Staphylococcus aureus CA-MRSA

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A Microbial Biorealm page on the genus Staphylococcus aureus CA-MRSA


Bacteria; Firmicutes; Cocci, Bacillales; Staphylococcaceae; Staphylococcus; Aureus

Description and significance

Methicillin-resistant Staphylococcus aureus (MRSA) is a super bug that has developed resistance to our strongest antibiotics including penicillin and amoxicillin. It emerged in the 1970’s and now accounts for 50-70% of S. aureus infections, which are the most prevalent of hospital pathogens. The MRSA mortality rate is estimated to be as high as 23 percent of patients, around 2.5 times higher than the methicillin susceptible strain of S. aureus. While MRSA is found most commonly in patients undergoing invasive surgery or in those with weakened immune systems, the type of infection classified as community-acquired MRSA (CA-MRSA) requires no contact with healthcare facilities. Since the spread of MRSA only requires skin to skin contact, it can occur among teams where athletes share equipment and even in childcare facilities where children are in close contact for long periods of time. Numbers indicate that around 50 percent of skin infections entering emergency rooms are caused by MRSA (5).

Vancomycin was originally used to combat the infection, but with new strains emerging an increased resistance has grown. Researchers are attempting to develop new ways to cope with this organism, hopefully with the aid of genome sequencing, so that this untreatable pathogen can be eradicated.

Genome structure

Two MRSA strains, methicillin-resistant N315 and vancomycin-resistant Mu 50, were sequenced in 1982 and 1997 respectively. The strain N315 has 2,839,469 bp, holds a plasmid of 25kb in size, and has a G-C content of 32.8% (7). The complex genes present in S. aureus were acquired through lateral gene transfer. The notorious antibiotic resistance of the MRSA pathogen is carried by plasmids or mobile genetic elements. The mobile genetic elements include a unique resistance island. Three new classes of pathogenicity islands were recognized along with the identification of 70 candidates for new virulence factors (1).

S. aureus is able to infect humans of many backgrounds and cause severe immune reactions due to its super antigens encoded by repeated duplication of genes. Research into these newly recognized genes will hopefully help the process of developing a way to fight back (4).

Cell structure, metabolism & life cycle

S. aureus is a gram-negative bacterium arranged in clusters of cocci shaped colonies. They form these grape-like clusters when they divide in succession, expanding on three perpendicular planes with their sister cell (3). When grown on nutrient rich media S. aureus forms a large yellow colony, which is the source of its name. S. aureus is always considered a potential pathogen. This genus is made of facultative anaerobes, meaning they produce ATP by aerobic respiration when oxygen is present but also can switch to fermentation.

S. aureus is associated with biofilm when attached to medical devices and other vectors for the disease. There is not a consensus on metabolic requirements for S. aureus in this environment. It is suggested that Glucose is catabolized to pyruvate and may follow the lactate dehydrogenase, pyruvate formate-lyase, and butanediol pathways (8).

Ecology (including pathogenesis)

S. aureus causes disease in humans and also in a variety of animals including ruminants such as cows, sheep, and goats (6). In a number of countries and settings domestic pets, livestock, and wild birds and animals were recently identified as carriers of MRSA (2). For humans, the spread of this infection through hand-to-hand contact makes it extremely hard to manage. As the most prevalent of hospital pathogens, it is most commonly present in invasive surgery patients and those patients with lowered immune systems, but also on sports teams and daycares. MRSA has a mortality rate of around 23 percent of patients (5).

Symptoms include red, swollen and painful areas on the skin similar to boils, skin abscesses, fever and warmth around the infected area. Other symptoms can result such as rashes, shortness of breath, chest pains, fatigue, muscle aches. These can elevate to even more severe symptoms including cellulitis (common skin infection), toxic shock syndrome, pneumonia, blood poisoning and endocarditis (inflammation of the inner layer of the heart).

Interesting feature

CA-MRSA is occurring more frequently than ever before, in the United States and all over the world. What makes it so prevalent is that it does not need a medical environment to spread. It is now being passed between athletes, soldiers, inmates, childcare workers, and in people living in long term resident homes. The close physical contact common in these environments is perfect for this pathogen to spread. Sharing towels, sports equipment and razors has added to the problem. Cases of CA-MRSA see very high prevalence in places where hygiene has been compromised.


1. "Comparative Genomics of Virulent Antibiotic Resistant Strains of Staphylococcus aureus". Pathogen Functional Genomics Resource Center sponcered by the National Institute of Allergy and Infectious Diseases (NIAID). 10/23/11.

2. "For Clinical Researchers-MRSA & Animals". The University of Chicago Medical Center. 10/24/11.

3. K. Todar. "Staphylococcus aureus and Staphylococcal Disease". Todar's Online Textbook of Bacteriology. 2011.

4. M. Kurudo. "Whole genome sequencing of methicillin-resistant Staphylococcus aureus". The Lancet. 2001. 357(9264), 1225-1240

5. "Methicillin-resistant Staphylococcus Aureus (MRSA) Backgrounder ". APIC- Associated for Professionals in Infection Control & Epidemiology, INC. 10/24/11.

6. N. L. Zakour, D. E. Sturdevant, S. Even, C.M. Guinane. “Genome-Wide Analysis of Ruminant Staphylococcus aureus Reveals Diversification of the Core Genome.”American Society for Microbiology. 2008.190(19): 6302–6317

7. "Providing genomic information: Staphylococcus aureus N315". Biotechnology Field. 10/25/2011.

8. Z. Yefei. Staphylococcus aureus metabolism in a biofilm: the influence of arginine on polysaccharide intercellular adhesin synthesis, biofilm formation, and pathogenesis. American Society for Microbiology. 2007. 10.1128/IAI.00509-07