Evolution of Methicillin-Resistant Staphylococcus Aureus

Contributed by Priya Chopra, Shoeb Lallani, Rahul Mohan, Vivek Sawhney, Matt Wu, Manal Zafar

Perhaps you may think that humans cannot influence the evolution of MRSA. However, this is not the case. For years, humans have used antibiotics to treat many types of bacterial infections, ranging from Staphylococcus aureus infection to Streptococcus. Antibiotics can be found in places you might not expect, such as hand soaps, cleaners, toothpaste, and in livestock that have contact with humans (Nerby et al., 2011). The use of antibiotics in a wide variety of places promotes the development of a diverse range antibiotic resistance in S.aureus.

A Video on The Evolution of MRSA

You may also think that MRSA evolved/continues to evolve randomly by chance. However, the fact that humans continually introduce numerous antibiotics to bacteria promotes the evolution of bacteria in a way that promotes its own survival. Humans provide the selective pressure to prompt bacteria to evolve characteristics that will maximize its fitness in its host. For example, if we introduce an antibiotic to a population, there may be a select few bacteria that have a mutation or gene that confers antibiotic resistance, which can then be passed onto future generations (vertical gene transfer). This leads to antibiotic resistance, and, to make things worse, resistance can then also be transferred by horizontal gene transfer (between different species) (Giedraitiene et al., 2011). For example, S. aureus can develop resistance to an antibiotic used to treat a nearby different bacterial infection, like tuberculosis, by means of horizontal gene transfer. This resistance can then be shared to the rest of the S. aureus population via vertical gene transfer.

Eventually, many strains of MRSA evolve, and new antibiotics need to be created in order to treat the strains. So, next time your doctor gives you antibiotics, think about the evolutionary consequences of introducing these antibiotics to your body.

To learn more…

Cogen A. L., Nizet V., Gallo R. L. (2009). Skin microbiota: a source of disease or defense? British Journal of Dermatology, 158(3): 442-455.

Fomda B. A., Thokar M. A., Ray P. (2014). Prevalence and genotypic relatedness of methicillin resistant Staphylococcus aureus in a tertiary care hospital. Journal of Postgraduate Medicine, 60(4): 386-9.

Giedraitiene A., Vitkauskiene A., Naginiene R., Pavilonis A. (2011). Antibiotic Resistance Mechanisms of Clinically Important Bacteria. Medicina, 47(3): 137-46.

McNulty C., Boyle P., Davey P. (2007). The public’s attitudes to and compliance with antibiotics. Journal of Antimicrobial Chemotherapy, 60: 63-68.

Micek S. T. (2007). Alternatives to Vancomycin for the Treatment of Methicillin-Resistant Staphylococcus aureus Infections. Clinical Infectious Diseases, 45: 184-190.

Nerby J.M., Gorwitz R., Harriman K. (2011). Risk factors for household transmission of community-associated methicillin-resistant Staphylococcus aureus. Pediatric Infectious Disease Journal, 30(11): 927-32.

Planet P. J., LaRussa S. J., Dana A., Smith H., Xu A. (2013). Emergence of the Epidemic Methicillin-Resistant Staphylococcus aureus Strain USA300 Coincides with Horizontal Transfer of the Arginine Catabolic Mobile Element and speG-mediated Adaptations for Survival on Skin. American Society for Microbiology, 4, 13.

Poole K. (2007) Efflux pumps as antimicrobial resistance mechanisms. Annals of Internal Medicine, 39(3): 162-76.

Wielders C. L., Fluit A., Schmitz F., mecA Gene Is Widely Disseminated in Staphylococcus aureus Population, Journal of Clinical Microbiology, 40(11): 3970-3975.  

Leave a Reply

Your email address will not be published. Required fields are marked *