All It Takes is One Mutation

A university research team from Scotland recently discovered a bacteria that has mutated and gained the ability to jump from humans to rabbits.  The scientists traced the evolution of a specific bacterium that causes skin infections in rabbits: Staphylococcus aureus (ST121).  Strangely enough, ST121 has been found in some humans as well and although it's relatively harmless, it can sometimes lead to meningitis or sepsis.  

This similarity allowed the scientists to track the evolution of the pathogen and discover that the rabbit-specific ST121 bacteria evolved from the human-specific version over 40 years ago and mutated enough to be able to jump from humans to rabbits.  One genetic mutation allowed this to happen.  One naturally occurring genetic mutation was enough to completely change the bacteria and let it change host species.  The fact that a genetic mutation this small can alter a pathogen so much brings up a lot of questions and a lot of places where more studies can be done to see what other bacteria, if any, may be able to jump so easily from another species to humans or vice versa.  This could also pose a problem for industrial animal businesses that keep many different species of animals in close quarters.

I think this is a very interesting topic because it's bizarre; a human probably wouldn't expect to get an infection from a rabbit.  I also think it's interesting how only one genetic mutation allowed the bacteria to do this.  Scientists know little about bacteria and viruses because they are all so complex and there are many variations of them so scientists may never learn everything there is to know about their makeups.  It's important that scientists research this in more detail with other species of animals if they ever want to help slow or stop the spread of these species-hopping pathogens for peoples' and animals' sake.

Viruses Are Less Effective to Genetically Diverse Populations

When a virus was allowed to spread through a group of five genetically identical mice, the virus became more effective. That is, it spread more quickly and became more severe with each mouse it infected. The same test was done, this time with the mice being genetically diverse. This time around, the virus became less virulent as it struggled to adapt to the dissimilar genomes of the mice.

The University of Utah uses this simple example to urge the owners of livestock and other bred animals to keep their genetic diversity up. A herd of genetically similar cows is the vertebrate version of a monoculture, and a single pathogen capable of killing one of them will affect all of them. Whereas a population of genetically diverse animals will cause a pathogen to kill less effectively, both on the individual level and on the level of the whole herd. The first author of the study, Jason Kubinak, believes that sexual reproduction may have evolved to keep pathogens at bay. Another hypothesis on the evolution of sexual reproduction is that it evolved to regulate the inevitable mutations that occur when DNA is replicated.




article: http://unews.utah.edu/news_releases/viruses-impaired-if-their-targets-have-diverse-genes/

How Bacteria Resist Antibiotics in Hospitals

Scientists have discovered why antibiotic-resistant bacteria thrive in hospitals.  By using advanced DNA sequencing of samples from over 1,000 patients, researchers were able to identify antibiotic-resistant genes.  This was possible as they were able to see the complete genome of bacteria samples.  Circular DNA known as plasmids appear to be the center of the issue.  Plasmids easily enter bacteria and have the ability to move from one bacteria to another.  This study indicates that some plasmids carry a gene responsible for making bacteria drug-resistant.  Plasmids are able to multiply independently and can integrate their DNA with the DNA of bacteria.  Scientists have found that plasmids containing the gene capable of inactivating certain antibiotics can be transferred to bacteria of various classifications.  Dr. Tara Palmore, an infection control specialist for the U.S. National Institute of Health and co-author of this study stated, "The plasmids we are talking about carry an antibiotic-resistant gene to a class of antibiotic called carbapenems."  The carbapenem class of antibiotics are essentially antibiotics of last resort.  Dr. Marc Siegel, an associate professor of medicine at NYU Langone Medical Center stated, "Carbapenems are the best we have. So if you've got carbapenem resistance, there is nowhere else for us to go.  We don't have a secret treatment up our sleeves."  

The image above displays the serious threat that 

antibiotic-resistant bacteria pose to humans.  

According to the study, carbapenem-resistant Enterobacteriaceae (CRE) are bacterial pathogens that pose an alarming threat to hospitalized patients.  The occurrence of CRE has quadrupled in the United States in the last ten years. Researchers claim that CRE are resistant to most, if not all antibiotics.  A death rate of 40-80% from infection has been reported.  According to the U.S. National Institute of Health, over the past two years, ten patients have been identified as having resistance to carbapenems.  Although patients who contain this bacteria may not be sick themselves, they have the ability to pass the drug-resistant bacteria to others.  Dr. Julie Segre, chief investigator at the U.S. National Human Genome Research Institute and co-author of this study stated, "We are trying to reinforce the message that these drug-resistant bacteria can't become so prevalent that we can no longer control them."  

Ultimately, drug companies need to manufacture new antibiotics in which doctors need to use more cautiously.  Hospitals also need to do a better job of disinfecting facilities.  The correlation between the use of antibiotics and the increasing level of antibiotic- resistant bacteria is extremely interesting. In particular, this article caught my eye, as I always read how important it is for medical personnel to be careful when prescribing antibiotics.  Antibiotics are often prescribed during unnecessary circumstances in which over usage leads to ineffectiveness.  The article supports that theory due to bacteria forming resistance over time to even the most potent antibiotics available in the world today.


[1] Article: http://health.usnews.com/health-news/articles/2014/09/17/researchers-discover-how-bacteria-resist-antibiotics-in-hospitals
Related articles: http://www.medpagetoday.com/MeetingCoverage/ICAAC/47541
                          http://www.medicalnewstoday.com/articles/282357.php

Deadly Human Pathogen Fully Sequenced

In this article, researchers have sequenced the entire genome and all the RNA products of the most important pathogenic lineage of Cryptococcus neoformans, a strain called H99.  The results describe numerous genetic changes that can take place after laboratory handling of H99 that cause it to be more susceptible to stress, affect its ability to sexually reproduce, and cause it to be less virulent.  The study describes how the pathogen causes diseases and how to keep it from becoming deadly.  By having a sequenced genome of H99, researchers now know why organisms like this aren't easily killed by antifungal medications.  Cryptococcus neoformans is a major human pathogen that mainly affects humans with compromised immune systems.  The best way for the researchers to study how the virulence of this pathogen could change over time was to develop a map of the H99 strain in both its original state and after it had been cultured.  The researchers discovered the molecules ability to produce genetic messages from both strands of DNA, which enables it to adapt and survive in changing conditions.  They also discovered that the original and cultured strains were very similar to each other.

The results from this study could help researchers study this organism and other organisms like it.  If more studies like this are performed, more genomes could be sequenced.  Genome sequencing could help us cure and possibly prevent deadly human pathogens from occurring in the future.











Original article: http://www.sciencedaily.com/releases/2014/04/140417191618.htm
To learn more about pathogens, visit: http://www.sciencedaily.com/articles/p/pathogen.htm

Gonorrhea gets even more personal

Researchers at the Feinburg School of Medicine have discovered a piece of human DNA incorporated in the DNA of the human pathogen Neisseria Gonorrhoeae, the microbe responsible for the sexually transmitted infection known as Gonorrhea. When the DNA of multiple N. Gonorrhoeae was sequenced it was observed that around 11% of them contained a small fragment of human L1 DNA element. Then the researchers sequenced the DNA of very closely related Neisseria species and found no human fragments at all. 
 It is proposed that the fragment of human DNA was incorporated by a horizontal gene transfer. Which up until now were only thought to occur between like types of cells, prokaryotic or eukaryotic. Since N. Gonorrhoeae is known to reside both intracellular and extracellular it is thought by researchers that it would be able to make its way into a position in which a HGE could occur. Also, that since only 11% of the tested population showed the fragment it implies that this transfer event could have happened recently. This observation alone has many implications in evolution as well as disease and immunity research. This could be a possible mechanism in which pathogens are able to build immunities to their hosts.
 I hope these discoveries bring about more research into Horizontal Gene Transfers between bacteria and mammals, not only for the implications into evolutionary mechanisms but also as a tool to better understand the pathogens around us.

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