MRSA for non-scientists

MRSA for non-scientists

History of MRSA and mechanisms against antibiotics

MRSA is a form of methicillin resistant staphylococcus aureus that has become a worry to many scientists in the past 30 years. The scary aspect of MRSA is its ability to not only resist methicillin, but its ability to seemingly resist any antibiotic humanity uses to kill it. Some of these other antibiotics include penicillin, vancomycin, fluoroquinolone and many more. Penicillin and methicillin work by permanently binding to the active site of penicillin binding protein (PBP) (a protein that builds the cell wall of gram positive bacteria by using peptidoglycans) and not allowing the cell to build its cell wall. Without a cell wall the cell loses all its structural integrity, which leads to the internal parts of the cell to spill out and to therefore kill the cell. To resist this MRSA has evolved a gene called the BlaZ gene that in the presence of penicillin makes a protein called penicillinase. This penicillinase then binds to penicillin and denatures it before it can bind to PBP. To resist methicillin many forms of MRSA have evolved a gene called the mecA gene. This gene encodes for a different kind of PBP that methicillin can not bind to and therefore the cell can continue to make its cell wall even in the presence of methicillin.

Fluoroquinolone works by over activating enzymes that help to maintain the structure of DNA within a bacterial cell. Fluoroquinolone binds to these enzymes and interacts with them in a way that makes them cut the DNA of the bacteria. With its DNA being in a bunch of little pieces the bacteria cannot produce any proteins that are critical for cell function. To counter this the enzymes in bacteria have changed their amino acid sequence in a way that does not allow fluoroquinolone to bind to it. This allows the bacteria to safely maintain its DNA even in the presence of fluoroquinolone.

Vancomycin works by binding specific amino acids (monomers that make up a proteins and other cellular structures) on peptidoglycan and not allowing PBP to form the cell wall. As stated before, PBP uses peptidoglycans to build the cell wall and to stop the cell wall from forming, vancomycin binds to the alanine (a type of amino acid) at the end of peptidoglycans. This stops the PBP enzyme from binding two peptidoglycan sequences and therefore the cell wall cannot be built. To resist this the cells evolved to change the amino acids on the ends of peptidoglycan that vancomycin binds to. This leads to vancomycin not being able to bind to peptidoglycan and the bacterial cell being able to form its cell wall.

Antibiotic resistance in humans

MRSA infections are classified into two subsections: community associated MRSA (CA-MRSA) and healthcare associated MRSA (HA-MRSA). CA-MRSA is a MRSA infection that came from outside a healthcare facility and these infections commonly occur in schools, athletic facilities, military barracks and any place where many people come into contact. HA-MRSA is any MRSA infection that occurs from a visit or surgery within a healthcare facility. The diversity and frequency of both infection types have been on a steep rise in the last two decades. HA-MRSA is of worry because these infections occur in healthcare facilities where many people have compromised immune systems from other diseases. These HA-MRSA strains tend to have more resistance to a wider form of antibiotics because they come into contact with sublethal dosages of antibiotics more often than other bacterium. This can lead to cases of HA-MRSA where almost no antibiotics can kill the MRSA bacteria, and therefore have a higher chance of killing the patient.

Prevention and Treatment

Many scientists nowadays are looking for new and better methods to fight MRSA. One new class of antibiotic in development is called diphenylureas that works to inhibit the growth of MRSA cells. Another extremely surprising antibiotic in testing is called lugdunin and is produced by Staphylococcus lugdunensis, a species of bacteria found in human nasal passages. This is very important because it would be the first case a commensal bacterium within a human host produces an antibiotic.

The best way to fight and prevent MRSA though is to follow the general prevention guidelines provided by the CDC. These involve washing your hands regularly, cleaning all clothes and linens especially after exercise and disinfecting heavily trafficked areas. Scientists have also been developing new materials that bacteria will die on if they stay on it too long. An example of this is Optifoam™ which is a polyurethane with silver chloride ions bonded to it. The silver creates an environment that kills the bacteria leaving a surface that is pretty much self-sanitizing.


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6 thoughts on “MRSA for non-scientists

    1. Staphylococcus lugdunensis is a naturally occurring bacteria in many environments. When certain non-pathogenic bacteria enter a part of the body they find to be a suitable environment they grow and form a mutually beneficial relation with the host. Staphylococcus lugdunensis benefits by having a stable, moist and protected environment to grow in while the host benefits by having Staphylococcus lugdunensis kill potentially dangerous bacteria like Staphylococcus aureus.

    1. An active site is the place within a protein where a substrate (a molecule that will somehow how be acted on by the enzyme) binds and goes through some form of a reaction. In the case of Penicillin Binding Protein, two seperate molecules of peptidoglycan come together and are connected to each other in a chemical reaction. This chemical reaction is a key reaction in building the cell wall.

    1. Flouroquinolone binds to a enzyme’s active site in a way that allows it cut DNA at a faster rate. Usually this enzyme cuts DNA at very specific times to keep the cells DNA intact, but when flouroquinolone binds it begins to cut very rapidly to the point where it destroys the cells DNA structure.

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