MRSA - a simple guide

Before the introduction of penicillin in 1941, almost all S.aureus were sensitive to penicillin but a few had the capacity to produce an enzyme (penicillinase) that broke down penicillin and protected the bacteria from its action;  thus making them resistant. By 1959, 90-95% of clinical isolates of S.aureus were resistant to penicillin. They had been selected according to Darwinian evolution by the widespread use of penicillin.

Methicillin and related antibiotics (all developed from the initial penicillin) were made to resist breakdown by penicillinase so that penicillin-resistant S.aureus would still be sensitive to these new agents. Within a year of the introduction of methicillin, the first MRSA was reported in England. MRSA has an altered (mutant) form of the target attacked by penicillin, methicillin etc, making it resistant.

MRSA was relatively uncommon through the 1960s and 1970s. A few more appeared in the 1980s, but the problem exploded in the mid-1990s when particular 'epidemic' strains of MRSA became established in hospitals in the UK. They have the property of easy transmissibility (i.e. they readily spread between patients and colonised both patients and attendants) and the capacity to cause serious disease (i.e. they were virulent). These are the ones that now represent over 40% of the S.aureus causing bloodstream infections in England.

The Staphylococcal family
S.aureus is one of a family of staphylococcal bacteria. Their normal home is on human skin. The commonest non-S.aureus staphylococcus on human skin is S.epidermidis. This is generally harmless and is called part of the 'normal commensal flora' of the human body. Many S.epidermidis are resistant to antibiotics including methicillin and they have the same resistance mechanism (the altered target) as MRSA.

Although present harmlessly on the skin of everyone, S.epidermidis can cause significant infections if implanted in deep wounds along with medical devices such as artificial hip joints or heart valves, or when they track along intravenous catheters into the bloodstream, especially in severely ill and/or immunosuppressed patients such as those in intensive care units or undergoing cancer chemotherapy.

S.epidermidis appears very similar to S.aureus when growing in the laboratory and MRSE will grow on the same selective culture medium as MRSA. Some simple, but crucial, laboratory tests must be done to confirm that a methicillin resistant Staphylococcus isolated from a patient or the environment is MRSA and not MRSE.

What does MRSA cause in patients?
Staphylococcus aureus (including MRSA) causes a wide range of infections from asymptomatic colonisation, i.e., the MRSA is doing no damage, to fatal septicaemia (the most severe blood stream infection).

Colonisation
Between 30% and 60% of the general, healthy population are colonised by S. aureus; in hospital the percentage is higher. S. aureus carriage is more likely to be MRSA in hospital populations (patients and staff) than in the community. Carriage sites are nose (most common) and skin, especially skin folds such as axilla (armpit) or groin. A carrier can be a source of infection for themselves (e.g. if they have a wound) or others.

In high risk situations, e.g. patients for elective orthopaedic or cardiovascular surgery, if screening shows MRSA carriage, decontamination with skin and nose treatment is recommended before surgery.

Infections
There is no specific 'MRSA disease', unlike tuberculosis, meningococcal meningitis or typhoid S. aureus infects a range of tissues and body systems giving general symptoms of infection that are common to infection with various different bacteria.

Wounds:- S. aureus/MRSA is the commonest cause of wound infection – either after accidental injury or surgery. This shows as a red, inflamed wound with yellow pus seeping from it. The wound may break down. A wound abscess may develop.

Intravenous line infections:- MRSA may infect the entry site of an intravenous line causing local inflammation and pus and tracking into the blood stream to cause a bacteraemia (blood stream infection).

Superficial ulcers:- Pressure ulcers, varicose ulcers and diabetic ulcers (all due to poor blood supply and superficial skin damage) are often infected with MRSA. There is further tissue damage with extension of the ulcer. Infection may spread deeper.

Deep abscesses:- If MRSA (or any S. aureus) spreads from a local site into the blood stream it can lodge at various sites in the body (e.g. lungs, kidneys, bones, liver, spleen) and cause one or more deep abscesses distant from the original site. These present with pain, high fever, a high white cell count in the blood and signs of inflammation related to the site. The patient will be very unwell and may have rigors (shivers) and low blood pressure (shock). Over a period, the body enters a catabolic state with breakdown of tissue, loss of weight and failure of essential organs. This is usually linked with an associated septicaemia.

Lung infection:- MRSA/S.aureus is a rare cause of lung infection except in Intensive Care Units. There, the patient is on a ventilator with a tube in the trachea, bypassing the defences of the nose and throat. MRSA can gain entry to the lungs via the tube and cause pneumonia which may be fatal.

Bacteraemia/septicaemia:- MRSA/S.aureus gains entry to the normally sterile blood stream either from a local site of infection (wound, ulcer, abscess) or via an intravenous catheter. Bacteraemia describes the presence of MRSA/S. aureus in the blood. Septicaemia is a clinical description of severe illness caused by bacteria in the blood stream. The signs and symptoms are not specific to MRSA and are the same for many different bacteria that cause septicaemia: high fever; raised white cell count; rigors (shaking); disturbance of blood clotting with a tendency to bleed; failure of vital organs (kidneys, liver, heart). This is the form of MRSA infection that has the highest mortality; it can develop from localised infections and often affects debilitated patients.