G re ws Pr BX Ape illed lesions, is facultatively anaerobic, is non-motile and non spore forn any ment NM tee / — Biol. 2905 As: 1. Describe the characteristics of MRSA and why itis resistant to methicillin. Staphylococcus curelee “S. aureus” is a type of bacteria fy iauren the Skin, hr, throat, and in the nasal cavities of healthy people alt has the potential to cause infection, in different parts of the body. depending on where it resides. There are over 30 different types of S. aureus that can cause infections including skin infections, pneumonia, food poisoning. toxic shock syndrome and blood poisoning (Webmd, 2013) S. aureus infections were commonly and successfully treated with the antibiotic penicillin, With the clinical overuse of penicillin, S. aureus microbes became resistant to the antibiotic by producing beta-lactamases that hydrolyze penicillin (Ji, 2007). Therefore the antibiotic methicillin, a synthetic form of penicillin, was created to resist the beta- lactamase degradation (tiraoo7 Afowever again with the overuse of methicillin to treat S. aureus infections, resistant strains of the bacteria began to emerge, these resistant strains of staph became known as Methicillin-resistant Staphylococeus aureus (MRSA). MRSA has several defining characteristics: it is a gram-positive bacteria, it produces pus- ing. MRSA has become resistant to an entire class of penicillin-like antibiotics called beta-lactams (NIH, 2007) Phere are three known ways by which S.aureus has developed resistance to methicillin: the hyperproduction of beta-lactamases, the egdification of normal penicillin-binding proteins (PBPs), and the acquired or inherited presence of the lin-binding protein PBP2a. PBP2a has a low affinity to beta-lactams that has been encoded by the mecA gene (Ji, 2014). PBP2a catalyzes the formation of cross-bridges in bacterial cell wall peptidoglycan creating an even more rigid cell wall. PBP2a is a unique = protein tha only produced by methicillin-resistant staphylococci (Hanssen, 2005). The bacterial evolution of MRSA has made it increasingly difficult to treat with antibiotics. Due to its high resistance, MRSA can now be referred to as a “superbu! "creating avery serious public health concern (WebMD, 2013) — 4 62. What does SCCmec refer to? (not just what the letters stand for but what + S¥Bies.this designation mean practically and molecularly?) +i e? - SSCmec stands for staphylococcal cassette chromosome mec. SSCmec is a mobile genetic clement of staphylococci. The genetic sequence includes the mec gene, which as described above, encodes the additional penicillin-binding protein, PBP2a that has a low affinity for all beta-lactam antibiotics (Ji, 2014). The SSC element acts as a vector, carrying the mecA gene which encodes the methicillin resistance in susceptible staphylococei st $SCmec elements are classified according to the type of recombinase they carry and their general genetic composition, for example there are have been five types of SSCmec (I-V) that have been described to carry antibiotic resistance (Hassen, 2005). SSCmec plays@ large role in horizontal gene transfer and ultimately the molecular change between and among staphylococci (Hanssen, 2005). From a practical standpoint we know that S. aureus is fron of our normal flora that has the potential to become a harmful and resistant pathogen, so it is important to understand how SSCmec changes staphyloccoci into a resistant organism. This will further our knowledge of the variants of SSCmrec and MRSA and how resistance is spreading among genes. MRSA infections increase the risk of mortality each year so understanding its genetic composition and mechanism of spread will hopefully increase methods of effective treatment. 3. How is VRSA related to MRSA and how did VRSA acquire vancomycin resistance? (environmental pressures and molecular mechanisms) ‘Vancomycin-resistant Staphylococcus aureus (VRSA), @ highly vacomycin resistant t S. aureus strain, emerged as a result of the genetic exchange of material from ae 5 vancomycin-resistant enteroccosci (VRE) to MRSA (CDC, 2014). The first reported case" oer of VRSA was in 2002 that involved a woman from Michigan who, undergoing dialysis ‘was hospitalized for several procedures. The patient was immunocompromised she had diabetes mellitus, hypertension, peripheral vascular disease, chronic renal failure, and developed chronic foot ulcers that became infected with MRSA (Tenover, 2006). Duringthe hospitalization the patient developed MRSA, and had to undergo several catheterizations and received extensive vancomycin therapy over a six-month period. Cultures of the catheter e: site and the catheter tip that were taken tested positive for both MRSA and VRE. Heel cultures also tested positive for VRSA. The detection of VRE and MRSA at the infection site suggested that the transfer of van avancemycin resistance gene from VRE to MRSA had occurred, giving rise to VRSA (Tenover, 2006). Vacomycin acts by binding irreversibly to the terminal D-alanyl-D-alanine of the bacterial cell wall precursor inhibiting cell wall production by attacking the sites responsible for cell wall synthesis (Appelbaum, 2006). There are three possible mechanisms of vancomycin resistance. First the trapping of vancomycin molecules by cell wall monomers (Ji, 2007). Secondly these trapped molecules then clog the outer layer of the peptidoglycan meshwork and form a physical barrier toward further incoming, vacomycin molecules therefore rendering the vancomycin ineffective (Appelbaum, 2006). Lastly the exchange of genetic material among VRSA bacteria involving the expression of the vand gene, that is associated with thgaaHtegation of the vancomycin binding cite in the cell wall (Tenover, 2006). 4, The Applelbaum article discusses only a few incidences of VRSA infeetions— but this paper was written in 2006. Use your research skills to find and describe new information on the prevalence and treatment of VRSA infections today. “4 A we’ The VRSA infection continues tobe Limited, Globally thgghave ben 3 stuns of > VRSA reported, 13 that have come from the USA to date (Moravvej Z et al, aD) Mee are some existing factors that will predispose a patient to contracting the VRSA infection, ‘These include: prior MRSA infections, enterococcal infections, diabetes, sand previous treatment with vancomycin (CDC, 2014). VRSA can be diagnosed through blood tests, examination of stool, urine, or wound site. The success of antibiotic treatment against VRSA is variable and there is currently no uniform protocol of antibiotic treatment, Treatment of VRSA should be based on its susS®Puil (Mazulli, 2015). There was some success found with the antimicrobials quinupristin- ity in laborstory testingdalfopristin, linezolid, and trimethoprm-sulfamethoxazole (TMP-SMX), in treating ‘VRSA that have been used alone or in combination for a synergistic effect (Mazzull, 2015). Ceftaroline-fosamil, its brand name Teflaro is a new medication apart of the cephalosporin class of antimicrobial agents that has proven to be effective at treating some strains of the gram-positive bacteria MRSA and VRSA. Ceftaroline-fosamil works by binding to the PBPs on the bacterial cell wall inhipiging the cell wall synthesis. Ceftaroline-fosamil is the only Food and Drugs Administration (FDA) approved cephalosporin that has activity against VRSA (Bassetti et al., 2013). Knowledge of VRSA is unfolding case by case, but more research is needed to fully understand the organisyy including its epidemiology, microbiology, and the clinical and infection control (2 procedures needed for optimal treatment. 5, Would you be likely to contract a VRSA infection if you were working with a VRSA patient? Why or why not? VRSA infections are still a rare occurrence, however VRSA can spread from person to person especially among those who have close physical contact with VRSA infected patients or contaminated materials. As a health care provider or someone who is caring fora patient with VRSA this is very important information to know. People who are more likely to contract VRSA are those who are immunocompromiset/fave had a prolonged hospital stay, surgery, been on long-term antibiotics, have had medical tubes in their bodies such as an IV or central line, or do not wash there hands thoroughly (CDC, 2013). To reduce the spread of VRSA the proper hygiene protocols should beefSllowed: ‘wash your hands often, keep the wound clean and covered, do not share items, clean surfaces well using a germ-killing cleaner, wash contaminated laundry, wear protective gloves, and adhere to the proper hand hygiene protocols recommended by the health care facility (CDC, 2013). Ifyou follow the proper hygiene protocols diligently and do not fit the desription of a typeal person prone to VRSA the chancesgn contracting VRSA should be low.beep References Appelbaum PC. The emergence of vancomycin-intermediate and vancomycin-resistant Staphylococcus aureus. Clinical Microbiology & Infection. 2006;12:16-23. Bassetti M, Merelli M, Temperoni C, Astilean A. New antibiotics for bad bugs: where are we? Annals of Clinical Microbiology and Antimicrobials 2013;12:22. doi: 10.1186/1476-0711-12-22. Capriotti T. Resistant 'Superbugs' Create Need for Novel Antibiotics. Dermatology ‘Nursing. 2007 02;19(1):65-70. CDC Centers for Disease Control and Preventions. General information about VISA/ ‘VRSA. Last updated, August 2015. [online] Retrieved. 27, Oct. 2015. CDC Centers for Disease Control and Preventions. Reminds Clinical Laboratories and Healthcare Infection Preventionists of their Role in the Search and Containment of ‘Vancomycin-Resistant Staphylococcus aureus (VRSA). Last updated, May, 2014. [online] Retrieved. 27, Oct. 2015. EDA approves Dalvance to treat skin infections. Clinical infectious diseases: an official publication of the Infectious Diseases Society of America. 2014;59:i. Gould IM. Treatment of bacteraemia: Meticillin-resistant Staphylococcus aureus (MRSA) to vancomycin-resistant S, aureus (VRSA). Int J Antimicrob Agents. 2013;42:817-S21. Hanssen A, Ericson Sollid JU. SCCmec in staphylococci: genes on the move. FEMS Immunology & Medical Microbiology. 2006;46:8-20. Ji, Yinduo. Methicillin-Resistant Staphylococcus Aureus (MRSA) Protocols. 391 Vol. Totowa, N.J: Humana Press, 2007. Mazzulli, Dr. Tony. Vancomycin Resistant Staphylococcus Aureus (Versa). Canadian Antimicrobial Resistance Alliance. Can-r.com, n.d. [online] Retrieved, 30, Oct. 2015. . Moravvej Z, Estaji F, Askari E, Solhjou K, Naderi Nasab M, Sadat S. Update on the global number of vancomycin-resistant Staphylococcus aureus (VRSA) strains. Int J Antimicrob Agents. 2013;42:370-, wks e _