Spoilers! Ebola worries are non-existent for us in South Central Pennsylvania. However, according to an email I received this week might lead one to believe that the risk is far, far worse. A notice to staff, faculty, and students at York College requires that anyone planning on traveling anywhere outside of the United States through the beginning of March 2015 self identify themselves to the Health Center, and monitor their temperature for the 3 week Ebola Hemorrhagic Fever incubation contagious period. The notice also contains several editorialized Ebola facts, which unfortunately convey a sense about the risks of contracting Ebola virus that are perhaps a bit exaggerated.
A posting in the Atlantic Monthly gives a concise summary of our current understanding. There is no indication today, and there never has been, any evidence to support the hypothesis that Ebola viruses can be transmitted between humans via any indirect means. Ebola virus is what is known as an enveloped virus, and contains a genome made of RNA; consequently, intact virus particles with these characteristics are unable to survive in an infectious state outside of a mammalian host. As a result, in contrast to many bacterial pathogens, inanimate objects (fomites) in the environment are very poor reservoirs for these types of viral pathogens, although virus shed via sneezing does pose a temporary risk.
The one study that examined the possibility of airborne transmission found that transmission between infected pigs and non-human primates can occur in specialized situations. This study has a big caveat (and indeed was followed up with an additional study to address this), in that in pigs Ebola virus has a hugely significant lung involvement, resulting in massive amounts of the virus in respiratory secretions. This doesn’t happen in primates, which show mainly hemorrhagic disease. The followup study looking at primate to primate aerosol transmission found no infection between test animals. Because of the very nature of Ebola virus in comparison to many respiratory viruses, we are not likely to see a change in these properties.
What about the risk to York College community members who are planning on traveling overseas in the near future? The Centers for Disease Control and Prevention and the Pennsylvania Department of Health remain the best sources of information to assess the risks of this scary disease to the general public. The CDC in fact has a page devoted to precautions that are recommended for college students planning travel abroad. All of these precautions are directed towards travel to those countries where the Ebola outbreak is occurring (Guinea, Liberia, Sierra Leone). The CDC also has a page which clearly indicates epidemiological risks for contracting Ebola virus for use in evaluating whether an individual has potentially been exposed. Class 4–No Identifiable Risk is indicated for persons traveling to a country without widespread Ebola virus transmission–this includes travel anywhere besides Guinea, Liberia, and Sierra Leone. Persons traveling to the Democratic Republic of the Congo should practice enhanced precautions, however the CDC risk assessment is very low for travel there. The Pennsylvania Department of Health echoes all of the CDC guidelines, and as of 27 October 2014, is monitoring a total of 105 residents of the Commonwealth who are considered “at some risk” for exposure to Ebola virus, due to recent travel to one of the afflicted countries. These individuals are being monitored for potential exposure to Ebola by local and state health officials. As indicated on the PA Department of Health page, travel into Pennsylvania from any other international origin is NOT considered a risk factor for Ebola exposure.
There is an awful lot of poorly cited information circulating and straight out disinformation about this epidemic at present. Advocating unwarranted steps in screening for potential exposure when the risk is non-existent creates an atmosphere of uncertainty, and this can be damaging in the long run. I urge all BIO230 students to follow the links they see on the Internet, and check to see whether they represent experimentally-supported science, or merely reflect someone’s opinion.
Google today is commemorating Jonas Salk’s birthday with a Google doodle. Salk was the developer of the first vaccine against polio, a disease which affected 58,000 people in 1952 in the United States alone, leading to over 3000 deaths and over 20,000 people with permanent levels of paralysis from the disease. Polio is a viral disease, and is passed from individual to individual via contaminated drinking water, and until the development of a vaccine it was essentially impossible to control. Previous attempts at creating vaccines generally used a strategy of attenuating pathogens, a method of laboriously reducing the virulence of the pathogen in the laboratory, with the hope that non-virulent organisms might still provide protection against the more virulent pathogens in the wild. Salk’s innovation was to pursue inactivated pathogens; virus that had been grown in the lab, and then was partially denatured so that it was then physically unable to cause disease. Fortunately, this approach worked for Salk, and in 1955 the first polio vaccine came to market worldwide. By 1962, the number of polio cases in the US had dropped to under 1000, and the last case of natural transmission domestically occurred in 1979 during an outbreak among several Amish communities.
Salk was hailed as a hero when the wide availability of the vaccine was announced. The Google doodle above is based on an actual photograph from 1955–I think that people today have little understanding how terrifying many infectious diseases were to society as a whole. Salk was recognized with many honors during his career, however he did not receive the Nobel Prize even though he was nominated during the late 1950’s. Vincent Racaniello at the Virology Blog suggests that the prevailing opinion among the community at the time was that Salk’s procedure didn’t really involve true innovation, which is an important component of the Nobel Prize. The 1954 Nobel Prize was awarded to a trio of polio researchers (John Enders, Thomas Weller, and Frederick Robbins) who discovered a method to grow polio virus in the laboratory. Indeed, without this innovation, Salk would have never been able to produce his vaccine.
I came across a second item about polio this morning as I went through my Twitter feed, linked to by @popehat, a politics/news site that helps me to get outside my political comfort zone on occasion. In this Boston Globe article detailing what is hopefully the final days of polio here on Planet Earth, the intrusion of world politics clearly is complicating global eradication efforts. Most recent outbreaks have been limited to a small geographic area in sub-Saharan Africa, however Pakistan is currently experiencing an epidemic, whereas neighboring India has been certified “polio-free” effective this year. The problems in Pakistan have been complicated by US anti-terror efforts in the region. Currently, Taliban leaders regard legitimate polio aid efforts as suspect, with vaccination efforts as an American plot to deliberately infect children or to gather intelligence information. The latter suspicion is not off base, as in 2011 CIA operatives used a vaccination program around Abbottabad near Osama bin Laden’s compound to collect DNA samples in hopes of confirming that bin Laden was there. Following exposure of the CIA’s involvement, later vaccination aid efforts were stymied, and aid workers have been threatened.
Global polio eradication will eventually occur, and like smallpox, within a generation the only place polio virus will be found will be in laboratories. Smallpox required an almost 200-year concerted effort to eliminate; polio by contrast has essentially disappeared within two generations. This story however is important to remind us that seemingly disconnected events (the war on terror, global public health measures) are in fact tightly intertwined. Unfortunately, the messy intrusion of politics into polio eradication has created a mistrust of the importance of public health measures outside of this county. I fear that this same mistrust is also at work with public health measures here at home.
Brittany Reichelt (11 AM Micro) is thinking outside the box with the treatment of Clostridium difficile infections. These infections are difficult to treat, in large part due to the fact that they can form endospores, and as a result are not easily eliminated by antibiotic treatment. This leads to many patients have long term gastrointestinal issues from the infection, and a generally unsatisfactory quality of life for the patients with these infections. Brittany found this summary via the National Institutes of Health news page (excellent choice!). FYI, the use of poop to treat C. difficile infections is not news to long time BIO230 fans–it is a topic near and dear to my heart (see here, here, or just search “poop” on the blog). Here is Brittany’s take and summary on this important topic:
The following summary is on an article from the National Institutes of Health on Clostridium difficile. We have heard about the genus Clostridium with infections, such as Clostridium botulinum and Clostridium tetani. Clostridium difficile has many of the same characteristics, such as endospore forming and is anaerobic. This bacterium C. difficile is most prevalent in people with prolonged use of antibiotics, since antibiotics kill the bad and good bacteria in the colon, it will be easier for C. difficile to make its home there. Normally for treatment, antibiotics are not effective in improving the symptoms. Instead, the recommended treatment is to transplant “microbe-rich stool samples from healthy people into the C. difficile patient to help improve the bacteria in their colon and improve their symptoms.”
In the study completed by National Institutes of Health funded researchers from Massachusetts General Hospital took a different approach. Rather than taking the poop of healthy individuals and transplanting it into the patients, they created a simple pill: “the poop pill, which is shown in the picture above.” Researchers completed this by first taking healthy poop samples, purifying them, and then concentrating the good bacteria it. The concentrated good bacteria was put into clear capsules and then froze, these poop pills were to be given to patients frozen. Researchers tested the effects of the poop pills on 20 patients who experienced “at least three C. difficile infections and did not respond to antibiotics normally used on this bacterium. Patients were given 30 pills over a period of two days. The results of this study showed in 2 days of treatment 14 out of 20 patients had a dramatic reduction in symptoms, such as frequent diarrhea went away. The resulting 8 patients were given a second round of treatment and 4 more patients had the same decrease in symptoms.
The results show that this may be a better alternative; it is much easier for a patient to take a pill then it is to transplant the poop from one human being to another human. Researchers say that someday, this treatment may even be beneficial for other gastrointestinal diseases.
(note added in proof by Singleton: this seems as good as an opportunity to bring out this old chestnut–any ideas why this graphic is completely relevant to Brittany’s story? First person to comment with the correct answer gets a free bonus point!)
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.”