action of penicillin drugs on gram negative , chlamydia?

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sadaca

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hey guys , I just want to clarify this, the reason penicillin agents cannot act on the following:

Chlamydia- b/c it lacks peptidoglycan cell walls
Mycoplasma- lacks a cell wall all together
Gram negative- B/c it has no nuclear membrane.

Could someone plz explain the reason penicillin agents can't treat all gram negative agents? I read it has to do with nuclear membrane but I don't know what that means.

Appreciate it as always,
thank you

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I thought all bacteria didn't have nuclear membrane? Gram negatives have LPS outer-membrane protecting the thin peptidoglycan wall. I would guess the relative inaccessibility of the peptidoglycan layer of the gram negatives makes penicillin a less desirable choice..
 
Surgok has it right, and that, for the most part, is the reason why penicillins are not the drug of choice for gram negative infections.
 
okay thank you so its the LPS thats the reason B lactams can't reach the peptidoglycan layer in gram neg? Thank you
 
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DIT said that you don't use beta-lactam abx on gram negs because they produce beta-lactamases that are stored in the periplasm.
 
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but then FA says gram negative bacilli are resistant to penicillin G and vanc because the outer membrane prohibits entry of those two, but they may be susceptible to aminopenicillins. So, who knows.
 
damn wow, as a former microbiologist, this is painful :)

penicillins do work on gram negatives, but they were historically abused. The drug of choice for gonorrhea was penicillin back in the day. Syphillis is just a fancy Gram negative (genetically speaking) and structurally is organized similarly, except that it's flagella is periplasmic instead of extracellular. However, the DOC is penicillin, even though T. pallidum has an outer membrane that would act as a barrier. So nowadays, most gram negatives (and most bugs actually) are resistant to straight penicillin. That's why we have penicillin derivatives such as amp/amox/carbapenam. Vanco never penetrates the outer membrane, so it's worthless against gram negatives.

Even though Gram negatives have a thin layer of peptidoglycan, that layer is necessary for structural integrity. The thing is that with the widespread antibiotic resistance, even bugs that are sensitive will become resistant because of horizontal gene transfer. There was a paper in Nature a few years ago that showed that your gut biome has resistance genes to just about every antibiotic out there. It doesn't take much to make pathogens resistant to antibiotics, which is why we go for the heavy hitters nowadays (cipro/azithro) because even if you don't finish your course, the bugs are less likely to develop resistance because you can kill the vast majority off (>99.9%) in the few days you do take the antibiotic.

Chlyamdia has a special mechanism behind it's suspectibility to penicillin, with the best hypothesis being that it converts the EBs to RBs, allowing for immune system killing.

Mycoplasmas have no cell wall, so yea, penicillin is worthless against them.

No bacteria have a nuclear membrane. That's one of the defining characteristics between the Eukarya and Bacteria (membrane bound organelles). They have a nucleoid, which is similar, but it's not contained within a membrane.
 
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hey friend, WOW I can see your passion for microbio. Thanks alot for the clarification
 
Don't forget about the bulky R group on some generations of Penicillins. A big, bulky R group decreases its ability to go through the porins of the outer membrane of gram negatives. But, the bigger the R group, the more its beta lactam ring is protected. This is why we give beta lactamase inhibitors with the generations that have smaller or absent R groups because once they fit through the porins, they are faced with the beta lactamases in the periplasmic space. Some bacteria also acquire resistance by altering the size of their porins.
 
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Don't forget about the bulky R group on some generations of Penicillins. A big, bulky R group decreases its ability to go through the porins of the outer membrane of gram negatives. But, the bigger the R group, the more its beta lactam ring is protected. This is why we give beta lactamase inhibitors with the generations that have smaller or absent R groups because once they fit through the porins, they are faced with the beta lactamases in the periplasmic space. Some bacteria also acquire resistance by altering the size of their porins.

To expand, the reason why extended-spectrum penicillins work better on Gram-negative organisms than your traditional penicillins is because they have better penetration through the outer membrane. Gram-negative organisms have the outer membrane as a first line of protection, and it does a good job on keeping water-soluble penicillin from rushing in except through porins. The second line of defense is its stockpile of beta-lactamases. Extended-spectrum penicillins work not by defending itself against beta-lactamases (because as DeeJay mentioned, a bulky R group = decreased ability to go through porins), but by increased penetration through the outer membrane so they overwhelm the beta-lactamase secondary line of defense.
 
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