Category Archives: Danger danger danger!

Jonas Salk’s 100th Birthday

downloadGoogle 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.


Coming Soon: No More Antibiotic Resistance!

New Picture (5)

This graphic shows a carbapenems molecule entering the carbapenemase enzyme (blue arrow), which is where the beta-lactam structure gets broken down. The orange arrow shows the ineffective molecule leaving the enzyme.

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.

Rethink your Decision to Play Contact Sports

staph2Ashley 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.

staphNatalia 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.”

Who Knew Feces Could Tell Us So Much?!

New Picture (2)Ashley Hiltebeitel (12 Micro) finds Ebola virus fascinating, and noted in the comment thread to the previous post that she is working on a research paper for her Academic Writing class on the topic! It is unclear exactly how big the outbreak is, and epidemiologists are using many approaches to define the size of it. Ashley presents one approach for finding out how significant the outbreak is in non-human primates, from a news alert on Science Daily summarizing a primary research article in the journal PLoS Neglected Tropical Diseases. Here is Ashley’s summary:

The Wildlife Conservation Society (WCS) has led a research that uses fecal samples from wild great apes to center in on the populations that have been infected with the Ebola virus. This discovery will change the way the Ebola virus is studied. Because it is hard to capture and sample the wildlife in West Africa, it makes it hard to figure out how it emerges and is maintained in wildlife. Using the feces from the great apes gives scientists a cheaper, more simple and non-invasive technique to acquiring information about the disease. This new methodology also gives scientists the fact that apes develop antibodies against a disease to survive just as humans do. They also developed a way to isolate the antibodies from the ape’s feces. 10% of samples from 80 free-ranging wild gorillas from five different habitats tested positive in showing the Ebola virus in their feces.

New Picture (3)The worst ever human epidemic of the Ebola virus is ongoing right now throughout West Africa in Guinea, Liberia, Nigeria, and the Sierra Leone. The zaire species of the Ebola virus is the one responsible. This species has been the cause of major human outbreaks before as well as major declines in the chimpanzee and gorillas populations all over central Africa. The human outbreaks have followed the wildlife outbreaks in the past. They transfer to humans from eating infected wildlife. including apes and fruit bats. Therefore, this spillover from wildlife to humans could easily be avoided by not consuming dead wildlife or buying the bats that are sold as food in markets. Because there is no cure for this disease yet, barrier nursing, supportive care, contact tracing, isolation of those who become ill, and education of the public is the only way to try and stop the spread of the disease from human to human. This is much harder to do in less developed nations than the United States where the Ebola virus has emerged repeatedly.

Alain Ondzie, a WCS veterinarian, made a great point by saying, “If scientists can better understand patterns of Ebola virus infection in wildlife, the public health sector can be more prepared to prevent human outbreaks.” The presence of the virus in the ape’s feces shows that some apes survive the Ebola virus. It also shows the regions where the Ebola virus has emerged and which populations of apes are more prone to getting it. Further investigation will need to be done to to see if antibodies persist or whether they pose protection against future infection of the disease.

The benefits of collecting ape feces include being able to cover large areas of forest more quickly without the expense of capturing and handling the animals. It also opens interest to better understand the ecology of the disease and some management options. This could include the study of immune response that could be compared with the genetic information of individuals after an outbreak. Scientists could use this technique with other species that play roles in the transmission of the Ebola virus as well, including wild pigs and antelope.


CDC update on Ebola

The Centers for Disease Control and Prevention have taken the unusual step of revamping their main website in response to the significant outbreak of Ebola Hemorrhagic Fever in central Africa. Traditionally, outbreaks of this disease have had epidemiologists worried when they occur, but fortunately the severity of the disease also means that it outbreaks have been contained rapidly, and the number of deaths historically have not been high with at most a few hundred deaths. The mortality in all outbreaks however has been high, with up to a 90% fatality rate in a 2003 outbreak in the Dem. Republic of the Congo. Currently, no treatment or preventative vaccine exists for Ebola virus.

The current outbreak is historic in its severity; as of late September, an outbreak in West Africa has affected over 6000 people with  about a 50% death rate. The origin of this and previous outbreaks is similar, with the virus moving from its native reservoir in bats to non-human primates, and then to humans. Outbreaks in human populations then occur when human to human transmission occurs with high frequency. The CDC estimates that this number of cases will continue to rise, with potentially 21,000 cases by the end of September, and estimates from the World Health Organization are similar in scope.

To curtail this rise in cases, immediate measures need to be instituted, primarily consisting of ensuring that sick individuals are cared for in equipped Ebola Treatment Units, or if full, in home/community settings with appropriate infection control procedures in place including safe burial procedures. The CDC currently has over 700 staff members actively working on the epidemic at labs in the US, and have deployed almost 100 specialists to offer assistance in the affected region. Part of their work oversees is to assist with screening measures to prevent the epidemic from spreading to other regions, and ensuring that medical and humanitarian resources can reach the affected areas. For US citizens, a non-essential travel alert for this region has been issued.

Public health investigators think that the current outbreak is so severe for a variety of reasons. Seasonal climate variation has potentially created an environment where the virus flourishes in its animal reservoir, or perhaps facilitates transfer from the bat to other transient animal carriers. Development into the jungle has eased the movement of people into regions where the virus is natively found, making animal-human transmission easier. Additionally, political turmoil makes it more difficult for health officials to rapidly respond when an outbreak occurs, and the current outbreak region spreads over several political jurisdictions. Together, these factors have combined for a perfect storm enabling a much greater outbreak than previously seen. The good news in all of this is that there is an international response to the outbreak, and the likelihood of the epidemic spreading to the United States remains very small, even when patients are brought to the US for treatment.

Beware of the brain eating amoeba -Naegleria fowleri

Maria Allera (11 AM Micro) is worried about parasitic diseases, and with good reason. She found a news alert about the brain eating amoeba, which has long been one of my favorites. Who can forget this classic episode of House which featured Nagleria, and was one of the last times I got to trot out the #BOGUS hashtag? Let’s see if Maria can make us feel better about Nagleria:

Naegleria fowleri is an amoeba that takes residence in warm, fresh water all over the world. Just two weeks ago N. fowleri turned up in a water supply in Louisiana, causing the town to go into a state of emergency to provide bottled water for all the residents. N. fowleri can be found in any body of water, such as lakes, ponds, rivers and even manmade structures like pools or waterparks. The amoeba thrives in hot water and can also be found in water discharges from industrial plants.

When N. fowleri comes in contact with a human it makes its way into the body through the nasal passage, swims to the brain and causes an often fatal infection called Primary Amebic Meningoencephalistis (PAM). Some symptoms of PAM include headaches, fever, nausea, vomiting, hallucinations and coma; all of these can lead to death. Since the 1960’s only 200 conditions have been reported, unfortunately less than 5% survive. The infection can be diagnosed when examining spinal fluid under a microscope to identify the amoeba. Under the microscope the amoeba appears as:

Naegleria fowler is elongated, 15-30 μm, and feeds on Gram-negative bacteria. The cytoplasm is granular, has a single nucleus with a prominent and contains vacuoles. Blunt lobular pseudopodia are formed at the widest point. The flagellated form is smaller, with a pear shape and two flagellae at the broad end. N. fowleri cysts are round, 7-15 μm in diameter and have a thick smooth double wall. N. fowleri is thermophilic, preferring water temperatures between 35 and 46ºC (link here)

Within the amoebas life there are three stages. The first two stages, the cyst and flagellate stage, require low food supply and low temperature. When an amoeba is in the cyst or flagellate stage it cannot survive in human tissue. The human body is the perfect living condition for the trophozoite stage. The amoeba feeds off of the human blood cells, it reproduces by binary fission and destroys other tissues. As dangerous as this microorganism sounds, it all depends how it is ingested to determine if it will cause harm or not. If you consume water with N. fowleri in it, it will process through your digestive system without any health problems. This amoeba is only dangerous when it gains nasal access.

Naegleria fowleri in its trophozoite stage, from the CDC

Just like any pathogenic disease everyone wants to know how to prevent acquiring it and how to treat it if acquired. To prevent contracting N. fowleri, it is smart to not submerge your head in fresh water, especially if it is a warm temperature. Try to always swim in treated waters and don’t wash your nose out with fresh water. Do not use a neti pot to clean your sinuses, the water goes straight up the nose so if the water is effected you’re putting your body directly at risk. Unfortunately most infections of N. fowleri end in death, there are a few survival stories. There have been four survival cases in North America, a laboratory did testing and the CDC released

It has been suggested that the original U.S. survivor’s strain of Naegleria fowleri was less virulent, which contributed to the patient’s recovery. In laboratory experiments, the original U.S. survivor’s strain did not cause damage to cells as rapidly as other strains, suggesting that it is less virulent than strains recovered from other fatal infections.

Amphotericin B  was the most common medicine to treat amoebas. It’s inserted directly into the brain; however, this treatment usually fails. The CDC also has an investigational drug on study called Miltefosine for three free living amoebas including N. fowleri and it has had much better results.

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