Editing Staphylococcus aureus (section)

== History ==

=== Discovery ===
In 1880, [[Alexander Ogston]], a Scottish surgeon, discovered that ''Staphylococcus'' can cause wound infections after noticing groups of bacteria in pus from a surgical abscess during a procedure he was performing. He named it ''Staphylococcus'' after its clustered appearance evident under a microscope. Then, in 1884, German scientist [[Friedrich Julius Rosenbach]] identified ''Staphylococcus aureus'', discriminating and separating it from ''[[Staphylococcus albus]]'', a related bacterium. In the early 1930s, doctors began to use a more streamlined test to detect the presence of an ''S. aureus'' infection by the means of [[coagulase]] testing, which enables detection of an enzyme produced by the bacterium. Prior to the 1940s, ''S. aureus'' infections were fatal in the majority of patients. However, doctors discovered that the use of penicillin could cure ''S. aureus'' infections. Unfortunately, by the end of the 1940s, [[antibiotic resistance|penicillin resistance]] became widespread amongst this bacterium population and outbreaks of the resistant strain began to occur.<ref>{{cite journal| vauthors = Orent W |date=2006|title=A Brief History of Staph|journal=Proto Magazine}}</ref>

=== Evolution ===
''Staphylococcus aureus'' can be sorted into ten dominant human lineages.<ref>{{Cite web |title=S. aureus clonal complex designation |url=https://pubmlst.org/organisms/staphylococcus-aureus/clonal-complexes |access-date=2024-02-28 |website=PubMLST |language=en}}</ref> There are numerous minor lineages as well, but these are not seen in the population as often. Genomes of bacteria within the same lineage are mostly conserved, with the exception of [[mobile genetic elements]]. Mobile genetic elements that are common in ''S. aureus'' include bacteriophages, [[pathogenicity island]]s, [[plasmids]], [[transposons]], and staphylococcal cassette chromosomes. These elements have enabled ''S. aureus'' to continually evolve and gain new traits. There is a great deal of genetic variation within the ''S. aureus'' species''.'' A study by Fitzgerald et al. (2001) revealed that approximately 22% of the ''S. aureus'' genome is non-coding and thus can differ from bacterium to bacterium. An example of this difference is seen in the species' virulence. Only a few strains of ''S. aureus'' are associated with infections in humans. This demonstrates that there is a large range of infectious ability within the species.<ref>{{cite journal | vauthors = Fitzgerald JR, Sturdevant DE, Mackie SM, Gill SR, Musser JM | title = Evolutionary genomics of ''Staphylococcus aureus'': insights into the origin of methicillin-resistant strains and the toxic shock syndrome epidemic | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 98 | issue = 15 | pages = 8821–6 | date = July 2001 | pmid = 11447287 | pmc = 37519 | doi = 10.1073/pnas.161098098 | doi-access = free | bibcode = 2001PNAS...98.8821F }}</ref>

It has been proposed that one possible reason for the great deal of heterogeneity within the species could be due to its reliance on heterogeneous infections. This occurs when multiple different types of ''S. aureus'' cause an infection within a host. The different strains can secrete different enzymes or bring different antibiotic resistances to the group, increasing its pathogenic ability.<ref name=":0">{{cite journal | vauthors = Lindsay JA | title = Genomic variation and evolution of ''Staphylococcus aureus'' | journal = International Journal of Medical Microbiology | volume = 300 | issue = 2–3 | pages = 98–103 | date = February 2010 | pmid = 19811948 | doi = 10.1016/j.ijmm.2009.08.013 }}</ref> Thus, there is a need for a large number of mutations and acquisitions of mobile genetic elements.{{citation needed|date=December 2022}}

Another notable evolutionary process within the ''S. aureus'' species is its co-evolution with its human hosts. Over time, this parasitic relationship has led to the bacterium's ability to be carried in the [[nasopharynx]] of humans without causing symptoms or infection. This allows it to be passed throughout the human population, increasing its fitness as a species.<ref>{{cite journal | vauthors = Fitzgerald JR | title = Evolution of ''Staphylococcus aureus'' during human colonization and infection | journal = Infection, Genetics and Evolution | volume = 21 | pages = 542–7 | date = January 2014 | pmid = 23624187 | doi = 10.1016/j.meegid.2013.04.020 | bibcode = 2014InfGE..21..542F }}</ref> However, only approximately 50% of the human population are carriers of ''S. aureus'', with 20% as continuous carriers and 30% as intermittent. This leads scientists to believe that there are many factors that determine whether ''S. aureus'' is carried asymptomatically in humans, including factors that are specific to an individual person. According to a 1995 study by Hofman et al., these factors may include age, sex, [[diabetes]], and smoking. They also determined some genetic variations in humans that lead to an increased ability for ''S. aureus'' to colonize, notably a polymorphism in the [[glucocorticoid receptor]] gene that results in larger [[corticosteroid]] production. In conclusion, there is evidence that any strain of this bacterium can become invasive, as this is highly dependent upon human factors.<ref>{{cite journal | vauthors = van Belkum A, Melles DC, Nouwen J, van Leeuwen WB, van Wamel W, Vos MC, Wertheim HF, Verbrugh HA | title = Co-evolutionary aspects of human colonisation and infection by ''Staphylococcus aureus'' | journal = Infection, Genetics and Evolution | volume = 9 | issue = 1 | pages = 32–47 | date = January 2009 | pmid = 19000784 | doi = 10.1016/j.meegid.2008.09.012 | bibcode = 2009InfGE...9...32V }}</ref>

Though ''S. aureus'' has quick reproductive and micro-evolutionary rates, there are multiple barriers that prevent evolution with the species. One such barrier is AGR, which is a global [[accessory gene regulator]] within the bacteria. This such regulator has been linked to the virulence level of the bacteria. Loss of function mutations within this gene have been found to increase the fitness of the bacterium containing it. Thus, ''S. aureus'' must make a trade-off to increase their success as a species, exchanging reduced virulence for increased drug resistance. Another barrier to evolution is the Sau1 Type I [[Restriction modification system|restriction modification]] (RM) system. This system exists to protect the bacterium from foreign DNA by digesting it. Exchange of DNA between the same lineage is not blocked, since they have the same enzymes and the RM system does not recognize the new DNA as foreign, but transfer between different lineages is blocked.<ref name=":0" />