Methicillin-resistant Staphylococcus aureus (MRSA) is a prokaryotic organism of
domain bacterium that causes infections which are hard to treat. MRSA disease has been
associated with a kind of staph bacteria that has proven to be hard to handle because most
antibiotics used to treat the usual staphylococcus infections are not effective against MRSA
due to resistance ("MRSA Infection – Symptoms and Causes"). Most MRSA is referred to as
nosocomial infection because they are often contracted due to pathogenic microbes that exists
in a hospital setting (Stubblefield). This essay illustrates the structure of MRSA and its
virulence factors in human host, mechanisms causing the antimicrobial resistance associated
with MRSA, the laboratory methods used to differentiate MARSA from MAAS and finally
analyze the factors responsible for development of genetically diverse MRSA.
The virulence factors include but not limited to the bacterial cell wall, toxicity,
adhesives, enzymes and immunomodulators. The intricate cell wall composition of S. aureus
contains a dense peptidoglycan coating and a polysaccharide. This functions as a protective
cover and also a point of attachment of surface proteins which are crucial usual cell division,
structural development of the microbes and eventual pathogenesis. In addition,
Staphylococcus aureus has an extensive array of toxin development and invasion systemic
that constitutes the furtive virulence factors and immune response evasion strategies.
Methicillin-resistant Staphylococcus aureus (MRSA) strains are particularly extreme and
potentially lethal pathogens with virulence mechanisms like toxins, adhesives, enzymes and
immunomodulators. For example, colonization of the nose of patients with MRSA toxins
known as Panton-Valentine leukocidin (PVL) is associated with abscess formation and severe
pneumonia mostly in hospital-acquired and ventilator-associated pneumonia (Siddiqui and
Koirala). The most important nasal carriage is likely because the microbe may spread to other
surfaces of the body and to other hosts effectively. Studies shows that over 20% of
individuals are colonized persistently (Lovering, et al. 32096). It is worth noting that,
persistent and transient transport depends on the trial but is generally described as a single
positive nasal swab (transient) crop versus at least one week apart of two consecutive
(persistent) positive cultures.
Under normal conditions, S. aureus is a normal microbiota of the skin, intestinal
mucosa and upper respiratory tract. However, due to risk factors such as prolonged
hospitalization, intensive care admission and recent hospitalization or other infections like
HIV and less often old age, Staphylococcus aureus can colonize and trigger infection.
Colonization and infection are often achieved by entire tissue invasion and thus referred to as
pathobiont. The first line of defense against infections involves the activation of the
innate immunity via a pattern recognition pathway that detect non-specific markers of
Staphylococcus aureus infection. However, the Staphylococcus aureus has evolved methods
of preventing eradication by the innate immune response. Neutrophils constitute a critical
component of innate immunity and primary cell protection from infections of the S. aureus.
The adaptive immune response targets specific S. aureus antigens through T cell activation
and B cell production of antibodies besides amplifying the activity of innate immune cell
through increasing phagocytotic killing and recruitment (Karauzum and Datta 419). The
recurrent of infection and possible resistance to antibiotic is an indication of ineffective
adaptive memory response.
The most common lab procedures used to distinguish MRSA from MSSA include
Xpert MRSA/SA assay and direct cefoxitin disk test. For example, for direct cefoxitin disk
test the results are interpreted as follows, a zone diameter that is ≤17-mm is identified as
MRSA, a zone diameter of ≥21-mm is an indication of MSSA and a zone diameter between
18- to 20-mm is concluded as an indeterminate result (Bennett and Sharp 3836).
Differentiation based on oxacillin minimum inhibitory concentration (MIC) relies on the
dosage which is often ≥4 micrograms/mL which is greatly based on Methicillin resistance
in S. aureus is (Siddiqui and Koirala). Another method which can be used to distinguish
MRSA from MSSA is using polymerase chain reaction to detect either
the mecA or orfX genes. The differentiation is important because it ensures appropriate and
rapid treating of patient with the most effective antibiotic thereby decreasing patient
Methicillin is β-lactam antibiotic and therefore they act by inhibiting proteins that are
involved in the formation of peptidoglycan such as the penicillin-binding proteins (PBPs)
(Stapleton and Taylor). The main reason why MRSA is resistance Methicillin antibiotics is
because of mecA gene sequence which is often associated with the formation of
transpeptidase PB2a or the methicillin-hydrolysing β-lactamase that reduces the ability of the
S. aureus to bind to β-lactam Methicillin and subsequent greater rates of release of the bound
antibiotic as compared to the usual PBP2 (Stapleton and Taylor). Methicillin, also known as
Staphcillin, is a semi synthesized penicillin-related antibiotic. In the past, Staphcillin has been
effective against resistant penicillin staphylococci that were producing penicillinase.
However, over the years it has been ineffective against various drug resistant Staphylococcus
aureus. This has been linked to mutation on various genes that are involved in affinity of the
microbe to the antibiotics and other internal and external factors that influence substrate
Factors that affect the formation of the substrate also influence methicillin resistance.
According to Stapleton and Taylor, PBP2a has specific substrate requirements (Stapleton and
Taylor). For example, Glycan chains of longer lengths have been associated with methicillin
resistance as compared to those with shorter lengths. Internal factors therefore, is based
entirely on peptidoglycan synthesis besides peptidoglycan remodelling and cell division.
Therefore. Effects of specific genes involved in methicillin resistance is often controlled via
regulation of genes involved in peptidoglycan synthesis. On the other hand, external factors
that are involved in methicillin resistance include temperature and pH (Stapleton and Taylor).
The risks associated with MRSA becoming a hospital acquired infection include having a
contaminated medical equipment and living in a long-term care home. Medical devices like
intravenous lines can act as a link for MRSA to enter into patient’s body. Additionally,
carriers of MRSA in nursing homes have the ability to spread it to others more easily.
In brief, MRSA infection has been associated with a kind of staph bacteria that has
proven to be difficult to handle due to its resistant to antibiotics. The virulence factors have
been linked to bacterial cell wall especially the peptidoglycan layer, adhesives, enzymes and
immunomodulators. These together with other factors enable the bacteria to evade the host’s
immune response and cause infection. The ability to differentiate MRSA from MSSA has
been crucial especially in administering timely medication for patients in hospitals.
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