Staphylococcus aureus is a gram-positive spherically shaped bacterium, a member of the Bacillota, and is a usual member of the microbiota of the body, frequently found in the upper respiratory tract and on the skin. It is often positive for catalase and nitrate reduction and is a facultative anaerobe, meaning that it can grow without oxygen. Although S. aureus usually acts as a commensal of the human microbiota, it can also become an opportunistic pathogen, being a common cause of skin infections including abscesses, respiratory infections such as sinusitis, and food poisoning. Pathogenic strains often promote infections by producing virulence factors such as potent protein toxins, and the expression of a cell-surface protein that binds and inactivates antibodies. S. aureus is one of the leading pathogens for deaths associated with antimicrobial resistance and the emergence of antibiotic-resistant strains, such as methicillin-resistant S. aureus (MRSA). The bacterium is a worldwide problem in clinical medicine. Despite much research and development, no vaccine for S. aureus has been approved. An estimated 21% to 30% of the human population are long-term carriers of S. aureus, which can be found as part of the normal skin microbiota, in the nostrils, and as a normal inhabitant of the lower reproductive tract of females. S. aureus can cause a range of illnesses, from minor skin infections, such as pimples, impetigo, boils, cellulitis, folliculitis, carbuncles, scalded skin syndrome, and abscesses, to life-threatening diseases such as pneumonia, meningitis, osteomyelitis, endocarditis, toxic shock syndrome, bacteremia, and sepsis. It is still one of the five most common causes of hospital-acquired infections and often the cause of wound infections following surgery. Each year, around 500,000 hospital patients in the United States contract a staphylococcal infection, chiefly by S. aureus. Up to 50,000 deaths each year in the U.S. are linked to staphylococcal infection.
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 means of coagulase testing, which detects an enzyme produced by the bacterium. Before the 1940s, S. aureus infections were fatal in most patients. However, doctors discovered that penicillin could cure S. aureus infections. Unfortunately, by the end of the 1940s, penicillin resistance became widespread amongst this bacterium population and outbreaks of the resistant strain began to occur.
Evolution Staphylococcus aureus can be sorted into ten dominant human lineages. 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, except for mobile genetic elements. Mobile genetic elements that are common in S. aureus include bacteriophages, pathogenicity islands, plasmids, transposons, and staphylococcal cassette chromosomes. These elements have enabled S. aureus to evolve and acquire new traits continually. 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. It has been proposed that one possible reason for the significant 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. Strains can secrete different enzymes or bring different antibiotic resistances to the group, increasing their pathogenic ability. Thus, there is a need for a large number of mutations and acquisitions of mobile genetic elements. 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. 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 many factors determine whether S. aureus is carried asymptomatically in humans, including individual-specific factors. According to a 1995 study by Hofman et al., these factors may include age, sex, diabetes, and smoking. They also noted genetic variations in humans that increase the likelihood of S. aureus colonization, 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. Although S. aureus has quick reproductive and micro-evolutionary rates, multiple barriers prevent evolution within the species. One such barrier is AGR, a global accessory gene regulator within the bacteria. This regulator has been linked to the bacteria's virulence level. 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 its success as a species, exchanging reduced virulence for increased drug resistance. Another barrier to evolution is the Sau1 Type I 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.
Microbiology
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