Ceftriaxon - good or bad in Cpn infections?

Because nobody knows what I have, I am treated with iv Ceftriaxon at this time. Does someone know if Ceftriaxon (a betalactam antibiotic) may worsen Cpn infection?

I think I've read that Stratton recommends Amoxicillin for Cpn treatment. Is this true? If so, than Ceftriaxon might also be of benefit, because both are cell wall antibiotics.

That's not why amoxicillin is recommended, though; it's recommended because it serves the same function as NAC, namely reducing disulfide bonds.

Anyway, penicillins do have an effect on Cpn, since while it doesn't have a cell wall it uses cell wall chemistry in the process of replicating (where one RB splits into two RBs).  But the effect is that RBs become really big without dividing; then when the penicillin is removed they divide.

Thanks, Norman.

"But the effect is that RBs become really big without dividing; then when the penicillin is removed they divide."

Did I get it right: This effect also occurs with Ceftriaxon? I ask because Ceftriaxon is not exactly a penicllin, but a cephalosporin. And is it a problem when the RBs become so big?

The study I saw was on penicillin, but ceftriaxone has a similar mechanism of action, so it can be expected to have a similar effect.

It's better to have enlarged RBs than to have the RBs divide and complete their life cycle (by turning into EBs and then leaving the host cell to infect other cells), but it doesn't represent a real cure for the infection, it just slows it down.

RBs are located IN the cells, right? I don't understand how an antibiotic like penicillin or a cephalosporin, which cannot get into human cells, may have any effect on something that is located inside a cell. Or am I wrong?

Yes, RBs are inside cells, but enough penicillin gets in to affect them.  Hmm, I've never paid much attention to what concentration these experiments used.  Taking a quick look, this paper


used 5 micrograms/milliliter of penicillin G in one experiment and 20 in another, which seems to be similar to the doses used in humans.  (This is something one has to watch out for: people claiming an effect when really it's only present at unrealistic doses.  But that doesn't seem to be the case here.)

ET lives outside cells: just stress/antibiotics doing this,that et going from extracelullar places to intracelullars places .... next stress RB going to fibroblastoms/cystics etc etc etc...

Penicilin G doesnt working for cells of chlamydia= Penicilin G no transformating to penicilamine transgenese...just betalactams AMOKSIKLAV/AUGMENTIN/AMOXICILIN can do it...

PEN G is good for boreliose cell walls

PEN G do resistance of bacteria on macrolides: be ware