. In contrast, marked variability is seen among proteins that are involved in specific processes, such as nutrient transport, metabolism, gene-specific transcription regulation, signal transduction, and host response. Differences in the gene complements encoded in the two spirochete genomes suggest active adaptive evolution for their distinct niches. Comparative analysis of the spirochete genomes produced evidence of gene exchanges with other bacteria, archaea, and eukaryotic hosts that seem to have occurred at different points in the evolution of the spirochetes. Examples are presented of the use of sequence profile analysis to predict proteins that are likely to play a role in pathogenesis, including secreted proteins that contain specific protein-protein interaction domains, such as von Willebrand A, YWTD, TPR, and PR1, some of which hitherto have been reported only in eukaryotes. We tentatively reconstruct the likely evolutionary process that has led to the divergence of the two spirochete lineages; this reconstruction seems to point to an ancestral state resembling the symbiotic spirochetes found in insect guts.
Top
Abstract
MATERIALS AND METHODS
RESULTS AND DISCUSSION
REFERENCES 
 
 
Comparative analysis of the protein products encoded in complete genomes provides a powerful tool for evaluating evolutionary trends and adaptive strategies in pathogenic microbes. Identification of metabolic and signaling pathways that are unique to pathogens offers novel targets for therapeutic intervention. Also, such unique determinants may prove useful in developing better diagnostic and prognostic indicators of infectious diseases in humans. Conclusions from such an analysis enhance understanding of the host-parasite interactions that enable pathogens to carve out unique ecological niches in nature.
 
Borrelia burgdorferi is the causative agent of Lyme disease, whereas the related spirochete Treponema pallidum causes syphilis. Both organisms are fastidious in their growth requirements, have small genomes, and manifest clinically as distinct, chronic, disseminated diseases. The clinical similarities (68) include progression of disease in stages following local inoculation either through a tick in Lyme disease or through sexual contact in syphilis. Involvement of the central nervous system is seen in both infections, with sequalae ranging from neurologic deficits to neuropsychiatric abnormalities (19). Chronic, recurrent joint involvement is classically associated with Lyme disease (64). The protean clinical manifestations of these pathogens and their propensity to cause chronic infection in the human host contribute to the ongoing diagnostic and therapeutic challenges offered by these spirochetes (22, 42).
 
The recent determinations of the complete genome sequences of B. burgdorferi (30) and T. pallidum (31) have made a comprehensive computer-based comparison of the two spirochete genomes a feasible exercise. Recent comparative genomic studies include comparisons between two closely related mycoplasma species (36) and between bacteria that belong to related genera but encode vastly different numbers of proteins, namely, Escherichia coli and Haemophilus influenzae (72). The complete genomes of T. pallidum and B. burgdorferi give us the first chance to compare two moderately related pathogenic bacteria with approximately equivalent coding capacities. In order to systematically compare the protein sets encoded in the two spirochete genomes, we devised a measure for evaluating evolutionary relationships between families and functional classes of proteins: the orthology coefficient. With regard to the two spirochetes, it seemed likely that differences observed across families and functional groups of proteins could be indicative of the distinct evolutionary pressures of the host environment.
 
Completely automated computational analysis of genome sequences is often plagued by errors arising from compositional bias in protein sequences, difficulties in automatic assessment of the domain organization of proteins, and the lack of in-depth predictive power (16). Therefore, in comparative analysis of the two spirochete genomes we used a semiautomated strategy that is based on recently developed, powerful tools for sequence analysis, particularly position-specific iterating BLAST (PSI-BLAST) (2, 3), and also involves case-by-case examination of protein families and individual protein sequences. Optimization of the functional annotation of proteins accompanied by reconstruction of metabolic and signaling pathways in the two spirochetes helped uncover a number of unique features that likely play a role in host response-related functions. In this report, we compare and contrast the gene complements of the two spirochetes and provide examples of shared and unique genes and functional systems.
Top
Abstract
 MATERIALS AND METHODS
RESULTS AND DISCUSSION
REFERENCES
MATERIALS AND METHODS
 
Databases. The complete protein sets of B. burgdorferi (30) and T. pallidum (31) were obtained from the genome division of the Entrez retrieval system at http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome. All database searches were carried out against the nonredundant (NR) sequence database maintained at the National Center for Biotechnology Information (National Institutes of Health, Bethesda, Md.).
 
Sequence analysis: detection and interpretation of varying levels of sequence similarity. Large-scale sequence analysis was handled using the SEALS program package (76). The first step of the analysis involved a search of the NR database of protein sequences at the National Center for Biotechnology Information using the gapped BLAST program (3), with the complete protein sets of B. burgdorferi and T. pallidum as queries. Compositionally biased regions in query sequences that tend to produce spurious hits in database searches were masked using the SEG program (81). Two different sets of parameters for SEG were used, namely, mild masking (window length, 12; trigger complexity, 2.2; extension complexity, 2.5) for routine searches and stringent masking (window length, 45; trigger complexity, 3.4; extension complexity, 3.75) for delineating particular globular domains (81). In-depth database searches were performed using the PSI-BLAST program (3) whenever specific annotation required detection of subtle relationships. Briefly, PSI-BLAST uses multiple alignments of sequences that show expectation values, or e-values, lower than a specified cutoff (in this case 0.01) in the first-pass gapped BLAST search to construct a position-specific scoring matrix (PSSM). The PSSM is then used as the input for further iterations of the database searches, which results in increased detection of subtle sequence similarities (2, 8). Statistical evaluation of the PSI-BLAST result is based on the empirical version of Karlin-Altschul statistics, modified for gapped alignments (3). The e-value indicates the number of sequences which show a certain level of similarity by chance alone for a database of the size equivalent to NR. The e-value reported on the first instance that PSI-BLAST detects the given sequence above the cutoff is a reliable indicator of statistical significance. Under the condition that properly filtered globular domains are used as queries, an e-value of less than 0.01 is generally suggestive of homology (8).
 
Structural features of proteins were analyzed using the FAMASK program of the SEALS package (76), which incorporates several prediction methods. Signal peptides were predicted using the SIGNALP program (49), transmembrane helices were predicted using the PHD topology program (57) or the TopPred II program (20), and coiled-coil regions were predicted using the COILS2 program with a window length of 21 (43).
 
The phyletic distribution of homologous proteins detected by gapped BLAST searches was evaluated using the TAX_COLLECTOR program (76) of SEALS. The hits with an e-value below 0.001 between each protein encoded in the two spirochete genomes and the NR databases were analyzed, and the best hits in the second spirochete as well as those in other bacteria, archaea, and eukarya, with their respective e-values, were tallied. This provided the starting point for identifying orthologous genes in the two genomes as well as a preliminary indication of the phyletic distribution of homologs for most of the proteins encoded in each genome. An attempt was made to delineate true orthologous relationships on the basis of symmetric best hits between the proteins from the two spirochetes as well as between the spirochete proteins and those from other bacteria, archaea, and eukaryotes. In problematic cases, phylogenetic tree analysis using multiple sequence alignments of conserved domains was carried out in order to evaluate the relationships. Phylogenetic trees were constructed using the PAUP3 or CLUSTALW programs (35) with the neighbor-joining and least squares (Fitch-Margoliash) methods, accompanied by bootstrap analysis (27).
 
A complementary approach was employed for case-by-case analysis of those spirochete proteins that failed to show statistically significant matches when used as queries for PSI-BLAST. These sequences were screened for the presence of known conserved domains using the previously developed libraries of PSSMs (18, 53) as well as newly developed PSSMs. Domain-family PSSMs were created by running PSI-BLAST against the NR database with the appropriate query and an e-value cutoff of 0.01 and saving the profile using the “−C” option. The resulting PSSM was rerun against the protein sequence sets of T. pallidum and B. burgdorferi using the −R option of PSI-BLAST, and hits with significant scores were detected. To test the robustness of this procedure, we prepared databases using randomized protein sequences from each of the spirochete proteomes and conducted similar searches with each of the PSSMs on them. No hits with significant e-values (<0.01) were detected in these searches, supporting the validity of the domains detected in the spirochete proteomes with the PSSMs. Additional database searches were performed with family-specific Hidden Markov models that were constructed and run using the HMMER2 program package (66). Multiple alignments of protein families were constructed using a combination of the −m4 option of PSI-BLAST and the CLUSTALW program (35).
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Abstract
MATERIALS AND METHODS
 RESULTS AND DISCUSSION
REFERENCES
RESULTS AND DISCUSSION
 
Orthology coefficient: functional classes and protein families. The proteins encoded by the genomes can be broadly categorized on the basis of either (predicted) cellular function (functional class) or shared conserved domains (protein families). Orthologs are genes (proteins) in different genomes that are related by vertical descent; i.e., they can be traced back to a common ancestor. Such orthologous proteins typically have similar, if not identical, biological functions in the respective organisms (71). Paralogs, in contrast, are genes related by duplication within a lineage (genome); paralogs are expected to possess generally similar biochemical functions but distinct biological roles. Given these differences in functional implications, careful delineation of orthologous and paralogous relationships between genes is of primary importance for predicting functions of proteins with an appropriate degree of precision. We adopted a quantitative measure of orthology that we termed the orthology coefficient (OC). This index can be applied to different protein categories, namely, superfamilies related by descent as opposed to functional classes of proteins, such as those involved in transcription or replication. In the simplest case of a one-to-one correspondence between genes in two genomes, OC = 2No/(N1 + N2) where No is the number of orthologs and N1 and N2 are the numbers of members of the given protein family or functional category in the two compared genomes (Fig. 1). If the gene complements in the two genomes are completely conserved, then the OC is 1.00; by contrast, in the hypothetical case where there are no orthologs, the OC is 0. If there is one or more duplications in one or both of the species that occurred after their divergence, then OC = (No1 + No2)/(N1 + N2) where No1 and No2 are the numbers of members in orthologous clusters from the two respective genomes (Fig. 1). Criteria used to identify orthologs included symmetry of retrieval in reciprocal BLAST searches, conservation of the domain organization of proteins, and, in problematic cases, phylogenetic tree analysis (71, 72).
 
Conservation and diversity of functional classes of proteins between the two spirochetes. Functional classes of proteins include core functions, such as replication and cell division, repair, transcription, and translation, that are shared by all bacteria and to a large extent also by archaea and eukaryotes, and more specialized functions, such as metabolism, metabolite transport, host and environment response, and signal transduction. Figure 2 shows the representation of the functional classes in the two genomes and the level of orthology in each class measured using OC. In order to assess the effects of specific adaptations of each of the spirochetes to their distinct niches, investigation of classes with low OC values appears to be critical. Below, we discuss the distribution of functional classes in the two spirochetes along the gradient of OC values. A selection of prominent differences in the functional systems of the two spirochetes is shown in Table 1, and examples of apparent spirochete synapomorphies are listed in Table 2.
 
Highly conserved functional classes with OCs close to 1. Not surprisingly, the core functional classes, namely, DNA replication and translation, had OCs of 0.94 and 0.98, respectively, which is indicative of largely vertical inheritance (Fig. 2). The limited differences observed in these conserved functional classes could be attributed to interesting cases of horizontal gene transfer, gene loss, or duplication with divergence.
 
Differences in the gene complement involved in DNA replication include the lack of topoisomerase IV (parC, parE) in T. pallidum, which is of interest given the conserved role of these proteins in chromosome partitioning in other bacteria (77). Conversely, the proofreading 3′-5′ exonuclease—the  subunit of DNA polymerase III (e.g., the E. coli DnaQ protein)—whose role in DNA replication seems to be conserved in all other bacteria (29), is missing in B. burgdorferi. The absence of this enzyme would result in error-prone replication, which seems to be compatible with the generation of new variants through mutation in the genes encoding variable antigens of Borrelia (58, 84). An alternative is nonorthologous displacement (E. V. Koonin, A. R. Mushegian, and P. Bork, Letter, Trends Genet. 12:334–336, 1996), that is, an unrelated or distantly related and so far unidentified exonuclease being recruited for the proofreading role. Interestingly, T. pallidum encodes a second copy of the single-stranded DNA-binding protein (TP0310), which might have a distinct function in replication or recombination.
 
In addition to these striking differences, we detected an interesting case of apparent displacement of an existing gene by its ortholog from a distant species, probably via horizontal gene transfer. Sequence searches showed that topoisomerase I (Topo I) from B. burgdorferi shares an insert within the TOPRIM domain (10) and a C-terminal repeat domain with actinomycetes and cyanobacteria. These features are lacking in other bacterial lineages and appear to be derived, shared characters (synapomorphies) within this protein superfamily. Phylogenetic analysis using multiple alignment of the conserved region of bacterial Topo I strongly supported grouping of B. burgdorferi with actinomycetes and cyanobacteria (Fig. 3 [bootstrap value, >90%]). This phylogenetic affinity of Topo I is in stark contrast to the typical clustering of the other spirochete proteins, particularly those from the core functional classes, and suggests horizontal gene transfer into the B. burgdorferi lineage followed by loss of the ancestral form. This phenomenon, which may be termed xenologous gene displacement, that is, displacement by an orthologous gene from a phylogenetically distant source (J. P. Gogarten, Letter and comment, J. Mol. Evol. 39:541–543, 1994), is seen also in several other instances in the two spirochetes (see below).
 
In spite of the high level of conservation in the translation apparatus, we did detect a few interesting examples of evolutionary divergence between the two species. One notable case was the prolyl-tRNA synthetase from B. burgdorferi, where phylogenetic analysis strongly suggested that the enzyme in B. burgdorferi has been acquired from a eukaryotic source by the xenologous displacement mechanism (78). The other aminoacyl-tRNA synthetases are strongly conserved between the spirochetes, but phylogenetic analysis provided evidence for likely ancient horizontal transfers into the ancestor of spirochetes accompanied by displacement of the original gene. One well-studied case in this category is class I lysyl-tRNA synthetase, which apparently was acquired from the archaea (37, 78); similar evidence of archaeal origin was obtained for the two subunits of phenylalanyl-tRNA synthetase (78). By contrast, the synthetases for arginine, glutamate, methionine, isoleucine, and serine showed evidence of likely horizontal transfer from eukaryotic sources (78).
 
Functional classes with intermediate OCs (0.6 to 0.8). The gene complements involved in repair, recombination, and transcription show significant differences between the two spirochetes, which is reflected in OC values of less than 0.8 (Fig. 2). A number of important repair genes are different in the two genomes. Thus, B. burgdorferi encodes the helicase-nuclease complex RecBCD, whereas T. pallidum lacks these genes but has instead a complement of recFGNR genes. Another repair enzyme unique to T. pallidum is the ERCC3-like eukaryotic-type DNA repair helicase that is also present in mycobacteria (54). It is likely that this gene was horizontally transferred from eukaryotes into a certain bacterial lineage and subsequently disseminated amidst the bacteria. The triplication of the C-terminal BRCT domain of DNA ligase in T. pallidum is a unique feature that is in contrast to the similarly located single copy of this domain present in all other bacteria (7, 15). The RecQ helicase gene is found in T. pallidum but not in B. burgdorferi. Conversely, B. burgdorferi but not T. pallidum retains the ancient duplication of the mutS gene, which is also seen in other bacteria. Interestingly, B. burgdorferi lacks RuvC, the endonuclease subunit of the Holliday junction resolvase complex, which suggests either that the Ruv complex is nonfunctional or that a distinct nuclease complements this function. Both spirochetes possess a novel mismatched-base DNA glycosylase (TP0229/BB0013), a base excision repair enzyme, orthologs of which are conserved in a number of bacteria and in all archaea (60), but the B. burgdorferi version is highly divergent from all other bacterial orthologs. The major disparities in the repertoires of repair proteins suggest a difference in the selective forces that act on this system in the two spirochetes. The fact that B. burgdorferi undergoes antigenic variation (58, 84) that may require both active recombination and error-prone repair provides a possible explanation for the retention of only certain of its repair pathways.
 
The intermediate OC of the transcriptional apparatus seems to reflect a bimodal effect of selective evolutionary forces. The core transcriptional machinery, which includes RNA polymerase subunits and components of the elongation and termination complexes, is highly conserved, whereas the repertoires of specific transcriptional regulators are largely different (Fig. 2). Within the shared heritage, there are some unique features that are likely to have been derived in the common ancestor of these spirochetes and may be considered signatures of this clade. In particular, the spirochete NusA protein (a part of the transcription termination complex) contains a C-terminal Zn ribbon domain in place of the helix-hairpin-helix (HhH) domain that is found in most other bacteria (data not shown). Similarly, the transcription elongation factor GreA (40) in both spirochetes possesses a long N-terminal extension which is shared only with chlamydiae (69). An orthologous pair of spirochete proteins (TP0511 and BB0355) are homologous to the transcription factor CarD from Myxococcus (48) and share a domain with the transcription repair-coupling helicase (TRCF) (Fig. 4A). Since the corresponding region in TRCF interacts with the RNA polymerase holoenzyme (63), these proteins are likely to be novel transcription factors, characteristic of the spirochete clade, that modulate transcription by interacting directly with the RNA polymerase.
 
Major differences between the two spirochetes were revealed even among the sigma factors. While they share ς70 (RpoD) and ς54 (RpoN), B. burgdorferi also encodes an RpoS ortholog, whereas T. pallidum possesses ς24 (RpoE), ς28, and ς43 (SigA). The three sigma factors present in T. pallidum but not in B. burgdorferi are likely to be involved in regulating multiple gene sets specific to the former. Of particular interest in this context is ς24, whose orthologs in other bacteria regulate gene batteries associated with stress response and pathogenesis (1). Consistent with the detection of multiple sigma factors, T. pallidum encodes elements of the system of sigma factor regulators similar to that seen in Bacillus, Chlamydia, Synechocystis, and the actinomycetes. These regulators include two phosphatases of the PP2C family and an anti-sigma factor antagonist (83), which suggests that T. pallidum senses a distinct environmental signal regulating the anti-sigma factor antagonist. However, T. pallidum does not encode an ortholog of the small serine kinase of the histidine kinase class (RsbV protein), which is an essential component of the anti-sigma factor regulatory system in other bacteria (83). If this system is to be functional, it must include a kinase other than conventional histidine or serine/threonine kinases, as none of them, with the exception of CheA (which is not known to participate in this pathway), are detectable in T. pallidum.
 
Each of the spirochetes encodes several predicted specific transcriptional regulators of the helix-turn-helix (HTH) class of DNA-binding proteins. In addition, B. burgdorferi encodes a member of the MetJ/Arc family of β-sheet-containing transcription factors (BBD22) on its linear plasmid. With the exception of a single, novel family of HTH proteins, none of these likely transcriptional regulators are orthologous in the two spirochetes, which is consistent with the diversification of the possible target metabolic pathway operons (see below). The shared HTH proteins are an unusual group of two orthologous protein pairs (TP0711/BB0265 and TP0408/BB0512) that contain a C-terminal HTH domain similar to the PAIRED domains of resolvases (Fig. 4B). In addition, they have a hydrophobic N-terminal region resembling a signal peptide that may be responsible for an unexpected membrane association and processing associated with their function. Orthologs of these proteins with the same domain arrangement are detectable in H. pylori, Bacillus subtilis, and Thermatoga maritima. As an example of the diversified transcriptional regulation for similar functions, T. pallidum encodes a winged-HTH protein, TroR (34), whereas B. burgdorferi encodes the unrelated Fur protein (75), both of which are predicted to negatively regulate metal uptake. Two HTH-containing regulators of sugar metabolism, XylR-1 and XylR-2, that combine the HTH domain with the Hsp-70 like sugar-kinase domain are present only in B. burgdorferi.
 
Functional classes with low OC (<0.6) signaling. The signal transduction systems in T. pallidum and B. burgdorferi show low OC values (Fig. 2), with only a few conserved features that seem to be remnants of the signaling apparatus of the common ancestor of the spirochetes. This shared core includes components of chemotactic signaling based on the histidine kinase CheA, which contains a C-terminal CheW domain (Fig. 5), and associated downstream signaling components, such as methyl-accepting and methyltransferase chemotaxis proteins. Even within this system, however, B. burgdorferi possesses specific methylesterase, methyltransferase, and methyl-accepting proteins with no counterparts in T. pallidum (Fig. 5). Furthermore, B. burgdorferi has a larger representation of the two-component relay systems, with two additional histidine kinases other than the two CheA paralogs and multiple additional receiver domain proteins. These histidine kinases are likely to function as sensors of different stimuli, since one of them contains a PAS domain that has been implicated in redox sensing and the other one contains a large, uncharacterized extracellular (periplasmic) domain (Fig. 5). Cross-talk between these kinases and other signaling systems is suggested by the fusion of the receiver domain of the two-component system with other signaling domains, such as methylesterase and diguanylate cyclase/phosphodiesterase. Of additional interest is the presence, in both spirochetes, of CheX proteins (TP0365/BB0671) (32). These proteins are homologs of the FliM protein of E. coli, which appears to provide a link between chemotactic signaling and the flagellar motor (46).
 
The phosphoenolpyruvate:sugar phosphotransferase system (PTS) (59) is fully represented in B. burgdorferi (Fig. 5). It includes multiple EII enzymes with different sugar specificities along with other PTS proteins, such as HPR and phosphoenolpyruvate-protein-phosphotransferase. By contrast, T. pallidum encodes an unusual motley of proteins from the PTS system which includes the phosphocarrier protein Hpr and its kinase, similar to the one involved in catabolite repression in gram-positive bacteria (56), and a single protein containing an EIIA domain but not the other PTS components (Fig. 5). It is possible that these remnants of the PTS system in T. pallidum are involved in a novel signal transduction mechanism.
 
T. pallidum possesses a well-developed cyclic AMP (cAMP) signaling system that is lacking in B. burgdorferi (Fig. 5). The presence, in T. pallidum, of four cAMP-binding domain-containing proteins and a classical “eukaryote-type” adenylyl cyclase similar to those present in some other bacteria, such as cyanobacteria, myxobacteria, and actinomycetes, indicates a prominent role for this system in signal transduction. The domain architectures of these proteins suggest functional diversity—these include duplication of the cAMP-binding domain (TP0089) and fusions to an HTH DNA-binding domain (TP0262) and to an alpha-helical domain distantly related to the tetratricopeptide repeats (TPR) (TP0261) (Fig. 5). Furthermore, diguanylate cyclase/phosphodiesterase from T. pallidum contains a GAF domain that in some instances binds cyclic nucleotides (12). This protein might participate in cross-talk between cyclic nucleotide signaling and cyclic diguanylate signaling. The adenylyl cyclase of T. pallidum (TP0485) contains a HAMP (for histidine kinases, adenylyl cyclases, methyl accepting chemotaxis receptors, and phosphatases) domain, a recently described module that is associated with the cytoplasmic face of several bacterial signaling proteins (11). This domain is predicted to transmit extracellular stimuli sensed by these receptor proteins to the respective intracellular signaling domains. All bacteria that contain this eukaryotic-type cAMP-dependent signaling system lack a counterpart to the eukaryotic cyclic nucleotide phosphodiesterase and, in addition, lack the proteobacterial-type phosphodiesterase Icc (44). However, T. pallidum encodes a predicted membrane protein with six transmembrane helices that contains a metal-dependent phosphodiesterase domain of the HD superfamily, which is distantly related to eukaryotic phosphodiesterases (9). This protein is a candidate for the cAMP phosphodiesterase function. B. burgdorferi lacks classical adenylyl cyclases and cAMP-binding proteins but encodes an unrelated adenylyl cyclase (BB0723) that belongs to a recently described class of adenylyl cyclases found in thermophilic archaea and Aeromonas hydrophila (65). The function of this protein in signal transduction remains unclear in the absence of any detectable downstream effector molecules that would recognize cAMP. It cannot be ruled out that a new class of cAMP-binding domains shared by archaea, eukaryotes, and some bacteria, including B. burgdorferi, remains to be discovered.
 
Most bacteria encode the SpoT protein, which is a guanosine-3′,5′-bispyrophosphate (ppGpp) 3′-pyrophosphohydrolaseguanosine 3′,5′-bispyrophosphohydrolase (62). This key enzyme is responsible for cellular (p)ppGpp degradation, which reverses ppGpp accumulation during the stringent response to amino acid deprivation. While B. burgdorferi possesses a SpoT ortholog (BB0198) (Fig. 5), with its characteristic catalytic HD domain (9) and regulatory TGS (78) and ACT (8) domains, T. pallidum surprisingly lacks this protein. The parasitic lifestyle of T. pallidum may differ from that of Borrelia, resulting in the loss of this stringent response signaling system. Of the published genomes of bacteria, only the two chlamydial species (38, 69) and T. pallidum lack this enzyme, whereas Rickettsia prowazekii encodes a degenerate and probably inactive version of the enzyme (5). This may reflect the superfluous nature of stringent response regulation in the nutrient-rich environments of these pathogens.
 
Functional classes with low OCs (<0.6): metabolic pathways and transport and other membrane components. Consistent with the picture emerging from other pathogenic bacteria, the genomes of the two spirochetes are noticeably reduced in terms of genes coding for metabolic enzymes, which suggests a general degeneration of metabolic systems that most likely were represented in their common ancestor. However, even in this degenerate state, there are striking differences in the predicted metabolic pathways between T. pallidum and B. burgdorferi, suggesting different adaptation strategies. The common metabolic heritage is largely restricted to the trunk of the glycolytic Embden-Meyerhof pathway, the phosphorylation steps of nucleotide interconversion, and a system for membrane potential generation, namely, the multisubunit V-type ATPase. The latter is the principal energy-generating ATPase in archaea; in bacteria, the V-ATPase subunits are encoded in a single operon that appears to be evolutionarily mobile and shows a scattered distribution, being found, in addition to in the spirochetes, in Chlamydia, Enterococcus, Deinococcus, and Thermus (55).
 
As already discussed for other, more conserved pathways, even within the shared core of metabolism there are instances of likely horizontal transfer and associated xenologous and nonorthologous (E. V. Koonin et al., Letter, Trends Genet. 12:334–336, 1996) gene displacement. Apparent lateral gene transfer accompanied by displacement is illustrated by fructose-1-6-bisphosphate aldolase and the glyceraldehyde 3-phosphate dehydrogenase that belong to the central glycolytic pathway. Phylogenetic analysis of the aldolases from the two spirochetes showed that, while both of them are class II aldolases, they belong to two entirely distinct, well-supported groups, which suggests independent acquisition via lateral gene transfer from other bacteria (Fig. 3). In phylogenetic trees, glyceraldehyde 3-phosphate dehydrogenase from T. pallidum groups strongly with the orthologs of this protein from kinetoplastid eukaryotes (Fig. 3). This points to horizontal gene transfer from this eukaryotic lineage to T. pallidum after the divergence of the two spirochetes, followed by displacement of the original spirochete version. An even more interesting case is T. pallidum uridine kinase, which not only shows the unexpected grouping with the ortholog from Thermotoga in phylogenetic trees but also possesses a unique domain architecture, with two domains, including the TGS domain, apparently acquired from threonyl-tRNA synthetases (78). In the threonyl-tRNA synthetases, these domains play a role in RNA binding (61), which suggests that these unique uridine kinases could regulate their own expression by binding to mRNA. Another notable case of likely horizontal transfer followed by gene displacement involves a pair of closely linked genes in an operon, namely glucose 6-phosphate dehydrogenase (G6-PDH) and the adjacent gene that encodes the DevB protein. In T. pallidum, both of these proteins are closely related to their counterparts from Haemophilus and Actinobacillus rather than to those from B. burgdorferi. Phylogenetic analysis (Fig. 3) provides strong bootstrap support for this lineage and suggests that the entire operon comprised of G6-PDH and DevB has been exchanged between T. pallidum and the proteobacterial lineage.
 
Even among the genes encoding components of metabolic pathways that have been vertically inherited by the two spirochetes, there are footprints of likely ancient horizontal transfer events. Horizontal transfer from eukaryotes to spirochetes is attested by the presence of a pyrophosphate-dependent phosphofructokinase (BB0020, TP0542) that otherwise is characteristic of plants and several protists, such as Entamoeba and Giardia. This enzyme is present in the spirochetes along with the original bacterial ATP-dependent phosphofructokinase (BB0727, TP0108) in the glycolytic pathway, suggesting functional partitioning of the two versions.
 
Each of the spirochetes encodes two cytidylate kinases. One of these appears to have been acquired by the common ancestor of the spirochetes from the archaea. This is strongly suggested by their highly significant relationship to the archaeal proteins in phylogenetic tree analysis (Fig. 3) and the modified P-loop ATPase motif (data not shown) that is uniquely shared by these proteins with their archaeal counterparts.
 
Both spirochetes encode an aminopeptidase M containing an N-terminal insert sequence that is specifically shared with eukaryotes; phylogenetic analysis indicates that it might have been horizontally transferred into the ancestral spirochete from a eukaryote (Fig. 3).
 
Some of the drastic differences in the gene complements for metabolic processes seem to reveal adaptive features unique to each spirochete. The ability to utilize glycerol and chitin as energy sources through the glycolytic pathway, which is unique to B. burgdorferi, is consistent with the existence of an arthropod-specific stage in the life cycle of this spirochete. This is supported by the presence of genes for glycerol uptake and the FAD-dependent glycerol-3-phosphate dehydrogenase (BB0243), the latter apparently being an unusual case of horizontal transfer from a eukaryotic source (Fig. 3). Utilization of N-acetylglucosamine polymers or chitin (available in the arthropod host) as a substrate for cell wall biosynthesis (glucosamine deacetylase, NagA; BB0151) and/or as an energy source (glucosamine deaminase, NagB; BB0152) could represent an adaptation of B. burgdorferi for survival in its specific niche, in this case the arthropod host. The presence of an additional pathway for conversion of dihydroxyacetone phosphate into lactate via a methylglyoxal intermediate also could be an adaptation for growth under certain environmental conditions and carbohydrate sources (28, 74).
 
Another interesting metabolic feature of B. burgdorferi inferred from sequence analysis is the presence of a pathway for the biosynthesis of isopentenyl pyrophosphate (IPP). All of the enzymes necessary for the formation of IPP from 3-hydroxymethyl glutaryl-coenzyme A (HMG-CoA), along with a novel glycolate oxidase-like, TIM barrel fold oxidoreductase (BB0684) that could participate in the same process, are encoded in a single long operon. With the exception of this oxidoreductase, the remaining proteins of this pathway show eukaryotic or archaeal affinities in phylogenetic analysis (data not shown), with no closely related proteins in bacteria. Taken together with the fact that Pseudomonas mevalonii is the only other bacterium to date that encodes an orthologous HMG-CoA reductase (14), these observations suggest that this pathway has been acquired by B. burgdorferi via horizontal transfer from either an archaeal or a eukaryotic source. The enzymes encoded in this unusual operon are likely to participate in the synthesis of still uncharacterized membrane/lipoprotein components in B. burgdorferi.
 
The repertoires of transporters encoded by the two spirochetes are significantly different and, with an OC of 0.38, are among the most divergent functional classes revealed in our analysis; this suggests distinct substrate requirements. In this class, it is notable that, unlike B. burgdorferi, T. pallidum appears to lack a transport mechanism for proline or glycine-betaine. Given the proposed osmoprotective role of proline and glycine-betaine in bacterial stress response (4, 23), the presence of a full complement of genes for proline biosynthesis in T. pallidum likely serves as an adaptive response to osmotic stress.
 
Finally, the surface lipoproteins and other, uncharacterized membrane proteins of the two spirochetes show very low OC values (Fig. 2), which is compatible with the different modes of parasite-host interaction.
 
Individual protein families in the two spirochetes. (i) Conserved and variable families. As an alternative approach to assessing the evolutionary forces acting on the spirochetes, we analyzed all of the largest families of paralogous proteins in the two genomes and calculated the OCs for each of them (Fig. 6). Like other bacteria and archaea (39, 80), the largest protein superfamily in the spirochetes includes P-loop-containing NTPases, with 86 members in B. burgdorferi and 69 in T. pallidum. Different families within this large superfamily show substantial variability in the degree of conservation. A number of ATPases, such as those involved in DNA replication, V-type ATPases, and GTPases, show a largely vertical inheritance pattern. By contrast, the ABC transporter ATPases show considerable diversity in the two spirochetes, which is consistent with the differences noted in nutrient transport and substrate specificity (see above). There is a specific expansion of the MinD family of ATPases, which are involved in chromosome partitioning in B. burgdorferi (12 members); this is consistent with the presence of several cosegregating plasmids that comprise parts of the B. burgdorferi genome (30).
 
Compared to the P-loop ATPase superfamily, all other protein families are much smaller and show widely varying degrees of orthology (Fig. 6). Some of these families, such as the pseudouridine synthetases, the PDZ domain proteins, and lysostaphin-like proteases, show OC values close to 1, which suggests functional coherence between the two organisms. The two classes of aminoacyl-tRNA synthetases and SAM-dependent methyltransferases have slightly lower OC values, which is due to the likely horizontal transfers discussed above or to relatively minor lineage-specific gene losses. Other families, such as HD superfamily hydrolases (9), metallo-β-lactamase fold hydrolases (6), calcineurin-like phosphatases (7), and peptidyl-prolyl cis-trans isomerases, show much lower OC values, which indicates major effects of lineage-specific gene loss, horizontal transfer, and rapid diversification. These families, unlike those associated with translation and replication, appear to participate in diverse roles that are under constant selection due to variations in the niches occupied by the two spirochetes. Certain protein families, such as the P-methylase/lipoate synthetase family, are seen only in T. pallidum. This raises the possibility of distinct metabolic options that are absent in B. burgdorferi.
 
(ii) Newly identified protein families. We identified several previously undetected protein families in the spirochetes by using family-specific PSSMs (see Materials and Methods). These include some secreted (or possibly periplasmic) and membrane proteins that could be involved in pathogen-host interactions. The most interesting of these are the von Willebrand A factor (vWA) domain-containing proteins (52), which, until recently, had been detected only in eukaryotes. The vWA domain is a Mg2+-binding protein module with an α/β fold that participates in adhesion and protein-protein interactions in a wide range of eukaryotic proteins, such as integrins (26). Using profile searches, we identified three vWA domain-containing proteins in each of the spirochetes (Fig. 4C). However, the vWA proteins from B. burgdorferi are not highly similar to those from T. pallidum, suggesting that they either have been independently acquired or have diverged rapidly due to selective forces acting on extracellular proteins. These secreted or membrane-associated vWA domain proteins are reminiscent of similar domains present in the extracellular adhesion molecule (TRAP) of a eukaryotic pathogen, the malarial genus Plasmodium (73). By analogy to TRAP, it is likely that the spirochete vWA proteins are involved in adhesion of these bacteria to the extracellular matrix or to cells of the host connective tissues. These proteins could be potential targets for specific antispirochete therapies. The similarity between the spirochete vWA domains and that of the LFA-1 integrin is of interest given the recent report identifying LFA-1 as an autoantigen in treatment-resistant Lyme arthritis (33).
 
Another interesting protein of B. burgdorferi is BB0689, a secreted or periplasmic protein containing a PR1 domain (70). This domain hitherto has been detected only in eukaryotes, namely in plant pathogenesis-related proteins (PR-1) and in proteins expressed in the animal immune system such as GliPR (70). One of the human proteins in this family has been suggested to be a novel trypsin inhibitor (82), whereas other members, such as helothermine, found in the toxins of Helodermid lizards and certain snakes, act as inhibitors of potassium and calcium channels (17, 50). Another protein of this family, TPX-1, is implicated in the interaction between spermatogenic and Sertoli cells (45). All of these observations indicate that PR-1 domain-containing proteins participate in diverse extracellular protein-protein interactions, suggesting a role for BB0689 in adhesion to host extracellular proteins and, accordingly, in pathogenesis.
 
Conversely, T. pallidum encodes an unusual, large, secreted (periplasmic) protein (TP0544) that contains an OB-fold domain (47). This protein might interact with host cells and act as a virulence factor like the OB-fold-containing toxins from a wide range of bacteria (25).
 
Both spirochetes encode proteins (BB0236 and TP0421) containing a modified version of the YWTD domain (67) that is seen in intracellular animal proteins, some of which also contain the RING finger domain (L. Aravind, unpublished data). This relationship to a class of animal proteins suggests lateral transfer from an animal host into the ancestor of the two spirochetes. YWTD domains assume a β-propeller structure similar, for example, to that in low-density lipoprotein receptors and in proteins from other parasites (e.g., Trypanosoma cruzi) that mediate extracellular adhesion (51). The presence of a predicted signal peptide suggests that, like the vWA and PR-1 domain-containing proteins, the spirochete YWTD domain proteins are secreted and interact with host cell surface molecules (52).
 
Another interesting family that is conserved between the two spirochetes, some of whose members appear to be secreted, are the tetratricopeptide repeat (TPR) domain-containing proteins (24). These domains form an alpha-helical superstructure and mediate protein-protein interactions. The use of TPR motifs in extracellular interactions might be a novel strategy of host interaction employed by the spirochetes and is reminiscent of a family of secreted Sel-1 repeat proteins in Helicobacter pylori (52; L. Aravind, unpublished data).
 
To add to this repertoire of previously undetected proteins that could be important for the pathogen's interaction with host cell surfaces, T. pallidum encodes two proteins with multiple ankyrin repeat motifs (TP0502, TP0835) (Fig. 5). At least TP0835, which contains 20 ankyrin repeats, has a canonical signal peptide, indicating that, unlike the eukaryotic ankyrin repeat proteins, this Treponema protein is secreted.
 
Evolutionary implications of comparative analysis of the two spirochete proteomes. The use of the OC concept, along with a case-by-case analysis of individual protein sequences, has provided considerable information that allows us to address several evolutionary issues: (i) the amount of shared heritage present in the spirochete genomes, (ii) the likely gene repertoire and lifestyle of the common ancestor, (iii) the role of horizontal transfer, and (iv) the strategies and adaptations used by these organisms in their interaction with the host, which are important for pathogenesis.
 
Likely orthologs comprise about 43% of the total number of proteins encoded by the two spirochetes (39.5% [495 of 1,256] of the B. burgdorferi proteins and 47% [486 of 1,031] of the T. pallidum proteins). This fairly low fraction of orthologs indicates that lineage-specific gene loss, horizontal gene transfer, and rapid divergence account for more than one-half of the gene repertoires of the two spirochetes. The relatively lower fraction of orthologs in Borrelia is to a large extent due to the fact that multiple plasmids harbored by this spirochete encode a number of highly variable proteins without counterparts in Treponema (30). Genome comparisons between two more closely related bacteria, namely H. influenzae and E. coli, have indicated that lineage-specific gene loss was a major force in the evolution of the parasitic organism, in this case H. influenzae (72). Given that both spirochetes are obligate parasites, it is likely that the two lineages have lost genes largely independently, resulting in major differences in the complement of genes eventually retained. However, the number of genes lost by the spirochetes is lower than that seen in some other obligate parasites, such as the mycoplasmas, chlamydiae, and rickettsiae (5, 69, 79).
 
The OC values for different functional classes of proteins (Fig. 2) illustrate the spectrum of genes that have retained identical or similar functions and were probably present in the common ancestor of the spirochetes. As expected, certain core functions, such as translation, RNA modification, and replication, are hardly affected by gene loss. By contrast, the DNA repair systems and the transcription systems show major differences, probably due to a combination of lineage-specific loss and horizontal gene transfer driven by different selective forces acting on the two organisms. The core of the glycolytic pathway and associated metabolic steps show a predominantly vertical inheritance. These systems with high OC values are very similar to their counterparts in other bacteria, which suggests a typical bacterial core physiology of the common ancestor. The presence of V-type ATPase operons in both spirochetes indicates that, like Thermus and Enterococcus (55), the common ancestor of the spirochetes used H+/Na+ exchange for ion gradient generation. The signal transduction systems in general show low OC values, but the elements involved in chemotactic response are conserved. Together with the conservation of the flagellar apparatus (Fig. 2), this suggests an actively motile chemoresponsive ancestral spirochete that used a mode of locomotion similar to that of the two extant species.
 
Even within the conserved systems, there are some striking cases of xenologous and nonorthologous gene displacement that are suggestive of horizontal transfer from distantly related bacteria and archaea. Some of these appear to have occurred in the common ancestor of the spirochetes, whereas others are lineage specific. Examples of apparent ancient gene transfers include the acquisition of certain aminoacyl-tRNA synthetases and cytidylate kinase from archaea. Likely xenologous displacements in one of the spirochete lineages were seen in a number of cases, such as fructose-1-6-bisphosphate aldolase, glyceraldehyde 3-phosphate dehydrogenase, glucose 6-phosphate dehydrogenase subunits, 6-phosphogluconate dehydrogenase, and topoisomerase I (Fig. 3). Other examples of likely gene exchange with distant bacteria include the small, primase-like TOPRIM domain protein (10), which is otherwise seen only in low-GC gram-positive bacteria and in archaea, and the unusual HTH proteins shared with Bacillus, Thermotoga, and Helicobacter. These observations suggest that, unlike the extant forms that lead a relatively isolated existence due to their specialized life cycles, the ancestors of B. burgdorferi and T. pallidum, both before and after their divergence from each other, existed in close proximity with other prokaryotes, which favored gene exchange.
 
There is considerable evidence of likely acquisition of genes from eukaryotic, and possibly animal, sources by the common ancestor of the spirochetes; on most occasions, such gene acquisitions apparently have been accompanied by displacement of the endogenous bacterial versions. Several of the aminoacyl-tRNA synthetases exemplify this phenomenon (78). Other striking cases include the YWTD domain proteins and the secreted vWA domain proteins, which until now appeared to be specific to animals, as well as predicted secreted proteins containing TPR repeats. Thus, it appears that the common ancestor of Treponema and Borrelia was already in contact with animal hosts. However, the evidence of gene exchange with other bacteria, archaea, and perhaps eukaryotic protists (see above) suggests that they were not specialized obligate parasites isolated from the rest of the microbial community. The lifestyle predicted for the common ancestor of B. burgdorferi and T. pallidum is consistent with that of the spirochetes in the microbial community in invertebrate guts (21, 41). These spirochetes are not only in contact with an animal host but also share the niche with other bacteria, methanogenic archaea, and eukaryotic protists. The alternative hypothesis, that the common ancestor of Treponema and Borrelia was a free-living spirochete and that the bacteria of these two lineages have independently established symbiosis with the eukaryotic host, cannot be ruled out but seems to be less strongly supported by the evidence. Indeed, many of the likely cases of horizontal gene transfer from eukaryotes are shared by the two spirochetes, which strongly suggests that their ancestor was already in contact with a eukaryotic host.
 
Subsequent to the divergence from its common ancestor, each lineage independently acquired the ability to infect vertebrate hosts. This is indicated by the presence of very different variant antigens in the two genera, a feature that might have enabled these organisms to evade the acquired immunity of the vertebrate hosts. The possibility that Borrelia has moved from arthropod parasitism to vertebrate parasitism is suggested by the presence of specific carbohydrate metabolism genes that provide for the utilization of arthropod chitin by this bacterium. The presence of commensal treponemes in vertebrates (21) suggests that the ancestors of T. pallidum were well adapted for life in a vertebrate host before the final step in the evolution of pathogenicity that might have been accompanied by the acquisition of specific variant antigens to evade the host immune system. T. pallidum lacks many of the carbohydrate metabolism genes and a functional PTS system; these systems might have been lost subsequent to its displacement from the carbohydrate-rich niches occupied by the ancestral treponeme, such as the vertebrate oral cavity.
 
Conclusions. By means of local sequence similarity searches, profile searches, and analysis of individual domains and protein families, we have conducted a detailed comparative analysis of the genomes of the spirochetes B. burgdorferi and T. pallidum. The level of conservation between functional classes and paralogous families of proteins was measured using the orthology coefficient. Using this measure, it was possible to characterize, in functional terms, the nature of the divergence between the two spirochetes and the common and distinct aspects of their physiological strategies. Protein profile searches resulted in the identification of hitherto undetected components of the signal transduction machinery and novel proteins containing domains previously seen only in eukaryotes. Secreted proteins containing these domains might mediate interactions between the spirochetes and host cells or the extracellular matrix. It appears possible to tentatively reconstruct the evolutionary steps leading from a common ancestor that might have been an invertebrate gut symbiont to the divergence of the two genera of spirochetes and adaptation to their specific niches.
 
Availability of complete results. The list of T. pallidum and B. burgdorferi orthologs classified by functional categories and by protein families is available by anonymous ftp at ftp://ncbi.nlm.nih.gov/pub/Koonin/Spirochetes.
Top
Abstract
MATERIALS AND METHODS
RESULTS AND DISCUSSION
 REFERENCES
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#1731 De: "juanca" <juancaqd@...>
Fecha: Lun, 25 de Abr, 2005 9:43 pm
Asunto: methods related to Borrelia burgdorferi toxin and antitoxin preparations
juancaqd
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United States Patent 6667038
Prevention, diagnosis and treatment of lyme disease
Issued on December 23, 2003
Abstract
 
 
The present invention provides compositions and methods related to Borrelia burgdorferi toxin and antitoxin preparations. In particular, the present invention provides methods and compositions for the diagnosis of Lyme disease, as well as for use in treating subjects infected with B. burgdorferi through passive immunization, and vaccine development.
...............
................
................
 
  
Inventor(s)
Sam T. Donta
Mark J. Cartwright
Assignee
Boston Medical Center Corp.
Application
 
No. 553863 filed on 2000-04-20
Current US Class
 
424/190.1, 424/184.1, 424/234.1, 424/236.1, 424/262.1, 424/9.2, 530/300, 530/350, 536/23.1, 536/23.7
Field of Search
 
424/184.1, 424/185.1, 424/190.1, 424/234.1, 424/236.1, 424/262.1, 424/9.2, 530/300, 530/350, 536/23.1, 536/23.7
Examiners
Primary: Rodney P Swartz
US Patent References
5530103
 
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#1730 De: "juanca" <juancaqd@...>
Fecha: Lun, 25 de Abr, 2005 7:01 pm
Asunto: Lyme Endotoxins & Biotoxins, rol de las toxians en lyme, artículos medline
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Al final se encuentran referencias a artículos de medline sobre borrelia,
toxinas y el rol que juegan en el desarrollo de la enfermedad.
 
 
James L. Schaller, MD, MAR, PA, DABPN, DABFM
 
Clinical and Research Psychiatry and Medicine
Adult Psychiatry and Psychotherapy Services
Subspecialty Child & Adolescent Psychiatry
Hormonal & Nutraceutical Consultation
 

www.personalconsult.com
Lyme Endotoxins & Biotoxins
 
Some physician's feel that Lyme is like a donut covered in powder, but the powder is a biotoxin or "endotoxin." And some patients are very poor at removing these toxins. These biotoxins mess up hormones, mess up your weight, weaken you ability to fight infections and cancer, lower your natural pain killing endorphins, undermine sleep and thinking. These are just a few examples. The bottom line is that biotoxins can leave you very ill and in an unknown percentage can kill.
 
Sincere physicians treat many patients with antibiotics, and yet this releases biotoxins and endotoxins from the Lyme, and these are biologically active chemicals that effect genes and commonly increase weight, increase mood trouble, and increase inflammation and forty other problems.
 
My opinion is that it is a proven fact that Lyme has endotoxins in the small abstracts below. But what is an endotoxin?
 
Simply, they are substances on the outside of the lyme bug, in its outer shell, which is typically released when the lyme bug is disrupted or destroyed. Endotoxins are very active molecules that cause severe allergic reactions, fever and influence your immune system significantly. Some endotoxins are so strong they cause you to lose your blood pressure and die from the loss of blood to vital organs, or from severe diarrhea if the endotoxin is in the intestines. Obviously, Lyme's endotoxins do not act this particular way.
 
Endotoxins are a made of two parts: a fat or lipid bound to a polysaccharide chain in the lyme bug's outer shell. Endotoxins are like other biotoxins in that their goal is to help the bug survive. Some endotoxins are released in the body to make it safe for new lyme bugs, or when attacked by your immune system attack cells. The full actions and types of Lyme's biotoxins and endotoxins is unknown.
 
Biotoxins exist in many types of creatures: tetanus, botulinum (botox), spiders, algae, ascaridin (gut parasites), staph, strept, babasia, lyme, special fish, clamydia, tuberculosis, fungus or molds and viruses. Biotoxins are proposed to be tiny molecules used to survive by effecting the host´s body in many ways that helps the infecting agent survive.
 
Labs that must be checked in all Lyme patients are:
Leptin (LabCorp test code 146712)
Alpha MSH or Melanocyte Stimulating Hormone (LabCorp test code 010421)
Biotoxin Processing Genes: HLA DRB, DBQ Disease Evaluation (LabCorp test code 012542)
 
The last lab listed, or the HLA lab has been found to provide some specific genetic abilities to removal Lyme toxins. Our new Mold Warrior book has the table that shows which people have trouble removing Lyme biotoxins -- so they just float around the body forever messing up DNA and the body.
 
MSH is a massively critical hormone that will be a hot new treatment in future years and help with acne, obesity, addiction, sleep, fatigue, etc. If your MSH is low you clearly have massive toxins or inflammation that is at a dangerous level. You will need treatment with someone with is up on this 2006 medicine.
 
Leptin helps you see if the biotoxins have messed with the fat cells. It is a sign common in Lyme biotoxins and massive inflammation. (Reading it is complex.).
 
Studies on clearly positive Lyme patients show a simple biotoxin binder that NEVER leaves the intestines improves the patient's health and they do better in brain tests that measure biotoxin disease. Most initially get much sicker as the fat-loving biotoxin is pulled out into the blood stream and inflames the body, but over many weeks or months they clearly improve -- with no antibiotic. Most have had extensive lyme killing antibiotics already. Of course, the biotoxin binder needs to be used at high doses or it is a false trial -- like licking an aspirin and expecting arthritis relief.
 
Of course, their improvement assumes they are not living in a home with toxic mold all over the walls, or hidden behind a wall. This has actually happened when someone is not getting better. I ask about the possibility of indoor mold and they say, "Oh, we killed all that stuff under our floors last year with some bleach and changing a few boards." I just shake my head. They sincerely do not understand that some indoor mold chemicals are biowarfare agents -- we are not talking about the 100,000 to 200,000 safe forms outside. They were not getting better and we found toxic mold species at work or home.
 
According to Internist and author, Dr. James Howenstine, Lyme disease "requently exhibits neurologic abnormalities because the Lyme neurotoxins are drawn to the fatty tissue found in the brain and peripheral nerves. As a consequence sudden deafness, Bells palsy, Parkinson's Disease, Multiple Sclerosis, reflex sympathetic dystrophy, peripheral neuritis, and chronic pain may appear."
ARTICLE ABSTRACTS POINTING TO
POSSIBLE ACTIVE PROTEINS OR
TOXINS COMING FROM LYME
 
All bolding italics are from me
 
23: Zentralbl Bakteriol Mikrobiol Hyg [A]. 1986 Dec;263(1-2):137-41.
 
Borrelia burgdorferi lipopolysaccharide and its role in the pathogenesis of Lyme disease.
 
Habicht GS, Beck G, Benach JL, Coleman JL.
 
Lipopolysaccharides (LPS) are a constitutive part of the outer wall of gram negative bacteria. Because many of the symptoms of Lyme disease could be explained by a spirochetal LPS we have subjected Borrelia burgdorferi to standard LPS extraction techniques which yielded a LPS which accounted for 1.5-4% of the dry weight. The LPS was very similar to classical gram negative bacterial LPS both chemically and in its biological activities which included pyrogenicity, mitogenicity for lymphocytes and the induction of Interleukin 1 production by macrophages. In addition, the LPS produced an acute inflammatory reaction when injected intradermally into rabbit skin. It could also prepare a skin site for the production of the local Shwartzman reaction. These results show that the Lyme disease spirochete contains a hitherto unknown LPS that is biologically active in vitro and in vivo. It is likely that this molecule plays an important role in the pathogenesis of Lyme disease.
 
PMID: 3577475 [PubMed - indexed for MEDLINE]
 
41: J Infect Dis. 1985 Jul;152(1):108-17.
 
Chemical and biologic characterization of a lipopolysaccharide extracted from the Lyme disease spirochete (Borrelia burgdorferi).
 
Beck G, Habicht GS, Benach JL, Coleman JL.
 
A lipopolysaccharide (LPS) was isolated from the Lyme disease spirochete by a modification of the hot phenol-water method. The material was composed of 45% carbohydrate, 8% protein, 44% lipid A, and 1% 3-deoxy-D-mannooctulosonic acid and accounted for approximately 1.5% of the cellular dry weight. The isolated LPS possessed several biologic activities characteristic of endotoxins. The LPS was pyrogenic for rabbits, mitogenic for human mononuclear cells and murine splenocytes, capable of clotting limulus lysate, and cytotoxic for murine macrophages. LPS extracted from Borrelia burgdorferi by the petroleum-ether:chloroform:liquid-phenol procedure was also characterized. The results show that the Lyme disease spirochete contains a hitherto unknown LPS that is biologically active in vitro, and the expression of such activities in vivo may play an important role in the pathogenesis of Lyme disease. Some of the clinical manifestations of other spirochetal disease may be explained by similar endotoxins in those organisms. To our knowledge this is the first report of an LPS extracted from a spirochete that is known to be a human pathogen.
 
PMID: 4008983 [PubMed - indexed for MEDLINE]
 
22: Zentralbl Bakteriol Mikrobiol Hyg [A]. 1986 Dec;263(1-2):142-5.
 
Endotoxin-like activity associated with Lyme disease Borrelia.
 
Fumarola D, Munno I, Marcuccio C, Miragliotta G.
 
The newly recognized spirochete, Borrelia burgdorferi, the causative agent of Lyme Disease, has been examined for endotoxin-like activities as measured by the standard Farmacopea Ufficiale della Republica Italiana rabbit fever test and the Limulus amoebocyte lysate assay. The suspension of heat-killed microorganism caused a febrile response at a dose of 1 X 10(8) bacteria pro kilo. Similar results were obtained in the Limulus assay where the heat-killed spirochetes stimulated formation of solid clot until the concentration of 1 X 10(5) per ml. Both in pyrogen test and in Limulus assay heat-killed Escherichia coli exhibited a higher degree of potency. These results show that LD-Borrelia possess endotoxin-like activities which could help in understanding the pathogenesis of the clinical symptomatology of the disease.
 
PMID: 3577476 [PubMed - indexed for MEDLINE]
 
Immunology. 2004 Nov;113(3):401-8.
 
Characterization of the B-cell inhibitory protein factor in Ixodes ricinus tick saliva: a potential role in enhanced Borrelia burgdoferi transmission.
 
Hannier S, Liversidge J, Sternberg JM, Bowman AS.
 
School of Biological Science, Zoology, University of Aberdeen, UK.
 
We recently described the inhibition of host B lymphocytes by Ixodes ricinus tick saliva. In this study, we characterized the factor responsible for this activity and examined the modulation of lipopolysaccharide (LPS)- and Borrelia burgdorferi outer surface protein (Osp)-induced proliferation of naive murine B lymphocytes by an enriched fraction of this factor. The B-lymphocyte inhibitory activity was destroyed by trypsin treatment, indicating that a proteinaceous factor was responsible for this activity. The removal of glutathione-S-transferase (GST) from tick salivary glands extracts (SGE) showed that this B-cell inhibitory protein (BIP) was not a GST. Gel filtration liquid chromatography indicated that BIP has a native molecular weight of approximately 18,000. An enrichment protocol, using a combination of anion-exchange and reverse-phase liquid chromatography, was established. BIP-enriched fractions did not suppress T-cell proliferation. Delayed addition of BIP-enriched fractions, up to 7 hr after LPS addition, inhibited the proliferation of isolated B cells. BIP-enriched fractions dramatically inhibited both OspA- and OspC-induced proliferation of isolated B cells. These results strongly suggest that BIP may facilitate B. burgdorferi transmission by preventing B-cell activation, and also highlights the potential of BIP as a therapeutic agent in B-cell maladies.
 
PMID: 15500628 [PubMed - indexed for MEDLINE]
 
2: Arthritis Rheum. 2004 Jul;50(7):2360-9.
 
Outer surface lipoproteins of Borrelia burgdorferi vary in their ability to induce experimental joint injury.
 
Batsford S, Dunn J, Mihatsch M.
 
Albert Ludwigs University, Freiburg, Germany. bats@...
 
To examine the ability of bacterial lipoproteins from the spirochete Borrelia burgdorferi to cause in vivo tissue injury (arthritis). METHODS: Outer surface proteins (OSPs) from B burgdorferi were used in a rat model of antigen-induced allergic arthritis. Intraarticular challenge with recombinant OspA, OspB, and OspC in nonlipidated (peptide) and lipidated forms was performed in the left knee joint; the contralateral joint received buffer as control. Inflammation was monitored by technetium scintigraphy and histology. RESULTS: Nonlipidated (peptide) OspA, OspB, and OspC did not induce arthritis; the only exception was polymerized OspA, which was tested in preimmunized rats. Lipidated OspA from 2 different strains and lipidated OspC induced severe arthritis, whereas lipidated OspB failed to induce injury. A synthetic analog of the OSP lipid modification, lipopeptide Pam(3)Cys-Ser-Lys(4)-OH, either alone or coupled to bovine serum albumin, also failed to induce injury. Injury did not develop in control groups that were given the appropriate buffers or lipopolysaccharide. This showed that lipidated borrelial OSPs can be potent arthritogens but vary greatly with respect to their injury-inducing potential. The possession of a lipid modification is essential but is not sufficient to render an OSP arthritogenic. CONCLUSION: This is the first study to demonstrate that individual lipoproteins from B burgdorferi can induce experimental joint injury in vivo. These results may help elucidate the pathogenesis of Lyme arthritis and, above all, underline the importance of bacterial lipoproteins as major virulence factors.
 
PMID: 15248237 [PubMed - indexed for MEDLINE]
 
12: J Immunol. 2001 Jan 1;166(1):473-80.
 
Borrelia burgdorferi and other bacterial products induce expression and release of the urokinase receptor (CD87).
 
Coleman JL, Gebbia JA, Benach JL.
 
State of New York Department of Health, State University of New York, Stony Brook, NY 11794-5120, USA. jcoleman@...
 
The urokinase-type plasminogen activator receptor (uPAR, CD87) is a highly glycosylated 55- to 60-kDa protein anchored to the cell membrane through a glycosylphosphatidylinositol moiety that promotes the acquisition of plasmin on the surface of cells and subsequent cell movement and migration by binding urokinase-type plasminogen activator. uPAR also occurs in a soluble form in body fluids and tumor extracts, and both membrane and soluble uPAR are overexpressed in patients with tumors. uPAR may be a factor in inflammatory disorders as well. We investigated whether Borrelia burgdorferi could stimulate up-regulation of cell membrane uPAR in vitro. B. burgdorferi, purified native outer surface protein A, and a synthetic outer surface protein A hexalipopeptide stimulated human monocytes to up-regulate membrane uPAR as measured by immunofluorescence/FACS and Western blot. The presence of soluble uPAR in culture supernatants, measured by Ag capture ELISA, was also observed. LPS from Salmonella typhimurium and lipotechoic acid from Streptococcus pyogenes also induced the up-regulation of both membrane and soluble uPAR protein by monocytes. Up-regulation of uPAR was induced by conditioned medium from B. burgdorferi/monocyte cocultures. The up-regulation of uPAR by B. burgdorferi was concomitant with an increase in uPAR mRNA, indicating that synthesis was de novo. The expression and release of uPAR in response to B. burgdorferi and other bacterial components suggests a role in the pathogenesis of Lyme disease as well as in other bacterial infections.
 
PMID: 11123326 [PubMed - indexed for MEDLINE]
 
13: Infect Immun. 2000 Dec;68(12):6663-9.
 
Interleukin-10 modulates proinflammatory cytokines in the human monocytic cell line THP-1 stimulated with Borrelia burgdorferi lipoproteins.
 
Murthy PK, Dennis VA, Lasater BL, Philipp MT.
 
Department of Parasitology, Tulane Regional Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana 70433, USA.
 
We determined previously that lipoproteins of Borrelia burgdorferi stimulate inflammatory and anti-inflammatory cytokines (interleukin-10 [IL-10]) in monocytes. IL-10 could have an effect on innate and acquired immune responses to B. burgdorferi and influence the magnitude of the infectious inoculum and disease outcome. To understand the mechanism(s) of IL-10 action during early infection, when innate immunity expressed chiefly by skin macrophages is key, we investigated the effect of exogenous and endogenous IL-10 on the production of the macrophage-derived cytokines IL-6, IL-1beta, IL-12, and tumor necrosis factor alpha (TNF-alpha). We used the THP-1 human monocytic cell line and recombinant lipidated OspA (L-OspA) as the model target cell and stimulant, respectively. To determine the kinetics of cytokine production by THP-1 cells, we stimulated them with L-OspA and also with heat-killed B. burgdorferi cells (HBb) and lipopolysaccharide (LPS). Exogenous IL-10 dampened production of inflammatory cytokines, as elicited by lipoproteins. The inhibition of endogenous IL-10 function by anti-IL-10 antibody reduced the production of IL-12 and IL-6 but not that of IL-1beta and TNF-alpha. An inspection of the kinetics of cytokine production clarified this finding. TNF-alpha was produced prior to, and IL-beta was produced at the same time as, IL-10, whereas IL-6 and IL-12 were produced later. HBb, LPS, and L-OspA yielded similar kinetics of cytokine production. This result reinforces the notion that lipoproteins are the functional molecules in HBb and perhaps in vivo. It indicates also that signaling pathways utilized by LPS and lipoproteins may be extensively shared. The results are consistent with a major role played by IL-10 in controlling the initial phase of infection with this spirochete.
 
PMID: 11083779 [PubMed - indexed for MEDLINE]
 
15: J Immunol. 1999 Sep 1;163(5):2382-6.
 
Cutting edge: inflammatory signaling by Borrelia burgdorferi lipoproteins is mediated by toll-like receptor 2.
 
Hirschfeld M, Kirschning CJ, Schwandner R, Wesche H, Weis JH, Wooten RM, Weis JJ.
 
Department of Pathology, University of Utah School of Medicine, Salt Lake City 84132, USA.
 
The agent of Lyme disease, Borrelia burgdorferi, produces membrane lipoproteins possessing potent inflammatory properties linked to disease pathology. The recent association of toll-like receptors (TLR) 2 and 4 with LPS responses prompted the examination of TLR involvement in lipoprotein signaling. The ability of human cell lines to respond to lipoproteins was correlated with the expression of TLR2. Transfection of TLR2 into cell lines conferred responsiveness to lipoproteins, lipopeptides, and sonicated B. burgdorferi, as measured by nuclear translocation of NF-kappaB and cytokine production. The physiological importance of this interaction was demonstrated by the 10-fold greater sensitivity of TLR2-transfected cells to lipoproteins than LPS. Futhermore, TLR2-dependent signaling by lipoproteins was facilitated by CD14. These data indicate that TLR2 facilitates the inflammatory events associated with Lyme arthritis. In addition, the widespread expression of lipoproteins by other bacterial species suggests that this interaction may have broad implications in microbial inflammation and pathogenesis.
 
PMID: 10452971 [PubMed - indexed for MEDLINE]
 
16: Infect Immun. 1999 Jan;67(1):140-7.
 
Induction of pro- and anti-inflammatory cytokines by Borrelia burgdorferi lipoproteins in monocytes is mediated by CD14.
 
Giambartolomei GH, Dennis VA, Lasater BL, Philipp MT.
 
Department of Parasitology, Tulane Regional Primate Research Center, Tulane University Medical Center, Covington, Louisiana 70433, USA.
 
We previously showed that heat-killed Borrelia burgdorferi spirochetes and lipidated outer surface protein A (L-OspA) stimulated the in vitro production of interleukin-10 (IL-10) in peripheral blood mononuclear cells (PBMC) from uninfected humans and rhesus monkeys (G. Giambartolomei et al., Infect. Immun. 66:2691-2697, 1998). Here we demonstrate that uninfected human peripheral blood monocytes, but not B or T cells, are the cells that transcribe the IL-10 cytokine gene in response to heat-killed B. burgdorferi. B. burgdorferi similarly induced an upregulation of the IL-1beta and IL-6 cytokine genes in monocytes and the production of IL-10 and IL-6 in culture supernatants of the human monocytic cell line THP-1. Purified L-OspA (but not unlipidated OspA [U-OspA] or U-OspC) also stimulated the production of both cytokines in THP-1 cells in a dose-dependent fashion, suggesting that acylation of the OspA protein molecule is required for the production of both anti- and pro-inflammatory cytokines in naive monocytes. A lipohexapeptide that contained the tripalmitoyl-modified cysteine motif (Pam3Cys-Hex) of B. burgdorferi lipoproteins but with an arbitrary peptide sequence had the same effect. Monoclonal antibodies (MAbs) MY4 and 60bca, both of which bind to CD14 and are known to block lipopolysaccharide (LPS)-mediated cytokine production, were able to block L-OspA-mediated IL-10 and IL-6 cytokine production. In contrast, MAb 26ic, which also binds to CD14 but does not block LPS function, failed to inhibit L-OspA-mediated cytokine production. These data suggest that activation of monocytes and production of both anti- and pro-inflammatory cytokines induced by lipoproteins proceeds via the CD14 receptor. LPS binding protein was not required for OspA-induced cytokine production. Our results demonstrate that pro- and anti-inflammatory cytokines induced by B. burgdorferi lipoproteins in PBMC are produced by monocytes and that lipoprotein and LPS signaling pathways share at least the initial signaling event that involves the CD14 receptor.
 
PMID: 9864208 [PubMed - indexed for MEDLINE]
 
6: Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7913-8. Epub 2003 Jun 10.
 
A newly discovered cholesteryl galactoside from Borrelia burgdorferi.
 
Ben-Menachem G, Kubler-Kielb J, Coxon B, Yergey A, Schneerson R.
 
Laboratory of Developmental and Molecular Immunity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. gilben@...
 
Two major glycolipids, which comprise approximately 36% of the total lipid mass from Borrelia burgdorferi, the etiological agent of Lyme disease, were investigated. We determined the fatty acid type, sugar identity, anomeric configuration, and substituent type and position. The structures were identified as cholesteryl 6-O-acyl-beta-d-galactopyranoside (B. burgdorferi glycolipid 1, BbGL-I), and 1,2-di-O-acyl-3-O-alpha-d-galactopyranosyl-sn-glycerol (BbGL-II). The major fatty acids were palmitate and oleate. The structures were corroborated by gas-liquid chromatography MS, matrix-assisted laser desorption/ionization time-of-flight spectroscopy, fast atom bombardment MS, detailed NMR spectrometry, and metabolic labeling. This is a previously undescribed demonstration of a cholesteryl galactoside in bacteria. Lipopolysaccharide was not detected in B. burgdorferi. The two glycolipids have several properties suggesting they may function as lipopolysaccharide: both are main components of the bacterial membrane, surface exposed, and have a three-domain structure. BbGL-I elicited specific antibodies in mice and rabbits, and BbGL-II elicited antibodies that reacted with both glycolipids.
 
PMID: 12799465 [PubMed - indexed for MEDLINE]
 
18: J Immunol. 1998 Jun 1;160(11):5485-92.
 
The role of CD14 in signaling mediated by outer membrane lipoproteins of Borrelia burgdorferi.
 
Wooten RM, Morrison TB, Weis JH, Wright SD, Thieringer R, Weis JJ.
 
Department of Pathology, University of Utah School of Medicine, Salt Lake City 84132, USA.
 
Borrelia burgdorferi possesses membrane lipoproteins that exhibit stimulatory properties and, consequently, have been implicated in the pathology related to Lyme disease. As CD14 has been shown to mediate signaling by a number of lipid-modified bacterial products, the involvement of CD14 in signaling mediated by two B. burgdorferi lipoproteins, outer surface protein A (OspA) and OspC, was determined. Lipoprotein-mediated induction of nuclear factor-kappaB nuclear translocation and production of IL-8 and IL-6 in HUVEC was enhanced in the presence of serum or soluble rCD14. CD14-specific Abs that block LPS-mediated signaling also inhibited lipoprotein-dependent signaling in HUVEC and neutrophils. The formation of stable complexes between OspA and CD14 was demonstrated by native gel electrophoresis. LPS was found to compete with OspA for binding with CD14, suggesting that LPS and OspA bind similar regions on CD14. The similarity in binding was further supported by the finding that a mutant soluble CD14, lacking the LPS binding site, did not facilitate lipoprotein signaling, nor did it form a complex with OspA. Binding of OspA to CD14 was dependent on the lipid modification, as unlipidated OspA did not form a complex with CD14 or stimulate cells. In contrast, the lipopeptide remaining after proteinase K digestion both formed a complex with CD14 and retained stimulatory properties. These findings indicate that CD14 facilitates bacterial lipoprotein signaling in mammalian cells.
 
PMID: 9605151 [PubMed - indexed for MEDLINE]
 
39: Clin Sci. 1972 Sep;43(3):343-54.
 
Studies of the mechanism of the Jarisch-Herxheimer reaction in louse-borne relapsing fever: evidence for the presence of circulating Borrelia endotoxin.
 
Bryceson AD, Cooper KE, Warrell DA, Perine PL, Parry EH.
 
PMID: 5077513 [PubMed - indexed for MEDLINE]
 
21: J Immunol. 1997 May 15;158(10):4838-45.
 
Borrelia burgdorferi outer surface protein A (OspA) activates and primes human neutrophils.
 
Morrison TB, Weis JH, Weis JJ.
 
Department of Pathology, University of Utah Health Sciences Center, Salt Lake City 84132, USA.
 
Lyme disease is caused by infection with the spirochete Borrelia burgdorferi and is characterized by bacterial persistence and inflammation of many host tissues. B. burgdorferi express outer surface lipoproteins, including OspA, with inflammatory properties that could contribute to the localized tissue inflammation. Neutrophils are the predominant infiltrate into the inflamed arthritic joints, and are crucial for controlling the spirochete infection. They may also contribute to the joint pathology associated with Lyme arthritis. This study examines the effect of OspA on the activities of the neutrophil. Picomolar concentrations of OspA induce surface markers associated with neutrophil activation: increased CD10 and CD11b expression; decreased CD62-L expression; and an increased adherence to extracellular matrix. These events were similar in kinetics and magnitude to those induced by the strong activators LPS and FMLP. Like LPS, OspA could prime neutrophils for FMLP-induced release of lysosomal granules and production of superoxide. Thus, models of Lyme arthritis should include the possible contribution of direct activation of neutrophils to both defense and disease.
 
PMID: 9144499 [PubMed - indexed for MEDLINE]
 
23: Infect Immun. 1996 Sep;64(9):3845-52.
 
Activation of human monocytic cells by Treponema pallidum and Borrelia burgdorferi lipoproteins and synthetic lipopeptides proceeds via a pathway distinct from that of lipopolysaccharide but involves the transcriptional activator NF-kappa B.
 
Norgard MV, Arndt LL, Akins DR, Curetty LL, Harrich DA, Radolf JD.
 
Department of Microbiology, University of Texas Southwestern Medical Center, Dallas 75235, USA.
 
There is increasing evidence that lipoproteins of Treponema pallidum and Borrelia burgdorferi are key inflammatory mediators during syphilis and Lyme disease. A principal objective of the present study was to identify more precisely similarities and divergences among lipopolysaccharide (LPS)- and lipoprotein-lipopeptide-induced immune cell signaling events. Like LPS, purified native B. burgdorferi OspA and synthetic analogs of OspA, OspB, and two T. pallidum lipoproteins (Tpp47 and Tpp17) all induced NF-kappa B translocation in THP-1 human monocytoid cells. Acylation of OspA and the synthetic peptides was requisite for cell activation. Polymyxin B abrogated only the response to LPS. By using 70Z/3-derived pre-B-cell lines either lacking or expressing human CD14 (the LPS receptor), it was observed that expression of human CD14 imparted responsiveness to LPS but not to OspA or spirochetal lipopeptides (assessed by induction of NF-kappa B and expression of surface immunoglobulin M). Finally, the biological relevance of the observation that T. pallidum lipoproteins-lipopeptides induce both NF-kappa B and cytokine production in monocytes was supported by the ability of the synthetic analogs to promote human immunodeficiency virus replication in chronically infected U1 monocytoid cells; these observations also suggest a potential mechanism whereby a syphilitic chancre can serve as a cofactor for human immunodeficiency virus transmission. The combined data lend additional support to the proposal that spirochetal lipoproteins and LPS initiate monocyte activation via different cell surface events but that the signaling pathways ultimately converge to produce qualitatively similar cellular responses.
 
PMID: 8751937 [PubMed - indexed for MEDLINE]
 
25: Immunology. 1994 Jul;82(3):389-96.
 
A 14,000 MW lipoprotein and a glycolipid-like structure of Borrelia burgdorferi induce proliferation and immunoglobulin production in mouse B cells at high frequencies.
 
Honarvar N, Schaible UE, Galanos C, Wallich R, Simon MM.
 
Max-Planck-Institut fur Immunbiologie, Freiburg, Germany.
 
Sonicated preparations of Borrelia burgdorferi are able to stimulate unselected resting BALB/c spleen cells to proliferate and to produce immunoglobulin in vitro. FACS analysis of target cells prestained with an integrated cell-surface marker as well as cell-depletion experiments demonstrate that the majority of responding lymphocytes are B cells. Limiting dilution analyses of resting B cells revealed high frequencies of cells producing IgM (F 1/11-1/62) or IgG (F 1/5-1/163) in response to B. burgdorferi sonicate (B.b. sonicate). These numbers were similar to those obtained with lipopolysaccharide (LPS) (IgM: F 1/20-1/84; IgG: F 1/14-1/85) or a synthetic lipopeptide of Braun's Escherichia coli lipoprotein (IgM: F 1/15, 1/19; IgG: F 1/148, 1/34). The mitogenic structure(s) expressed by B. burgdorferi is distinct from LPS, as similar proliferative responses were obtained with B cells from LPS-resistant (C57BL/10ScCr and C3H/HeJ) and LPS-susceptible (C57BL/10ScSn, C3H/HeN) mice.
 
Furthermore, B-cell mitogenic properties were also found in two distinct fractions of a phenol-chloroform-petroleum ether extract of B. burgdorferi: they consisted of a lipoprotein distinct from the outer surface proteins (Osp) A and B and glycolipid-like structures, respectively. These data suggest that spirochetes express a multitude of distinct structures with mitogenic activity for B cells including various lipoproteins as well as glycolipid(s).
 
PMID: 7959873 [PubMed - indexed for MEDLINE]
 
28: FASEB J. 1992 Apr;6(7):2482-6.
 
Interleukin-1 (IL-1) receptor blockade reduces endotoxin and Borrelia burgdorferi-stimulated IL-8 synthesis in human mononuclear cells.
 
Porat R, Poutsiaka DD, Miller LC, Granowitz EV, Dinarello CA.
 
Department of Medicine, New England Medical Center, Boston, Massachusetts 02111.
 
Interleukin-1 (IL-1) is a potent stimulator of IL-8 production by fibroblasts and monocytes. In the present study, we asked how much of endotoxin (LPS)-induced IL-8 production by human peripheral blood mononuclear cells was due to IL-1 induced by LPS. Cells were stimulated with either IL-1 beta, LPS, or Borrelia burgdorferi, and total IL-8 was determined by a specific radioimmunoassay. The addition of saturating concentrations of IL-1 receptor antagonist protein (IRAP) reduced the IL-1 beta-, LPS-, and B. burgdorferi-induced IL-8 synthesis by 85, 50, and 40%, respectively. Increasing the concentration of LPS did not affect the reduction in IL-8 synthesis observed in the presence of IRAP. Significant inhibition of the IL-1 beta-induced IL-8 synthesis was observed when IRAP was added 60 or 90 min after IL-1 beta; similarly, IL-8 synthesis after LPS was also reduced by delayed addition of IRAP. These data suggest that the ameliorative effects of IL-1 receptor blockade in models of inflammation and infection may be due, in part, to suppression of IL-1-induced IL-8.
 
PMID: 1532945 [PubMed - indexed for MEDLINE]
 
30: J Infect Dis. 1992 Mar;165(3):471-8.
 
Comment in: J Infect Dis. 1992 Oct;166(4):938-9.
 
Nonspecific proliferative responses of murine lymphocytes to Borrelia burgdorferi antigens.
 
de Souza MS, Fikrig E, Smith AL, Flavell RA, Barthold SW.
 
Section of Comparative Medicine; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06510.
 
Proliferative responses of naive splenocytes to Borrelia burgdorferi antigens from mice susceptible (C3H) and resistant (BALB) to Lyme borreliosis were investigated. B. burgdorferi spirochetes and recombinant outer surface proteins, OspA and OspB, were found to induce nonspecific proliferation of naive splenocytes from both strains of mice. Cell purification studies localized nonspecific proliferation to the B cell-enriched fraction. B. burgdorferi, OspA, and OspB were found to induce IgM and IgG synthesis in vitro. The mitogenic effect of B. burgdorferi was dissimilar to that of lipopolysaccharide (LPS), in that B cells from C3H/HeJ mice (LPS-unresponsive) responded at levels comparable to those from C3H/HeNCrlBr mice. These results emphasize the need for caution in the study of antigen-specific proliferation for B. burgdorferi.
 
PMID: 1531672 [PubMed - indexed for MEDLINE]
 
38: Zentralbl Bakteriol Mikrobiol Hyg [A]. 1986 Dec;263(1-2):137-41
 
Borrelia burgdorferi lipopolysaccharide and its role in the pathogenesis of Lyme disease.
 
Habicht GS, Beck G, Benach JL, Coleman JL.
 
Lipopolysaccharides (LPS) are a constitutive part of the outer wall of gram negative bacteria. Because many of the symptoms of Lyme disease could be explained by a spirochetal LPS we have subjected Borrelia burgdorferi to standard LPS extraction techniques which yielded a LPS which accounted for 1.5-4% of the dry weight. The LPS was very similar to classical gram negative bacterial LPS both chemically and in its biological activities which included pyrogenicity, mitogenicity for lymphocytes and the induction of Interleukin 1 production by macrophages. In addition, the LPS produced an acute inflammatory reaction when injected intradermally into rabbit skin. It could also prepare a skin site for the production of the local Shwartzman reaction. These results show that the Lyme disease spirochete contains a hitherto unknown LPS that is biologically active in vitro and in vivo. It is likely that this molecule plays an important role in the pathogenesis of Lyme disease.
 
PMID: 3577475 [PubMed - indexed for MEDLINE]
 
40: Microbiologica. 1986 Apr;9(2):249-52.
 
Endotoxicity associated with the Lyme disease Borrelia: recent findings.
 
Fumarola D, Munno I, Marcuccio C, Miragliotta G.
 
The endotoxicity of Borrelia burgdorferi, the causative agent of Lyme Disease, a tick-borne spirochetosis, was studied using Limulus assay and pyrogen test in rabbit. Some suspensions of Ixodes ricinus and Ixodes dammini associated Borrelia were able to gelify Limulus lysate and demonstrated a febrile response in rabbit. These findings and other recent data demonstrating an endotoxin-like activity of the Lyme Disease agent are discussed in the context of the pathogenic mechanisms of the illness.
 
PMID: 3713546 [PubMed - indexed for MEDLINE]
 
42: Infection. 1983 Nov-Dec;11(6):345.
 
"Endotoxicity" of the Lyme disease spirochete.
 
Fumarola D, Munno I, Miragliotta G.
 
Publication Types: Letter
 
PMID: 6668073 [PubMed - indexed for MEDLINE]
 
8: Vaccine. 1997 Jun;15(9):988-96.
 
OspA lipoprotein of Borrelia burgdorferi is a mucosal immunogen and adjuvant.
 
Erdile LF, Guy B.
 
Pasteur Merieux Connaught, Marcy L'Etoile, France.
 
The outer surface protein A (OspA) lipoprotein of Borrelia burgdorferi, like cholera toxin and the heat-labile enterotoxin of Escherichia coli, induces pro-inflammatory cytokines. This suggested that, like those toxins, OspA might be a mucosal immunogen and adjuvant. OspA, administered intranasally (i.n.) or intragastrically, induced strong serum IgG and salivary gland IgA responses. The serum IgG isotypes were indicative of a mixed T helper 1 and T helper 2 response, the latter being more pronounced. The N-terminal tripalmitoyl-S-glyceryl-cysteine (Pam3Cys) lipid moiety was absolutely required. OspA strongly enhanced the serum IgG and salivary gland IgA responses to jack bean urease co-administered by the i.n. route. OspA also enhanced the response to tetanus toxoid and induced limited protection against challenge. A synthetic lipopeptide also adjuvanted the response to urease by the i.n. route, but was ca 500-fold less potent on a molar basis than OspA. These results suggest that OspA or other lipoproteins may be useful in mucosal vaccines.
 
PMID: 9261945 [PubMed - indexed for MEDLINE]
 
Immunology. 2004 Nov;113(3):401-8.
 
Characterization of the B-cell inhibitory protein factor in Ixodes ricinus tick saliva: a potential role in enhanced Borrelia burgdoferi transmission.
 
Hannier S, Liversidge J, Sternberg JM, Bowman AS.
 
School of Biological Science, Zoology, University of Aberdeen, UK.
 
We recently described the inhibition of host B lymphocytes by Ixodes ricinus tick saliva. In this study, we characterized the factor responsible for this activity and examined the modulation of lipopolysaccharide (LPS)- and Borrelia burgdorferi outer surface protein (Osp)-induced proliferation of naive murine B lymphocytes by an enriched fraction of this factor. The B-lymphocyte inhibitory activity was destroyed by trypsin treatment, indicating that a proteinaceous factor was responsible for this activity. The removal of glutathione-S-transferase (GST) from tick salivary glands extracts (SGE) showed that this B-cell inhibitory protein (BIP) was not a GST. Gel filtration liquid chromatography indicated that BIP has a native molecular weight of approximately 18,000. An enrichment protocol, using a combination of anion-exchange and reverse-phase liquid chromatography, was established. BIP-enriched fractions did not suppress T-cell proliferation. Delayed addition of BIP-enriched fractions, up to 7 hr after LPS addition, inhibited the proliferation of isolated B cells. BIP-enriched fractions dramatically inhibited both OspA- and OspC-induced proliferation of isolated B cells. These results strongly suggest that BIP may facilitate B. burgdorferi transmission by preventing B-cell activation, and also highlights the potential of BIP as a therapeutic agent in B-cell maladies.
 
PMID: 15500628 [PubMed - indexed for MEDLINE]
 
25: Microbiologica. 1986 Apr;9(2):249-52.
 
Endotoxicity associated with the Lyme disease Borrelia: recent findings.
 
Fumarola D, Munno I, Marcuccio C, Miragliotta G.
 
The endotoxicity of Borrelia burgdorferi, the causative agent of Lyme Disease, a tick-borne spirochetosis, was studied using Limulus assay and pyrogen test in rabbit. Some suspensions of Ixodes ricinus and Ixodes dammini associated Borrelia were able to gelify Limulus lysate and demonstrated a febrile response in rabbit. These findings and other recent data demonstrating an endotoxin-like activity of the Lyme Disease agent are discussed in the context of the pathogenic mechanisms of the illness.
 
PMID: 3713546 [PubMed - indexed for MEDLINE]
 
2: Arthritis Rheum. 2004 Jul;50(7):2360-9.
 
Outer surface lipoproteins of Borrelia burgdorferi vary in their ability to induce experimental joint injury.
 
Batsford S, Dunn J, Mihatsch M.
 
Albert Ludwigs University, Freiburg, Germany. bats@...
 
OBJECTIVE: To examine the ability of bacterial lipoproteins from the spirochete Borrelia burgdorferi to cause in vivo tissue injury (arthritis). METHODS: Outer surface proteins (OSPs) from B burgdorferi were used in a rat model of antigen-induced allergic arthritis. Intraarticular challenge with recombinant OspA, OspB, and OspC in nonlipidated (peptide) and lipidated forms was performed in the left knee joint; the contralateral joint received buffer as control. Inflammation was monitored by technetium scintigraphy and histology. RESULTS: Nonlipidated (peptide) OspA, OspB, and OspC did not induce arthritis; the only exception was polymerized OspA, which was tested in preimmunized rats. Lipidated OspA from 2 different strains and lipidated OspC induced severe arthritis, whereas lipidated OspB failed to induce injury. A synthetic analog of the OSP lipid modification, lipopeptide Pam(3)Cys-Ser-Lys(4)-OH, either alone or coupled to bovine serum albumin, also failed to induce injury. Injury did not develop in control groups that were given the appropriate buffers or lipopolysaccharide. This showed that lipidated borrelial OSPs can be potent arthritogens, but vary greatly with respect to their injury-inducing potential. The possession of a lipid modification is essential but is not sufficient to render an OSP arthritogenic. CONCLUSION: This is the first study to demonstrate that individual lipoproteins from B burgdorferi can induce experimental joint injury in vivo. These results may help elucidate the pathogenesis of Lyme arthritis and, above all, underline the importance of bacterial lipoproteins as major virulence factors.
 
PMID: 15248237 [PubMed - indexed for MEDLINE]
 
4: Infect Immun. 2003 Jul;71(7):3979-87.
 
Borrelia burgdorferi-induced tolerance as a model of persistence via immunosuppression.
 
Diterich I, Rauter C, Kirschning CJ, Hartung T.
 
Biochemical Pharmacology, Faculty of Biology, University of Konstanz, Konstanz, Germany.
 
If left untreated, infection with Borrelia burgdorferi sensu lato may lead to chronic Lyme borreliosis. It is still unknown how this pathogen manages to persist in the host in the presence of competent immune cells. It was recently reported that Borrelia suppresses the host's immune response, thus perhaps preventing the elimination of the pathogen (I. Diterich, L. Harter, D. Hassler, A. Wendel, and T. Hartung, Infect. Immun. 69:687-694, 2001). Here, we further characterize Borrelia-induced immunomodulation in order to develop a model of this anergy. We observed that the different Borrelia preparations that we tested, i.e., live, heat-inactivated, and sonicated Borrelia, could desensitize human blood monocytes, as shown by attenuated cytokine release upon restimulation with any of the different preparations. Next, we investigated whether these Borrelia-specific stimuli render monocytes tolerant, i.e. hyporesponsive, towards another Toll-like receptor 2 (TLR2) agonist, such as lipoteichoic acid from gram-positive bacteria, or towards the TLR4 agonist lipopolysaccharide. Cross-tolerance towards all tested stimuli was induced. Furthermore, using primary bone marrow cells from TLR2-deficient mice and from mice with a nonfunctional TLR4 (strain C3H/HeJ), we demonstrated that the TLR2 was required for tolerance induction by Borrelia, and using neutralizing antibodies, we identified interleukin-10 as the key mediator involved. Although peripheral blood mononuclear cells tolerized by Borrelia exhibited reduced TLR2 and TLR4 mRNA levels, the expression of the respective proteins on monocytes was not decreased, ruling out the possibility that tolerance to Borrelia is attributed to a reduced TLR2 expression. In summary, we characterized tolerance induced by B. burgdorferi, describing a model of desensitization which might mirror the immunosuppression recently attributed to the persistence of Borrelia in immunocompetent hosts.
 
PMID: 12819085 [PubMed - indexed for MEDLINE]
 
5: Dtsch Med Wochenschr. 2003 Mar 7;128(10):513.
 
[What is to be made of the therapy of borreliosis with cholestyramine and pioglitazone?]
 
[Article in German]
 
Hassler D.
 
PMID: 12627347 [PubMed - indexed for MEDLINE]
 
11: Semin Neurol. 1994 Dec;14(4):313-9.
 
Central nervous system vasculitis secondary to infections, toxins, and neoplasms.
 
Giang DW.
 
Department of Neurology, University of Rochester Medical Center, New York, USA.
 
Publication Types: Review
 
PMID: 7709082 [PubMed - indexed for MEDLINE]
 
12: Infect Immun. 1992 Aug;60(8):3224-30.
 
Hemolytic activity of Borrelia burgdorferi.
 
Williams LR, Austin FE.
 
Department of Microbiology and Immunology, School of Medicine, University of Louisville, Kentucky 40292.
 
Zones of beta-hemolysis occurred around colonies of Borrelia burgdorferi grown on Barbour-Stoenner-Kelly medium containing agarose and horse blood. Blood plates were inoculated with either the infective strain Sh-2-82 or noninfective strain B-31 in an overlay and incubated in a candle jar. Both strains of B. burgdorferi displayed beta-hemolysis after 1 to 2 weeks of incubation. The hemolytic activity diffused out from the borrelial colonies, eventually resulting in lysis of the entire blood plate. Hemolysis was most pronounced with horse blood and was less intense with bovine, sheep, and rabbit blood. Hemolysis was enhanced by hot-cold incubation, which is typical of phospholipase-like activities in other bacteria. Further characterization of the borrelial hemolysin by using a spectrophotometric assay revealed its presence in the supernatant fluids of stationary-phase cultures. Detection of the borrelial hemolytic activity was dependent on activation of the hemolysin by the reducing agent cysteine. This study provides the first evidence of hemolytic activity associated with B. burgdorferi.
 
PMID: 1639493 [PubMed - indexed for MEDLINE]
 
13: Infect Immun. 1992 Mar;60(3):1109-13.
 
In vitro and in vivo induction of tumor necrosis factor alpha by Borrelia burgdorferi.
 
Defosse DL, Johnson RC.
 
Department of Microbiology, University of Minnesota, Minneapolis 55455.
 
Tumor necrosis factor alpha (TNF-alpha) is an immunoregulatory cytokine with many biological activities including the mediation of inflammation. We examined sera and synovial fluids from patients seropositive for infection with Borrelia burgdorferi using a radioimmunoassay specific for TNF-alpha. Significant elevation of TNF-alpha was found in the sera and synovial fluids of patients examined, while controls showed no elevation. Sera of mice infected with B. burgdorferi contained elevated levels of TNF-alpha which varied during the course of a 24-day infection. To determine whether B. burgdorferi is capable of inducing TNF-alpha production, spirochetes were added to adherent human peripheral blood mononuclear cells or mouse peritoneal exudate cells and 24 h later supernatants were assayed. TNF-alpha induction occurred in a dose-dependent manner. The maximum stimulation occurred when a ratio of 1 to 10 spirochetes per mononuclear cell was used. At optimal concentrations, induction was not diminished by inactivation of spirochetes or pretreatment with polymyxin B. These results suggest that an increase in TNF-alpha production may occur as a result of infection with B. burgdorferi.
 
PMID: 1541526 [PubMed - indexed for MEDLINE]
 
14: J Infect Dis. 1992 Mar;165(3):471-8.
 
Comment in: J Infect Dis. 1992 Oct;166(4):938-9.
 
Nonspecific proliferative responses of murine lymphocytes to Borrelia burgdorferi antigens.
 
de Souza MS, Fikrig E, Smith AL, Flavell RA, Barthold SW.
 
Section of Comparative Medicine; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06510.
 
Proliferative responses of naive splenocytes to Borrelia burgdorferi antigens from mice susceptible (C3H) and resistant (BALB) to Lyme borreliosis were investigated. B. burgdorferi spirochetes and recombinant outer surface proteins, OspA and OspB, were found to induce nonspecific proliferation of naive splenocytes from both strains of mice. Cell purification studies localized nonspecific proliferation to the B cell-enriched fraction. B. burgdorferi, OspA, and OspB were found to induce IgM and IgG synthesis in vitro. The mitogenic effect of B. burgdorferi was dissimilar to that of lipopolysaccharide (LPS), in that B cells from C3H/HeJ mice (LPS-unresponsive) responded at levels comparable to those from C3H/HeNCrlBr mice. These results emphasize the need for caution in the study of antigen-specific proliferation for B. burgdorferi.
 
PMID: 1531672 [PubMed - indexed for MEDLINE]
 
15: J Infect Dis. 1991 Sep;164(3):568-74.
 
Cytokines and the pathogenesis of neuroborreliosis: Borrelia burgdorferi induces glioma cells to secrete interleukin-6.
 
Habicht GS, Katona LI, Benach JL.
 
Department of Pathology, State University of New York, Stony Brook 11794-8691.
 
Lyme disease is a multisystemic disease caused by a tickborne spirochete, Borrelia burgdorferi. Neuroborreliosis is characterized by intrathecal production of antibodies specific for the spirochete. This suggests that spirochetal infection of the central nervous system produces conditions that support the maturation of B lymphocytes to immunoglobulin-secreting cells. Interleukin 6 (IL-6) stimulates B cell differentiation into antibody-secreting cells. The present study was undertaken to determine whether B. burgdorferi can stimulate cells of central nervous system origin to secrete IL-6. C6 rat glioma cells cultured with spirochetes induced secretion of IL-6 activity. Peak stimulation was achieved at 24 h with 25 spirochetes per glioma cell. Glioma cells were also stimulated to produce IL-6 by interleukin 1 and tumor necrosis factor. That very few spirochetes are found in Lyme disease patients suggests that biologic amplification factors derived from the organism or the host, or both, are responsible for the pathogenesis of this disease. IL-6 can now be added to the growing list of such factors.
 
PMID: 1908002 [PubMed - indexed for MEDLINE]
 
16: Rev Infect Dis. 1991 Jul-Aug;13(4):658-65.
 
Plagues--what's past is present: thoughts on the origin and history of new infectious diseases.
 
Ampel NM.
 
Medical Service, Tucson Veterans Affairs Medical Center, Arizona 85723.
 
Medical science has made tremendous strides in overcoming infectious diseases in the 20th century. Despite this, several epidemics of previously unrecognized diseases have occurred during the last 15 years. These diseases include Lyme disease, Legionnaires' disease, toxic shock syndrome, and AIDS. Examination of past epidemics, including the plague of Athens, the black death, syphilis, and influenza, suggests that the sudden occurrence of diseases that were previously unrecognized is not unusual. Analysis of the new infectious disease indicates that while all four appeared suddenly, isolated cases of the disease occurred before the actual epidemic. Further, all four new diseases were found to be due to agents or toxins that were not previously recognized. Epidemics due to new infectious diseases may arise by several mechanisms, including mutation of the pathogen to a virulent form and introduction of an infectious agent into a nonimmune population. Environmental and behavioral factors may play an important role, as illustrated by toxic shock syndrome, Legionnaires' disease, and AIDS. On the other hand, epidemic diseases tend to abate over time because of changes in the infecting pathogen and in the host. Hence, epidemics can be seen as cycles; new diseases will arise periodically, occasionally with a devastating outcome. With time the effects of these diseases on the population will ameliorate. The cycle will begin again when a new disease emerges.
 
Publication Types: Review; Review, Tutorial
 
PMID: 1925288 [PubMed - indexed for MEDLINE]
 
17: FEMS Microbiol Immunol. 1991 Feb;3(1):33-8. Related Articles, Links
 
Evidence for (lipo) oligosaccharides in Borrelia burgdorferi and their serological specificity.
 
Cinco M, Banfi E, Balanzin D, Godeas C, Panfili E.
 
Istituto di Microbiologia, Universita degli Studi, Trieste, Italy.
 
SDS-PAGE and Western immunoblot profiles have been determined for different strains of Borrelia burgdorferi. Major proteins of 60 kDa, 41 kDa corresponding to flagellin, 34-36 kDa and 30-31 kDa corresponding to OspB and OspA respectively, and 18-20 kDa corresponding to 'pC' fractions were detected. A "rough" lipopolysaccharide which we called lipooligosaccharide (LOS) of 8-11 kDa appeared to be present, being detected by specific silver staining, as in crude Borrelia lysates as in proteinase K digested Borrelia strains, quite similar in shape among the different strains examined. The LOS reacted in Western blotting with immune anti-B. burgdorferi rabbit serum and also with sera collected from humans affected by Lyme borreliosis. The LOS did not react with sera positive for syphilis or leptospirosis, and their immunological specificity is discussed.
 
PMID: 1711876 [PubMed - indexed for MEDLINE]
 
19: Ann N Y Acad Sci. 1988;539:80-6.
 
The role of interleukin-1 in the pathogenesis of Lyme disease.
 
Habicht GS, Beck G, Benach JL.
 
Department of Pathology, State University of New York, Stony Brook 11794.
 
PMID: 3263828 [PubMed - indexed for MEDLINE]
 
21: Sci Am. 1987 Jul;257(1):78-83.
 
Lyme disease.
 
Habicht GS, Beck G, Benach JL.
 
PMID: 3496660 [PubMed - indexed for MEDLINE]
 
25: Microbiologica. 1986 Apr;9(2):249-52.
 
Endotoxicity associated with the Lyme disease Borrelia: recent findings.
 
Fumarola D, Munno I, Marcuccio C, Miragliotta G.
 
The endotoxicity of Borrelia burgdorferi, the causative agent of Lyme Disease, a tick-borne spirochetosis, was studied using Limulus assay and pyrogen test in rabbit. Some suspensions of Ixodes ricinus and Ixodes dammini associated Borrelia were able to gelify Limulus lysate and demonstrated a febrile response in rabbit. These findings and other recent data demonstrating an endotoxin-like activity of the Lyme Disease agent are discussed in the context of the pathogenic mechanisms of the illness.
 
PMID: 3713546 [PubMed - indexed for MEDLINE]
 
26: Eur J Clin Microbiol. 1985 Aug;4(4):440.
 
Lyme arthritis: does endotoxin play a role?
 
Fumarola D, Munno I, Miragliotta G, Marcuccio C.
 
Publication Types: Letter
 
PMID: 4043072 [PubMed - indexed for MEDLINE]
 
27: J Infect Dis. 1985 Jul;152(1):108-17.
 
Chemical and biologic characterization of a lipopolysaccharide extracted from the Lyme disease spirochete (Borrelia burgdorferi).
 
Beck G, Habicht GS, Benach JL, Coleman JL.
 
A lipopolysaccharide (LPS) was isolated from the Lyme disease spirochete by a modification of the hot phenol-water method. The material was composed of 45% carbohydrate, 8% protein, 44% lipid A, and 1% 3-deoxy-D-mannooctulosonic acid and accounted for approximately 1.5% of the cellular dry weight. The isolated LPS possessed several biologic activities characteristic of endotoxins. The LPS was pyrogenic for rabbits, mitogenic for human mononuclear cells and murine splenocytes, capable of clotting limulus lysate, and cytotoxic for murine macrophages. LPS extracted from Borrelia burgdorferi by the petroleum-ether:chloroform:liquid-phenol procedure was also characterized. The results show that the Lyme disease spirochete contains a hitherto unknown LPS that is biologically active in vitro, and the expression of such activities in vivo may play an important role in the pathogenesis of Lyme disease. Some of the clinical manifestations of other spirochetal disease may be explained by similar endotoxins in those organisms. To our knowledge this is the first report of an LPS extracted from a spirochete that is known to be a human pathogen.
 
PMID: 4008983 [PubMed - indexed for MEDLINE]
 
29: Ann Intern Med. 1985 Mar;102(3):397-9.
 
Relapsing fever: new lessons about antibiotic action.
 
Butler TC.
 
PMID: 3970476 [PubMed - indexed for MEDLINE]
 
30: J Infect Dis. 1984 Oct;150(4):616.
 
Failure to detect endotoxin in sera from patients with Lyme disease.
 
Schmid GP, Verardo L, Highsmith AK, Weisfeld JS.
 
Publication Types: Letter
 
PMID: 6491371 [PubMed - indexed for MEDLINE]
 
32: Lancet. 1983 Apr 16;1(8329):835-9.
 
Meptazinol diminishes the Jarisch-Herxheimer reaction of relapsing fever.
 
Teklu B, Habte-Michael A, Warrell DA, White NJ, Wright DJ.
 
Naloxone, an opioid antagonist, and meptazinol, an opioid antagonist with agonist properties, were tested in a double-blind placebo-controlled trial in 24 Ethiopian patients with louse-borne relapsing fever. The potentially fatal Jarisch-Herxheimer reaction (J-HR), which invariably follows tetracycline treatment of the disease, was unaffected by naloxone, 30-40 mg intravenously, but was diminished by meptazinol, 300-500 mg intravenously. Compared with naloxone and placebo, meptazinol reduced the clinical severity of the reaction, significantly delayed and shortened its chill phase, delayed the rise in temperature, and reduced peak temperature and changes in pulse and respiratory rates and leucocyte count. High-dose corticosteroids given before or at the time of tetracycline treatment failed to alter the reaction, which is thought to result from release of endotoxin-like substances. Meptazinol is the first effective treatment for the J-HR of louse-borne relapsing fever. This finding suggests a role for endogenous opioids in the pathogenesis of the J-HR.
 
Publication Types: Clinical Trial; Randomized Controlled Trial
 
PMID: 6132178 [PubMed - indexed for MEDLINE]
 
34: Parasite Immunol. 1980 Autumn;2(3):201-21.
 
Reaction following treatment of murine borreliosis and Shwartzman type reacion with borrelial sonicates.
 
Wright DJ.
 
Treatment of experimental murine borreliosis induced an acute transient fall in temperature, leucopenia and thrombocytopenia with appearance of circulating 'endotoxin-like' material. This reaction to treatment could be reproduced by the inoculatioh of borrelial sonicates into infected mice or by two injections of the same sonicate given 24 hours apart, into normal mice. Sensitization or precipitation of the reaction could not be induced by E. coli lipopolysaccharide, although a reaction indistinguishable from the reaction to treatment could be provoked in mice by two successive injections of lipopolysaccharide given 24 hours apart. The nature of this reaction in mice was investigated and the relation of both reactions to the Shwartzman reaction, Endotoxin.
 
PMID: 7413246 [PubMed - indexed for MEDLINE]
 
37: Am J Med. 1977 Dec;63(6):933-8.
 
Activation of protein mediators of inflammation and evidence for endotoxemia in Borrelia recurrentis infection.
 
Galloway RE, Levin J, Butler T, Naff GB, Goldsmith GH, Saito H, Awoke S, Wallace CK.
 
Fifteen patients with Borrelia recurrentis infection were studied to evaluate the role of certain plasma proteins and endotoxin in the pathophysiology of both the acute illness and the Jarisch-Herxheimer-like reaction. The causative spirochetes disappeared from the blood during the Jarisch-Herxheimer-like reaction, which occurred about 2 hours after antibiotic therapy. The mean titers of Hageman factor, plasma prekallikrein and serum hemolytic complement activity were decreased at the time of admission and 2 hours after treatment, and rose to normal values during convalescence. Serum properdin titers were decreased in 14 patients at the time of admission, in 12 patients 2 hours after treatment, and in none during convalescence. The frequency of elevated levels of fibrinogen-related antigens increased from three patients at the time of admission to 12 patients 2 hours after treatment. Results of plasma limulus tests for endotoxin-like material were positive in 11 patients at the time of admission and in 13 patients 2 hours after treatment. These findings demonstrated that Hageman factor, prekallikrein and proteins of the complement system are activated in B. recurrentis infection and that endotoxin may play a role in both the acute illness and in the development of the Jarisch-Herxheimer-like reaction after treatment.
 
PMID: 605915 [PubMed - indexed for MEDLINE]
 
38: J Infect Dis. 1976 Jun;133(6):696-704.
 
Clinical pathology of the Jarisch-Herxheimer reaction.
 
Bryceson AD.
 
The Jarisch-Herxheimer reaction is a complication that can follow treatment of several infectious diseases. Its most severe form is in louse-borne relapsing fever; in this syndrome the reaction can cause death. Information from studies in Ethiopia during the past eight years is presented, and clinical, physiological, pathological, and immunological features of the reaction are described. Possible causative mechanisms of the reaction are discussed, especially in relation to the role of endotoxin, and an attempt is made to consider this reaction in relation to other endotoxin-associated states.
 
PMID: 932495 [PubMed - indexed for MEDLINE]
 
The quote in the introduction from Dr. James Howenstine is from: http://69.93.158.250/forums/m.asp?f=58&i=444
 
He is a specialist in internal medicine. He is author of A Physician's Guide to Natural Health Products that Work, 328 pg. $17.95. His book can be obtained from Amazon.com, naturalhealthteam.com or by calling 1-800-416-2806. Dr. Howenstine can be reached at jimhow@... or by writing Dr. James Howenstine c/o Remarsa USA SB 37, P.O. Box 25292, Miami, Florida 33102-5292
 
My Hope For Your Healing!! Full Healing!!
 
Dr. J
 
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#1729 De: "juanca" <juancaqd@...>
Fecha: Lun, 25 de Abr, 2005 5:43 pm
Asunto: Syndromes of continuous muscular activity
juancaqd
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
19: Rev Neurol. 1995 Jan-Feb;23(119):129-33. Related Articles,Links  
 
[Syndromes of continuous muscular activity: report of a central case (stiff-man) and a peripheral case (neuromyotonia) associated with neuroborreliosis]
 
[Article in Spanish]
 
Requena I, Arias M, Pardo J, Portela M, Alvarez JA.
 
Departamento de Medicina, Universidad de Santiago de Compostela, SERGAS.
 
We describe two cases of continuous muscular activity: one which is central (the stiff-man syndrome), and another which is peripheral (neuromiotony), the latter in a patient suffering from diabetic neuropathy and with positive Borrellia burgdorferi serology in the bloodstream, as well as CSF. Both cases reacted favourably to medical treatment. In the first case botulinic toxin was used as a simultaneous treatment for focal pseudodystonia in one foot. Response was good.
 
Publication Types:
Case Reports
 
PMID: 8548606 [PubMed - indexed for MEDLINE]
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#1728 De: virginia anez <virginia_anez@...>
Fecha: Lun, 25 de Abr, 2005 2:08 pm
Asunto: Re: [Lyme-E] virginia, como tienes el colesterol?
virginia_anez
Sin conexión Sin conexión
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No me ordenaron ningun examen para controlar el colesterol que yo sepa.
La dieta es la del Lyme más otra dieta mas detallada hecha en base a unos analisis de sangre que ordeno burrascano donde por primera vez supe que era alergica a ciertos alimentos.Como el huevo, las mussels ,string beans, lentils,etc.

antsettler <sacorroto@...> wrote:

virginia, como tienes los analisis de los colesteroles? te van a
hacer seguimiento de ellos mientras estas con la colestiramina? te
han puesto alguna dieta?
pablo

--- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
virginia anez <virginia_anez@y...> escribió:
> Gracias por el ofrecimiento de tus habilidades que en algun
momento te pueda consultar con respecto al estudio de JOnes.

> Tomo el colesteramine 2 veces al dia. Son sobresitos que contienen
un polvo parecido al metamucil.
> Lo puedo hacer con las comidas, pero dos horas antes o despues de
abx y vitaminas.

> Lo tengo que tomar por lo menos 4 meses.

> Yo vi unprograma en The Learning Channel y Dicovery Channel donde
Shoemaker salia explicando su teoria junto con otros pacientes.
Estos pacientes eran pescadores y parece que padecian de otro tippo
de toxina pero tambien muy mala.

> Hablando del colon Burrascano ordeno que colectara por tres dias
seguidos poops cada vez que fuera al baño .Esta muestra fue
conservada en liquidos de alto riesgo (tenia que usar gloves para
almacenar la muestra en estos tubos previamente llenados)......a lo
mejo querian examinar algo de lo que tu mencionas en cuanto a la
absorcion de mis intestinos.

> Yo, me siento super differente y lo unico que a cambiado en mi
tratamiento es este cholesteramyne....sino son toxinas, no lo se ni
mi importa, pero de que me esta mejorando y me disminuye casi
completo muchsimos symptomas es verdad y noes un painkiller o
antinflmatorio.....

> Espero que cuando lo pare no regresen los symptomas.!!!

> Si he estado un poco estreñida pero la dieta ayuda.

> Quiero que sepan que estoy a la orden para responder cualquier
curiosidad y les dejare saber si esta mejoria tiene relapse.
>
> antsettler <sacorroto@h...> wrote:
>
> hola,
>
> todo ese conocimiento acumulado que mencionas es oro puro para los
> enfermos de lyme; si yo puedo aportar algo cuenta conmigo, aunque
> estoy limitado, estadisticas, sistemas expertos o analizar
> dinamicas, en la medida que pueda
>
> sobre las neurotoxinas de la borrelia hay que decir que nadie ha
> aislado nunca ninguna, y que no hace falta la teoria de las
toxinas
> para explicar daños en organos, la bacteria misma los ocasiona; si
> el herx es una respuesta inmune a bacterias muertas, tampoco
tienen
> nada que ver las toxinas; los ciclos se explican con variacion de
> antigenos, y la resistencia con la forma cistica; sobre la
> inmunomodulacion hay estudios en alemania que muestran que se debe
> principalmente a saturacion de receptores toll-like para el
> reclutamiento de macrofagos y neutrofilos, estimulando la il-10
> (como hace tambien el ebv),no hace falta inventarse toxinas
> misteriosas de la borrelia, y menos que lo haga un medico de
familia
> (shoemaker (zapatero?)), sin ningun estudio firmado;
>
> la colestiramina tampoco es trigo limpio del todo, intercambia en
el
> colon iones cloro por bicarbonato organico, acidificando el
> organismo; y arrastran todo antibiotico o vitamina liposoluble
> orales; lo digo por ser excepticos mientras no haya un estudio
> serio, como tantos otros remedios; ahora, si te va bien, estupendo!
>
> cuanto tiempo vas a tomarlo? notaste mejoria en breve? lo tomas
con
> el estomago vacio o con las comidas? te provoca estreñimiento?
>
> encantado de oir tus mejorias, dan animos, un saludo a todos,
> pablo
>   
>
>
> --- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
> virginia anez <virginia_anez@y...> escribió:
> > Fijate:
> > 
> > Empe'ze hace 10 dias el colesteramine+levaquin+omeprazole al
mismo
> tiempo.
> > Tengo entendido (dime que opinas porfavor) de que la bart hay
que
> tratarla minimo 3 meses, pues como cualquier otra lyme-co-
> infection ,pero menos severa, lo que quiere de cir que es deficil
> tener  tanta mejoria en este lapso de tiempo .Tambien de que el
> levaquin es bueno contra el Lyme (me lo dijo JOnes)...ahora sino
he
> ni siquiera tenido herx ni del Lyme, ni bart  antes de sentirme
> mejor (aunque burrascano dijo que el bart no causa herxes).... Lo
> que he tenido es mas bien como un lifting o disminucion de los
> sintomas hasta cierto punto magico.... por eso pense que el
> colesteramine me lo hizo excretar de mi organismo y ya.
> > Tambien yo como he tenido muchas infecciones urinarias en el
2004
> yo ya habia tomado incluso por 14 dias el leva y de 500mgs en vez
de
> 250 como me mando burrascano.
> > 
> > Tambien pienso que como de alguna manera he usado buenos
> antibioticos desde el principio y atacado casi todas las co-
> infections (espero que burrascano no me diga que no encontro algo
> mas en los examenes que me practico) y nunca habia addressed las
> neurotoxinas.
> > 
> > El medijo en la cita del 24 de marzo que a la tercera o cuarta
> semana de tratamiento me hiba a sentir mejor. Las primeras dos
> semanas fueron de puras vitaminas recetadas por el asi como b12
> injections.
> > Me dijo que el sospechaba de neurotoxinas de bart pero que el
lyme
> itself lo tenia en la minima expresion.
> > 
> > Me dijo que fortalezer el sistema inmunologico es clave para
> seqguir recuperandose.
> > 
> > MIGUEL:dejame saber tu opinion por favor.
> > 
> > Tambien queria preguntarte si tubieras las historias medicas de
Dr
> Jones en una base de datos que le pidirias al systema que te
> arrojara..por ejemplo"Cual fue el antibiotico de mayor empleo en
> niños de 5 a 8 anos que resolvio mas symptomas??? o Cuales eran
los
> cinco symptomas comunes en los ninos que llegaban al consultorio
sin
> saber que tenian lyme???
> > 
> > Te pregunto esto por que Jones quiere dejar su legado de alguna
> manera y para que le otorguen un grant o donacion para ese estudio
> de recolection de data, analisis, clasificacion necesita que la
> investigacion tenga un objetivo specifico y claro. Jones tiene una
> mina de oro en su consultorio (todos las historias medicas paso
por
> paso) pero el esta muy ocupado tratando a sus pacientes..es obvio
> que el tiene la palabra final y el conocimiento supremo en cuanto
a
> cual deberia de ser el mejor objetivo para su estudio, pero por
> curiosisdad seria bueno saber que quisieras tu u otras personas
que
> ese estudio respondiera.
> >
> > Miguel Angel Ramírez <ramirezortega@t...> wrote:
> > Virginia,
> > 
> > ¿Por qué estas tan segura de que es la colestiramina la
> responsable de tu mejoría espectacular y no el levaquin? Según
> entiendo has comenzado los dos tratamientos a la vez y los
mantienes
> ambos ¿No es así?¿Cuánto tiempo llevas tomándolos?
> > 
> > Miguel
> > ----- Original Message -----
> > From: virginia anez
> > To: lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com
> > Sent: Friday, April 22, 2005 3:32 AM
> > Subject: Re: [Lyme-E] donde estas herx?
> >
> >
> > Migue:
> > 
> > No tenia ni idea de esta reaccion.
> > 
> > Gracias por la informacion........pero es que yo no senti esa
> molestia o  intensification the los symptomas..sera que esta por
> venir en las siguientes semanas????
> > 
> > Pero queria contribuir con mi testimonio acerca del
> cholesteramyne.Ya yo habia oido antes acerca de este medicamento y
> sus beneficios a los lyme sufferers pero nunca me imagine que de
> verdad, por lo menos en mi caso ,eran las neurotoxins mi gran
> molestia y que releasing them de mi cuerpo la mejoria hiba a ser
tan
> rapida y significativa.
> >
> >
> >
> >
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> >
> >
> >
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#1727 De: "juanca" <juancaqd@...>
Fecha: Do, 24 de Abr, 2005 11:19 pm
Asunto: Re: [Lyme-E] neurotoxinas, colestiramina, muchos estudios y la gente enferma
juancaqd
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
 
Lo mas fiable son los estudios doble ciego con placebo pero esto
es muy poco ético si además es por un periodo largo.
El problema es que no hay estudios por periodos largos porque
todavía muchos piensan que no es crónica y los estudios
que se hacen doble ciego con placebo como el de Fallon
son por periodos breves que solo van a atestiguar que hay un cierto
grado de mejoría.
El macrólido in vitro es mas eficaz que la mayoria de hecho a mi es
lo que mas reacción me dió pero hazte la pregunta si será bueno para
tu organismo esas reacciones tan fuertes sean producidas por 
toxinas o no.
En todo caso una vez que hayas reducido carga bacteriana siempre podrás
pasarte a un tratamiento más agresivo .
 
La idea es que las toxinas del lyme son capaces de permanecer por tiempo
indefinido a causa de la reabsorcion en el intestino pero podría pasar que ocurriera
como con el estudio que hicieron con el sida y las estatinas que impedian
la penetracion del virus en las células.
 
Aquí nadie vende tratamientos solo se exponen opiniones a título personal y
cada cual que haga lo que estime mas oportuno, porque las alternativas que
dan muchos médicos son pocas o ninguna.
 
No es que me guste el tratamiento Marshall pero hay muchísmos tratamientos
mas peligrosos como los corticoides que dan alegremente los médicos para
muchos con fibromialgia y SFC.
 
Me pregunto de que serviría matar de hambre a la bacteria si uno mismo
empeora y bajan sus defensas.
Ademas la borrelia puede permanecer largo tiempo en su forma quística.
 
A mi personalmente los esfuerzos extremos siempre han ido seguidos
de un empeoramiento notable, a ver que dicen los demas.
 
Los suplementos de Magnesio y multivitaminas-minerales en dosis cdr
me han dado mas energia pero a largo plazo no se lo que ocurrirá.
 
Yo elegi la tetra por el estudio de Donta pero sobre todo porque me da
mas confianza conocer a alguien que lo lleva utilizando años y sigue
mejorando.
 
J.C
----- Original Message -----
From: antsettler
Sent: Sunday, April 24, 2005 11:11 PM
Subject: RE: [Lyme-E] neurotoxinas, colestiramina, muchos estudios y la gente enferma


hola juanca,

no he decidido tomar tetraciclina porque le vaya bien a otros, sino
solo y exclusivamente porque es la unica droga probada en un
estudio, el de donta; la otra opcion era macrolidos, qu eme parecen
mejor porque protegen los leucocitos (tengo luc y atipicos muy
altos), pero se me van de presupuesto; en algo tan brusco como meses
de antibiotico con final abierto no me puedo fiar de testimonios,
solo de estudios serios, y donta es lo poquito que hay en vivo con
cientos de pacientes;

redefine eficaz como aquello que queda constatado con placebo y
doble ciego, con muestra y tiempo suficientes; el resto a la
cuarentena, y a tomarlo por decision individual; todos en momentos
de debilidad somos susceptibles de aceptar cualquier remedio-
milagro, hay que cuidar por nosotros, y por no influir al
desesperado que piense que de lo que se habla es inocuo y eficaz,
son todo drogas, y hay protocolos peligrosos como el de marshall; 

la colestiramina se usa para absorber toxinas intestinales, como de
clostridia, o intoxicaciones alimentarias, no internas; aqui se
habla de hipoteticas toxinas, hipoteticamente liposolubles,
hipoteticamente en bucle higado-bilis-sangre, y ningun estudio de la
eficacia de la colestiramina; 

ojala funcione, ademas que esta resina no es muy agresiva, aunque yo
creo que tiene mas que ver con la bajada de colesterol; 

aqui me entra siempre la misma duda, cuando la infeccion ha agotado
recursos como colesterol, fosfolipidos, manganeso, magnesio, etc,
deberiamos recargarlos o intentar matar de hambre al alien? yo soy
un suplemento-adicto desde hace años, pero a la vez noto que me es
mas dificil prescindir de ellos, como si estuviera alimentando a la
bestia hambrienta; no encuentro ningun articulo sobre cultivos de BB
con distintos nutrientes; para mi la diferencia es estar en la cama
o no, pero me da miedo estar inflando al alien

que notais con los suplementos? sentis que os es dificil dejarlos?
habeis tenido recaidas tras periodos de hacer deporte? recaidas tras
haber tomado multivitaminicos, o mucha b12, o mucha vit c?  

un saludo a todos,
pablo


--- En
lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com, "juanca"
<juancaqd@t...> escribió:
> Pablo,
> no creo que nadie las tenga del todo claras por eso nos tenemos
> que guiar por lo que es eficaz y se ha visto que funciona en otros
> enfermos y como tu dices casi todo lo demás son conjeturas.
>
> Estudios hay muchos, luego que sean correctos será otro tema.
> Tampoco conocemos todos los estudios sobre este tema.
> Si tenemos que esperar a que haya un consenso general sobre
> tratamiento etc, en lyme estamos listos.
>
> Shoemaker no es el único que utiliza la colestiramina, para
> otras bacterias tambien se ha utilizado por gastroenterólogos.
>
> Te dije que no tenias claro al igual que yo cuando empeoras si es
> por herx o simplemente porque vas a peor, no por otro motivo y
> que deberíamos decidir con un tiempo prudencial.
>
> Es lógico pensar que si en otras bacterias las toxinas juegan un
papel primordial ,
> se conoce la existencia de las mismas referidas a borrelia y
muchos pacientes
> cuando hacen tratamientos para eliminar toxinas mejoran su estado,
que tengan
> un papel importante.
>
> Bienvenido sea cualquier intento de mejorar estas patologias, sea
marshall o
> perico de los palotes.
> Antes de encontrar la solución al problema hay que hacer muchos
intentos y
> alguien en algún intento lo logrará y habrá que probar porque si
no jamás
> llegaremos a nada.
>
> Mientras llegan los estudios definitivos probaré tratamientos que
están
> ayudando y tengan una cierta lógica.
>
> Espero que te vaya bien el tratamiento con tetraciclina aunque lo
hayas
> seleccionado porque le haya ido bien a otros.
>
> Aunque no tengamos las cosa claras espero que entre todos nos
aclaremos
> un poco y toda información que creamos útil la aportemos al foro y
creo
> que tu puedes aportar mucha con tus conocimientos.
>
> Saludos,
> J.C
>
>
>
>
>
>   ----- Original Message -----
>   From: antsettler
>   To: lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com
>   Sent: Sunday, April 24, 2005 8:12 PM
>   Subject: [Lyme-E] neurotoxinas, colestiramina, y cero estudios
>
>
>
>   juanca, me dices que no tengo las cosas claras; si las tuviera
ya
>   estaria curado
>
>   para cero estudios todo vale: rife, plata coloidal, saunas,
>   colestiramina, etc etc; somos libres y no nos ceñimos a los
>   protocolos medicos, y probamos estos metodos, y a veces se
mejora,
>   pero tanto testimonio no es ciencia, tanto testimoniono no es
dato
>
>   que haya alguna neurotoxina no implica que tenga un papel
principal,
>   el aluminio lo es y nadie se lia a tomar edta por tener ciertos
>   niveles, todos tenemos; en los articulos sobre neurotoxinas de
lyme
>   siempre aparecen palabras como 'se cree','parece', etc; nunca
hay
>   una relacion clara, un estudio serio, nada; que existan no
aporta
>   informacion sin profundizar en ello, bien pudieran ser inocuas,
no
>   basta con citarlas;
>
>   para mi los daños de la borrelia son reales, fisicos, causados
por
>   la infeccion,por la propia bacteria, no por bloqueos de
receptores o
>   por las neurotoxinas; el mismo daño al cerebro se explica bien,
y
>   hay pruebas de ello,por el agotamiento del colesterol reservado
en
>   las glial cells, y su destruccion, se lo comen
>
>   bien pudiera ser este el efecto beneficioso de la colestiramina,
>   rebajar el colesterol disponible para la borrelia, que es para
lo
>   que se prescribe esta droga; es algo similar a los estudios
sobre
>   bloqueadres de citocromo p450, como los antimicoticos, habria
que
>   ver si el efecto beneficioso es sobre la borrelia o sobre la
>   proliferacion de levaduras que estamos todos servidos con tanto
>   antibiotico, o cualquier otro efecto ,dificil de determinar como
>   bloquear otra via de citocromo de la borrelia
>
>   mientras no haya estudio claros, relacion cierta, mejor meter en
>   cuarentena; probar con uno mismo y testimoniar la sensacion,
pero
>   nada mas,
>
>   mas de un marshall protocoll (otro sin ningun estudio hecho) se
va
>   al otro barrio;
>
>   un saludo a todos
>   pablo
>
>
>
>
>
>
>
>
>
>
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#1726 De: "antsettler" <sacorroto@...>
Fecha: Do, 24 de Abr, 2005 9:15 pm
Asunto: virginia, como tienes el colesterol?
antsettler
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
virginia, como tienes los analisis de los colesteroles? te van a
hacer seguimiento de ellos mientras estas con la colestiramina? te
han puesto alguna dieta?
pablo

--- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
virginia anez <virginia_anez@y...> escribió:
> Gracias por el ofrecimiento de tus habilidades que en algun
momento te pueda consultar con respecto al estudio de JOnes.
>
> Tomo el colesteramine 2 veces al dia. Son sobresitos que contienen
un polvo parecido al metamucil.
> Lo puedo hacer con las comidas, pero dos horas antes o despues de
abx y vitaminas.
>
> Lo tengo que tomar por lo menos 4 meses.
>
> Yo vi unprograma en The Learning Channel y Dicovery Channel donde
Shoemaker salia explicando su teoria junto con otros pacientes.
Estos pacientes eran pescadores y parece que padecian de otro tippo
de toxina pero tambien muy mala.
>
> Hablando del colon Burrascano ordeno que colectara por tres dias
seguidos poops cada vez que fuera al baño .Esta muestra fue
conservada en liquidos de alto riesgo (tenia que usar gloves para
almacenar la muestra en estos tubos previamente llenados)......a lo
mejo querian examinar algo de lo que tu mencionas en cuanto a la
absorcion de mis intestinos.
>
> Yo, me siento super differente y lo unico que a cambiado en mi
tratamiento es este cholesteramyne....sino son toxinas, no lo se ni
mi importa, pero de que me esta mejorando y me disminuye casi
completo muchsimos symptomas es verdad y noes un painkiller o
antinflmatorio.....
>
> Espero que cuando lo pare no regresen los symptomas.!!!
>
> Si he estado un poco estreñida pero la dieta ayuda.
>
> Quiero que sepan que estoy a la orden para responder cualquier
curiosidad y les dejare saber si esta mejoria tiene relapse.
>
> antsettler <sacorroto@h...> wrote:
>
> hola,
>
> todo ese conocimiento acumulado que mencionas es oro puro para los
> enfermos de lyme; si yo puedo aportar algo cuenta conmigo, aunque
> estoy limitado, estadisticas, sistemas expertos o analizar
> dinamicas, en la medida que pueda
>
> sobre las neurotoxinas de la borrelia hay que decir que nadie ha
> aislado nunca ninguna, y que no hace falta la teoria de las
toxinas
> para explicar daños en organos, la bacteria misma los ocasiona; si
> el herx es una respuesta inmune a bacterias muertas, tampoco
tienen
> nada que ver las toxinas; los ciclos se explican con variacion de
> antigenos, y la resistencia con la forma cistica; sobre la
> inmunomodulacion hay estudios en alemania que muestran que se debe
> principalmente a saturacion de receptores toll-like para el
> reclutamiento de macrofagos y neutrofilos, estimulando la il-10
> (como hace tambien el ebv),no hace falta inventarse toxinas
> misteriosas de la borrelia, y menos que lo haga un medico de
familia
> (shoemaker (zapatero?)), sin ningun estudio firmado;
>
> la colestiramina tampoco es trigo limpio del todo, intercambia en
el
> colon iones cloro por bicarbonato organico, acidificando el
> organismo; y arrastran todo antibiotico o vitamina liposoluble
> orales; lo digo por ser excepticos mientras no haya un estudio
> serio, como tantos otros remedios; ahora, si te va bien, estupendo!
>
> cuanto tiempo vas a tomarlo? notaste mejoria en breve? lo tomas
con
> el estomago vacio o con las comidas? te provoca estreñimiento?
>
> encantado de oir tus mejorias, dan animos, un saludo a todos,
> pablo
>
>
>
> --- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
> virginia anez <virginia_anez@y...> escribió:
> > Fijate:
> >
> > Empe'ze hace 10 dias el colesteramine+levaquin+omeprazole al
mismo
> tiempo.
> > Tengo entendido (dime que opinas porfavor) de que la bart hay
que
> tratarla minimo 3 meses, pues como cualquier otra lyme-co-
> infection ,pero menos severa, lo que quiere de cir que es deficil
> tener  tanta mejoria en este lapso de tiempo .Tambien de que el
> levaquin es bueno contra el Lyme (me lo dijo JOnes)...ahora sino
he
> ni siquiera tenido herx ni del Lyme, ni bart  antes de sentirme
> mejor (aunque burrascano dijo que el bart no causa herxes).... Lo
> que he tenido es mas bien como un lifting o disminucion de los
> sintomas hasta cierto punto magico.... por eso pense que el
> colesteramine me lo hizo excretar de mi organismo y ya.
> > Tambien yo como he tenido muchas infecciones urinarias en el
2004
> yo ya habia tomado incluso por 14 dias el leva y de 500mgs en vez
de
> 250 como me mando burrascano.
> >
> > Tambien pienso que como de alguna manera he usado buenos
> antibioticos desde el principio y atacado casi todas las co-
> infections (espero que burrascano no me diga que no encontro algo
> mas en los examenes que me practico) y nunca habia addressed las
> neurotoxinas.
> >
> > El medijo en la cita del 24 de marzo que a la tercera o cuarta
> semana de tratamiento me hiba a sentir mejor. Las primeras dos
> semanas fueron de puras vitaminas recetadas por el asi como b12
> injections.
> > Me dijo que el sospechaba de neurotoxinas de bart pero que el
lyme
> itself lo tenia en la minima expresion.
> >
> > Me dijo que fortalezer el sistema inmunologico es clave para
> seqguir recuperandose.
> >
> > MIGUEL:dejame saber tu opinion por favor.
> >
> > Tambien queria preguntarte si tubieras las historias medicas de
Dr
> Jones en una base de datos que le pidirias al systema que te
> arrojara..por ejemplo"Cual fue el antibiotico de mayor empleo en
> niños de 5 a 8 anos que resolvio mas symptomas??? o Cuales eran
los
> cinco symptomas comunes en los ninos que llegaban al consultorio
sin
> saber que tenian lyme???
> >
> > Te pregunto esto por que Jones quiere dejar su legado de alguna
> manera y para que le otorguen un grant o donacion para ese estudio
> de recolection de data, analisis, clasificacion necesita que la
> investigacion tenga un objetivo specifico y claro. Jones tiene una
> mina de oro en su consultorio (todos las historias medicas paso
por
> paso) pero el esta muy ocupado tratando a sus pacientes..es obvio
> que el tiene la palabra final y el conocimiento supremo en cuanto
a
> cual deberia de ser el mejor objetivo para su estudio, pero por
> curiosisdad seria bueno saber que quisieras tu u otras personas
que
> ese estudio respondiera.
> >
> > Miguel Angel Ramírez <ramirezortega@t...> wrote:
> > Virginia,
> >
> > ¿Por qué estas tan segura de que es la colestiramina la
> responsable de tu mejoría espectacular y no el levaquin? Según
> entiendo has comenzado los dos tratamientos a la vez y los
mantienes
> ambos ¿No es así?¿Cuánto tiempo llevas tomándolos?
> >
> > Miguel
> > ----- Original Message -----
> > From: virginia anez
> > To: lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com
> > Sent: Friday, April 22, 2005 3:32 AM
> > Subject: Re: [Lyme-E] donde estas herx?
> >
> >
> > Migue:
> >
> > No tenia ni idea de esta reaccion.
> >
> > Gracias por la informacion........pero es que yo no senti esa
> molestia o  intensification the los symptomas..sera que esta por
> venir en las siguientes semanas????
> >
> > Pero queria contribuir con mi testimonio acerca del
> cholesteramyne.Ya yo habia oido antes acerca de este medicamento y
> sus beneficios a los lyme sufferers pero nunca me imagine que de
> verdad, por lo menos en mi caso ,eran las neurotoxins mi gran
> molestia y que releasing them de mi cuerpo la mejoria hiba a ser
tan
> rapida y significativa.
> >
> >
> >
> >
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> >
> >
> >
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#1725 De: "antsettler" <sacorroto@...>
Fecha: Do, 24 de Abr, 2005 9:11 pm
Asunto: RE: [Lyme-E] neurotoxinas, colestiramina, muchos estudios y la gente enferma
antsettler
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
hola juanca,

no he decidido tomar tetraciclina porque le vaya bien a otros, sino
solo y exclusivamente porque es la unica droga probada en un
estudio, el de donta; la otra opcion era macrolidos, qu eme parecen
mejor porque protegen los leucocitos (tengo luc y atipicos muy
altos), pero se me van de presupuesto; en algo tan brusco como meses
de antibiotico con final abierto no me puedo fiar de testimonios,
solo de estudios serios, y donta es lo poquito que hay en vivo con
cientos de pacientes;

redefine eficaz como aquello que queda constatado con placebo y
doble ciego, con muestra y tiempo suficientes; el resto a la
cuarentena, y a tomarlo por decision individual; todos en momentos
de debilidad somos susceptibles de aceptar cualquier remedio-
milagro, hay que cuidar por nosotros, y por no influir al
desesperado que piense que de lo que se habla es inocuo y eficaz,
son todo drogas, y hay protocolos peligrosos como el de marshall;

la colestiramina se usa para absorber toxinas intestinales, como de
clostridia, o intoxicaciones alimentarias, no internas; aqui se
habla de hipoteticas toxinas, hipoteticamente liposolubles,
hipoteticamente en bucle higado-bilis-sangre, y ningun estudio de la
eficacia de la colestiramina;

ojala funcione, ademas que esta resina no es muy agresiva, aunque yo
creo que tiene mas que ver con la bajada de colesterol;

aqui me entra siempre la misma duda, cuando la infeccion ha agotado
recursos como colesterol, fosfolipidos, manganeso, magnesio, etc,
deberiamos recargarlos o intentar matar de hambre al alien? yo soy
un suplemento-adicto desde hace años, pero a la vez noto que me es
mas dificil prescindir de ellos, como si estuviera alimentando a la
bestia hambrienta; no encuentro ningun articulo sobre cultivos de BB
con distintos nutrientes; para mi la diferencia es estar en la cama
o no, pero me da miedo estar inflando al alien

que notais con los suplementos? sentis que os es dificil dejarlos?
habeis tenido recaidas tras periodos de hacer deporte? recaidas tras
haber tomado multivitaminicos, o mucha b12, o mucha vit c?

un saludo a todos,
pablo


--- En
lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com, "juanca"
<juancaqd@t...> escribió:
> Pablo,
> no creo que nadie las tenga del todo claras por eso nos tenemos
> que guiar por lo que es eficaz y se ha visto que funciona en otros
> enfermos y como tu dices casi todo lo demás son conjeturas.
>
> Estudios hay muchos, luego que sean correctos será otro tema.
> Tampoco conocemos todos los estudios sobre este tema.
> Si tenemos que esperar a que haya un consenso general sobre
> tratamiento etc, en lyme estamos listos.
>
> Shoemaker no es el único que utiliza la colestiramina, para
> otras bacterias tambien se ha utilizado por gastroenterólogos.
>
> Te dije que no tenias claro al igual que yo cuando empeoras si es
> por herx o simplemente porque vas a peor, no por otro motivo y
> que deberíamos decidir con un tiempo prudencial.
>
> Es lógico pensar que si en otras bacterias las toxinas juegan un
papel primordial ,
> se conoce la existencia de las mismas referidas a borrelia y
muchos pacientes
> cuando hacen tratamientos para eliminar toxinas mejoran su estado,
que tengan
> un papel importante.
>
> Bienvenido sea cualquier intento de mejorar estas patologias, sea
marshall o
> perico de los palotes.
> Antes de encontrar la solución al problema hay que hacer muchos
intentos y
> alguien en algún intento lo logrará y habrá que probar porque si
no jamás
> llegaremos a nada.
>
> Mientras llegan los estudios definitivos probaré tratamientos que
están
> ayudando y tengan una cierta lógica.
>
> Espero que te vaya bien el tratamiento con tetraciclina aunque lo
hayas
> seleccionado porque le haya ido bien a otros.
>
> Aunque no tengamos las cosa claras espero que entre todos nos
aclaremos
> un poco y toda información que creamos útil la aportemos al foro y
creo
> que tu puedes aportar mucha con tus conocimientos.
>
> Saludos,
> J.C
>
>
>
>
>
>   ----- Original Message -----
>   From: antsettler
>   To: lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com
>   Sent: Sunday, April 24, 2005 8:12 PM
>   Subject: [Lyme-E] neurotoxinas, colestiramina, y cero estudios
>
>
>
>   juanca, me dices que no tengo las cosas claras; si las tuviera
ya
>   estaria curado
>
>   para cero estudios todo vale: rife, plata coloidal, saunas,
>   colestiramina, etc etc; somos libres y no nos ceñimos a los
>   protocolos medicos, y probamos estos metodos, y a veces se
mejora,
>   pero tanto testimonio no es ciencia, tanto testimoniono no es
dato
>
>   que haya alguna neurotoxina no implica que tenga un papel
principal,
>   el aluminio lo es y nadie se lia a tomar edta por tener ciertos
>   niveles, todos tenemos; en los articulos sobre neurotoxinas de
lyme
>   siempre aparecen palabras como 'se cree','parece', etc; nunca
hay
>   una relacion clara, un estudio serio, nada; que existan no
aporta
>   informacion sin profundizar en ello, bien pudieran ser inocuas,
no
>   basta con citarlas;
>
>   para mi los daños de la borrelia son reales, fisicos, causados
por
>   la infeccion,por la propia bacteria, no por bloqueos de
receptores o
>   por las neurotoxinas; el mismo daño al cerebro se explica bien,
y
>   hay pruebas de ello,por el agotamiento del colesterol reservado
en
>   las glial cells, y su destruccion, se lo comen
>
>   bien pudiera ser este el efecto beneficioso de la colestiramina,
>   rebajar el colesterol disponible para la borrelia, que es para
lo
>   que se prescribe esta droga; es algo similar a los estudios
sobre
>   bloqueadres de citocromo p450, como los antimicoticos, habria
que
>   ver si el efecto beneficioso es sobre la borrelia o sobre la
>   proliferacion de levaduras que estamos todos servidos con tanto
>   antibiotico, o cualquier otro efecto ,dificil de determinar como
>   bloquear otra via de citocromo de la borrelia
>
>   mientras no haya estudio claros, relacion cierta, mejor meter en
>   cuarentena; probar con uno mismo y testimoniar la sensacion,
pero
>   nada mas,
>
>   mas de un marshall protocoll (otro sin ningun estudio hecho) se
va
>   al otro barrio;
>
>   un saludo a todos
>   pablo
>
>
>
>
>
>
>
>
>
>
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#1724 De: "juanca" <juancaqd@...>
Fecha: Do, 24 de Abr, 2005 7:22 pm
Asunto: Re: [Lyme-E] neurotoxinas, colestiramina, muchos estudios y la gente enferma
juancaqd
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
Pablo,
no creo que nadie las tenga del todo claras por eso nos tenemos
que guiar por lo que es eficaz y se ha visto que funciona en otros
enfermos y como tu dices casi todo lo demás son conjeturas.
 
Estudios hay muchos, luego que sean correctos será otro tema.
Tampoco conocemos todos los estudios sobre este tema.
Si tenemos que esperar a que haya un consenso general sobre
tratamiento etc, en lyme estamos listos.
 
Shoemaker no es el único que utiliza la colestiramina, para
otras bacterias tambien se ha utilizado por gastroenterólogos.
 
Te dije que no tenias claro al igual que yo cuando empeoras si es
por herx o simplemente porque vas a peor, no por otro motivo y
que deberíamos decidir con un tiempo prudencial.
 
Es lógico pensar que si en otras bacterias las toxinas juegan un papel primordial ,
se conoce la existencia de las mismas referidas a borrelia y muchos pacientes
cuando hacen tratamientos para eliminar toxinas mejoran su estado, que tengan
un papel importante.
 
Bienvenido sea cualquier intento de mejorar estas patologias, sea marshall o
perico de los palotes.
Antes de encontrar la solución al problema hay que hacer muchos intentos y
alguien en algún intento lo logrará y habrá que probar porque si no jamás
llegaremos a nada.
 
Mientras llegan los estudios definitivos probaré tratamientos que están
ayudando y tengan una cierta lógica.
 
Espero que te vaya bien el tratamiento con tetraciclina aunque lo hayas
seleccionado porque le haya ido bien a otros.
 
Aunque no tengamos las cosa claras espero que entre todos nos aclaremos
un poco y toda información que creamos útil la aportemos al foro y creo
que tu puedes aportar mucha con tus conocimientos.
 
Saludos,
J.C
 
 
 
 
 
----- Original Message -----
From: antsettler
Sent: Sunday, April 24, 2005 8:12 PM
Subject: [Lyme-E] neurotoxinas, colestiramina, y cero estudios


juanca, me dices que no tengo las cosas claras; si las tuviera ya
estaria curado

para cero estudios todo vale: rife, plata coloidal, saunas,
colestiramina, etc etc; somos libres y no nos ceñimos a los
protocolos medicos, y probamos estos metodos, y a veces se mejora,
pero tanto testimonio no es ciencia, tanto testimoniono no es dato

que haya alguna neurotoxina no implica que tenga un papel principal,
el aluminio lo es y nadie se lia a tomar edta por tener ciertos
niveles, todos tenemos; en los articulos sobre neurotoxinas de lyme
siempre aparecen palabras como 'se cree','parece', etc; nunca hay
una relacion clara, un estudio serio, nada; que existan no aporta
informacion sin profundizar en ello, bien pudieran ser inocuas, no
basta con citarlas;

para mi los daños de la borrelia son reales, fisicos, causados por
la infeccion,por la propia bacteria, no por bloqueos de receptores o
por las neurotoxinas; el mismo daño al cerebro se explica bien, y
hay pruebas de ello,por el agotamiento del colesterol reservado en
las glial cells, y su destruccion, se lo comen

bien pudiera ser este el efecto beneficioso de la colestiramina,
rebajar el colesterol disponible para la borrelia, que es para lo
que se prescribe esta droga; es algo similar a los estudios sobre
bloqueadres de citocromo p450, como los antimicoticos, habria que
ver si el efecto beneficioso es sobre la borrelia o sobre la
proliferacion de levaduras que estamos todos servidos con tanto
antibiotico, o cualquier otro efecto ,dificil de determinar como
bloquear otra via de citocromo de la borrelia

mientras no haya estudio claros, relacion cierta, mejor meter en
cuarentena; probar con uno mismo y testimoniar la sensacion, pero
nada mas,

mas de un marshall protocoll (otro sin ningun estudio hecho) se va
al otro barrio;

un saludo a todos
pablo










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Version: 7.0.300 / Virus Database: 266.9.10 - Release Date: 14/04/2005
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Version: 7.0.300 / Virus Database: 266.9.10 - Release Date: 14/04/2005

#1723 De: "antsettler" <sacorroto@...>
Fecha: Do, 24 de Abr, 2005 6:12 pm
Asunto: neurotoxinas, colestiramina, y cero estudios
antsettler
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
juanca, me dices que no tengo las cosas claras; si las tuviera ya
estaria curado

para cero estudios todo vale: rife, plata coloidal, saunas,
colestiramina, etc etc; somos libres y no nos ceñimos a los
protocolos medicos, y probamos estos metodos, y a veces se mejora,
pero tanto testimonio no es ciencia, tanto testimoniono no es dato

que haya alguna neurotoxina no implica que tenga un papel principal,
el aluminio lo es y nadie se lia a tomar edta por tener ciertos
niveles, todos tenemos; en los articulos sobre neurotoxinas de lyme
siempre aparecen palabras como 'se cree','parece', etc; nunca hay
una relacion clara, un estudio serio, nada; que existan no aporta
informacion sin profundizar en ello, bien pudieran ser inocuas, no
basta con citarlas;

para mi los daños de la borrelia son reales, fisicos, causados por
la infeccion,por la propia bacteria, no por bloqueos de receptores o
por las neurotoxinas; el mismo daño al cerebro se explica bien, y
hay pruebas de ello,por el agotamiento del colesterol reservado en
las glial cells, y su destruccion, se lo comen

bien pudiera ser este el efecto beneficioso de la colestiramina,
rebajar el colesterol disponible para la borrelia, que es para lo
que se prescribe esta droga; es algo similar a los estudios sobre
bloqueadres de citocromo p450, como los antimicoticos, habria que
ver si el efecto beneficioso es sobre la borrelia o sobre la
proliferacion de levaduras que estamos todos servidos con tanto
antibiotico, o cualquier otro efecto ,dificil de determinar como
bloquear otra via de citocromo de la borrelia

mientras no haya estudio claros, relacion cierta, mejor meter en
cuarentena; probar con uno mismo y testimoniar la sensacion, pero
nada mas,

mas de un marshall protocoll (otro sin ningun estudio hecho) se va
al otro barrio;

un saludo a todos
pablo

#1722 De: virginia anez <virginia_anez@...>
Fecha: Do, 24 de Abr, 2005 4:31 pm
Asunto: RE: [Lyme-E] donde estas herx?
virginia_anez
Sin conexión Sin conexión
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Gracias por el ofrecimiento de tus habilidades que en algun momento te pueda consultar con respecto al estudio de JOnes.
 
Tomo el colesteramine 2 veces al dia. Son sobresitos que contienen un polvo parecido al metamucil.
Lo puedo hacer con las comidas, pero dos horas antes o despues de abx y vitaminas.
 
Lo tengo que tomar por lo menos 4 meses.
 
Yo vi unprograma en The Learning Channel y Dicovery Channel donde Shoemaker salia explicando su teoria junto con otros pacientes. Estos pacientes eran pescadores y parece que padecian de otro tippo de toxina pero tambien muy mala.
 
Hablando del colon Burrascano ordeno que colectara por tres dias seguidos poops cada vez que fuera al baño .Esta muestra fue conservada en liquidos de alto riesgo (tenia que usar gloves para almacenar la muestra en estos tubos previamente llenados)......a lo mejo querian examinar algo de lo que tu mencionas en cuanto a la absorcion de mis intestinos.
 
Yo, me siento super differente y lo unico que a cambiado en mi tratamiento es este cholesteramyne....sino son toxinas, no lo se ni mi importa, pero de que me esta mejorando y me disminuye casi completo muchsimos symptomas es verdad y noes un painkiller o antinflmatorio.....
 
Espero que cuando lo pare no regresen los symptomas.!!!
 
Si he estado un poco estreñida pero la dieta ayuda.
 
Quiero que sepan que estoy a la orden para responder cualquier curiosidad y les dejare saber si esta mejoria tiene relapse.

antsettler <sacorroto@...> wrote:

hola,

todo ese conocimiento acumulado que mencionas es oro puro para los
enfermos de lyme; si yo puedo aportar algo cuenta conmigo, aunque
estoy limitado, estadisticas, sistemas expertos o analizar
dinamicas, en la medida que pueda

sobre las neurotoxinas de la borrelia hay que decir que nadie ha
aislado nunca ninguna, y que no hace falta la teoria de las toxinas
para explicar daños en organos, la bacteria misma los ocasiona; si
el herx es una respuesta inmune a bacterias muertas, tampoco tienen
nada que ver las toxinas; los ciclos se explican con variacion de
antigenos, y la resistencia con la forma cistica; sobre la
inmunomodulacion hay estudios en alemania que muestran que se debe
principalmente a saturacion de receptores toll-like para el
reclutamiento de macrofagos y neutrofilos, estimulando la il-10
(como hace tambien el ebv),no hace falta inventarse toxinas
misteriosas de la borrelia, y menos que lo haga un medico de familia
(shoemaker (zapatero?)), sin ningun estudio firmado;

la colestiramina tampoco es trigo limpio del todo, intercambia en el
colon iones cloro por bicarbonato organico, acidificando el
organismo; y arrastran todo antibiotico o vitamina liposoluble
orales; lo digo por ser excepticos mientras no haya un estudio
serio, como tantos otros remedios; ahora, si te va bien, estupendo!

cuanto tiempo vas a tomarlo? notaste mejoria en breve? lo tomas con
el estomago vacio o con las comidas? te provoca estreñimiento?

encantado de oir tus mejorias, dan animos, un saludo a todos,
pablo
  


--- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
virginia anez <virginia_anez@y...> escribió:
> Fijate:

> Empe'ze hace 10 dias el colesteramine+levaquin+omeprazole al mismo
tiempo.
> Tengo entendido (dime que opinas porfavor) de que la bart hay que
tratarla minimo 3 meses, pues como cualquier otra lyme-co-
infection ,pero menos severa, lo que quiere de cir que es deficil
tener  tanta mejoria en este lapso de tiempo .Tambien de que el
levaquin es bueno contra el Lyme (me lo dijo JOnes)...ahora sino he
ni siquiera tenido herx ni del Lyme, ni bart  antes de sentirme
mejor (aunque burrascano dijo que el bart no causa herxes).... Lo
que he tenido es mas bien como un lifting o disminucion de los
sintomas hasta cierto punto magico.... por eso pense que el
colesteramine me lo hizo excretar de mi organismo y ya.
> Tambien yo como he tenido muchas infecciones urinarias en el 2004
yo ya habia tomado incluso por 14 dias el leva y de 500mgs en vez de
250 como me mando burrascano.

> Tambien pienso que como de alguna manera he usado buenos
antibioticos desde el principio y atacado casi todas las co-
infections (espero que burrascano no me diga que no encontro algo
mas en los examenes que me practico) y nunca habia addressed las
neurotoxinas.

> El medijo en la cita del 24 de marzo que a la tercera o cuarta
semana de tratamiento me hiba a sentir mejor. Las primeras dos
semanas fueron de puras vitaminas recetadas por el asi como b12
injections.
> Me dijo que el sospechaba de neurotoxinas de bart pero que el lyme
itself lo tenia en la minima expresion.

> Me dijo que fortalezer el sistema inmunologico es clave para
seqguir recuperandose.

> MIGUEL:dejame saber tu opinion por favor.

> Tambien queria preguntarte si tubieras las historias medicas de Dr
Jones en una base de datos que le pidirias al systema que te
arrojara..por ejemplo"Cual fue el antibiotico de mayor empleo en
niños de 5 a 8 anos que resolvio mas symptomas??? o Cuales eran los
cinco symptomas comunes en los ninos que llegaban al consultorio sin
saber que tenian lyme???

> Te pregunto esto por que Jones quiere dejar su legado de alguna
manera y para que le otorguen un grant o donacion para ese estudio
de recolection de data, analisis, clasificacion necesita que la
investigacion tenga un objetivo specifico y claro. Jones tiene una
mina de oro en su consultorio (todos las historias medicas paso por
paso) pero el esta muy ocupado tratando a sus pacientes..es obvio
que el tiene la palabra final y el conocimiento supremo en cuanto a
cual deberia de ser el mejor objetivo para su estudio, pero por
curiosisdad seria bueno saber que quisieras tu u otras personas que
ese estudio respondiera.
>
> Miguel Angel Ramírez <ramirezortega@t...> wrote:
> Virginia,

> ¿Por qué estas tan segura de que es la colestiramina la
responsable de tu mejoría espectacular y no el levaquin? Según
entiendo has comenzado los dos tratamientos a la vez y los mantienes
ambos ¿No es así?¿Cuánto tiempo llevas tomándolos?

> Miguel
> ----- Original Message -----
> From: virginia anez
> To: lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com
> Sent: Friday, April 22, 2005 3:32 AM
> Subject: Re: [Lyme-E] donde estas herx?
>
>
> Migue:

> No tenia ni idea de esta reaccion.

> Gracias por la informacion........pero es que yo no senti esa
molestia o  intensification the los symptomas..sera que esta por
venir en las siguientes semanas????

> Pero queria contribuir con mi testimonio acerca del
cholesteramyne.Ya yo habia oido antes acerca de este medicamento y
sus beneficios a los lyme sufferers pero nunca me imagine que de
verdad, por lo menos en mi caso ,eran las neurotoxins mi gran
molestia y que releasing them de mi cuerpo la mejoria hiba a ser tan
rapida y significativa.
>
>
>
>
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#1721 De: "juanca" <juancaqd@...>
Fecha: Do, 24 de Abr, 2005 10:11 am
Asunto: neurotoxins
juancaqd
Sin conexión Sin conexión
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El mas rápido del foro M.A, pues ya no lo busco lo de Donta.
Creo que lo de las toxinas ha quedado claro que no es un invento,
 
 
Esto está en la guia del 2002 de burrascano.
 
"Two different researchers have provided evidence that B. burgdorferi, like many other pathogenic bacteria, can produce neurotoxins. Early clinical trials aimed at removing these toxins have proven quite promising. I will discuss this in more detail in a later section."
-----------------------------------------------------------------------------
 
AEG asociacion española de gastroeterologia
 
Sección IV: Intestino grueso Volver  
Capítulo 35: Colitis colágena y linfocítica
Fernández Bañares F. y  Viver Pi-Sunyer J. 
 
Colestiramina
 
La colestiramina se ha utilizado en la colitis microscópica basándose en su efecto quelante de citotoxinas bacterianas y de ácidos biliares. Recientemente, se ha demostrado que un 40-65 % de los pacientes con colitis colágena y linfocítica presentan de forma concomitante malabsorción de ácidos biliares, idiopática o asociada a colecistectomía. En esta situación la colestiramina ha mostrado ser altamente eficaz con tasas de remisión clínica entre el 85 y el 92 %. La dosis inicial de colestiramina recomendada es de 8 g/día que se modificará en función de la respuesta clínica (dosis entre 4 y 12 g/día). En algunos pacientes se puede suspender el fármaco tras unos 3 a 6 meses de tratamiento sin recurrencia de la diarrea; sin embargo, en la mayoría es necesario continuar con colestiramina que se ha mostrado muy eficaz para mantener la remisión en estos pacientes.
 
Por otro lado, en un estudio reciente se ha administrado colestiramina a pacientes sin malabsorción de ácidos biliares a dosis de hasta 16 g/día, consiguiéndose una respuesta clínica en un 60 % de los pacientes.
 
Como con los anteriores fármacos, también, en este caso son necesarios estudios controlados que confirmen estos resultados.
-----------------------------------------------------------------------------------------------------------------
 

The Klinghardt Neurotoxin Elimination Protocol

 

Approved by:
American Academy of Neural Therapy and
Institute of Neurobiology (Bellevue, WA, USA)
Institute for Neurobiologie (Stuttgart, Germany)

Academy for Balanced NeuroBiology Ltd (London, United Kingdom)

 

This lecture was presented by Dietrich Klinghardt M.D., Ph.D. at the Jean Piaget Department at the University of Geneva, Switzerland Oct.2002 to physicians and dentists from Europe, Israel, several Arab countries and Asia

 

 

What are Neurotoxins?

Neurotoxins are substances attracted to the mammalian nervous system. They are absorbed by nerve endings and travel inside the neuron to the cell body. On their way they distrupt vital functions of the nerve cell, such as axonal transport of nutrients, mitochondrial respiration and proper DNAtranscription. The body is constantly trying to eliminate neurotoxins via the available exit routes: the liver, kidney, skin and exhaled air. Detox mechanisms include acetylation, sulfation, glucuronidation, oxidation and others. The liver is most important in these processes. Here most elimination products are expelled with the bile into the small intestine and should leave the body via the digestive tract. However, because of the lipophilic/neurotropic nature of the neurotoxins, most are reabsorbed by the abundant nerve endings of the enteric nervous system (ENS) in the intestinal wall. The ENS has more neurons than the spinal chord. From the moment of mucosal uptake the toxins can potentially take 4 different paths:

1.     neuronal uptake and via axonal transport to the spinal chord (sympathetic neurons) or brainstem (parasympathetics) – from here back to the brain.

2.     Venous uptake and via the portal vein back to the liver 

3.     Lymphatic uptake and via the thoracic duct to the subclavian vein 

4.     Uptake by bowel bacteria and tissues of the intestinal tract

 

Here is an incomplete list of common neurotoxins in order of importance:

 

(i)  Heavy metals: such as mercury, lead, cadmium and aluminium.

 

(ii) Biotoxins: such as tetanus toxin, botulinum toxin (botox), ascaridin (from intestinal parasites), unspecified toxins from streptococci, staphylococci, lyme disease, clamydia, tuberculosis, fungal toxins and toxins produced by viruses. Biotoxins are minute molecules (200-1000 kilodaltons) containing nitrogen and sulfur. They belong to a group of chemical messengers which microorganisms use to control the host´s immune system, host behaviour and the host´s eating habits.

 

(iii) Xenobiotics (man-made environmental toxins): such as dioxin, formaldehyde, insecticides, wood preservatives, PCBs etc.

 

(iv) Food Preservatives, excitotoxins and cosmetics: such as aspartame (diet sweeteners) food colourings, flouride,  methyl-and propyl-paraben, etc.

 

I have found that mercury in it´s different chemical forms has a synergistic amplifying effect with all other neurotoxins. When mercury is removed, the body starts to more effectively eliminate all other neurotoxins, even if they are not adressed.

 

 

What are the symptoms?

Any illness can be caused by, or contributed to, or exagerated by neurotoxins. Fatigue, depression, insomnia, memory loss and blunting of the senses are common early symptoms (see list of mercury related symptoms on the following pages).

 

How is the diagnosis established?

1.     History of Exposure: (Did you ever have any amalgam fillings? A tick bite? etc)

2.     Symptoms: (How is your short term memory? Do you have areas of numbness, strange sensations,etc)

3.     Laboratory Testing: (Metals: hair, stool, serum, whole blood, urine analysis, xenobiotics: fatty tissue biopsy, urine)

4.     Autonomic Response Testing: (Dr. Dietrich Klinghardt M.D., Ph.D.)

5.     BioEnergetic Testing (EAV, kinesiology etc.)

6.     Response to Therapeutic Trial

7.     Functional Acuity Contrast Test (measure of Retinal Blood Flow)

 

 

 

TREATMENT

 

Why would we want to treat anyone at all? Is it really needed? Can the body not eliminate these toxins naturally on its own?

 

Here is a short list of  independent risk factors which can either cause accumulation of metals in an otherwise healthy body - or slow down, or inhibit the bodys own elimination processes.

 

·        genetics

·        occupational exposure to toxic material

·        prior illnesses

·        surgical operations

·        medication or ´recreational´ drug use

·        emotional trauma, especially in eary childhood

·        social status

·        high carbohydrate intake combined with protein malnutrition (especially in vegetarians)

·        use of homeopathic mercury

·        food allergies

·        the patients electromagnetic environment (mobile phone use, home close to power lines etc)

·        constipation

·        compromise of head/neck lymphatic drainage (sinusitis, tonsil ectomy scars, poor dental occusion)

·        number of dental amalgam fillings over the patients life-time, number of the patients mothers amalgam fillings

 

We will discuss here only those elimination agents, which are natural, safe  and have also been shown to be as effective (or more effective) than the few available pharmaceuticals. Because these products cannot be patented and exploited for unethical personal gain, little attention has been given to them by European or North American medical researchers. Many of the best scientific studies on this topic are from Asian countries.

 

The basic program:

 

High protein, mineral, fatty acid and fluid intake

Rationale:

·        proteins provide the important precursors to the endogenous metal detox and shuttle agents, such as coeruloplasmin, metallothioneine, glutathione and others. The branched-chain amino acids in cow and goat whey have valuable independent detox effects.

·        Metals attach themselves only in places that are programmed for attachment of metal ions. Mineral deficiency provides the opportunity for toxic metals to attach themselves to vacant binding sites. A healthy mineral base is a prerequisite for all metal detox attempts (selenium, zinc, manganese, germanium, molybdenum etc.). Substituting minerals can detoxify the body by itself. Just as important are electrolytes (sodium, potassium, calcium, magnesium), which help to transport toxic waste across the extracellular space towards the lymphatic and venous vessels.

·        Lipids (made from fatty acids) make up 60-80 % of the central nervous system and need to be constantly replenished. Deficiency makes the nervous system vulnerabe to the fat soluble metals, such as metallic mercury constantly escaping as odorless and invisible vapour evapourating from the amalgam fillings.

·        Without enough fluid intake the kidneys may become contaminated with metals. The basal membranes swell up and the kidneys can no longer efficiently filtrate toxins. Adding a balanced electrolyte solution in small amounts to water helps to restore intra-and extracellular fluid balance

 

Cilantro (chinese parsley)

This kitchen herb is capable of mobilizing mercury, cadmium, lead and aluminum in both bones and the central nervous system. It is probably the only effective agent in mobilizing mercury stored in the inracellular space (attached to mitochondria, tubulin, liposomes etc) and in the nucleus of the cell (reversing DNA damage of mercury). Because cilantro mobilizes more toxins then it can carry out of the body, it may flood the connective tissue (where the nerves reside) with metals, that were previously stored in safer hiding places. This process is called re-toxification. It can easily be avoided by simultaneously giving an intestinal toxin-absorbing agent. Our definite choice is the algal organism chlorella. A recent animal study demonstrated rapid removal of aluminum from the skeleton superior to any known other detox agent.

 

Dosage and application of cilantro tincture: give 2 drops 2 times /day in the

beginning, taken just before a meal or 30 minutes after taking chlorella (cilantro causes the gallbadder to dump bile - containing the excreted neurotoxins - into the small intestine. The bile-release occurs naturally as we are eating and is much enhanced by cilantro. If no chlorella is taken, most neurotoxins are reabsorbed on the way down the small intestine by the abundant nerve endings of the enteric nervous system). Gradually increase dose to 10 drops 3 times/day for full benefit. During the initial phase of the detox cilantro should be given 1 week on, 2 –3 weeks off.

 

Other ways of taking cilantro: rub 5 drops twice/day into ankles for mobilization of metals in all organs, joints and structures below the diaphragm, and into the wrists for organs, joints and structures above the diaphragm. The wrists have dense autonomic innervation (axonal uptake of cilantro) and are crossed by the main lymphatic channels (lymphatic uptake).

 

Cilantro tea: use 10 to 20 drops in cup of hot water. Sip slowly. Clears the brain quickly of many neurotoxins. Good for headaches and other acute syptoms (joint pains, angina, headache): rub 10 –15 drops into painful area. Often achieves almost instant pain relief.

 

 

Chlorella:

Both C.pyreneidosa (better absorption of toxins, but harder to digest) and C.vulgaris (higher CGF content – see below, easier to digest, less metal absorbing capability) are available. Chlorella has multiple health inducing effects:

 

Antiviral (especially effective against the cytomegaly virus from the herpes family)

·        Toxin binding (mucopolysaccharide membrane)

      all known toxic metals, environmental toxins such as dioxin and others

·        Repairs and activates the bodys detoxification functions:

·        Dramatically increases reduced glutathion,

·        Sporopollein is as effective as cholestyramin in binding neurotoxins and more effective in binding toxic metals then any other natural substance found.

·        Various peptides restore coeruloplasmin and metallothioneine,

·        Lipids (12.4 %) alpha-and gamma-linoleic acid help to balance the increased intake of fish oil during our detox program and are necessary for a multitude of functions, including formation of ther peroxisomes.

·        Methyl-coblolamine is food for the nervous system, restores damaged neurons and has ist own detoxifying efect.

·        Chlorella growth factor helps the body detoxify itself in a yet not understood profound way. It appears that over millions of years chlorella has developed specific detoxifying proteins and peptides for every existing toxic metal.

·        The porphyrins in chlorophyl have their own strong metal binding effect. Chlorophyll also activates the PPAR-receptor on the nucleus of the cell which is responsible for the transcription of Dna and coding the formation of the peroxisomes (see fish oil), opening of the cell wall (unknown mechanism) which is necessary for all detox procedures, normalizes insulin resistance and much more. Medical drugs that activate the PPAR receptor (such as pioglitazone) have been effective in the treatment of breast and prostate cancer.

·        Super nutrient: 50-60% aminoacid content, ideal nutrient for vegetarians, methylcobolamin - the most easily absorbed and utilized form of B12, B6, minerals, chlorophyll, beta carotene etc.

·        Immune system strengthening

·        Restores bowel flora

·        Digestive aid (bulking agent)

·        Alkalinizing agent (important for patients with malignancies)

 

Dosage: start with 1 gram (=4 tabl) 3-4 times/day. This is the standard maintainance dosage for grown ups for the 6-24 months of active detox. During the more active phase of the detox (every 2-4 weeks for 1 week), whenever cilantro is given, the dose can be increased to 3 grams 3-4 times per day (1 week on, 2-4 weeks back down to the maintainance dosage). Take 30 minutes before the main meals and at bedtime. This way chlorella is exactly in that portion of the small intestine where the bile squirts into the gut at the beginning of the meal, carrying with it toxic metals and other toxic waste. These are  bound by the chlorella cell wall and carried out via the digestive tract. When amalgam fillings are removed, the higher dose should be given for 2 days before and 2-5 days after the procedure (the more fillings are removed, the longer the higher dose should be given). No cilantro should be given around the time of dental work. During this time we do not want to moblize deeply stored metals in addition to the expected new exposure. If you take Vitamin C during your detox program, take it as far away from Chlorella as possible (best after meals).

Side effects: most side effects reflect the toxic effect of the mobilized metals which are shuttled through the organism. This problem is instantly avoided by significantly increasing the chlorella dosage, not by reducing it, which would worsen the problem (small chlorella doses mobilize more metals then are bound in the gut, large chlorella doses bind more toxins then are mobilized). Some people have problems digesting the cell membrane of chlorella. The enzyme cellulase resolves this problem. Cellulase is available in many health food stores in digestive enzyme products. Taking chlorella together with food also helps in some cases, even though it is less effective that way. C.vulgaris has a thinner cell wall and is better toerated by people with digestive problems. Some manufactures have created cell wall free chlorella extracts (NDF, PCA) which are very expensive, less effective - but easily absorbed.

 

Chlorella growth factor

This is a heat extract from chlorella that concentrates certain peptides, proteins and other ingredients. The research on CGF shows that children develop no tooth decay and their dentition (maxillary-facial development) is near perfect. There are less illnesses and children grow earlier to a larger size with higher I.Q and are socially more skilled. There are case reports of patients with dramatic tumor remissions after taking CGF in higher amounts. In our experience, CGF makes the detox experience for the patient much easier, shorter and more effective.

 

Recommended dosage: 1 cap. CGF for each 20 tabl.chlorella

 

 

 

 

Garlic (allium sativum) and wild garlic (allium ursinum)

Garlic has been shown to protect the white and red blood cells from oxidative damage, caused by metals in the blood stream - on their way out – and also has ist own valid detoxification functions. Garlic contains numerous sulphur components, including the most valuable sulph-hydryl groups which oxidize mercury, cadmium and lead and make these metals water soluble. This makes it easy for the organism to excrete these subastances. Garlic also contains alliin whis is enzymatically transformed into allicin, natures most potent antimicrobial agent. Metal toxic patients almost always suffer from secondary infections, which are often responsible for part of the symptoms. Garlic also contains the most important mineral which protects from mercury toxicity, bio active selenium. Most selemium products are poorly absorbable and do not reach those body compartments in need for it. Garlic selenium is the most beneficial natural bioavailable source. Garlic is also protectice for against heart disease and cancer.

The half life of allicin (after crushing garlic) is less then 14 days. Most commercial garlic products have no allicin releasing potential left. This distinguishes freeze dried garlic from all other products. Bear garlic tincture is excellent for use in detox, but less effective as antimicrobial agent.

 

Dosage: 1-3 capsules freeze dried garlic after each meal. Start with 1 capsule after the main meal per day, slowly increase to the higher dosage. Initially the patient may experience die-off reactions (from killing pathogenic fungal or bacterial organisms). Use 5-10 drops bear-garlic on food at least 3 times per day.

 

Fish oil:

The fatty acid complexes EPA and DHA in fish oil make the red and white blood cells more flexible thus improving the microcirculation of the brain, heart and other tissues. All detoxification functions depend on optimal oxygen delivery and blood flow. EPA and DHA protect the brain from viral infections and are needed for the development of intelligence and eye-sight. The most vital cell organelle for detoxification is the peroxisome. These small structures are also responsible for the specific job each cell has: in the pineal gland the meltonin is produced in the peroxisome, in the neurons dopamine and norepinephrine, etc. It is here, where mercury and other toxic metal attach and disable the cell from doing its work. Other researchers have focussed on the mitochondria and other cellorganelles, which in our experience are damaged much later. The cell is constantly trying to make new peroxisomes to replace the damaged ones– for that task it needs an abundance of fatty acids, especially EPA and DHA. Until recently it was believed, that the body can manufacture ist own EPA/DHA from other Omega 3 fatty acids such as fish oil. Today we know, that this process is slow and cannot keep up with the enormous demand for EPA/DHA our systems have in todays toxic environment. Fish oil is now considered an essential nutrient, even for vegetarians. Recent research also revealed, that the transformation humans underwent when apes became intelligent and turned into humans happened only in coastal regions, where the apes started to consume large amounts of fish. Why not benefit from that knowledge and consume more fish oil?

The fatty acids in fish oil are very sensitive to exposure to electromagnetic fields, temperature, light and various aspects of handling and processing. Trans fatty acids, long chain fatty acids, renegade fats and other oxydation products and contaminants are frequently found in most commercial products. Ideally, fish oil should be kept in an uninterrupted cooling chain until it ends up in the patients fridge. The fish-source should be mercury and contaminant free, which is becoming harder and harder. Fish oil should tast slightly fishy but not too much. If there is no fish taste, too much processing and manipulation has destroyed the vitality of the oil. If it tastes too fishy, oxydation products are present. I recommend to use the product recommended below (grade I), where meticulous care has been taken to comply with all the necessary parameters. The clinical results are outstanding.

 

Dosage: 1 capsule Omega 3 taken 4 times/day during the active phase of treatment, 1 caps. twice/day for maintainance

Best if taken together with chlorella

The VegiPearls contain half the amount of EPA/DHA. The vegetarian capsules eliminate even the most remote possibility of containing prions and make the idea of taking fish oil more easily acceptable for vegetarians. Recently a fatty acid receptor has been discovred on the tongue, joining the other more known taste receptors. If the capsules are chewed, the stomach and pancreas start to prepare the digestive tract in exactly the right way to prepare for maximum absorption. Children love chewing the VegiPearls.

To treat bipolar depression, post partum depression and other forms of mental disease, 2000 mg of EPA are needed/day (David Horrobin). For the modulation of malignancies, 120 mg of EPA 4 times/day are needed. The calculations can easily be done with the information given on the label.

 

Balanced electolyte solution (Selectrolyte)

The autonomic nervous system in most toxic patients is dysfunctional. Electric messages in the organism are not received, are misunderstood or misinterpreted. Toxins cannot be shuttled through the extracellular space. Increased intake of natural ocean salt (celtic sea salt) – and avoidance of regular table salt - has been found to be very effective in resolving some of these problems. Most effective is a solution pioneered by the American chemist Ketkovsky. He created the formula for the most effective electrolyte replacement, which was further improved by Morin Labs, and is now called „selectrolyte“. I recommend this to all my patients and have observed, that every aspect of the detoxification process seems to be enhanced. 5 % of the population is sodium or chloride sensitive – the blood pressure goes up (easily reversible). In these patients the detox process takes longer and is more difficult.

 

Dosage: 1 tsp in a cup of good water 1-3 times/day During times of greater stress the dosage can be temporarily increased to 1 tbsp 3 times/day

 

More agressive approaches, such as i.v Glutathione, Vit.C, DMPS, CaEDTA and others have a place in reasonably healthy people but often worsen the condition in patients with advanced illness.

Most valuable is the addition of psychotherapeutic interventions such as applied psychoneurobiology (APN) and mental field therapy (MFT) to trigger the release of toxins from their hiding places.

 

Chlorella, cilantro, garlic-products and fatty acids vary greatly in quality and nutrient content, also in content of contaminants.  I no longer recommend BioReurella and other products that have not undergone or passed our quality control screening process.

 

 

Heavy metal detox has to be done carefully and right!

 

October 2002                                       

Dietrich Klinghardt, MD, PhD

Bellevue, Washington, USA

www.neuraltherapy.com

 
 
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#1720 De: Miguel Angel Ramírez <ramirezortega@...>
Fecha: Do, 24 de Abr, 2005 9:52 am
Asunto: Bbtox1: neurotoxina producida por Borrelia Burgdorferi.
miguelramire...
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
 

 

Mark J. Cartwright, Ph.D.
Boston University Medical Center
Boston VA Medical Center
88 East Newton Street, E-639
Boston, MA 02118

A Novel Toxin (Bb Tox 1) of Borrelia burgdorferi
Mark J. Cartwright, Ph.D.*, Suzanne E. Martin, Ph.D. and Sam T. Donta, M.D.

The mechanisms responsible for many of the symptoms of Lyme disease remain to be delineated. Because many of the symptoms involve the nervous system, we postulated that the Lyme spirochetes produce a toxin that interferes with normal neurophysiological function. We have identified and cloned a gene of B. burgdorferi which encodes a protein that is a neurotoxin.

Initially, degenerate primers were designed to highly conserved regions within various toxin groups. These primers were used for amplification of DNA extracted from B. burgdorferi strain 2591 to identify genes that express proteins analogous to existing toxins. Degenerate primers designed to the highly conserved catalytic domains of diphtheria and pertussis toxins yielded an amplification product. The product was cloned, sequenced, and subsequently identified in The Institute of Genomic Research (TIGR) database as BB0755, a 37 kD protein of unknown function. The full length gene for BB0755 was cloned, expressed and purified using epitope tags in the pET30a expression system, and the resultant recombinant protein renamed Bbtox1. Using the synthetic target agmantine, Bbtox1 exhibited ADP-ribosyltransferase activity. No ADP-ribosyltransferase activity was detected using elongation factor 2 as the target. In tissue culture, Bbtox1 affected the morphology (rounding) of Y1 mouse adrenal cells and C6 rat glial cells. Bbtox1 induced cell death in both Y1 and C6 cells. C6 glial cells responded to Bbtox1 in a dose and time dependent manner. Brefeldin A, an inhibitor of the trans-golgi network, accelerated the onset of action of Bbtox1 an Y1 adrenal cells.

The effects of Bbtox1 are consistent with a mechanism of action similar to that of botulinum C2 and other cytoskeletal toxins. Studies are underway to identify the cellular target of Bbtox1 and its role in Lyme Disease. In addition, a homologous gene in Treponema pallidum of undefined function is being analyzed to determine if it codes for a toxin similar to Bbtox1.

 


#1719 De: Miguel Angel Ramírez <ramirezortega@...>
Fecha: Do, 24 de Abr, 2005 9:51 am
Asunto: Bbtox1: neurotoxina producida por Borrelia Burgdorferi.
miguelramire...
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
 
Research Briefs

Possible key to Lyme disease. A toxin that may be responsible for many of the symptoms associated with Lyme disease has been identified by Boston University Medical Center (BUMC) researchers. The study results were presented November 13 at the annual meeting of the Infectious Diseases Society of America.

Dr. Sam Donta, professor of medicine and director of the BUMC Lyme Disease Center, and his research team recently identified a substance produced by the Lyme disease bacterium (B. burgdorferi) that appears to kill nervous system cells. "If we can learn precisely how the toxin works, we may be able to revolutionize the diagnosis and treatment of this debilitating disease," he says.

Lyme disease was first identified in 1975 and has been discovered in every region of the United States as well as in Europe, Asia, Africa, and Australia. The bacterium is transmitted to humans by the bite of an infected tick.

Members of the research team don't completely understand how the toxin acts, but believe that it may work similarly to botulism, tetanus, and cholera toxins. "Lyme disease patients suffer from many symptoms, and if this toxin is at the root of those, it may be possible to make a vaccine, or antitoxin, like the ones available for botulism and tetanus," says Donta.

It may also be possible to develop a better test for the disease using the newly identified toxin. "Antibodies to the toxin may appear in the blood, urine, or spinal fluid," he explains. Studies are already under way to identify the specific target of the toxin and its precise role in Lyme disease.

The research was conducted with the help of a grant from the Thaler Family and Pasiss Family Foundation.


#1718 De: Miguel Angel Ramírez <ramirezortega@...>
Fecha: Do, 24 de Abr, 2005 9:34 am
Asunto: Patogenia de la Borreliosis de Lyme
miguelramire...
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=12194230&dopt=Abstract

Przegl Epidemiol. 2002;56 Suppl 1:57-67. Related Articles, Links


[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 mielin production cells, probably by antibodies, induced in
cross reaction.

Publication Types:
Review
Review, Tutorial

PMID: 12194230 [PubMed - indexed for MEDLINE]

#1717 De: "juanca" <juancaqd@...>
Fecha: Do, 24 de Abr, 2005 9:22 am
Asunto: Re: [Lyme-E] donde estas herx?
juancaqd
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
Las toxinas del lyme fueron aisladas y descubiertas por Donta, no
son ningun invento y hay multitud de bacterias que producen toxinas
peligrosas como una de las variantes del E.coli.
Shoemaker no es el único que cree en las toxinas del lyme.
 
J.C
----- Original Message -----
From: antsettler
Sent: Sunday, April 24, 2005 4:20 AM
Subject: RE: [Lyme-E] donde estas herx?


hola,

todo ese conocimiento acumulado que mencionas es oro puro para los
enfermos de lyme; si yo puedo aportar algo cuenta conmigo, aunque
estoy limitado, estadisticas, sistemas expertos o analizar
dinamicas, en la medida que pueda

sobre las neurotoxinas de la borrelia hay que decir que nadie ha
aislado nunca ninguna, y que no hace falta la teoria de las toxinas
para explicar daños en organos, la bacteria misma los ocasiona; si
el herx es una respuesta inmune a bacterias muertas, tampoco tienen
nada que ver las toxinas; los ciclos se explican con variacion de
antigenos, y la resistencia con la forma cistica; sobre la
inmunomodulacion hay estudios en alemania que muestran que se debe
principalmente a saturacion de receptores toll-like para el
reclutamiento de macrofagos y neutrofilos, estimulando la il-10
(como hace tambien el ebv),no hace falta inventarse toxinas
misteriosas de la borrelia, y menos que lo haga un medico de familia
(shoemaker (zapatero?)), sin ningun estudio firmado;

la colestiramina tampoco es trigo limpio del todo, intercambia en el
colon iones cloro por bicarbonato organico, acidificando el
organismo; y arrastran todo antibiotico o vitamina liposoluble
orales; lo digo por ser excepticos mientras no haya un estudio
serio, como tantos otros remedios; ahora, si te va bien, estupendo!

cuanto tiempo vas a tomarlo? notaste mejoria en breve? lo tomas con
el estomago vacio o con las comidas? te provoca estreñimiento?

encantado de oir tus mejorias, dan animos, un saludo a todos,
pablo
  


--- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
virginia anez <virginia_anez@y...> escribió:
> Fijate:

> Empe'ze hace 10 dias el colesteramine+levaquin+omeprazole al mismo
tiempo.
> Tengo entendido (dime que opinas porfavor) de que la bart hay que
tratarla minimo 3 meses, pues como cualquier otra lyme-co-
infection ,pero menos severa, lo que quiere de cir que es deficil
tener  tanta mejoria en este lapso de tiempo .Tambien de que el
levaquin es bueno contra el Lyme (me lo dijo JOnes)...ahora sino he
ni siquiera tenido herx ni del Lyme, ni bart  antes de sentirme
mejor (aunque burrascano dijo que el bart no causa herxes).... Lo
que he tenido es mas bien como un lifting o disminucion de los
sintomas hasta cierto punto magico.... por eso pense que el
colesteramine me lo hizo excretar de mi organismo y ya.
> Tambien yo como he tenido muchas infecciones urinarias en el 2004
yo ya habia tomado incluso por 14 dias el leva y de 500mgs en vez de
250 como me mando burrascano.

> Tambien pienso que como de alguna manera he usado buenos
antibioticos desde el principio y atacado casi todas las co-
infections (espero que burrascano no me diga que no encontro algo
mas en los examenes que me practico) y nunca habia addressed las
neurotoxinas.

> El medijo en la cita del 24 de marzo que a la tercera o cuarta
semana de tratamiento me hiba a sentir mejor. Las primeras dos
semanas fueron de puras vitaminas recetadas por el asi como b12
injections.
> Me dijo que el sospechaba de neurotoxinas de bart pero que el lyme
itself lo tenia en la minima expresion.

> Me dijo que fortalezer el sistema inmunologico es clave para
seqguir recuperandose.

> MIGUEL:dejame saber tu opinion por favor.

> Tambien queria preguntarte si tubieras las historias medicas de Dr
Jones en una base de datos que le pidirias al systema que te
arrojara..por ejemplo"Cual fue el antibiotico de mayor empleo en
niños de 5 a 8 anos que resolvio mas symptomas??? o Cuales eran los
cinco symptomas comunes en los ninos que llegaban al consultorio sin
saber que tenian lyme???

> Te pregunto esto por que Jones quiere dejar su legado de alguna
manera y para que le otorguen un grant o donacion para ese estudio
de recolection de data, analisis, clasificacion necesita que la
investigacion tenga un objetivo specifico y claro. Jones tiene una
mina de oro en su consultorio (todos las historias medicas paso por
paso) pero el esta muy ocupado tratando a sus pacientes..es obvio
que el tiene la palabra final y el conocimiento supremo en cuanto a
cual deberia de ser el mejor objetivo para su estudio, pero por
curiosisdad seria bueno saber que quisieras tu u otras personas que
ese estudio respondiera.
>
> Miguel Angel Ramírez <ramirezortega@t...> wrote:
> Virginia,

> ¿Por qué estas tan segura de que es la colestiramina la
responsable de tu mejoría espectacular y no el levaquin? Según
entiendo has comenzado los dos tratamientos a la vez y los mantienes
ambos ¿No es así?¿Cuánto tiempo llevas tomándolos?

> Miguel
> ----- Original Message -----
> From: virginia anez
> To: lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com
> Sent: Friday, April 22, 2005 3:32 AM
> Subject: Re: [Lyme-E] donde estas herx?
>
>
> Migue:

> No tenia ni idea de esta reaccion.

> Gracias por la informacion........pero es que yo no senti esa
molestia o  intensification the los symptomas..sera que esta por
venir en las siguientes semanas????

> Pero queria contribuir con mi testimonio acerca del
cholesteramyne.Ya yo habia oido antes acerca de este medicamento y
sus beneficios a los lyme sufferers pero nunca me imagine que de
verdad, por lo menos en mi caso ,eran las neurotoxins mi gran
molestia y que releasing them de mi cuerpo la mejoria hiba a ser tan
rapida y significativa.
>
>
>
>
> Para cancelar su suscripción a este grupo, envíe un mensaje de
correo-e a:
> lyme_y_otras_zoonosis_cronicas_espanol-unsubscribe@yahoogroups.com
>
>
>
>
> Patrocinio de Yahoo! Grupos
>
> ---------------------------------
> Enlaces a Yahoo! Grupos
>
>    Para visitar tu grupo en la web, accede a :
>
http://es.groups.yahoo.com/group/lyme_y_otras_zoonosis_cronicas_espan
ol/
>  
>    Para cancelar tu suscripción a este grupo, envía un mensaje a:
> lyme_y_otras_zoonosis_cronicas_espanol-unsubscribe@yahoogroups.com
>  
>    El uso que hagas de Yahoo! Grupos está sujeto a las Condiciones
del servicio de Yahoo!.
>
>
>            
> ---------------------------------





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Checked by AVG Anti-Virus.
Version: 7.0.300 / Virus Database: 266.9.10 - Release Date: 14/04/2005

#1716 De: "antsettler" <sacorroto@...>
Fecha: Do, 24 de Abr, 2005 2:20 am
Asunto: RE: [Lyme-E] donde estas herx?
antsettler
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
hola,

todo ese conocimiento acumulado que mencionas es oro puro para los
enfermos de lyme; si yo puedo aportar algo cuenta conmigo, aunque
estoy limitado, estadisticas, sistemas expertos o analizar
dinamicas, en la medida que pueda

sobre las neurotoxinas de la borrelia hay que decir que nadie ha
aislado nunca ninguna, y que no hace falta la teoria de las toxinas
para explicar daños en organos, la bacteria misma los ocasiona; si
el herx es una respuesta inmune a bacterias muertas, tampoco tienen
nada que ver las toxinas; los ciclos se explican con variacion de
antigenos, y la resistencia con la forma cistica; sobre la
inmunomodulacion hay estudios en alemania que muestran que se debe
principalmente a saturacion de receptores toll-like para el
reclutamiento de macrofagos y neutrofilos, estimulando la il-10
(como hace tambien el ebv),no hace falta inventarse toxinas
misteriosas de la borrelia, y menos que lo haga un medico de familia
(shoemaker (zapatero?)), sin ningun estudio firmado;

la colestiramina tampoco es trigo limpio del todo, intercambia en el
colon iones cloro por bicarbonato organico, acidificando el
organismo; y arrastran todo antibiotico o vitamina liposoluble
orales; lo digo por ser excepticos mientras no haya un estudio
serio, como tantos otros remedios; ahora, si te va bien, estupendo!

cuanto tiempo vas a tomarlo? notaste mejoria en breve? lo tomas con
el estomago vacio o con las comidas? te provoca estreñimiento?

encantado de oir tus mejorias, dan animos, un saludo a todos,
pablo



--- En lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com,
virginia anez <virginia_anez@y...> escribió:
> Fijate:
>
> Empe'ze hace 10 dias el colesteramine+levaquin+omeprazole al mismo
tiempo.
> Tengo entendido (dime que opinas porfavor) de que la bart hay que
tratarla minimo 3 meses, pues como cualquier otra lyme-co-
infection ,pero menos severa, lo que quiere de cir que es deficil
tener  tanta mejoria en este lapso de tiempo .Tambien de que el
levaquin es bueno contra el Lyme (me lo dijo JOnes)...ahora sino he
ni siquiera tenido herx ni del Lyme, ni bart  antes de sentirme
mejor (aunque burrascano dijo que el bart no causa herxes).... Lo
que he tenido es mas bien como un lifting o disminucion de los
sintomas hasta cierto punto magico.... por eso pense que el
colesteramine me lo hizo excretar de mi organismo y ya.
> Tambien yo como he tenido muchas infecciones urinarias en el 2004
yo ya habia tomado incluso por 14 dias el leva y de 500mgs en vez de
250 como me mando burrascano.
>
> Tambien pienso que como de alguna manera he usado buenos
antibioticos desde el principio y atacado casi todas las co-
infections (espero que burrascano no me diga que no encontro algo
mas en los examenes que me practico) y nunca habia addressed las
neurotoxinas.
>
> El medijo en la cita del 24 de marzo que a la tercera o cuarta
semana de tratamiento me hiba a sentir mejor. Las primeras dos
semanas fueron de puras vitaminas recetadas por el asi como b12
injections.
> Me dijo que el sospechaba de neurotoxinas de bart pero que el lyme
itself lo tenia en la minima expresion.
>
> Me dijo que fortalezer el sistema inmunologico es clave para
seqguir recuperandose.
>
> MIGUEL:dejame saber tu opinion por favor.
>
> Tambien queria preguntarte si tubieras las historias medicas de Dr
Jones en una base de datos que le pidirias al systema que te
arrojara..por ejemplo"Cual fue el antibiotico de mayor empleo en
niños de 5 a 8 anos que resolvio mas symptomas??? o Cuales eran los
cinco symptomas comunes en los ninos que llegaban al consultorio sin
saber que tenian lyme???
>
> Te pregunto esto por que Jones quiere dejar su legado de alguna
manera y para que le otorguen un grant o donacion para ese estudio
de recolection de data, analisis, clasificacion necesita que la
investigacion tenga un objetivo specifico y claro. Jones tiene una
mina de oro en su consultorio (todos las historias medicas paso por
paso) pero el esta muy ocupado tratando a sus pacientes..es obvio
que el tiene la palabra final y el conocimiento supremo en cuanto a
cual deberia de ser el mejor objetivo para su estudio, pero por
curiosisdad seria bueno saber que quisieras tu u otras personas que
ese estudio respondiera.
>
> Miguel Angel Ramírez <ramirezortega@t...> wrote:
> Virginia,
>
> ¿Por qué estas tan segura de que es la colestiramina la
responsable de tu mejoría espectacular y no el levaquin? Según
entiendo has comenzado los dos tratamientos a la vez y los mantienes
ambos ¿No es así?¿Cuánto tiempo llevas tomándolos?
>
> Miguel
> ----- Original Message -----
> From: virginia anez
> To: lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com
> Sent: Friday, April 22, 2005 3:32 AM
> Subject: Re: [Lyme-E] donde estas herx?
>
>
> Migue:
>
> No tenia ni idea de esta reaccion.
>
> Gracias por la informacion........pero es que yo no senti esa
molestia o  intensification the los symptomas..sera que esta por
venir en las siguientes semanas????
>
> Pero queria contribuir con mi testimonio acerca del
cholesteramyne.Ya yo habia oido antes acerca de este medicamento y
sus beneficios a los lyme sufferers pero nunca me imagine que de
verdad, por lo menos en mi caso ,eran las neurotoxins mi gran
molestia y que releasing them de mi cuerpo la mejoria hiba a ser tan
rapida y significativa.
>
>
>
>
> Para cancelar su suscripción a este grupo, envíe un mensaje de
correo-e a:
> lyme_y_otras_zoonosis_cronicas_espanol-unsubscribe@yahoogroups.com
>
>
>
>
> Patrocinio de Yahoo! Grupos
>
> ---------------------------------
> Enlaces a Yahoo! Grupos
>
>    Para visitar tu grupo en la web, accede a :
>
http://es.groups.yahoo.com/group/lyme_y_otras_zoonosis_cronicas_espan
ol/
>
>    Para cancelar tu suscripción a este grupo, envía un mensaje a:
> lyme_y_otras_zoonosis_cronicas_espanol-unsubscribe@yahoogroups.com
>
>    El uso que hagas de Yahoo! Grupos está sujeto a las Condiciones
del servicio de Yahoo!.
>
>
>
> ---------------------------------

#1715 De: Miguel Angel Ramírez <ramirezortega@...>
Fecha: Sáb, 23 de Abr, 2005 8:10 pm
Asunto: Diseases produced by Borrelia
miguelramire...
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
1: Enferm Infecc Microbiol Clin. 2005 Apr;23(4):232-40. Links


[Diseases produced by Borrelia.]

[Article in Spanish]

Escudero-Nieto R, Guerrero-Espejo A.

Laboratorio de Espiroquetas y Patogenos Especiales. Servicio de
Bacteriologia. Centro Nacional de Microbiologia. ISCIII. Majadahonda.
Madrid. Spain.

Lyme borreliosis, caused by Borrelia burgdorferi sensu lato, is a
multi-organ infection with dermatological, rheumatological,
neurological, and cardiac manifestations. The main characteristic is a
skin lesion, named erythema migrans. Relapsing fever, caused by
numerous species of Borrelia, is characterized by a periodic cycle of
acute and afebrile episodes. The serological diagnosis of these
infections has limited value in sensitivity, specificity and predictive
values. Lyme borreliosis is usually diagnosed by recognition of a
characterisic clinical picture with serological confirmation, and the
diagnosis of relapsing fever relies on direct observation of
spirochetes in peripherical blood. The elected treatment is almost
always tetracycline for the young or for adults but not for pregnant
women, although betalactamic (such as penicillin or 3rd generation
cephalosporin for the central nervious system) or macrolides are
indicated in several situations. The prognosis, with adequate
treatment, is good. In the majority of Spanish regions, due to the low
incidence of these diseases, the prophylactic antimicrobial treatment
after a tick bite is not indicated.

PMID: 15826549 [PubMed - in process]


#1714 De: "anapieraa" <anapieraa@...>
Fecha: Sáb, 23 de Abr, 2005 2:03 am
Asunto: he cambiado mi ID
anapieraa
Sin conexión Sin conexión
Enviar mensaje Enviar mensaje
 
Hola Miguel y todos,

Soy anap_sfc, he cambiado de ID de Yahoo y también un nuevo correo.

Si utilizais el messenger de Yahoo y me quereís añadir, estaré
encantada.

Gracias,

Ana.

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