how do bacteria become resistant to certain antibiotics?

[Guest guest]

I asked this question several times and no one wanted to

answer so I found the answer here:

How do bacteria become resistant to antibiotics?

http://science.howstuffworks.com/question561.htm

Maybe someone else has other good answers but for some of us

with staph and other infection resistant to scores of antibiotics, we need

answers.

Anyway here is the text from the link above:

Antibiotics are compounds that either:

kill bacteria directly (bacteriocidal)

hamper their ability to grow and reproduce (bacteriostatic)

When you are fighting off a bacterial infection, your immune

system can be overwhelmed by the invading bugs. Antibiotics are thrown into the

fray to mount a defense against the invaders until your immune system can

recover and finish off the remaining bacteria.

How do antibiotics stave off bacterial growth? Antibiotics

stop or interfere with a number of everyday cellular processes that bacteria

rely on for growth and survival, such as:

crippling production of the bacterial cell wall that

protects the cell from the external environment

interfering with protein synthesis by binding to the

machinery that builds proteins, amino acid by amino acid

wreaking havoc with metabolic processes, such as the

synthesis of folic acid, a B vitamin that bacteria need to thrive

blocking synthesis of DNA and RNA

Antibiotics stop working because bacteria come up with

various ways of countering these actions, such as:

Preventing the antibiotic from getting to its target

When you really don't want to see someone, you might find

yourself doing things like hiding from them or avoiding their phone calls.

Bacteria employ similar strategies to keep antibiotics at bay. One effective

way to keep a drug from reaching its target is to prevent it from being taken

up at all. Bacteria do this by changing the permeability of their membranes or

by reducing the number of channels available for drugs to diffuse through.

Another strategy is to create the molecular equivalent of a club bouncer to

escort antibiotics out the door if it gets in. Some bacteria use energy from

ATP to power pumps that shoot antibiotics out of the cell.

Changing the target

Many antibiotics work by sticking to their target and

preventing it from interacting with other molecules inside the cell. Some

bacteria respond by changing the structure of the target (or even replacing it

within another molecule altogether) so that the antibiotic can no longer

recognize it or bind to it.

Destroying the antibiotic

This tactic takes interfering with the antibiotic to an

extreme. Rather than simply pushing the drug aside or setting up molecular

blockades, some bacteria survive by neutralizing their enemy directly. For

example, some kinds of bacteria produce enzymes called beta-lactamases that

chew up penicillin.

How do bacteria pick up these drug-fighting habits? In some

cases, they don't. Some bacteria are simply making use of their own inherent

capabilities. However, there are many bacteria that didn't start out resistant

to a particular antibiotic. Bacteria can acquire resistance by getting a copy

of a gene encoding an altered protein or an enzyme like beta lactamase from

other bacteria, even from those of a different species. There are a number of

ways to get a resistance gene:

During transformation - in this process, akin to bacterial

sex, microbes can join together and transfer DNA to each other.

On a small, circular, extrachromosomal piece of DNA, called

a plasmid - one plasmid can encode resistance to many different antibiotics.

Through a transposon - transposons are " jumping

genes, " small pieces of DNA that can hop from DNA molecule to DNA molecule.

Once in a chromosome or plasmid, they can be integrated stably.

By scavenging DNA remnants from degraded, dead bacteria.

Unfortunately, if a bacterium gets a resistance gene stuck

into its chromosomal DNA or picks one up in a free-floating plasmid, all of its

progeny will inherit the gene and the resistance it confers. Why do resistance

genes persist and spread throughout bacterial populations? It's basically just Darwin's idea of the

survival of the fittest, reduced to a microscopic level -- bacteria with these

genes survive and outgrow susceptible variants. And our own less than judicious

use of antibiotics actually selects for these resistant types! Here's how we

contribute to the problem:

Ignoring the brightly colored labels on the pill bottle and

the doctor's admonitions to take all of the medicine that you get, even if you

start to feel better. If you stop taking your medicine too early, your immune

system may not be capable of killing off the stragglers, and any resistant

bacteria left unscathed will be able to proliferate and spread to other people.

Insisting on getting antibiotics from the doctor to treat a

cold or the flu. Antibiotics are completely ineffective against viruses, so you

actually accomplish nothing by popping a pill. Worse yet, antibiotics can't

discriminate between bacteria that are good for us and bacteria that cause

disease. Our preoccupation with cleanliness notwithstanding, we actually

peacefully co-exist with a wide variety of bacteria each day. For example, our

intestines are lined with bacteria that break down foods that we can't digest.

Whenever you take antibiotics, you kill off some of these beneficial bugs.

Using antibiotics indiscriminately can blow away most of the bacteria normally

in your body, opening the door for more sinister strains to establish

themselves in their place.

Stockpiling leftover antibiotics and trying to medicate

ourselves - not every antibiotic will work for every infection. Your doctor

prescribes a specific drug for you based on what kind of infection you have. He

or she also selects a specific dose and length for your treatment. The old

antibiotic you have may not work at all against the infection you have, so it's

best to seek a doctor's advice before trying to treat yourself.