I called one of the pharmacists that I work with and there are still antibiotic treatment options for MRSA. If the infection is intranasal then this ointment Bactroban is used. Depending on the strain and susceptibility of MRSA then other antibiotics are used which include; clindamycin, Bactrim, vancomycin and/or Zyvox. Zyvox was approved for use in the market in 2000, so it is a very new antibiotic, it is also very powerful and a last resort (we almost never see this drug prescribed even though our patients are about 99% nursing home residents).
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Just a quick question about antibiotics. Can one antibiotic be used with another? Say to prevent mutation and adaptations from the antibiotic itself (i.e. vancomycin with Zyvox), is that healthy? I guess it wouldn’t be, but in my opinion, that would ensure that no genetic mutations can happen. Just a thought!
I think that you could use two antibiotics at the same time. However, if they work differently (vancomycin does different things than penicillin does, for example), you might have even more side effects because it would target wider ranges of bacteria. And many bacteria are resistant to more than one antibiotic, so some bacteria could still end up living after exposure.
I thought the people with MRSA also use wound vacs which is a suction tube like thihg that attaches at the point where the MRSA is at if it is on a wound and it sucks it out.
Also, my blog from November 17th never got published. Wonder what happened? I’ll post it within this comment box.
Sorry about the late blog guys! November 17 was my birthday (big 23) and Thanksgiving week was hectic (don’t work retail during Thanksgiving break). This is my first time blogging, so if it sucks, bear with me…
Anyways on with the blog….
Today we started the Evolution unit when it comes to both the evolution of the pathogen as well as the host as well. The 3 main points we started out with was 1.) How does virulence change over time? 2.) What are the possible effects on vaccination when it comes to pathogen evolution? and 3.) What are the effects of antimicrobial and antibacterical medicines on pathogen evolution?
Taking these 3 main focuses, we began the lecture going over some things about evolution itself. Defining evolution in lecture, evolution is simply the change in gene frequency over time. However, one of the main questions I have had during this lecture (and hoping some of you can answer) is how can gene frequency and its changes be measured? The answer to that may be simple, but what I am challenging change over time to be is actually the breaking down of a gene over time. In a nutshell, it is fact that nothing has the possibility or the ability to better itself, but rather to adapt. In the lecture notes, 3 things are needed to make natural selection work: Heritability, Selection, Variability, and Time. I may be getting this wrong, or failing to describe it correctly, but evolution to me is adaptations, forcing a host to either compete with the pathogen, or die. Maybe some of you can help me explain it if you understand what I am saying as well!
Anyways, the most important concept presented today was the Red Queen hypothesis. Stolen from Alice in Wonderland, the Red Queen hypothesis is basically, in layman terms, each organism competing with each other to stay alive. One must strive to get past each other, or ahead of the other, in order to have a better chance of survival. Again, I run into another problem here (maybe you guys can help me understand again). The question I have for that is how can a host evolve defenses? It has been an understanding of mine that matter can’t come from nowhere. Evolution, and the Red Queen hypothesis, states that an organism can develop defenses within a certain pathogen, but a pathogen can’t be viralent enough to kill it, but still viralent enough to infect it as well as others, and a battle of a sort ensues. This may get way complicated and intricate, but I like to ask the question of why and how? How does a pathogen know when to say “oh, I can’t be that viralent, but still stay viralent enough to get the host sick.” And how does the host start building other defenses than antibodies, and where do those antibodies come from? As you all can see, it is kind of a hard concept to grasp, because to me, the body doesn’t change that much (like genetic make-up to fight a disease) or that quickly over time. I think it is just the presence of more antibodies and may the biggest army win! Cool to think about though…
Moving on…
The evolution of virulence is what is next on the list. First, we defined virulence, which is the parasite mediated morbidity and mortality. Two paradigms were presented, the new and the old. The old states simply that virulence was a deleterious side effect of new host-parasite associations that would evolve to low levels with time. The new paradigm states that it depends on how virulent a pathogen will be. The term “it depends” corresponds to factors like host and pathogen interactions, variance in their interactions, and host and pathogen physiology. This in turn can effect the phases of host-pathogen associations. Taken from lecture, there are 3 phases or host-pathogen associations: Phase 1 – first contact of a disease agent with a new host, disease dies out. Phase 2 – pathogen has established itself in a new host, but the virulence level is not at an optimum for the pathogen. Phase 3 – applies to parasites that are established for a prolonged period of time in a host species and population and evolve in response to changes in the environment, including host demography. Phase 1 is usually accredited to having been used to develop vaccines. Because the pathogen is allowed to sit in the vaccine, and adapt to the conditions, its virulence was lowered when it comes to the human environment. An example of this is taking a fish from cold water and introducing it to warm water, it might kill it or severely disable it. Phase 2 explains accidental infections, or the pathogen makes it into the host but is not viralent enough to have a significant infection. If this happens, a chain of infection will result due to the rapid adaption of the pathogen or parasite within the host. Phase 3 is allowing everything to come to equilibrium, and the trade off model is introduced (how long and how fast it can transmit).
We then answered the questions on the slide after the explanation of Phase 3. Answers? Sure
higher, higher, more, decrease, higher, higher (check those)
As with all models, this one will again serve to be insufficient in certain circumstances. The trade off model doesn’t take into accounts of adaptation, and other things (on slide).
That would be it for the November 17th class. Good luck with finals and with the grant proposals!
Travis signing off….
That was a awesome blog and thank you for clearing up the evolution term. Those questions that we answered in class were a bit difficult and you really had to think about it. It seemed like for some of the questions it could be both answers.
Thanks for posting this information! This is cool to know!
Morning! Does anyone know where to find the instructions for the cover sheet of the grant proposal? I looked in the grant proposal file and I could not find it. I may have my head somewhere it shouldn’t be…..
I guess just do it as a regular scientific paper (i.e. title, author, and an abstract). Thats what I did, and I guess it was okay!
So does the antibiotic treat the MRSA completely or does it stop working after a while? In other words, can the MRSA come back? I always wonder about drugs because there always seems to be some side effect or a list of them.
I found this information on the mayo clinic website:
Staph bacteria are normally found on the skin or in the nose of about one-third of the population. If you have staph on your skin or in your nose but aren’t sick, you are said to be “colonized” but not infected. Healthy people can be colonized and have no ill effects. However, they can pass the germ to others.
In the hospital, you may be tested for MRSA if you show signs of infection or if you are transferred into a hospital from another health care setting where MRSA is known to be present. You may also be tested if you have had a previous history of MRSA.
http://www.mayoclinic.com/health/mrsa/DS00735
It seems that the bacteria may not lay dormant per se, but it seems like the bacteria is so prevalent one can be reinfected at anytime. I did see that if one had previous history they should be tested. I cannot find any other info online about it….anyone else find anything?
I also found this on another website, it is not an edu or org, but it does have information that is backed up by other info I have found on more credible sites.
Can MRSA be cured?
With treatment, most localized MRSA skin infections will go away. However, a certain number of these infections may be recurrent- usually with more of the same; boils, boils, boils! About 30% of the general population is colonized with staph organisms and a growing number of those colonized have MRSA. Staph often “hangs out” in the nose- not causing problems. After localized treatment, some recommend trying to “eradicate” the organism. There are a variety of attempts to do this. Some doctors will try antibiotic pills for a few weeks. Since MRSA often in colonized in the nose, some suggest usuing Bactroban ointment in the nostrils twice a day for a week or so. Others have tried Hibiclens, an antiseptic lotion, as both a shampoo and body wash. However, these methods appear to be doomed to failure. Once colonized with MRSA, many people may remain so for years. This is a tough bug to get rid of.
Found on http://www.birdmd.com/emergingthreats/mrsa.htm
found this one as well, it was also helpful for me:
http://www.earthclinic.com/CURES/MRSA.html