Staphylococcus aureus (SA)
Antibiotic-resistant superbugs are headline news. We are all familiar with the letters MRSA but perhaps not everyone knows that the SA stands for staphylococcus aureus.
Staph aureus is a germ or bacterium that is frequently found on the skin. It is a formidable opponent to medicine and its cunning behaviour on the skin is the subject of a recently published article by Dr Arden-Jones from the Division of Infection, Inflammation and Immunity at Southampton University¹.
If the success of a bacterium is measured by its ability to survive despite the body’s immune system and antibiotics, then staph aureus is one of the very best. Confusingly it can live on the skin of up to 30% of the population without causing a problem, and yet it is responsible for approximately 45% of skin infections in hospitalised patients.
The secret of its success is its amazing ability to protect itself and adapt to different environments. When it comes into contact with skin it immediately sets about multiplying and defending itself against our immune system. It already has a strong cell wall but this is strengthened further by a substance called fibrin which is produced by the bacterium when it secretes an enzyme called coagulase. It also produces a series of specific molecules which inactivate human antibodies sent to destroy it by the immune system. The net result is a well defended fortress.
Staph aureus can adopt many different guises or strains. The potential for these strains to sit harmlessly on the skin or suddenly turn nasty and start attacking us seems to lie in their ability to make ‘virulence factors’. Once a colony of staph aureus reaches an optimum size, it decides to turn nasty.
This is a clever mechanism known as quorum sensing, in simple words, knowing when there are enough! The microorganisms are then switched by a gene to start causing harm. The mechanism of causing damage involves the production of a series of enzymes and toxins which assist invasion. Each strain of staph aureus produces individual enzymes and hence different strains cause different clinical effects.
Although staph aureus was sensitive to penicillin when it was first developed for widespread use in the 1950s, some strains quickly developed resistance. Methicillin resistant staph aureus (MRSA) was first discovered in 1961. Since then the microorganism has gone on to become resistant to other antibiotics such as fusidic acid which is frequently used in cream or ointment form to treat skin infections.
Staph aureus has an interesting association with atopic eczema. Apart from causing clinical infection of the skin, it is known that over 90% of people with atopic eczema carry staph aureus. Furthermore the type of staph aureus they carry is more likely to express ‘virulence factors’, ie turn nasty. It has a tendency to produce toxins called superantigens which stir up the immune system and cause inflammation.
The treatment for staph aureus on the skin is directed by the clinical problem – if there’s no problem, there’s no need for treatment; if there are signs of clinical infection, appropriate antibiotics are required. In atopic eczema, however, it is not so clear cut. There is an argument to treat the bacteria even if there are no signs of clinical infection because this stops their number reaching the level needed for quorum sensing to take place.
A number of emollients contain antiseptic agents such as chlorhexidine to assist in the control of staph aureus. These are becoming increasingly recognised in the management of atopic eczema although more clinical trials are needed to confirm their utility. One thing is for sure. Staph aureus is a tricky customer particularly in atopic eczema, and any developments towards combating it are welcome.
1. Ardern-Jones M Advances in Clinical Dermatology 2010;2:1-8
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Last revised: 9 December 2012
Next review: 16 November 2014