HealingWell
Search Close Search
☰

.

Support Forums
>
Lyme Disease
✚ New Topic ✚ Reply
❬ ❬ Previous Thread |Next Thread ❭ ❭
Posted 5/22/2023 6:05 AM (GMT -5)
.

Post Edited (RainyCloud) : 5/22/2023 6:02:13 AM (GMT-8)

Posted 5/22/2023 7:01 AM (GMT -5)
i only read the abstract Rainy - but its not a surprising finding

remember - true antimicrobial resistance is one thing - it results from genetic adaptation to antibiotics via the natural selection process to create a mutated version of the bacteria that has specific new enzymes that can break down, pump out or resist the action of a given class of antibiotics (or in the case of multiple mutations - multiple classes of antibiotics)

whereas persistence after antibiotic therapy - for instance as we see in lyme - is via a variety of other mechanisms - not related to new genetic adaptations in response to selection pressure due to exposure to antibiotics
eg
1, persister cells - dormant - very low metabolic states - that do not use the pathways targeted by antibiotics - -and as a result render the bacteria immune to abx doses up to 1500x higher than their faster growing / higher metabolising counterparts of the same species. these microbes have always done this - its not a new adaptation to antibiotics.
2, intracellular infection - where the cells membranes provide a barrier protecting the organisms inside - again intracellular organisms have always done this.
3, biofilms- cells inside bacterial biofilms include persister cells - but also have the added survival advantage of the physical barrier presented by the outer bacteria protecting the inner bacteria from the actions of the immune system.

many of these bacteria such a bartonella have other specialised mechanisms of survival - for instance stimulating the host to produce fibrin that presents physical barrier to immune cells from attacking infected cells - and also causes infected cells to stick in the capillaries prevents them from travelling to the spleen where they would be detected as abnormal and removed.
and borrelia change their outer surface proteins to evade recognition by the host immune system
ete etc

overall it makes sense that samples taken from wild animals will have lower actual antimicrobial resistance - as in theory these animals will have had little exposure to antibiotics - and therefore v little natural selection pressure on the microbes inside them - while farm animals that are routinely exposed to antibiotics will have higher levels of true antimicrobial resistance
Posted 5/22/2023 12:06 PM (GMT -5)
i was just reacting to the article itself Rainy.

if i am not mistaken - there have been multiple efforts to try to stimulate borrelia to produce antimicrobial resistance in the past - and to my knowledge - no one has been able to demonstrate it does this.

the way these trails are usually done is by growing a culture of the bacteria - treating it with enough antibiotics to kill 50% or more of the cells- then remove those still living - culture them for a while - and dose them again with abx - and so on - so you are effectively selecting those more tolerant - until you have fully resistant strains.
different bacterial reach this point easier than others

but - when they do this with borrelia - they have not been able to generate true antimicrobial resistant strains - just lots of persister cells i think.

the antibiotic combination issue is an interesting one

to my mind - the LLMDs that are rotating abx are mainly doing so to address different infections along the route of their treatment path
like Dr J that girlie sees - first "gently" treating lyme - while hitting babesia - then later different dugs for lyme persisters and bart - rather than a true ongoing rotation for borrelia alone

i guess you could argue that Dr J does rotate abx when he uses tinidazole/metronidazole after ceftin etc - here the theory is that these mild abx like doxy and ceftin tend to cause the spirochetes to form round body forms / cysts in large numbers - and so the azoles are used as they are known to kill round body forms. thsi approach is used to try to defeat the persister mechanisms - rather than abx resistance

Horovitz tends to use the same drug combos continuously - rather than rotating

some doctors pulse the abx for lyme and co - but again here i think they are mainly pulsing the same drugs - rather than rotating - and as i understand it - the theory here is that the stress the bacteria experience from having to enter and recover from their persister state is metabolically taxing for them and so its a method used to increase the stress on the bacteria to weaken their defences/defeat the persister mechanism.

its a good topic - ( discussions around how to design the most effective abx regimen for lyme ) so this is just my brain dump on the subject

hope its of some use
✚ New Topic ✚ Reply