Please note, BioLabTests are UNABLE TO TEST ANY VIRUSES including SARS-CoV-2 (COVID-19)
Please note, BioLabTests are UNABLE TO TEST ANY VIRUSES including SARS-CoV-2 (COVID-19)

The molecular and genetic differences: Staphylococcus aureus vs MRSA

4.1 min readPublished On: April 26th, 2022Categories: Microbiology
Staphylococcus aureus vs MRSA

At BioLabTests, we offer a wide range of testing services to clients such as environmental testing, product testing and microbiological research. In this blog, we would like to delve deeper into the testing method ISO 22196 and the key differences between the strains of bacteria used – Staphylococcus aureus vs MRSA. Commonly BioLabTests test against MRSA, but we can also test against Staphylococcus aureus.

Introducing both bacteria

S.aureus is an aerobic, Gram-positive bacterium that makes up 50–60% of the skin’s natural microbiome, populating the hands, face and nose. S. aureus can lead to more serious infections causing abscesses and septicaemia if the skin is broken, either by surgery or cuts and/or grazes. MRSA (Methicillin-Resistant Staphylococcus Aureus) can include any strain of S. aureus that has acquired resistance to penicillin, methicillin or types of antibiotics called cephalosporins over time. MRSA is now classed as a superbug, which means many antibiotics are not effective treatment options, making infections harder and more difficult to treat.

The discovery of Staphylococcus aureus

S.aureus was first discovered in 1880 by Sir Alexander Ogston, after having identified the bacteria in pus-filled abscesses during a surgical operation. S. aureus infections were found to be fatal in the majority of patients before the discovery and production of penicillin in the 1940s. Penicillin was found to be highly effective in treating infections caused by S. aureus and prevented many fatalities. However, 2 years after its discovery, some strains had already developed a resistance to the antibiotic.

What can Staphylococcus aureus cause?

S.aureus is one of the most common causes of skin infections and can cause more serious infections like toxic shock syndrome and sepsis. S. aureus has many virulence factors such as hemolysins, leukocidins, and protein A, that are advantageous in initiating an infection. It is able to regulate the expression of these virulence factors by a system called quorum-sensing (agr system).

Protein A is an extremely important adhesion protein and promotes colonisation on host cells to initiate an infection. Furthermore, S. aureus releases many cytotoxic agents, for example α-toxin which can cause severe lung damage and pneumonia. Additionally, α-toxin is classed as a pore former, which means it forms pores on host cell membranes, which in return causes structural damage and eventually leads to cell apoptosis. However, S. aureus can still be treated quite easily with various forms of penicillin such as methicillin and flucloxacillin. This is because they work by inhibiting the formation of peptidoglycan cross linkages in bacterial cell walls, without which the cell wall becomes incredibly weak.

Staphylococcus aureus vs MRSA: The key differences

MRSA is a group of Gram-positive bacteria that are genetically distinct from other strains of Staphylococcus aureus. MRSA has become resistant to several widely used antibiotics. This means infections with MRSA can be harder to treat than other bacterial infections.

MRSA strains have become very virulent. A reason for this is that MRSA possesses many pathogenicity islands (SaPIs) which are a family of genetic mobile elements. MRSA also encodes super-antigen genes such as enterotoxin C.

A key difference between strains of S. aureus and MRSA is the acquisition of the mecA gen which is located on a large mobile genetic element called Staphylococcal Chromosome Cassette mec or SCCmec, of which there at least 11 distinct types. It is thought to be within a pathogenicity island (SaPI). As penicillin was found to be ineffective in treating strains of S. aureus in the 1950s, methicillin was designed in 1959 to resist the action of β-lactamase.

The first incidence of MRSA was identified in the 1961, and was found to be resistant to methicillin due to the mecA gene. Acquiring the mec gene (mecA, mecB, and mecC) meant that MRSA could block the action of methicillin due to the gene coding for an altered penicillin-binding protein (PBP2a). This in turn meant MRSA was resistant to all β-lactam antibiotics, cephalosporins and carbapenems. Furthermore, the SSCmec genetic element is thought to highly increase MRSA virulence and capability to transfer resistance genes to other strains and species.

To conclude, many strains of S. aureus have evolved over the years and antibiotic use has led to increasing incidence of MRSA infection. Both strains have various genetic and molecular differences that affect virulence and transmission.

References

Adame-Gómez, R. et al. (2020) Genetic Diversity and Virulence Factors of S. aureus. Available at: https://www.hindawi.com/journals/ijmicro/2020/1048097/

Novick, R. P., and Ram, G. (2017) Staphylococcal pathogenicity islands – movers and shakers in the genomic firmament. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5884141/

Babek, A. et al. (2014) Staphylococcus aureus mobile genetic elements. Available at: https://www.proquest.com/scholarly-journals/staphylococcus-aureus-mobile-genetic-elements/docview/1548176263/se-2

Liu, J. (2016) Staphylococcal chromosomal cassettes mec (SCCmec): A mobile genetic element in methicillin-resistant Staphylococcus aureus. Available at: https://www.sciencedirect.com/science/article/abs/pii/S0882401016301760

Oogai, Y. (2011) Expression of Virulence Factors by Staphylococcus aureus Grown in Serum. Available at: https://doi.org/10.1128/AEM.05316-11

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