«We need to make sure the genes that make these strategies possible aren't shared with infectious bacteria, because they could make the problem of drug -
resistant infections much worse.»
Not exact matches
Given that natural selection has held up since Darwin's time and wonderfully explains what we see and do in the lab and things like why it's hard to treat viral
infections and why there are an increasing number of antibiotic
resistant bacteria, I don't expect it to change
much in the next 10 years.
This is no different than hundreds of stories from across the country that that I get sent each month, but this caught my attention because it talked about a Methicillin -
resistant Staphylococcus Aureus (MRSA)
infection which is a potentially fatal bacterium that too few sports parents know
much about.
In fact, the rate of
infections resistant to two different antibiotics declined nearly twice as
much as
infections that could be treated with antibiotics.
According to the U.S. Centers for Disease Control and Prevention, about 23,000 Americans die from 17 antibiotic -
resistant infections each year (although it's difficult to parse out how
much is due to vancomycin resistance).
Globally, the situation is
much worse: More than 700,000 die annually from drug -
resistant infections, particularly in parts of Europe, Asia and South Asia.
We therefore questioned whether the naive, predisposed B6 Prf1 − / − model would develop alterations in disease upon immunization prior to
infection,
much like the BALB / c model switches from
resistant to permissive with immunization.
For instance, too little or too
much estrogen can contribute to a vaginal yeast
infection as proper estrogen levels keep the vaginal tract more
resistant to
infection.
I am in no way trying to say that food sensitivities aren't real and that individual systems vary — I myself do
much much better without any wheat at all (clears up my otherwise highly recurrent and occasionally drug
resistant sinus
infections) and on a very low carb diet.