Most skin infections will heal within a few weeks. More serious skin infections can take longer to heal if treatment is delayed or if ineffective treatment is given. Some serious S. Transmission S. The skin and mucous membranes are usually an effective barrier against infection. However, if these barriers are breached e. Persons who are immunocompromised or who have invasive medical devices are particularly vulnerable to infection.
In recent years physicians and other health care providers have observed an increasing number of people with MRSA infections who lack traditional health care-associated risk factors. These people appear to have community-associated infections. Complications Most skin infections resolve without treatment, however, some infections require incision and drainage or antibiotic treatment to cure the infection.
Three decades after its introduction into clinics, no clinical resistance to vancomycin was reported. The first report of a MRSA strain showing reduced susceptibility to vancomycin was reported in The strain had thickened cell wall when observed under electron microscopy and did not carry vanA or vanB genes as found in vancomycin-resistant enterococci VRE [ 79 ].
Subsequently, there were more reports of clinical infections due to MRSA strains with decreased vancomycin susceptibility similar to that of Mu50 strain. The S. The genetic basis of emergence of VISA appears complex. The increased MRSA infection in hospitals has led to extensive use of vancomycin resulting in the selection of MRSA strains with reduced vancomycin susceptibility [ 83 ].
Different diagnostic methods showed variable sensitivity and specificity leading to contradictory reports in prevalence [ 80 , 84 — 86 ]. However, by optimizing the dose regimen and drug delivery, thereby, achieving the desired blood plasma concentration which would give the clinical efficacy is the way forward in preserving the clinical utility of vancomycin [ 88 , 89 ].
Unlike VRE, these strains do not carry vanA or vanB type of genes to confer resistance to vancomycin. In , first report of a S. The strain was methicillin resistant and carried vanA gene which was responsible for high-level resistance to vancomycin [ 90 ]. This report was followed by sporadic incidences of isolation of S. VRSA strains carried copies of the transposon Tn , which was acquired from vancomycin-resistant Enterococcus faecalis.
The resulting D-Ala-D-Lac depsipeptide replaces the D-Ala-D-Ala dipeptide in peptidoglycan synthesis, a substitution that decreases the affinity of the molecule for vancomycin and other glycopeptide antibiotic, teicoplanin, considerably [ 92 , 93 ]. Since HA-MRSA strains are often MDR phenotype, drugs such as sulphonamides, tetracyclines, aminoglycosides, chloramphenicol and clindamycin were sidelined due to lack of activity, while vancomycin remained the mainstay of therapy.
Resistance to sulphonamides and trimethoprim [ 94 ], tetracyclines [ 95 — 97 ], aminoglycosides [ 98 — ], chloramphenicol [ ] and clindamycin [ ], occurring in S. Therapeutic approach to S. Various drugs as single agent and drug combinations have been used to treat S. There are guidelines and reviews to help in the treatment of community and hospital infections of MRSA. Mupirocin is used as topical antibiotic to treat impetigo due to S.
The drug is also used for nasal decolonization of S. Mupirocin belongs to monoxycarbolic acid class and it exerts antibacterial action by binding to isoleucyl t-RNA synthetase, thereby, inhibiting the protein synthesis [ ].
The antibiotic shows excellent activity against Staphylococci and most Streptococci [ ]. Clinical efficacy of mupirocin ointment in treating S. Various reports also demonstrated effectiveness of mupirocin in nasal decolonization of S. Fusidic acid is an antibiotic, which belongs to a class referred to as fusidanes. Chemically it is a tetracyclic triterpenoid [ ] and it binds to bacterial elongation factor G EF-G , which results in impaired translocation process and inhibition of protein synthesis [ ].
It has potent activity against S. The efficacy of fusidic acid ointment in treatment of S. The drug has also been used systemically to treat invasive S.
As discussed earlier, vancomycin remained the mainstay of therapy against MRSA infections in hospitalized patients for decades. Though the antibiotic was available for clinical use since , it gained prominence among clinicians only after the surge in nosocomial MRSA infections in s [ 73 , 75 ].
Numerous reports documented the clinical efficacy of vancomycin in treating various MRSA infections in hospitalized patients [ — ]. In addition, over the years, the mean MIC of vancomycin against susceptible MRSA populations has increased but within the susceptible range.
This phenomenon is referred to as vancomycin MIC creep. Optimizing the dose regimen and drug delivery, in order to achieve the desired blood plasma concentration which would give the clinical efficacy is the way forward in preserving the clinical utility of vancomycin [ 91 , 92 ]. The problem of MRSA infections in hospitals and lack of effective antibiotics other than vancomycin to treat them necessitated the discovery of novel anti-MRSA drugs.
The continued efforts of researchers in discovering novel anti-MRSA drugs fructified resulting in arrival of number of newer anti-MRSA drugs for clinical use in the last 15 years [ 78 , — ]. FDA for clinical use. Apart from chemotherapeutic approach to tackle the S.
Various phytochemical are also found to have anti-MRSA activity. All these are at investigational stages and more research is necessary to bring promising candidates for clinical usage. Clinical use of agents which are not conventional antibiotics but able to inhibit the expression or function of the virulence factors, rendering the bacteria non-pathogenic is considered an alternative approach to tackle MRSA.
Stripping microorganisms of their virulence properties without threatening their existence may offer a reduced selection pressure for drug-resistant mutations. Virulence-specific therapeutics would also avoid the undesirable dramatic alterations of the host microbiota that are associated with current antibiotics [ , ]. Accessory gene regulator agr -mediated quorum sensing system of S. Scientists identified small molecules which inhibited the agr system [ — ].
Active and passive immunization strategies targeting the virulence factors of S. Plants have immune system and other defensive mechanisms against microorganisms that cause plant diseases. Hence, the plants with huge diversity provide a vast source for exploration of anti-MRSA phytochemicals. In vitro Anti-MRSA activity of crude extracts of medicinal plants has been extensively reported [ ].
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Edited by Shymaa Enany. We are IntechOpen, the world's leading publisher of Open Access books. Built by scientists, for scientists. Our readership spans scientists, professors, researchers, librarians, and students, as well as business professionals. Downloaded: Abstract Staphylococcus aureus is an important human pathogen that causes wide range of infectious conditions both in nosocomial and community settings.
Introduction Staphylococcus aureus is a Gram-positive bacterium and causative agent of wide range of infectious diseases such as skin infections, bacteremia, endocarditis, pneumonia and food poisoning. Microscopic morphology S. General cultural and biochemical characteristics S. Medical laboratory diagnosis The primary objective in laboratory diagnosis is to identify whether the diagnosed S.
Pathogenesis The process of S. Hospital and community infections S. Virulence factors S. They are also involved in host immune evasion [ 13 ]. PVL belongs to group of membrane pores forming proteins.
It consists of two protein components LukS-PV and LukF-PV which act together as subunits and form porins on cell membrane of host cells, leading to leakage of cell contents and cell death [ 17 ].
Chemotaxis-inhibitory protein of S. In addition to the roles of adhesion and invasion, it also has immune-modulatory activity [ 20 ]. Induces toxinosis Enterotoxins S. The Staphylococcal food poisoning is an intoxication which results from consumption of foods containing sufficient amount of preformed enterotoxins [ 21 ].
TSST-1 causes toxic shock syndrome especially in menstrual women [ 7 ]. Most of the time, staph does not cause any harm; however, sometimes staph causes infections. In healthcare settings, these staph infections can be serious or fatal, including:. Although MRSA is often better known, any staph infection can be dangerous even if it is not resistant to antibiotics. Anyone can develop a staph infection, although certain groups of people are at greater risk, including people with chronic conditions such as diabetes, cancer, vascular disease, eczema, lung disease, and people who inject drugs.
In healthcare facilities, the risk of more serious staph infection is higher because many patients have weakened immune systems or have undergone procedures. In healthcare, the risk of more serious staph infection is higher for patients in intensive care units ICUs , patients who have undergone certain types of surgeries and patients with medical devices inserted in their bodies.
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