Difference Between Methicillin-Resistant Staphylococcus Aureus (MRSA) and Staphylococcus Aureus Re

Methicillin-Resistant Staphylococcus aureus versus Staphylococcus aureus

Definition

Our skin, nose, and respiratory tract provide a home for the gram-positive bacterium known as Staphylococcus aureus. This bacteria is not normally pathogenic i.e. disease causing. However, persons whom are immunocompromised, are at higher risk of infection through staphylococcus aureus. These infections include skin infections, respiratory infections, and food poisoning. Any strain of staphylococcus aureus that has developed multi-resistance towards beta-lactum antibiotics, is named Methicillin-resistant Staphylococcus aureus (MRSA). MRSA is responsible for a number of difficult to treat infections such as sepsis, necrotising pneumonia, infective endocarditis, and osteomyelitis.i

Microbiology

S. Aureus was identified by Sir Alexander Ogston in 1880. Since then it is carried by approximately 30% of the population, and can be found as a normal inhabitant of the skin flora viz. in the nostrils and reproductive tract of women. S. Aureus is non-motile and anaerobic, while being viewed as a “grape-cluster berry” under the microscope. Reproducing asexually by means of binary fission. Its non motility characteristic, causes it to be spread through human to human contact, or by contact of contaminated surfaces and foodsii. Similarly, MRSA is spread mostly by human to human contact through the hands and infrequently through the cough of patient infected with MRSA pneumonia iii.

MRSA is the evolution of S. Aureus into a minimum of 5 different multi resistant strains. This resistance increases the difficulty to treat the infection. The resistance is mainly due to MRSA thriving in the company of penicillin like antibiotics, due to a resistance gene in the evolved S. Aureus which prevents the antibiotics from deactivating enzymes responsible for cell wall synthesis. Synthesis of cell wall material is critical in bacterial growth. MRSA was first identified by British scientists in 1960. The next finding was a vancomycin resistant strain of S. Aureus, discovered in Japan in 2002. The drug resistant S. Aureus infections comprise of:

1. Methicillin-resistant Staphylococcus Aureus (MRSA)
2. Vancomycin-resistant Staphylococcus Aureus (VRSA)
3. Vancomycin-intermediate Staphylococcus Aureus (VISA)

Related Diseases

S. Aureus causes the following infections:

• Dermatitis
• Folliculitis
• Cellulitis
• Abscesses
• Pneumonia
• Staphylococcal endocarditis
• Food poisoning (gastroenteritis)
• Septic arthritis
• Osteomyelitis
• Bacteremia

S. Aureus is the foremost cause of infective endocarditis, bacteremia, skin infections, and device related infections.

MRSA causes the following diseases:

• Sepsis
• Necrotising pneumonia
• Necrotising fasciitis
• Impetigo
• Abscesses
• Cellulitis
• Folliculitis
• Infective endocarditis

Epidemiology

In developed nations, the S. Aureus incidence ranges between 10 to 30 per 100 000 population, with hospital acquired infections being the key contributor. It was suggested that the bacteria is carried via healthcare workers from pets, to working environments. Due to S. Aureus being found as inhabitants of domestic pets. Additionally, it can be transferred from infected patients to non infected patients, through healthcare workers. Studies show that S. Aureus can survive for up to three months on polyester fabric, i.e. hospital privacy curtains. Simarlarly, MRSA can survive on surfaces and fabrics.

MRSA infection incidence rate has fluctuated, increasing from 0 to 7.4 per 100 000 population in Quebec, Canada. Since 2005, there has been reduced incidence of MRSA, possibly due to improved infection control procedures. Incidence of S. Aureus is highest in infants and rising with advancing age (above 70 years of age). Those individuals with HIV/AIDS have a significantly higher incident rate viz. 494 per 100 000 population and 1960 per 100 000 population according to two separate studies.

With regards to MRSA incidence rates, the Center for Disease Control and Prevention states that two per 100 population are carriers for MRSA. Unfortunately there is a lack of data regarding MRSA skin infections. However, studies show that incidence of MRSA infections, in healthcare settings, have declined by 50%.iv

Diagnosis

S. Aureus is diagnosed through laboratory testing of appropriate specimen samples. The bacteria is identified by utilising a biochemical or an enzyme based test. Whereas, MRSA is diagnosed through quantitative PCR procedures, broth microdultion tests, cefoxitin disk screen test, and the latex agglutination test in order to promptly identify strains.

Treatment

The first line of treatment for S. Aureus infections is penicillin or penicillinase-stable penicillin, which inhibits the formation of peptidoglycan cross-linkages, that give strength to the cell wall of bacterium. Therefore, cell wall formation is impaired resulting in cell death. However, some strains of S. Aureus re resistant to penicillin, such as in MRSA. These strains are then treated with vancomycin, which also inhibits peptidoglycan by binding to amino acids in cell wall.v

Infection control

S. Aureus is spread via human to human contact, as well as through pets. Therefore, great emphasis should be placed on hand washing, to limit the bacterium’s transmission. Healthcare facilities and workers should employ the use of disposable gloves and aprons, thereby reducing bodily contact and transmission.vi

MRSA can be reduced / prevented by using ethanol as a surface sanitising agent, as well as quaternary ammonium. Other measures are screening patients for MRSA (using nasal cultures) prior to hospital admissions, in order to prevent cohabitation of MRSA. Those infected with MRSA, should be decolonized and / or isolated from non infected patients. These clinical areas need to be subjected to terminal cleaning methods.





Conclusion

S. Aureus clinical infections are likely to persist, due to its increasing antimicrobial resistance and evolution. In the last 20 years there has been an increase in nosocomial infections, especially prosthetic device infections and infective endocarditis, not to mention the epidemic of community associated skin and soft tissue infections. At this stage the old adage prevails i.e. prevention is better than cure.



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