Paper type: Report Pages: 6 (1415 words)
In 2007 Center for Disease Control (CDC) report stated that in USA the most serious and fatal infections are caused by Staphylococcus aureus. MRSA as customarily considered a Hospital Acquired infection but the increased infections of MRSA in Community are not initiating from hospital as the CA-MRSA are genetically distinct and diverse and can be tracked by Genotyping.32The first CA-MRSA infection with unique genetic elements occurred in aboriginal in Australia in early 1990s.33 Later Centers for Disease Control and Prevention (CDC) reported first CA-MRSA deaths of four children in USA Minnesota 1997-1999 by the CA-MRSA strain MW2 that acquired staphylococcal cassette chromosome (SCC) mec type IV, SaPI3 (Staphylococcus aureus pathogenicity island, and Sa2 (bacteriophage) in its evolution from MSSA476.
34Several lineages of CA-MRSA have emerged on every continent, quite a lot of which have spread internationally, most notably community-associated MRSA strain USA300 carrying genes for the Panton-Valentine leukocidin (PVL) and the staphylococcal cassette chromosome mec (SCCmec) type IV, became the predominant strain type of MRSA circulating in the United States by 2011.
35 USA300 probably emerged during the early 1990s and was isolated during 2000 in several states, including California, Texas, and Midwestern states. The geographic mean center of USA300 MRSA then shifted eastward from 2000 to 2013 and then disseminated rapidly worldwide.36 USA300 isolates that spreads to Europe, South America and Australia are becoming more resistant to antimicrobial agents, including mupirocin, erythromycin, levofloxacin, and tetracycline. Figure 4: Worldwide dissemination of CA-MRSAFigure 5: Global distribution of predominant successful clones of community-associated methicillin-resistant Staphylococcus aureus. PVL+ =Panton-Valentine leukocidin positive. PVL”=PVL negative. SWP=southwest Pacific. WA=Western Australia. 37In neonates and children up to one year of age the emergence of CA-MRSA strains has recently become a major public health concern and increased mortality rates in low-income countries are estimated to be up to 50%.HA-MRSA and CA-MRSA are comparable in numerous ways, still distinct38Table: 3 Cell comparison of the two major MRSA epivars types (after Fox 2015; Weigelt 2008). MRSA in Health Care MRSA in the CommunityMajor Genotypes USA100/200 USA300/400Growth Rate Slow compared to wild-type Intermediate*Antibiotic Resistance Many antibiotics Few antibiotics Cipro-sensitive Cipro-resistantVirulence Factor Toxins HA-MRSA CA-MRSASCC Mec Types I”III Types IV, VCytolytic, ‘ ” Hemolysins ” +Leukocidin (PVL) ” +Exfoliative ” some strainsEnzymesІ-lactamase ” 90% of strainsCoagulase + +Hyaluronidase ” +Staphylokinase + +Phagocytic InhibitorsPolysaccharide slime layer + +The single gene mutation results in Cipro resistance. on the other hand, via horizontal gene transfer, primarily transduction via phage the leukocidin toxin is acquired. Plasmid transfers may be the reason for other antibiotic resistant traits. But, all the strains must adapt to a host and the environment and would be subject to selection pressures. (Purdom and Anderson 2008).*Intermediate: Faster than CA-MRSA; Table: 4 Clinical differences between HA-MRSA and CA-MRSA (after Fox 2015; Weigelt 2008).CA-MRSA HA-MRSABlood stream ImmunocompromisedSurgical site Residency in long-term care facilitiesSite of implant Recent hospitalizations, recent surgeryArea affected skin and soft tissues Dialysis patients, kidney, lungs causing pneumoniaThe Molecular evidence supports the complex evolution of CA-MRSA strain developed in several decades. To the genomes of MRSA strains the horizontal transfer of SCCmec elements and PVL genes with other virulence and resistance factors resulted in CA-MRSA clones in the community.CA-MRSA that is PVL positive causes recurrent, chronic or severe skin and soft tissue infection. CA-MRSA positive PVL Pneumonia infection is more complicated, aggressive and very difficult to treat. As CA-MRSA is now becoming more prevalent PVL positive CA-MRSA must be chased by Genotyping Figure 6: Global distribution of CA-MRSA as indicated by Multi Locus Sequence Type (ST)Dotted lines indicated possible route of dissemination for the indicated clones. Major CA-MRSA clones are indicated by larger font and color. Colored regions are an estimate of the area in which infections have been reported for the indicated clone (not all are shown). ST1, green; ST8, red; ST30, blue; ST80, gray hatched. +, PVL-positive; €’, PVL-negative; ±, combination of PVL-positive and PVL-negative strains isolated from the region.the most abundant CA-MRSA strains in Europe are distinct from those in North America, Oceania, or other parts of the world Since the late 1960s, five major MLST defined MRSA pandemic clones ST5, ST8, ST22, ST36, and ST45 caused significant nosocomial disease and spreaded in different regions of the world, with the exception of ST22, reported as SCCmecIV.39CA-MRSA clones identified in the US, Europe and Australia carried SCCmec IV a recent recombinant element is smaller and much more mobile than SCCmec”III present in HA-MRSA strains and have moved repeatedly into diverse lineages of MSSA.40 and it is widely dispersed among numerous MRSA lineages.The epidemiology of CA- MRSA has not been fully described. Furthermore, there are limited data comparing community-associated with health care”associated MRSA cases, and no studies from multiple geographic locations.Literature Review:Table: 5 Nasal carriage rates of Methicillin-Sensitive Staphylococcus aureus (MSSA) and Methicillin-Resistant Staphylococcus aureus (MRSA) in literature 41Author Year of Publication Country Age group Setting Sample size MSSA(%) MRSA(%)Adler l30 2010 Israel 2 to 12 months Community 555 48 5.7Buck37 2008 USA (Minnesota) Kinder to Grade 3 School 611 33 0.5Chaterjee29 2009 India 5 to 15 years Community 489 52.3 3.89Chen15 2011 Taiwan 2 to 60months Community 6,057 15.4 7.8Ciftci39 2007 Turkey 4 to 6 years Community 1,134 28.4 0.3Creech27 2005 USA(Nashville) 2 weeks to 21 years Outpatient clinic 500 36.4 9.2Datta20 2008 Switzerland Not specified Hospital 1350 41.2 1 childErdenizmenili4 2004 Turkey 1 to 16 years Outpatient clinics 115 19.1 not specifiedFaden41 2010 USA (New York) Newborn to18 yrs Hospital 90(control group) 21 not specifiedFan42 2011 China Kindergarten School 801 18.4 1.1Fritz43 2008 USA (Washington) Birth to 18years Outpatient clinics 1,300 24.2 2.6Gorwitz25 2008 USA (nationwide) 1-19 years Community 4772 (2001-02); 4338 (2003-04) 36.9;34.6 0.6;1.3Halabhab14 2010 Lebanon 6 to 10 years Community not specified 57.1 not specifiedHisata44 2005 Japan Nursery and Kindergarten School 818 28.2 4.3Huang45 2007 Taiwan 2 months to 5 years Outpatient Clinic 3,046 23 7.3Hussain46 2001 USA (Chicago) ‰¤16 years Outpatient clinic 500 24.4 2.5Lamaro-Cardoso17 2009 Brazil 2 months to 5 years Day care centers 1,192 31.1 1.2Lear47 2011 USA (Ohio) 14-18 years School (football players) 190 23.1 NoneLo48 2008 Taiwan Birth to ‰¤14 Outpatient Clinic or School 3,200 25.8 11.6Lu49 2005 Taiwan 2 to 18 years Community 987 31.8 3.3Miller28 2011 USA (Virginia and North Carolina) Birth to 6 years Child care centers 1,163 18.1 1.3Nakamura1 2002 USA (Nashville) 2 weeks to 21 years Outpatient Clinic 500 29 0.8Ogzukaya-Artan50 2008 Turkey 5 to 7 years Day care center 200 18 5.6Ozguven26 2008 Turkey Not specified Primary school and High school 2,015 14.7 NonePathak13 2010 India 1 month to 5 years Outpatient clinics 1,562 6.3 16.3% of Staphylococcus aureus isolatesRamana51 2009 India 5 to 15 years School 392 16 19% of Staphylococcus aureus isolatesRijal52 2008 Nepal less than 15 years School 184 31 56.1% of Staphylococcus aureus isolatesSahr53 2010 Sierra Leone Less than 2 years Hospital 116 34.5 NoneSchlesinger34 2003 Israel 0.5 to 17 years ER, Outpatient Clinics and chronic care institutions 831 healthy 118 chronically institutionalized 23.5 36.4 2.6 21Shopsin54 2000 USA (New York) 1 week to 20 years Outpatient clinic 275 35 1 patientStaphylococcus infection and Classification.Staphylococci are intrinsically not pathogenic organisms they colonize the host remain dormant and maintains the normal flora providing a safeguard for opportunistic organisms; they do not possess any such single virulence factor that is sufficient for the establishment of an infection, but as a result of any abrasion or trauma of the skin or mucous membrane the colonizing strain gain entrance to the sterile site and depending on the infective or lethal dose causes staphylococcal infection.Formerly Staphylococcus infection classification was based on the site of infection, such as lung, blood stream, urinary tract, etc. and later on the classification that is followed is on the location of the patient where the pathogen was acquired.The Centers for Disease Control and Prevention (CDC) Active Bacterial Core Surveillance Program defines CA-MRSA infection by as a patient with an MRSA infection and no history of the following: surgery, hospitalization, or residence in a long-term care facility within the year before infection, presence of a percutaneous device or indwelling catheter, dialysis within the previous year, hospitalization >48 h before MRSA culture, or previous MRSA infection or colonization.42 On the other hand, various MRSA clones have spread between the community and hospitals, mainly CA-MRSA transmitted in hospital settings, making the distinction between CA-MRSA and HA-MRSA difficult. The community-acquired (CA-MRSA) strains shows enhanced virulence can affect vital organs leading to sepsis, toxic shock syndrome and pneumonia. Figure 7: Centers for Disease Control and Prevention (CDC) Active Bacterial Core Surveillance Program CA-MRSA definition.Transmission
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