so here's my big question

[Guest guest]

I've asked it before. Do bacteria like the ones I may have, sense

their own density, and/or host inflammation, and stop growing?

[Footnote: If so, why didn't they *start* growing, and thus become

more abx-sensitive, when I killed off ~90% of them, if not more like

99.99% - and felt 95% better? In that scenario, my improvement should

have just gotten faster and faster all the way to completion instead

of slowing down. This is assuming a monotonic, " veeeery roughly

linear " function from bacteria to sickness over the relevant range, so

to speak.]

I used to wonder about this in 2004 before I knew much about ecology -

how can there even *be* a chronic infection? It's a struggle, right, a

conflict? And someone's got to get the upper hand at some point. So

why don't I either get progressively better, or progressively worse?

Then I would think, I guess, about the dynamics of trench warfare in

WWI...

But WWI, static though it may have been, did eventually end. Albiet

mainly because the central powers ran out of people and/or dough, as I

recall, but microbes synthesize " people " (cells) and " dough " (ATP)

ever anew. Anyway...

I kind of stopped asking this question once I started thinking of a

near-zero-turnover infection causing my illness. That would be like a

war with no killing - easy to see why that kind of struggle doesn't

change much on the timescale of my life.

Of course, even for an infection with lots of turnover, there can

still be equilibrium. Because it's not a war, not a struggle for

*conquest* - the microbes instead struggle to *exploit*, so they'd

rather not carry out the conquest by killing the host. That's the

ecological reason - but there's still the need for a mechanism.

That's where Blaser's thoughts are interesting. He'd like to

know how helicobacter negotiates with the human host. As he says, if

stable equilibrium is to occur - rather than eradication of the

parasite or infinite proliferation of the parasite - there must be

some kind of *negative* feedback somewhere in the host-parasite system.

But nowhere in his writings do I find anything on helicobacter

actually reducing its growth. He does mention it getting pruned by the

host immune system...

Relatedly, I once read one about how Bb multiplies in the tick gut. It

mightve been this one, but I don't have full-text right now:

Am J Trop Med Hyg. 1990 Apr;42(4):352-7.

Growth kinetics of the Lyme disease spirochete (Borrelia

burgdorferi) in vector ticks (Ixodes dammini).

Piesman J, Oliver JR, Sinsky RJ.

PMID: 2331043 [PubMed - indexed for MEDLINE]

I seem to remember the authors suggesting, perhaps in an opinionish,

no-citation sort of way, that the Bb had to stop replicating at some

point or the tick would be killed. All the abstract says is:

" Lyme disease spirochetes (Borrelia burgdorferi) multiplied rapidly in

larval Ixodes dammini, reaching a mean density of 2,735

spirochetes/tick on day 15 post-repletion. A 5-fold drop in spirochete

levels occurred during the subsequent premolting period. Recently

molted nymphs contained a mean of less than 300 spirochetes/tick.

Following nymphal repletion, spirochete multiplication renewed,

reaching a mean abundance of 61,275 spirochetes/nymph on day 75

post-repletion. A 10-fold drop in spirochete abundance occurred again

when ticks molted to the adult stage. "

" Pruning " by the host (with the implicit consent of Bb), or

self-regulation by Bb? I think insects probably have inducible

(nonspecific) immunity, but could it really take 15 days to rev up? I

doubt it...

[Guest guest]

I think you do get progressively worse. You're just not aware of it, especially when your youth compensates for the damage being done. Or perhaps you don't make the connection with various other conditions that develop over time, such as hormonal issues or heart conditions, some which take a long time to appear. I used to think I was just severely fatigued all the time, nothing much else. Seemed mysterious. Eventually being dx'd and treating thyroid & adrenal issues didn't help much. Still seemed like a mystery. Eventually the fatigue has progressed to chronic inflammation, arthritic type conditions, and constant migraines and I think they're all related to my underlying infection and the stress it puts on my body. I used to think I'd live to be a 100 easily. Now I wouldn't be surprised if I don't make 60. penny <usenethod@...>

wrote: I've asked it before. Do bacteria like the ones I may have, sensetheir own density, and/or host inflammation, and stop growing? [Footnote: If so, why didn't they *start* growing, and thus becomemore abx-sensitive, when I killed off ~90% of them, if not more like99.99% - and felt 95% better? In that scenario, my improvement shouldhave just gotten faster and faster all the way to completion insteadof slowing down. This is assuming a monotonic, "veeeery roughlylinear" function from bacteria to sickness over the relevant range, soto

speak.]I used to wonder about this in 2004 before I knew much about ecology -how can there even *be* a chronic infection? It's a struggle, right, aconflict? And someone's got to get the upper hand at some point. Sowhy don't I either get progressively better, or progressively worse?Then I would think, I guess, about the dynamics of trench warfare inWWI...But WWI, static though it may have been, did eventually end. Albietmainly because the central powers ran out of people and/or dough, as Irecall, but microbes synthesize "people" (cells) and "dough" (ATP)ever anew. Anyway...I kind of stopped asking this question once I started thinking of anear-zero-turnover infection causing my illness. That would be like awar with no killing - easy to see why that kind of struggle doesn'tchange much on the timescale of my life.Of course, even for an infection with lots of turnover, there canstill be

equilibrium. Because it's not a war, not a struggle for*conquest* - the microbes instead struggle to *exploit*, so they'drather not carry out the conquest by killing the host. That's theecological reason - but there's still the need for a mechanism. That's where Blaser's thoughts are interesting. He'd like toknow how helicobacter negotiates with the human host. As he says, ifstable equilibrium is to occur - rather than eradication of theparasite or infinite proliferation of the parasite - there must besome kind of *negative* feedback somewhere in the host-parasite system.But nowhere in his writings do I find anything on helicobacteractually reducing its growth. He does mention it getting pruned by thehost immune system...Relatedly, I once read one about how Bb multiplies in the tick gut. Itmightve been this one, but I don't have full-text right now:Am J Trop Med Hyg. 1990

Apr;42(4):352-7.Growth kinetics of the Lyme disease spirochete (Borreliaburgdorferi) in vector ticks (Ixodes dammini).Piesman J, Oliver JR, Sinsky RJ.PMID: 2331043 [PubMed - indexed for MEDLINE]I seem to remember the authors suggesting, perhaps in an opinionish,no-citation sort of way, that the Bb had to stop replicating at somepoint or the tick would be killed. All the abstract says is:"Lyme disease spirochetes (Borrelia burgdorferi) multiplied rapidly inlarval Ixodes dammini, reaching a mean density of 2,735spirochetes/tick on day 15 post-repletion. A 5-fold drop in spirochetelevels occurred during the subsequent premolting period. Recentlymolted nymphs contained a mean of less than 300 spirochetes/tick.Following nymphal repletion, spirochete multiplication renewed,reaching a mean abundance of 61,275 spirochetes/nymph on day 75post-repletion. A 10-fold drop in spirochete abundance

occurred againwhen ticks molted to the adult stage.""Pruning" by the host (with the implicit consent of Bb), orself-regulation by Bb? I think insects probably have inducible(nonspecific) immunity, but could it really take 15 days to rev up? Idoubt it...