• What is Methicillin Resistant Staphylococcus aureus and how do we manage it?
• MRSA down but not out
• Management of ulcers in the diabetic patient

What Is Methicillin Resistant Staphylococcus aureus and how do we manage it?

Speaker: Ms. Elizabeth Aubrecht RN

Staphylococcus aureus microbiology

The epidemiology of Methicillin Resistant Staphylococcus aureus (MRSA) is similar toStaphylococcus aureus (S. aureus). Microscopically, S. aureus are gram-positive cocci that tend to appear as "clusters" or "groups" of cocci when viewed under the microscope. Macroscopically, the species name aureus refers to the organism's golden coloured colonies on blood agar hence the term 'Golden Staph'. Different strains of MRSA can be detected using polimerase chain reaction (PCR) which is a laboratory technique used to amplify DNA genes so they can be seen; different strains of MRSA have different gene sizes. Knowing this will help trace the source of infection more accurately than just following antibiotic sensitivity patterns.

History of Staphylococcus aureus

In 1880 a surgeon noted that most abscesses were infected with S. aureus. Today, over 100 years later, S. aureus is still the most common organism associated with wound infections. Penicillin was discovered by Fleming in 1928 and later taken up by Florey in the 1930s, it was introduced into general medical use in 1941 as the preferred treatment for S. aureus infections. However, by 1948 most Staphylococci in British hospitals were resistant to Penicillin, so in 1960 semi-synthetic penicillin's (e.g. methicillin & flucloxacillin) were introduced and had an immediate clinical impact but within 12 months the first methicillin resistant Staphylococcus aureus was detected in British hospitals. Sydney saw Australia's first MRSA in 1967. The 1970s to 1990s have seen further resistance develop (e.g. gentamicin, ciprofloxacin, rifampicin and others) and 1997 has seen the beginning of a strain with so called 'intermediary resistance' to Vancomycin, the drug of choice for treatment of MRSA infections.

Epidemiology and, transmission of Staphylococcus aureus

20% - 40% of adults at any given time have S. aureus nasal carriage; carriage will be prolonged in 30% of the population and intermittent in 50%. Colonisation is unlikely to lead to infection if the colonised person is well. Health-care workers have a higher S. aureus nasal carriage rate (50% - 90%) than the general population. Diabetics receiving insulin, patients receiving long-term haemodialysis, and users of illicit drugs also have higher rates thin the general population. Nasal shedding of organisms does not appear to be important in direct dispersion of S. aureus to others.

MRSA is most frequently spread from one patient to another via the hands of health care workers by direct contact transmission. The hands of health-care workers become transiently colonised while performing patient care activities on patients colonised or infected with MRSA. Airborne transmission of MRSA is not considered to be a significant mode of transmission. Over the past 20 years it has been increasingly recognised that environmental surveillance contributes little to the control of infections in hospitals. S. aureus can survive in a dry environment, however they do not replicate and will gradually die.

Risk Factors

MRSA tends to be an opportunistic pathogen, which is more likely to cause infection in patients with severe underlying disease e.g.

malignancy
steroid therapy (impairs fibroblast function with long-term use)
diabetes (impairs fibroblast function)
poor circulation (oxygen & nutrients needed for collagen formation)
older age
Extended hospital stay and an ICU or Bums Unit admission are also risk factors.

MRSA Control Strategies

1. Notify Infection Control of patient's admission and obtain institution specific control strategies

2. Standard and Additional Precautions including:

a 15 second soap and water handwash before and after patient contact, and in-between procedures on a patient
single room and 'Stop' sign to reinforce the need for handwashing and remind visitors to talk with nurses regarding handwashing
masks/protective eye wear for MRSA isolated in tracheal aspirate, and with risk of exposure to any blood and body fluids
gloves for patient contact, to be removed immediately after use and, before touching non-contaminated items and environmental surfaces and before leaving the room (gloves do not take place of handwashing)
gowns for direct patient contact, to be removed before leaving the room
linen is treated in the usual manner
equipment should be appropriately cleaned with detergent and water before use on another patient
reduce clutter and clean the room daily with detergent and water

3. Control antibiotic use

The excessive or inappropriate use of broad-spectrum antimicrobial therapy within the hospital or community encourages the selection of MRSA and antibiotics should not be given to treat colonisation. The drug of choice for treatment of MRSA infection is intravenous Vancomycin or combined oral therapy depending on sensitivities and clinical findings.

4. Staff/ patient screening

Patient screening on admission differs between institutions; usually for previously colonised or infected patients or patients transferred from interstate or overseas or from a hospital with endemic MRSA (wound/nasal swab). Staff screening is not recommended routinely but may be considered in a suspected outbreak (check with your Infection Control Officer)

5. Reduce microbial load

Antimicrobial solutions such as chlorhexidine or triclosan can be used as a body wash for patients who are heavily colonised or infected with MRSA, and/or for staff handwashing. Both solutions are effective in reducing microbial load, but the extent to which they contribute to eradication of MRSA carriage is not clear and again there is potential for resistance to these agents to develop (seek advice from your Infection Control Officer). Promote wound healing, contain exudate with an appropriate dressing and reduce frequency of dressing changes. Wound drainage or surgery may be necessary in some instances. Systemic antibiotics are used to treat MRSA infection where necessary, based on the microbiology culture result.

6. Patient Advocate

We are all patient advocates, so a tactful reminder to colleagues who fail to follow the necessary precautions is a very important infection control measure.

Clinical Determinants of a Wound Infection

redness*
pain*
localised heat (cf. surrounding skin)*
swelling*
purulent discharge (foul odour)
febrile
wound dehiscence or wound deliberately opened by a surgeon
whole picture: vital signs, WBC count, deep tissue culture, bacteraemia, X Ray findings etc.
*characteristics of a healing wound in the first few days post-surgery

Treatment of Infected Wounds

define wound aetiology
control factors that delay healing (smoking, diabetes, malnutrition)
appropriate moist wound dressing
plan wound healing maintenance
appropriate systemic antibiotics
cleansing and debridement. Antiseptics were the mainstay of wound management in the 1800s and in 1867 Lister published the benefits of Carbolic Acid for wound cleansing. Antiseptics have been found to be potentially harmful to tissue especially hypochlorite solutions (e.g. Eusol) and delay healing. There is little indication for ongoing treatment and routine use. Antiseptics may however have some use in cleansing acute wounds with a high bacterial load (e.g. abrasions and lacerations).
antibacterials such as Mupirocin ointment have been applied to wounds and anterior nares, however resistance to Mupirocin has been noted so long-term use is not recommended. Short-term use in an outbreak situation may be deemed appropriate. Silver sulfadiazine has low toxicity and a wide antibacterial spectrum, it can be used alone or combined with a Hydrogel for short term use on infected wounds to reduce bacterial load.

Challenges for the Future

There is a need to become proactive rather than reactive in controlling the spread of MRSA, particularly at a time when early discharge and day surgery concentrates the more susceptible older and sicker patients in the hospitals.

Unknown MRSA patients present a substantial risk to susceptible patients. Surveillance activities aim to determine who is at risk of MRSA (nosocomial) infection and will provide information on which to base appropriate prevention strategies to reduce that risk. Controlled, institution specific patient screening programs may be necessary to determine unknown cases, particularly during an outbreak.

Constant reinforcement of Standard and Additional Precautions is paramount in controlling cross infection from known cases.

Nosocomial infections are associated with increased morbidity and mortality and result in substantial personal, hospital and community costs. Limited resources combined with a fear of litigation make prevention of nosocomial infections everyone's responsibility.

MRSA - down but not out

Speaker: Ms. Marilyn Leaver RN

Multiresistant Staphylococcus aureus has never quite disappeared from our hospitals since the epidemic in the 1980's. S aureus has been one of the major causes of infection in hospitals since it first captured our attention during the epidemic of antibiotic sensitive S aureus in the United States of America, United Kingdom, Australia and New Zealand in the 1950's. As a result of this epidemic, a need for programs for the prevention and control of hospital acquired (nosocomial) infection (HAI) was first identified, Why is MRSA still perceived as a problem in the 1990's?

'Golden staph' or S aureus was named for the shiny yellow colonies formed by these bacteria when grown on culture medium, as distinct from the more common S epidermidis previously called S alba or 'white staph' which forms pale creamy colonies. S epidermidis is part of our normal flora - the bacteria which can be found on human skin, S aureus can also be normal flora, but is less widespread being found on approximately one person in three. S aureus has the greater potential for deep wound infection while S epidermidis is more likely to colonise intravenous and central venous lines.

Where does MRSA come from? Three main sources can be identified. First, 'spontaneous' emergence following antibiotic therapy especially if prolonged. Second, person to person or contact spread and third, environmental reservoirs. Risk factors include

frequent or prolonged antibiotic therapy
age, either very young or very old, diabetes, alcohol or drug use
serious underlying illness
prior hospitalisation especially ICU admission
presence of invasive or prosthetic devices

Identification of the presence of S aureus (whether multiresistant or not) does not necessarily require treatment, Superficial infection such as a stitch abscess or colonisation of an ulcer should not be treated either topically or by administration of oral or intravenous antibiotics. The stitch abscess will resolve when the suture is removed and the ulcer will heal while colonised. Systemic infection - deep wound or bloodstream - with accompanying signs and symptoms such as pyrexia and inflammation will require antibiotic therapy. If the infecting organism is multiresistant then either oral or intravenous Vancomycin or a combination of Fucidin plus Rifampicin are the drugs of choice. However if MRSA infection occurs in the presence of a prosthetic device, then the only solution may be the removal of that prosthesis. If that happens to be a heart valve, vein graft or a joint replacement, then treatment choices are very limited and tend to be 'least harm' rather than curative.

How then does multiresistant Staphylococcus aureus or MRSA become a problem? If S aureus is found to be resistant to penicillin and/or Ampicillin, this is simply taken into consideration when prescribing antibiotics, if these are indicated. These resistances are common and do not present a problem. If resistance to four or more antibiotics is reported, then the S aureus (or S epidermidis) becomes characterised as 'multiresistant'. Multiresistant S aureus is no more virulent than antibiotic sensitive S aureus but is much more visible because of its resistance to commonly used antibiotics and therefore more difficult to treat requiring careful monitoring of antibiotic use by the attending medical officer. At this point it is essential to undertake a thorough assessment so that the potential for cross infection is minimised.

When MRSA is confirmed, the person with the infection or colonisation should be assessed to establish the potential for transmission, It is usual to take specimens using a sterile swab stick moistened in sterile normal saline to sample any wound, area of broken skin, nostrils and groin or axilla (whichever is closer) in addition to the original site.

Evaluate the potential for transmission - are the site(s) superficial or deep, colonised or is there systemic infection? Does the person have dry skin or a skin condition such as eczema or psoriasis?

Calculate the potential environmental reservoirs - horizontal surfaces and ledges on which dust (and skin scales) may collect. Make sure that damp dusting of all these areas is undertaken daily. Assess the potential for cross infection by considering the human and environmental and collaborate with the Senior Registered Nurse to plan appropriately. Check that if antibiotics are being prescribed for the condition, that they are appropriate.

Inform the patient of the need for preventative measures and explain what these will be. Ensure that visitors are also aware of the situation. Explain what is required to all staff who have contact with the patient.

All of these measures may sound simple, even familiar. It is surprising how frequently these basic actions can be overlooked when a multiresistant organism is first identified. Equally important is the necessity to continue to employ these strategies until complete resolution is reached That is, when the patient has been discharged or the site has healed and/or is no longer positive, With the rapid growth of day surgery and home care, hospitals will continue to house greater proportions of patients who are acutely ill and who will be likely to require antibiotic therapy over a longer period, thus increasing their susceptibility to this organism.

References

Benenson AS (ed) (1995)Control of Communicable Diseases Manual (16th ed) American Public Health Association Washington DC

Soule BA, Larson EL, Preston GA (1995) Infections and Nursing Practice Mosby St Louis

A copy of this paper is published in the Collegian October 1996 Volume 3(4):3839

Management of ulcers in the diabetic patient

Speaker:

The diabetic patient is at risk of a number of complications including:

1. Vascular disease. This includes peripheral vascular disease, coronary artery disease and cerebrovascular disease.

2. Neuropathy. This may be sensory, motor, autonomic and/or a mononeuropathy.

3. Nephropathy

4. Vision disorders

5. Infection.

6. Metabolic complications.

7. Foot ulceration

The patient with diabetes is at risk of foot problems and ulceration because of the change in foot structure, loss of sweating and loss of sensation which occurs with the neuropathies. In these circumstances the ulceration is usually due to abnormal pressures an the feet, or pressure, friction or shear which goes undetected because of reduced sensation. Foot ulceration can also occur because of ischaemia due to peripheral vascular disease (large and small vessel disease). A diabetic with a foot ulcer may therefore have an ulcer because of pressure problems (and neuropathy), ischaemia or have a mixed picture of pressure with neuropathy and ischaemia.

These factors need to be correctly identified and managed Thus when assessing and managing foot ulceration in the diabetic patient it is important to return to basic principles.

Assessment

Pressure problems/neuropathy and ischaemia can be identified clinically on examination.

An ABI can also aid the diagnosis of ischaemia (ABI < 0.75). Care must be taken however with interpreting the ABI in a diabetic patient. Diabetic patients are more likely to have arterial wall calcification resulting in a false high ABI. This may be obvious if it is not possible to occlude the pulse in the lower limb, or if the ABI is abnormally high eg > 1.2. However a "normal" ABI result in a diabetic patient may actually be a false high reading which provides false reassurance. The ABI therefore should be interpreted along with the clinical picture. Where doubt exists it is possible to obtain more accurate information with toe pressures.

Management

Having identified the main aetiology factor, management is directed at eliminating or controlling this factor. In the presence of peripheral vascular disease further investigation and definitive surgical intervention to improve blood flow is the main aim of treatment.

Where pressure is the main aetiological factor then management must be directed at pressure elimination. Regular debridement of callous will reduce pressure. Improving footwear can also be valuable. However, the most important component to controlling pressure, is pressure redistribution. Without consistent and constant pressure redistribution it is unlikely that the ulceration will heal. To achieve this either plaster casting or compressed felt padding can be used Where felt padding is used the padding must be more prominent than the lesion with a larger surface area compared to the lesion It must have appropriate anatomical borders, with an appropriate size hole and bevelled edges. The bevelled edges reduce discontinuity between the foot and the pad improve adhesion of pad and tape and allow the padding to conform to the contour of the foot Finally the padding needs to be hypoallergenic and have good adhesion.

The involvement of the podiatrist is essential to both debride callous and to provide pressure redistribution. It is important for other health professionals and patients to recognise that in debriding callous the podiatrist does not usually "cause ulcers". Rather, they are exposing underlying ulceration which was not obvious. Having debrided the callous the ulcer can be more effectively treated

Infection

Wound infection significantly inhibits healing and needs to be identified and treated appropriately. This is particularly important in the diabetic patient who is at five times more risk of developing a wound infection. The clinical signs of infection include increasing inflammation increasing pain, increasing ulcer size and increasing exudate but in the diabetic patient these signs may be less obvious. The presence of peripheral vascular disease can reduce the signs of inflammation because of the reduced blood flow, while neuropathy can mask pain. The health professional needs therefore, to have a high index of suspicion for infection Treatment often requires antibiotics which cover mixed infections - Gram +ve, -ve and anaerobes.

The likelihood of an underlying osteomyelitis also needs to be considered in the diabetic patient with a chronic ulcer. Probing to bone in the base of an ulcer can be indicative of the presence of osteomyelitis. Diagnosis is not easy but x-ray and bone scans can aid the diagnosis. Treatment requires long term antibiotics and may include the use of hyperbaric oxygen.

Maintenance/prevention

With appropriate attention to the aetiological factors and other factors contributing to poor healing it is possible to heal a large number of the foot ulcers which present in the diabetic patient, and reduce the likelihood of amputation.

Prevention, however, is better than cue. This role involves both the patient and health professionals.