Resource Packages: Methicillin Resistant Staphylococcal Aureus (MRSA)

Historical Overview

Staphylococcus aureus (S. aureus) is one of the most versatile human pathogens. In the late 1930’s, sulphonamides offered the first challenge to S. aureus, but they failed because of their poor clinical performance in the presence of pus and the acquisition of resistance by the bacteria.

In the 1940’s the introduction of benzylpenicillin (penicillin G) temporarily solved the problem of staphylococcal infections, but the continued use of this agent caused the selection of resistant strains. By 1948 the prevalence of resistant strains had seriously reduced the value of penicillin G.

By the end of the 1950’s, S. aureus had acquired resistance to virtually all available systemic antibiotics, including erythromycin, streptomycin and the tetracyclines, and its virulence remained undiminished.

When the antibiotic methicillin first underwent clinical trials in England in 1959, it was seen as a major advance in the treatment of penicillin-resistant staphylococcal infections. Unfortunately, resistance quickly arose, the first case being reported in 1961.

In the late 1960’s and early 1970’s, Methicillin Resistant Staphylococcus aureus (MRSA) was frequently a problem in England and other European hospitals but rarely in the USA and Australia. These strains eventually disappeared in the mid to late 1970’s for no obvious reason, although the reduced usage of tetracyclines is considered a possibility. Infection control also improved at this time.

In 1964 a new antibiotic, gentamicin, was introduced but although sporadic cases of resistance were reported, resistance to both gentamicin and methicillin did not arise until 1976.

In 1979, hospitals in Victoria (Australia) first began to report serious problems with a new strain of MRSA, the first epidemic strain to cause major clinical problems.

Similar strains subsequently have been reported worldwide but mainly from Australia, USA, South Africa, Greece, the Middle East, Ireland and England.

MRSA includes a great many strains, not all of which cause epidemics. Phage typing is the usual way to identify strains. Although too slow for routine detection and not always reliable, it is still the quickest way to differentiate between the epidemic strain and other strains that may not be epidemic.

The term “methicillin resistance” implies resistance to all penicillinase-resistant penicillins (methicillin, oxacillin, cloxacillin) to name but a few.

MRSA is often referred to as Multi-Resistant Staphylococcus aureus, or GMRSA (gentamicin plus methicillin resistant).

Recent Developments

Although the molecular mechanism of methicillin resistance is not completely understood it appears that some strains of S. aureus have altered cell wall structures which impair the effectiveness of antibiotics.

Over the past 15 years MRSA and other resistant strains of S. aureus have become one of the common causes of hospital and community acquired infections. MRSA is feared because it has demonstrated its virulence and its resistance to many antibiotics.

There has been a recent discovery of a S. aureus intermediately resistant to vancomycin (known by the acronym VISA)

MRSA strains often spread among the most severely ill, antibiotic treated patients by several modes of transmission. These include:

Patient to patient contact transmission via transient contamination on the unwashed hands of medical and nursing staff
Airborne spread from patients with MRSA pneumonia or those on ventilators
Contact spread from health care workers (health care workers) by asymptomatic nasal colonisation, on the hands, or with frank infections such as paronychia

Patients at risk for MRSA infection include:

The aged and debilitated
Those undergoing surgery with lengthy hospitalisations
Those receiving multiple antibiotics
Those having multiple invasive procedures
Those treated in intensive care units, trauma centres and burns units
Patients with indwelling catheters, endotracheal tubes, ventilatory support and intravascular devices are also significantly at risk

When MRSA causes severe infection it has the added problem of being resistant to effective antimicrobials, with the exception of vancomycin, rifampicin and fusidic acid. These antibiotics are expensive, more toxic and usually require parenteral administration.

Outbreaks of MRSA have resulted in huge costs because of increased hospital stay, and elective surgery may often be cancelled or re-scheduled. Contact precautions need to be instigated, so the patient requires the use of a single room.

If the patient is particularly susceptible, eg premature neonate or an adult in intensive care, a life threatening infection can ensue. There is sometimes the need for further surgery, eg the orthopaedic patient with an infected prosthesis. While colonisation produces no ill-effects, infection can lead to fatal bacteraemia, endocarditis or pneumonia. Bacteraemia is particularly associated with intravenous devices which are major portals of entry.

The spread of MRSA is often introduced into a hospital by admission of a patient who is either colonised or infected with MRSA. The patient may have previously been in another hospital, but usually no evidence of previous hospital admission can be found.

It is recognised that staff play a major role in the transmission of infection within hospitals. Contemporary strategies to prevent and control MRSA continue to rely on traditional measures including handwashing. Handwashing is of particular importance in preventing the spread of MRSA in hospitals because of the organism’s propensity to colonise and infect wounds, and because the likely mechanism of transmission appears to be the carriage of the organism on the hands and in the noses of hospital personnel. It is important to conduct continuing educational programs for all categories of personnel involved in direct patient care.

Pathogenic gram-negative bacilli may survive on the hands for over 2 hours. A hand disinfection system using an antimicrobial agent (chlorhexidine) reduces the rate of nosocomial infections more effectively than one using alcohol and soap. Chlorhexadine gluconate is frequently recommended because of its broad antimicrobial spectrum, low toxicity and residual activity.

Standard and contact precautions should be practised at all times.

Contact precautions require a single room. If a single room is not available cohort with patient(s) who has active infection or colonisation with MRSA but no other transmissible infection.

Gowns/aprons and gloves should be worn for patient contact.

When transferring patients notify area receiving the patient of their MRSA status.

Future Trends

It does appear from all the literature that MRSA is here to stay. The factors that appear to predispose patients to infection with MRSA should be avoided, for instance, the hospital stay should be made as short as possible, and the use of antibiotics should be controlled much more closely.

Since prevention is always better than cure there is a need for stricter epidemiologic surveillance of patients entering hospitals, possibly involving the pre-screening of patients in cases of non-urgent admissions.

All health care workers must be made aware of the dangers entailed by the spread of infection and instructed on methods of control.

Control of MRSA Outbreaks

When an outbreak of MRSA infection occurs, an epidemiological assessment should be initiated to identify risk factors for MRSA acquisition in the institution. Clinical isolates of MRSA should be saved and submitted for strain typing. Colonised or infected patients should be identified as quickly as possible and appropriate precautions should be instituted.

All personnel should be re-instructed on appropriate precautions and the importance of handwashing in preventing contact transmission.

Notification to the Public Health Unit - MRSA is not a notifiable disease.

References

Bennett, Brahman and Sandford, eds, 1992 3rd edition, Hospital Infections. Little, Brown and Company, Boston.

Brumfitt W, Hamilton-Miller J, 1989, Methicillin-Resistant Staphylococcus aureus. The New England Journal of Medicine, London, pp 1188-1196.

Doebbeling BN, et al,1992, Comparative Efficacy of Alternative Handwashing Agents in Reducing Nosocomial Infections in Intensive Care Units. The New England Journal of Medicine, Iowa, pp 88-91.

Manly Hospital and Community Health Services, 1992, Infection Control Manual. Manly.

NSW Health Department, 1999, Infection Control Policy, 99/87 AIDS/Infectious Diseases Branch, Sydney.

Pavillard R,et al, 1982, Epidemic of Hospital-Acquired Infection due to Methicillin-Resistant Staphylococcus aureus in Major Victorian Hospitals. Medical Journal of Australia.

Shiff B, VRE and MRSA, Putting Bad Bugs Out Of Business, Nursing Management 1999:30 (6)

Shovein J, Shelley Young M, 1992, MRSA: Pandora’s Box For Hospitals. American Journal of Nursing, California.

The Sutherland Hospital, Caringbah, 1993, Infection Control Manual. Sutherland.

Thompson RL, Cabezudo MD, Wenzel RP, 1982, Epidemiology of Nosocomial Infections Caused by Methicillin-Resistant Staphylococcus aureus. Annals of Internal Medicine, Virginia, pp309-316.

Wenzel RP, Nettleman MD, Jones RN, 1991, Methicillin-Resistant Staphylococcus aureus: Implications for the 1990’s and Effective Control Measures. The American Journal of Medicine, Iowa. Vol.91, pp 221-226.

Wenzel RP, 1993, 2nd ed, Prevention and Control of Nosocomial Infections. Williams and Wilkins, Baltimore.

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