Sarah Yeager (11 AM Micro) has taken my dire warnings about the future of medicine to heart, specifically our increasing problems in treating bacterial infections with antibiotics. However, she is unwilling to just sit there and do nothing about it; she has found research that may be able to help this problem, at least for a while. Spoilers though, Sarah, this will only work for a little while–the bacteria are always going to win, although we may be able to kick the can down the road a bit. She found this work via an article in Science Daily. Here is Sarah’s summary:
The issue of antibiotic resistance may not be a major issue now, but in twenty to thirty years, some of the diseases that people receive immunizations for might be prevalent in America again. The idea of antibiotic resistance may not be well known by everybody, but those involved in science and medical fields know the threat that this poses and I believe that everybody should realize that this could happen in their lifetime. This issue is due to fact that diseases are beginning to become antibiotic resistance since they have been introduced to the same treatment for multiple years now. Antibiotic resistance of bacteria is not an evolutionary adaptation, instead it is a variation of another bacteria. Antibiotic-resistant bacteria are created through alterations or mutations in their DNA.
At the University of Bristol, researchers have shown how bacteria can destroy antibiotics with the use of an enzyme. This is an interesting topic because this discovery can eventually help to develop drugs that can treat infections in the future without allowing the bacteria to become resistant to the antibiotic. The researchers used a Nobel Prize-winning technique called quantum mechanics/molecular mechanics (QM/MM) simulations in order to see how an enzyme, beta-lactamases, reacts to antibiotics. Using QM/MM simulations, they discovered that the most important step in the process occurs when the enzyme ‘spits out’ the broken down antibiotic. This process can occur either quickly or slowly. If it happens quickly, the bacteria becomes antibiotic resistance because the enzyme is able to continue to destroy the antibiotic. However, if the process occurs slowly, the enzyme is not able to become antibiotic resistant due to the amount of time that it takes for it to ‘spit out’ the antibiotic. Since different enzymes take different amounts of time, it is important to figure out which ones are contributing to creating antibiotic resistant bacteria.
Using a computer simulation at the University of Bristol’s school of Chemistry, the researchers were able to identify the enzymes that spit out carbapenems quickly and those who do not. Right now, they are focused on understanding how bacteria becomes resistance to carbapenems, “last resort” antibiotics, for infections and super bugs like Escherichia coli. The resistance to carbapenems is a huge issue because it can cause a minor infection to turn into a major one since it cannot be treated with the usual antibiotics. In the future, the computer simulations will hopefully help to test enzymes in order to predict the possibility for resistance to carbapenems and other antibiotics. This tool will be useful in identifying how different bacteria respond to different drugs in the case of an outbreak.
This discovery will greatly contribute to the on-going process of finding a way to create antibiotics that will work on bacteria and will not become antibiotic resistant. Hopefully, with this discovery, scientists will be able to create antibiotics for diseases before they become antibiotic resistant and create a major problem across the world.
Ashley Hiltebeitel (12:00 Micro) found another summary of microbes in the news from Science Daily. This one details the occurrence of MRSA in student athletes. This should come as no surprise to BIO230 students, who have been the subjects of scientific experiments looking at Staphylococcus aureus on YCP students in the past–click through to see how much Staphylococcus is in Nurses who have already gone through this class. Here is Ashley’s summary:
Even without showing signs and symptoms of of an infection, IDWeek2014 is presenting a study that Staphyloccocus aureus, more commonly known as MRSA, can be carried within college athletes who play contact sports such as football and soccer. This study shows that carrying the infection without showing symptoms puts them at a higher risk to obtain infection or spreading it to their peers or teammates. This disease can cause a serious infection which could lead to death. IDWeek2014 is the first to study athletes in college who are not part of a larger MRSA outbreak.
While carrying this microorganism in their noses and throats, contact athletes are twice as likely to be colonized with MRSA than people who do not play contact sports such as tennis and golf. To show the extreme difference, the two year long study performed by IDWeek2014 showed an 8 to 31 percent range of colonization of MRSA in those who play football, soccer, or other contact sports compared to 0 to 23 percent of those athletes who do not contact their opponent.
Natalia Jimenez-Truque, PhD, MSCI, research instructor, Vanderbilt University Medical Center, Nashville, Tenn. states that even without the full scale of the outbreak, a substantial number of athletes are being colonized with the harmful bacteria. She is convinced that the spread of the disease can be decreased within sports teams by reminding athletes to have good hygiene which includes more hand washing and not sharing personal items in the locker rooms such as towels, soaps, and razors.
The study being presented by IDWeek2014 researched the time it takes for Staphylococcus aureus to be colonized within an athlete. 377 male and female Vanderbilt University varsity athletes were observed. This group included 14 different sports. The contact sports observed were football, soccer, basketball, and lacrosse, while the non-contact sports included baseball, cross country, and golf. The number of participants for the contact sports were 224 and the the number for the non-contact sports were 153. Monthly nasal and throat swabs occurred over two academic years for each athlete. MRSA was found to be acquired more quickly and longer in contact athletes over non-contact athletes.
Skin and soft tissue infections are the result of MRSA. The infections usually heal on their own or can be easily treated. Pneumonia and infections of the blood, heart, bone, joints, and central nervous system can come from the invasive form of MRSA and kill about 18,000 people every year. This is harder to treat than the skin and soft tissue infections because doctors use powerful antibiotics delivered through an I.V.
When an athlete who plays a contact sport has cuts and scrapes on their body, they have a higher risk of getting colonized or infected with MRSA. Researchers suggest that this can be avoided by covering open wounds, regularly washings hands, showering after all practice and games, and not sharing personal items as mentioned before. They also suggest that athletes with scratches and cut should not be allowed to practice or play in games. MRSA is often spread person to person because researchers found little staph in a clean athletic environment.
In conclusion, Jimenez-Truque states that, “Staph is a problematic germ for us — always has been, always will be — and we need to do all we can to reduce the risk of infection in those at highest risk, such as college athletes.”
Erin Mensch (11 AM Micro) found another article she found interesting, from Science Daily. In this story, scientists from Michigan State University identified a gene from algae in research about biofuel production that also appears to be involved in the development of human cancers. As Erin notes, it is much easier to grow things like algae in the lab, and if you can get information about human diseases at the same time, that’s a great thing. Here is Erin’s summary:
Michigan State University has discovered what they think could help solve many problems in the world such as tumor growth and oil production. A man by the name of Christoph Benning is a professor at Michigan State University and teaches biochemistry and molecular biology. He and his team were working in the laboratory trying to find a way to make algae’s capacity as a biofuel expand. In the process of trying to do that, they discovered the protein CHT7. They believe this protein is able to decide when the cells are resting or hard at work reproducing rapidly. They called it the “cellular snooze button”. This could help the oil production industry and the cancer research tremendously. The protein could enhance the production of oil and could make the tumor cells in “resting state”.
Christoph Benning explained how he was working with algae because like yeast it is easy to work with in a laboratory setting whereas many human cells are not able to grow in laboratory setting. This makes studying human disease so much harder. He says algae are able to be manipulated in the lab which helps scientists study them closely. He believes algae are able to do the same if not even more for us than yeast can. He claims he discovered this protein when noticed that when algae are essentially awake they are able to grow and when they are asleep they are able to make oil. In order to have algae able to make viable biofuel they would have to be able to grow and make oil at the same time. Benning figured out that the way to have the algae producing oil and growing at the same time is the protein CHT7. This protein would be able to tell the cells to either be awake or asleep. Depending if they were awake or asleep they would either be producing oil or growing. This is a fascinating concept and could be the start of something that changes medicine and the oil industry forever.
Benning’s next step in this process is to create an organism that does not rest and is always active. This could then help scientists able to make an enormous amount of viable oil. More importantly is could help with suppressing the growth of tumors. Ultimately this protein CHT7 could make the cancer cells not able to divide. First, they would have to look at it from the other perspective, which is how to get a cell to grow rapidly and uncontrollably. This would then explain to us about tumor growth. Once we understand tumor growth it would be easier to figure out how to prevent the rapid growth all together. I found this article very interesting because it is always exciting when scientists find out new research that could possibly stop cancer. I hope that Benning is able to keep going with this experiment and find out more about the protein CHT7. I also found it interesting that algae have to do with oil production. I hope to read an article in the future about this being a successful protein that is able to tell tumor cells to stop rapidly dividing.
Gregory Gable (12:00 Micro) is interested in genetics, and how cells can keep cancer from occurring. He found the following article via Science Daily which summarizes work from the University of North Carolina School of Medicine about the role of gene regulation plays in the development of cancer. Here is Gregory’s story:
In a healthy cell, certain genes will be turned on if they are used, and turned off if they are not. If one of the genes that is not needed, the cell can grow uncontrollably, and become cancerous. Researchers have recently discovered that Bre1is the key protein that regulates which genes are turned on in which cells. These proteins are the biggest aid (much like enzymes are) to genes working in the first place, as they are the behind the scenes to make sure operation runs smoothly.
The field of cancer research has now been changed. A greater focus will now be placed on the epigenetic portion of research. The best way to visualize the way epigenetics works is to view it like a stage production. The protein Bre1 is the director who provides offstage cues for the main actors, the genes, to do or not do something. They are the ones who read off the script, RNA. If a single line is missed, catastrophe could be a potential outcome. The show could be ruined – in this case, rampant growth of cells.
Brian Strahl, Ph.D., is a member of the UNC Lineberger Comprehensive Cancer Center who is currently in the process of researching these histones. His goal is to figure out precisely what these histones do to contribute to biological regulations and, in turn, to cancer. Bre1 is a histone, and histones are used to wrap out or exclude genetic material in our cells. Ubiquitin is able to help histones in their task by exposing genetic material in the chromatin of cells. These proteins can also be tagged with chemicals that further allow control of genetic replication. Now all that needs to be learned is what these histones do exactly.
There is a Goldilocks range for these proteins. Too much, and the gene doesn’t turn off. Too little, and the gene is never on. If the gene isn’t needed at all, it simply leaves, creating other big issues. Before this day, it wasn’t known whether it promoted or prevented cancer, but now it is known that this protein has its own Goldilocks range. Bre1 protein could be a wonderful target for cancer drugs to help prevent rampant growth. This discovery is very important in showing specifically how these cells function, and how they need to be regulated.
With this new discovery, cell division by genetic replication can be better controlled. Not only is their function now known (and to be researched further), but it is also known that they have their own specifics for functioning as well. Pursuing drugs that target this specific protein should definitely be looked into. Whereas chemotherapy annihilates cells both good and bad, perhaps by using this to target down one specific regulator, life can better be maintained.
Well, it’s heading into flu season, and what’s a Micro prof to do? Get a flu shot, that’s what. As part of the YCP Wellness Fair on Monday during Fall Break, I went over to the Grum and received my flu shot from a very competent nurse, and now am ready to say “Bring it on, Influenza!”
— David Singleton (@drsingleton) October 13, 2014
The same day that I did this positive step for public health, I came across a little bit of craziness about the Ebola outbreak, via the science blog io9.com. Writer Mark Strauss spent some time among the seedier conspiracy theory websites over the weekend, and documented that in addition to the hysteria and mistaken information that is available, there is also some outright disinformation about the Ebola outbreak. Members of the anti-vaccination network have proposed that the spread of Ebola to Texas is part of a concerted government effort to shift attention away from a discredited “whistleblower,” who was going to make a statement about a vaccine/autism link that supposedly had been covered up by the CDC. Another site claims that the initial outbreak of Ebola in discrete regions in Guinea is indicative of a deliberate release of the virus by pharmaceutical companies, so that they could test a secret antidote on an unsuspecting population. Finally, the Vaccine Information Network doesn’t seem to believe that Ebola virus is real, and that the reports in the media are attributed to purposeful misinformation on the part of authorities ultimately “to poison us with drugs and vaccines.”
So after we all take a deep, cleansing breath to clear our minds after that, here’s a bonus opportunity. Simply do as I did up above–go get a flu shot. Document it if you can as I did, by tweeting it or posting it on Instagram with hashtag #ycpmicro, and paste the link in the comment thread below. Offer goes through the end of October, when we should all have gotten our flu shots anyway.