How is Staphylococcus Aureus infection treated?
Question:
Answers:
Does your friend have MRSA?
Many types of staphylococcus aureus (golden staph) can be treated with antibiotics - usually of the penicillin family (methicillin, cloxacillin (dicloxacillin, flucloxacillin), etc) but others are useful also.
If the infection is bad or life threatening, your friend SHOULD be treated. If she is very sick with high fevers and poor appetite, etc. she should see a doctor and get antibiotics.
If she is just carrying the staph (eg on her skin, in a wound or in her nose) and it is not a particularly bad infection then some doctors would not treat with antibiotics - particularly if this is a nasty form of staph called MRSA (multi-resistant staph aureus).
There ARE antibiotics to kill MRSA if your friend becomes very unwell ("septic"). These should be used if she is very sick.
Many people carry MRSA without much incident and if it is causing no trouble, then perhaps it is better not to treat.
Antibiotic resistance in S. aureus was almost unknown when penicillin was first introduced in 1943; indeed, the original petri dish on which Alexander Fleming observed the antibacterial activity of the penicillium mould was growing a culture of S. aureus. By 1950, 40% of hospital S. aureus isolates were penicillin reisistant; and by 1960, this had risen to 80%.[2]
Today, S. aureus has become resistant to many commonly used antibiotics. In the UK, only 2% of all S. aureus isolates are sensitive to penicillin with a similar picture in the rest of the world. The β-lactamase resistant penicillins (methicillin, oxacillin, cloxacillin and flucloxacillin) were developed to treat penicillin-resistant S. aureus and are still used as first-line treatment. Methicillin was the first antibiotic in this class to be used (it was introduced in 1959), but only two years later, the first case of methicillin-resistant S. aureus (MRSA) was reported in England.[3] Despite this, MRSA generally remained an uncommon finding even in hospital settings until the 1990's when there was an explosion in MRSA prevalence in hospitals where it is now endemic.[4]
First line treatment for MRSA is currently glycopeptide antibiotics (vancomycin and teicoplanin). There are number of problems with these antibiotics, mainly centred around the need for intravenous administration (there is no oral preparation available), toxicity and the need to monitor drug levels regularly by means of blood tests. There are also concerns that glycopeptide antibiotics do not penetrate very well into infected tissues (this is a particular concern with infections of the brain and meninges and in endocarditis). Glycopeptides must not be used to treat methicillin-sensitive S. aureus as outcomes are inferior.[5]
Because of the high level of resistance to penicillins, and because of the potential for MRSA to develop resistance to vancomycin, the Centers for Disease Control and Prevention have published guidelines for the appropriate use of vancomycin. In situations where the incidence of MRSA infections is known to be high, the attending physician may choose to use a glycopeptide antibiotic until the identity of the infecting organism is known. When the infection is confirmed to be due to a methicillin-susceptible strain of S. aureus, then treatment can be changed to flucloxacillin or even penicillin as appropriate.
Vancomycin-resistant S. aureus (VRSA) is a strain of S. aureus that has become resistant to the glycopeptides. The first case of vancomycin-intermediate S. aureus (VISA) was reported in Japan in 1996;[6] but the first case of S. aureus truly resistant to glycopeptide antibiotics was only reported in 2002.[7] Three cases of VRSA infection have been reported in the United States.[8]
Mechanisms of antibiotic resistance
For more details on this topic, see Methicillin-resistant Staphylococcus aureus.
Staphylococcal resistance to penicillin and cephalosporins is mediated by β-lactamase production: enzymes which break down the β-lactam ring of the penicillin molecule. β-lactamase-resistant penicillins such as methicillin, oxacillin, cloxacillin, dicloxacillin and flucloxacillin are able to resist degradation by staphylococcal β-lacatamase.
The mechanism of resistance to methicillin is by the acquisition of the mecA gene, which codes for an altered penicillin-binding protein (PBP) that has a lower affinity for binding β-lactams (penicillins, cephalosporins and carbapenems).
Glycopeptide resistance is mediated by acquisition of the vanA gene. The vanA gene originates from the enterococci and codes for an enzyme that produces an alternative peptidoglycan that vancomycin will not bind to.
The last thing we need anymore is to be giving out strong antibiotics for illnesses that will go away. More and more resistant bacteria are emerging and getting stronger.
More Questions and Answers
- Anyone had or heard of Ross River Virus in Australia?
- shouldn't there be background checks on your health on some job applications?
- What is the easiest and best diabetes monitoring kit?
- where can one locate std statistics for spain?
- It sounds teribel in my brain, like i have tinitusit is terible and i cannot relaks a minut. What is the cur
- red bumps on skin?
- I've had colon surgery and still have same complaint?
- Can Anyone please Help ME? Crazy Heart Rythum!?