Re: Barb - Andy s must-see amazing micro-cinema of horror

[Guest guest]

<usenethod@y...> wrote:

> But anyway, those are both piroplasmoses... so what else can we

> compare to, to get a broader picture? I dont know any other

> intra-red-cell infections? I guess bacteremia (in the serum, not the

> cells) is usually/always(?) pretty febrile - is that a fact thats

> contributing to your assessment?

Re the latter... its worth noting that J Radolf considers it likely

that the BLPs on the outside of the outer mebrane are severely

downregulated in vivo, and that the OM lipids are essentially not

antigenic. If so, then the outside is not intrinsically highly

antigenic - the bulk of the BLP antigens that are powerful TLR ligands

being covered in the living beast. In Radolfs opinion, this may

explain why passive antibody transfer does not protect the mouse from

infection, in spite of the observation that specific antibody can be

nicely borrelicidal in vitro - in vitro the BLPs are perhaps much more

present on the exterior.

This could conceivably contribute to the intact organism having low

antigenicity in blood. And indeed I believe it has been remarked that

in vivo, areas where the living spirochetal forms are visualized are

not necessarily that inflamed?

Of course, there are other possible angles on these observations....

[Guest guest]

This Rad Elf guy seems to be onto something.

>

> > But anyway, those are both piroplasmoses... so what else can we

> > compare to, to get a broader picture? I dont know any other

> > intra-red-cell infections? I guess bacteremia (in the serum, not

the

> > cells) is usually/always(?) pretty febrile - is that a fact thats

> > contributing to your assessment?

>

> Re the latter... its worth noting that J Radolf considers it likely

> that the BLPs on the outside of the outer mebrane are severely

> downregulated in vivo, and that the OM lipids are essentially not

> antigenic. If so, then the outside is not intrinsically highly

> antigenic - the bulk of the BLP antigens that are powerful TLR

ligands

> being covered in the living beast. In Radolfs opinion, this may

> explain why passive antibody transfer does not protect the mouse

from

> infection, in spite of the observation that specific antibody can

be

> nicely borrelicidal in vitro - in vitro the BLPs are perhaps much

more

> present on the exterior.

>

> This could conceivably contribute to the intact organism having low

> antigenicity in blood. And indeed I believe it has been remarked

that

> in vivo, areas where the living spirochetal forms are visualized

are

> not necessarily that inflamed?

>

> Of course, there are other possible angles on these

observations....

[Guest guest]

I didn't mean to apply one has to accompany the other -

I was making the point that my disease presentation, was acute -

and my periodic flares were acute.

And later down the road when I had supressed Lymphocytes, the

profile of the CBC changed, and the neutrophils had to take over, but

during flares I had fever and a very high WBC.

Acute is the key word - Presentation was acute, and flares were

actute with high out of range WBCs... as are seen in acute infections

of any type (but not mecessarilty chronic ones). Fever usually

accompanies extremely high WBC (and of course malaise).

In Malaria the terms 'complicated' and 'un complicated' are used to

denote the % RBCs infected- which in turn determines how risky

therapy is (there's a 5% death rate with treated complicated Malaria,

and a that's higher in the slpeen less. Matter of fact the b-

artemether drugs carry substantial risk when used on the spleenless

in malaria because the efficacy in killing is so high. And you are

correct, that in complicated malaria, the flares put people in bed,

and can kill children with underdeveloped immune systems, but in

uncomplicated, the person may just lay low for a day - but fever is

still present.

I'm making a distinction between my case while untreated ( high WBC

during flares/with fever - and a relatively higher WBC in general

(about 8K) with periodic modeerate fevers during the chronic stages)

and people lacking these symptoms........ like CFIDS

Which brings me to a question that just popped into my head -

(Does the ID in CFIDS stand for immunodeficiency?)

Will a person get a CFIDS dx if they present with high fever- or have

elevated WBCs??? Or is a low WBC a prerequisite for a CFIDS dx?

Barb

> > Re Bowen & the videos:

> > IMO, if a very

> > large percentage of RBCs are infected with anything, the patient

is

> > going to be very sick- and by sick I mean fever and high WBC.

> > Sometimes I see on Lymenet people talk about high WBcs- but now

> > often..mostly it's the reverse of me (low WBCs)

>

> Why necessarily a fever and leucocytosis? Certainly sustained or

> intermittant fever is the rule in malaria... Homers article on

> babs says fever is not a necessary charecteristic of babs, but then

> again many people with chronic babesiosis might have substantially

> lower infection mass compared to acute malaria (I'm not sure).

> Concurrent infections could also be a factor there.

>

> But anyway, those are both piroplasmoses... so what else can we

> compare to, to get a broader picture? I dont know any other

> intra-red-cell infections? I guess bacteremia (in the serum, not the

> cells) is usually/always(?) pretty febrile - is that a fact thats

> contributing to your assessment?

[Guest guest]

I think the ID in CFIDS stands for immune disfunction

rather than deficiency. This makes more sense in my

case because although I am immune deficient (hosting a

number of opportunistic infections) I also present as

hyper immune with lots of allergies and chemical

sensitivities.

This is my understanding. Don't have all the

scientific terms for this though. I am an artist not a

scientist.

Marie

Marie

--- Barb Peck <egroups1bp@...> wrote:

> I didn't mean to apply one has to accompany the

> other -

>

> I was making the point that my disease

> presentation, was acute -

> and my periodic flares were acute.

> And later down the road when I had supressed

> Lymphocytes, the

> profile of the CBC changed, and the neutrophils had

> to take over, but

> during flares I had fever and a very high WBC.

> Acute is the key word - Presentation was acute,

> and flares were

> actute with high out of range WBCs... as are seen in

> acute infections

> of any type (but not mecessarilty chronic ones).

> Fever usually

> accompanies extremely high WBC (and of course

> malaise).

>

> In Malaria the terms 'complicated' and 'un

> complicated' are used to

> denote the % RBCs infected- which in turn determines

> how risky

> therapy is (there's a 5% death rate with treated

> complicated Malaria,

> and a that's higher in the slpeen less. Matter of

> fact the b-

> artemether drugs carry substantial risk when used on

> the spleenless

> in malaria because the efficacy in killing is so

> high. And you are

> correct, that in complicated malaria, the flares put

> people in bed,

> and can kill children with underdeveloped immune

> systems, but in

> uncomplicated, the person may just lay low for a day

> - but fever is

> still present.

>

> I'm making a distinction between my case while

> untreated ( high WBC

> during flares/with fever - and a relatively higher

> WBC in general

> (about 8K) with periodic modeerate fevers during the

> chronic stages)

> and people lacking these symptoms........ like CFIDS

>

> Which brings me to a question that just popped into

> my head -

> (Does the ID in CFIDS stand for immunodeficiency?)

>

> Will a person get a CFIDS dx if they present with

> high fever- or have

> elevated WBCs??? Or is a low WBC a prerequisite for

> a CFIDS dx?

>

> Barb

>

>

>

>

>

>

> > > Re Bowen & the videos:

> > > IMO, if a very

> > > large percentage of RBCs are infected with

> anything, the patient

> is

> > > going to be very sick- and by sick I mean fever

> and high WBC.

> > > Sometimes I see on Lymenet people talk about

> high WBcs- but now

> > > often..mostly it's the reverse of me (low WBCs)

> >

> > Why necessarily a fever and leucocytosis?

> Certainly sustained or

> > intermittant fever is the rule in malaria...

> Homers article on

> > babs says fever is not a necessary charecteristic

> of babs, but then

> > again many people with chronic babesiosis might

> have substantially

> > lower infection mass compared to acute malaria

> (I'm not sure).

> > Concurrent infections could also be a factor

> there.

> >

> > But anyway, those are both piroplasmoses... so

> what else can we

> > compare to, to get a broader picture? I dont know

> any other

> > intra-red-cell infections? I guess bacteremia (in

> the serum, not the

> > cells) is usually/always(?) pretty febrile - is

> that a fact thats

> > contributing to your assessment?

>

>

>

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