Saturday, December 1, 2012

Superbugs Around Us and How They Come About

As we know, anything in life is not 100% perfect. Computers “act up”, Disinfectant sprays reading “kills 99.9% of germs”, and even human error prevents things being totally precise. It’s safe to say when regarding bacteria and infections, all people want 100% results. However, because of miscalculations, natural occurrences, and environmental cesspools, “superbugs”, have formed. Sounding like something out of a comic book, superbugs are formed as a result of the use of antibiotics. Some bacteria cells survive the exposure to antibiotics, and in turn, become immune to certain widely used drugs to treat bacterial infections.
These bacterial species can become stronger due to the stress that antibiotics inflict on bacterial cells, causing them to mutate. In general, the probability of mutation occurring by chance is about one out of every million copies of a gene of a bacterium. The ability for these prokaryotic cells to change offers harmful effects on humans because 100% of them are not dying. Vancomycin-resistant Staphylococcus aureus (VRSA), a strain of MRSA, or otherwise known as staph infection, arose from mutation. Vancomycin is the drug of last resort for this infection, proposing the educated guess of the possibility of more mutations and another antibiotic-resistant strain, leaving no drug to treat it.
Resistant genes are also made apparent by gene transfer. Humans reproduce sexually; traits are transferred vertically from parent to child. Prokaryotes do not reproduce sexually, but they exchange DNA between cells. This is known as horizontal gene transfer.  There are three ways horizontal gene transfer can occur: conjugation, transduction, and transformation.  
Conjugation requires cell-to-cell contact, and is common with E. coli. When E. coli cells become in contact with one another, plasmids are transferred. The best known plasmid capable of transfer is the F Plasmid, F for fertility factor. Cells that contain F plasmids are known as F+ cells, and cells that do not have the F plasmid cells are called F- cells. During the process of conjugation in E. coli, the F+ donor cell comes in contact with the F- recipient cell, and a pilus is formed on the F+ cell, acting as a the conjugation bridge. The F plasmid is replicated in the donor cell, displacing a parental strand, which gets transferred to the recipient cell and replicated once more. The F plasmid’s DNA is copied into the F- cell, changing it to an F+ cell. The new F+ cell then has the capability to use the same technique to transfer DNA as the original donor cell. The process is known as the rolling-circle replication.
Transduction is seen as an accident. When a phage infects a cell, it injects its DNA into the cell, and the phage DNA is replicated, and the host DNA is degraded. Phage particles are then packaged with DNA and released. When the phage package their DNA, they can package host DNA instead of phage DNA, producing a transducing phage. When the transducing phage infects a new cell, it only injects a piece of chromosomal DNA, which is incorporated by homologous recombination. The new cell contains DNA from the donor. The transducing phage incorporates its DNA into a cell, resulting in change in the genetic makeup of the cell to be like the donor cell, rather than phages being released as explained before.
Transformation occurs when one cell dies and releases its contents to its surroundings. These DNA fragments and be taken up in another cell and the DNA is incorporated by homologous recombination. The cell then contains DNA from the donor cell.
Antibiotic resistance can also occur due to contact with animals. Animals raised for food are given antibiotics either to promote growth, like Ractopamine, which promotes lean muscle growth, or to treat infections. “When you give low-dose antibiotics for growth promotion or for prophylaxis of infection, you end up killing off the susceptible bacteria, whether they’re E. coli, salmonella, campylobacter, or other bacteria,” says Robert S. Lawrence, M.D., director of the Center for a Livable Future at the Johns Hopkins Bloomberg School of Public Health in Baltimore. “And you continue to select for those bacteria that, through spontaneous mutations or transfer of genes from other resistant bacteria, allow them to be resistant to antibiotics.” This is an example for the “cesspools” mentioned before. Because of the close living quarters of the animals, it is a breeding ground for new antibiotic resistant bacteria cells to form.
Another breeding ground is hospitals. Since superbugs evolve from the heavy use of antibiotics, hospitals are a culprit. Also, considering the amount of open wounds and tubes carrying blood, that is another reason why hospitals are susceptible to antibiotic resistant superbugs. College campuses are another environment superbugs enjoy because of the unwashed clothing and sheets, being exposed to so many people, frequently used cafeteria trays, and even beer pong cups.
http://www.consumerreports.org/cro/pork0113.htm
http://www.thedailybeast.com/articles/2010/08/12/superbug-facts-to-know-as-ndm-1-emerges.html

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