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The not so golden Golden Staph

Staphylococcus aureus, *S. aureus*, commonly known as Golden Staph, may not be so golden as its name suggests. Let’s find out why.
Two petrie dishes with bacterial samples depicting bacterial multiplication
© Griffith University
Staphylococcus aureus (S.aureus), commonly known as Golden Staph, may not be so golden as its name suggests. Let’s find out why.

The Golden Staph

S.aureus (also known as Golden Staph) is a bacterial organism commonly found as part of one’s normal flora, or naturally occurring in our body.

However, it is an opportunistic pathogen, causing mostly skin infections amongst numerous others, usually gaining entry through cuts in the skin or mucous membranes. Because of this, S.aureus infection can be acquired in hospital and other healthcare settings (known as healthcare associated infections or (HAIs). Infections can occur due to invasive medical interventions and the high ratio of people with compromised immune systems. Treatment is often with a penicillin based drug, one of many different classes of antibiotics.

Antibiotics and resistance

The accidental discovery of penicillins in 1928 sparked a healthcare revolution. It was quickly followed by the discovery and subsequent widespread clinical use of other classes of antibiotics in order to treat bacterial infections. Complete eradication of bacterial diseases seemed inevitable. That is, until some species developed antibiotic resistance. Penicillins were first clinically used in 1942 with great success. However, bacterial resistance to penicillin was already observed before 1950. Since the 1970s, resistance to new antibiotics has been rapid. Figure 1 on page 5 of the Australian Commission on Safety and Quality in Healthcare Report shows that the lifespan of antibiotics is growing shorter and shorter (ACSQHC, 2013).

The emergence of multi drug resistant organisma (MROs) or ‘superbugs’ is of particular concern. Methicillin-resistant S.aureus (MRSA) is one such organism. By 1950, 40% of hospital S.aureus infections were penicillin-resistant; rising to 80% by 1960 (Chambers, 2001). Don’t be fooled by the name; MRSA is not only resistant to methicillin (a type of penicillin), but to other penicillins as well. Penicillins work by disrupting the formation of the cell wall, which results in the death of the bacterium. The surviving bacteria were those that had the ability to produce β-lactamase (penicillinase), an enzyme that breaks down penicillin and other β-lactam antibiotics. Scientists then discovered β-lactam antibiotics that were resistant to β-lactamase such as methicillin, but now resistance exists for these as well.

How do bacteria gain antibiotic resistance?

So how is it that bacteria can gain and spread antibiotic resistance at such astonishing rates? Bacteria have small genomes and reproduce rapidly so evolution via spontaneous genetic mutations is much more successful and quicker than in larger organisms such as humans. Bacteria also have the ability to transfer these new genes not only to their offspring (vertical gene transfer), but also directly to other bacteria (whether same or different species) through horizontal gene transfer. This can occur in one of three ways:

  1. Conjugation: This involves direct contact between two bacteria, usually via a tube-like bridge called a pilus.
  2. Transformation: The intake of loose genetic matter from dead bacteria and its subsequent incorporation into the genome of the live one.
  3. Transduction: The injection of new genetic material via a bacteriophage. Bacteriophages are viruses that infect bacteria. Similar to vectors that carry infectious agents from one organism to another, bacteriophages can carry genetic material from one bacterium to another.

The overuse and misuse of antibacterials has contributed greatly to antibiotic resistance. Unnecessary and prolonged exposure of bacteria to antibiotics gives them the chance to develop resistance. Examples include:

  1. Inappropriate dosage: Too little fails to kill the bacteria.
  2. Inappropriate use: Antibiotics are useless on illnesses caused by other classes of infectious agent such as viruses.
  3. Patient non-compliance: Even when told to take every single antibiotic, some patients stop when their symptoms improve, leading to the possibility of not entirely eliminating the infection.
  4. Antibiotics use in livestock: Antibiotics are commonly used as growth promoters and prophylactics for animals bred for our food supply.

Although this activity focused on bacterial resistance to antibacterials, antimicrobial resistance exists across other classes of infectious agents as well, and is just as concerning. However, the ability to develop antimicrobial resistance is not the only problem we face in the war against infectious diseases. Learn more in the next step.

Your Task

We asked you back in step 1.5 what kind of infectious diseases you or anyone you know have experienced. Now we’d like to ask, were any of these infections drug resistant or otherwise difficult to treat? Share your experiences in the discussion area.

References

Chambers, H.F (2001). The changing epidemiology of Staphylococcus aureus?. Emerging Infectious Diseases, 7 (2): 178–82. <doi:10.3201/eid0702.010204. PMC 2631711 . PMID 11294701>.

Australian Commission on Safety and Quality in Healthcare (ACSQHC). (2013). Antimicrobial resistance: A report of the Australian One Health Antimicrobial Resistance Colloquium. Retrieved from https://safetyandquality.gov.au/wp-content/uploads/2013/07/Briefing-paper-for-One-Health-AMR-Colloquium-participants-Final-Jul-2013.pdf

© Griffith University
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