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Penicillin vs. Sulfa Drugs vs. Phage Therapy

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Sulfa drugs (among the most famous of which was Prontosil) were the first truly effective antibacterial agents, and were widely used in the West in the years preceding World War II, and remained in widespread use in Germany until the end of the war.

Penicillin, discovered by Fleming and made practical by Chain and Florey, was the first antibiotic to be discovered. It replaced sulfa drugs in the second half of World War II among the Allied forces after tremendous problems with mass production were overcome.

Phage therapy (the use of bacteriophage viruses to destroy harmful bacteria) remained popular in the Soviet Union long after the West switched over to sulfa drugs and, later, antibiotics. It is still in use today in the former USSR, though concerns with using an evolving, self-replicating entity in medical treatments has thus far prevented their use in the West.

Discuss them here.


 

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My understanding is that phage therapy has a lot of potential, but some pretty severe limitations as well.

 

A given phage will only attack a very narrow range of bacteria, whereas antibiotics will nuke a wide spectrum of bugs.  This means that accurate diagnosis is crucial for phage therapy to be effective.

 

Interestingly, animal mucus contains bacteriaphages.

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It is, but there are also advantages in specificity. For example, they would not wipe out gut flora if used for gastrointestinal infections. On the other hand, as you mentioned, accurate diagnosis is crucial.

There are also concerns about the fact that phages can also transfer genes between bacteria, which can have unintended effects.

Incidentally, one of Gerhard Domagk's first patients for Prontosil was dyed permanently pink by the drug (it was developed from a dye), though she survived the infection. She was his daughter.

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Sadly anything medical is mostly outside of my pay grade which is compounded since so many members of my extended family have medical training, I've lucked out on relying on them and have focused my attention elsewhere.

I am glad about antibiotics, being given a dose for a bout of pneumonia that I had two winters ago. Although it does play havoc with the stomach critters, I've found that the inclusion of good yoghurt in the diet got my system back on an even keel.

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This is a completely terrifying article on resistant bacteria in cattle feces getting stirred up by dust storms in Texas and Oklahoma.

 

Some choice quotes:

 

 

In addition to a steady diet of flaked corn and sorghum silage, cattle are regularly administered steroids, some portion of which is excreted in their feces. Eight years ago, a Texas Tech professor, Philip Smith, funded by a U.S. Department of Agriculture grant and with the cooperation of local feeders, tried to figure out if those steroid remnants went airborne, and what happened to them if they did.

 

Smith eventually determined that steroids were indeed blowing off of feedlots and settling into the local environment, where they could act as endocrine disrupters among nearby aquatic species. All in all, it was a good bit of science, the sort of thing that not only meets professional standards but might make a difference outside of the academy.

 

 

 

Between August and December 2012, the two men—this time without any help from feed yards or the USDA—carried out a new round of sampling. In the bed of a truck that they parked on county roads adjacent to ten Lubbock-area feed yards, they set up small, generator-powered vacuums. On a number of windy days, they collected upwind and downwind air samples. The results confirmed their suspicions: downwind, they found antibiotics—specifically tetracycline—present at significantly higher levels than in the upwind samples. Yet as they dug deeper, they discovered something even more worrisome. Along with the antibiotics, they found another hitchhiker: remnants of bacteria that had acquired a gene that made them resistant to tetracycline.

 

“The tetracycline resistance was 400,000 percent more prevalent downwind than upwind,” said Smith. At some of the locations, there was tetracycline resistance in 100 percent of the samples. “That was really the wow moment,” said Mayer.

 

 

Studies have estimated that every day the average cow generates about 28.5 grams of PM10particles—fecal matter dried in the sun, aerosolized, and suspended in the air. PM10 particles, which are 10 micrometers in diameter or less, are of concern to the EPA because of their ability to pass through the nose and into the lungs. Of even greater concern are the smaller PM2.5particles, which can remain suspended by the wind for much longer and pass deeper into the lungs. Many of the particulates that Smith and Mayer studied were smaller still.

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How stable is HGH in the environment? Especially that area of the world. I would have to do more research, but the more stable it became the less bio-availabile it would become.

 

As for antibiotic resistance, yeah that's no bueno. Local populations of bacteria that are resistant would not be good. Although, I'm not sure what kind of evolutionary advantage it would give a certain population over another in an open environment (aka, not a feed lot), so I don't see the resistant plasmids completely overtaking very quickly. 

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The use of antibiotics on feed lots is problematic because it isn't used to cure any particular disease but rather to artificially cause weight gain in the animals before slaughter.

It is unethical on so many different levels.

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I'm writing a paper right now on antibiotics. Might end up writing more on SH about it when I finish.

 

As for antibiotic resistance, yeah that's no bueno. Local populations of bacteria that are resistant would not be good. Although, I'm not sure what kind of evolutionary advantage it would give a certain population over another in an open environment (aka, not a feed lot), so I don't see the resistant plasmids completely overtaking very quickly. 

An antibiotic resistant bacteria survives against the antibiotic by having a slightly different mechanism of action in place of the old mechanism that is targeted by the antibiotic. This is highly problematic due to the low generational time of bacteria and plasmid nature of DNA transfer. Low generation time means that a large amount of bacteria will be quickly produced and increases the probably that a bacteria will survive and replicate with a mutation. Now to answer the question, since many antibiotics are biosynthesized, having antibiotic resistance does give them a small selective advantage against the other bacteria that do not have the resistance.

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Just off the top of my head, most antibiotic resistant mutations don't impose substantial costs once they've fully developed. So you'd expect genetic drift to operate outside of the selecting environment.

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I'm writing a paper right now on antibiotics. Might end up writing more on SH about it when I finish.

 

An antibiotic resistant bacteria survives against the antibiotic by having a slightly different mechanism of action in place of the old mechanism that is targeted by the antibiotic. This is highly problematic due to the low generational time of bacteria and plasmid nature of DNA transfer. Low generation time means that a large amount of bacteria will be quickly produced and increases the probably that a bacteria will survive and replicate with a mutation. Now to answer the question, since many antibiotics are biosynthesized, having antibiotic resistance does give them a small selective advantage against the other bacteria that do not have the resistance.

Sometimes it's a slightly different mechanism. Other times they create a molecule that can disable the antibiotic in question. 

 

If you need help with the paper, hit me up. I studied the stuff for a while.

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Just finished my paper so I will post a bit about infection treatment. First let's talk about sulfa drugs.

 

Sulfa drugs are compounds that produce sulfonamides. They were not antibiotics but antimicrobials since they inhibited further growth of microbes rather than killing them. The first sulfa drug was arsephenamine (Salvarsan), introduced in 1910 and was a pretty shitty drug with terrible adverse effects and were a pain to store and administer. Although it was a shitty drug, it was a good treatment to syphilis, dubbed the 'magic bullet' because it was toxic to certain microbes but not humans. It was the most used antimicrobial until the 1940s.

 

Sulfa drugs became famous due to Prontosil, discovered in 1932. It was widely known because it successfully and quickly treated Franklin Delano Roosevelt's son who had a bad case of strep throat infection. Although it had awful side effects such as vomitting and kidney damage, it became famous and grabbed world wide attention as it was synthetic, showing that synthetic drugs had huge potential and directly killed off phage therapy in the West as the former was much easier to administer and had rapid results.

 

How do sulfa drugs work? Sulfa drugs are either sulfonamides or are pro drugs that break down into sulfonamides. They work by the competitive inhibition of dihydropteroate synthetase (DHPS), responsible for folate synthesis, inhibiting DNA, RNA and protein synthesis. They are broad spectrum against both Gram positive and Gram negative bacteria and are generally used to cure minor infections, especially in the urinary tract. They are terrible for anyone with compromised immune systems because they are bacteriostatic instead of bactericidal.

 

Resistance is very common, with different mechanisms such as decreased membrane permeability, mutated enzymes for the synthesis of folate and increased PABA production to compete for the active sites that the inhibitor takes.

 

Next time, I will post about beta-lactam antibiotics, the most famous of which being penicillin.

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