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Emerging Threat: Methicillin-Resistant Staphylococcus Aureus (MRSA)

Learn about the transformation of MRSA from a hospital-acquired pathogen to a community threat. Understand its mechanisms, epidemiology, and treatment options for HA-MRSA and CA-MRSA. Discover control measures and the differentiation between the two strains.

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Emerging Threat: Methicillin-Resistant Staphylococcus Aureus (MRSA)

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  1. Methicillin-resistant Staphylococcus Aureus - (MRSA): not just a health-care associated multi-drug resistant pathogen anymore Presenter: ZipporahMachuki

  2. Background S. aureus: • Facultative anaerobic • gram-positivecoccalbacterium. • forms large, round, golden-yellow colonies on BA often with hemolysis. • Reproduces asexually by binary fission • cells are arranged in cluster. • catalase-positive, • coagulase test was used to differentiate S. aureus from other staphylococci epidermidis. However it is now known that not all S. aureus are coagulase-positive.

  3. S.aureus commonly colonizes Survives for a long time on skin or environment. Mortality 80% prior to introduction of Penicillin. Resistance to penicillin usually mediated by beta-lactamase,

  4. Methicillin A penicillinase-resistant penicillin First used in 1959 and 2 years later S.aureus developed methicillin-resistance. Due to acquisition of the mecA gene. Traditionally recognized as a nosocomial pathogen Epidemiology has radically changed

  5. Mode of action of methicillin • Bind to the native PBPs that are present in the S. aureus cell wall • Leads to the disruption of the synthesis of the peptidoglycan layer and therefore lysis of the S.aureus.

  6. Methicillin Resistant S.aureus(MRSA) • Has a mecA gene which is 2.1kb in length • mecA gene codes for the 78-kDa penicillin binding protein (PBP) 2a (or PBP2’), • PBP2 has decreased affinity for most beta-lactam antibiotics.

  7. Mechanism of resistance • When PBP2a is produced, • thebinding of the b-lactam antibiotics is hindered and • PBP2A (a transpeptidase), assisted by the transglycosylase domain of the native PBP2 of S aureus, takes over the function of biosynthesis of cell-walls • Result in the growth of MRSA

  8. staphylococcal cassette chromosome mec (SCCmec) • A mobile genomic island where mecA gene is located. • Carries chromosome recombinances genes called ccrA/ccrB and ccrCthat enable excision and intergrationinto the host chromosome. • seven types main of SCCmec (SCCmec I to VII)

  9. Epidemiology of MRSA • MRSA first identified in 1960 • became a common nosocomial infection in 1980. • Previously known to be only a nosocomial pathogen. • Risk factors associated with development of MRSA infections: • surgery, dialysis, hospitalization or residence in a long-term care facility within the prior year; • indwelling percutaneous devices such as central venous catheters or feeding tubes; • an MRSA infection identified more than 48 hours after hospital admission; or • Had previously hadMRSA cultured

  10. MRSA cultured from patients with these risk factors are known as HA-MRSA. • major clones that disseminated internationally:Iberian, • Brazilian, • Hungarian, • New York/Japan, and • Paediatric clones • CA-MRSA is cultured from healthy and young individuals without any of these clinical risk factors.

  11. Control of HA-MRSA • Screening of staff Health-care workers who are nasal carriers can serve as sources of MRSA transmission, • Isolation and barrier nursing Patients colonised or infected with MRSA • Hand hygiene Transient contamination of health-care workers’ hands • Environmental cleaning How important are contaminated environmental surfacesasa reservoir for MRSA?

  12. Treatment of HA-MRSA • Laptomycin, • Linezolid, • Tigecyclineand • Vancomycin Zhanelet al. 2013

  13. Differences between HA-MRSA and CA-MRSA BassettiM et al 2009

  14. Transmission of CA-MRSA • colonize the nose and nares (Reservoir)- risk of developing a subsequent infection is 10.7%(Ellis MW 2et al 200) • Transmission between individuals is likely to be facilitated by: • crowded living conditions, • activities that involve skin-to-skin contact, • poor hygiene practices and • sharing of contaminated household items (towels, combs etc.).

  15. Groups at risk of CA-MRSA Zetola N et al 2005

  16. CA-MRSA causes: • skin and soft tissue infections and • invasive disease such as • sepsis and • necrotizing pneumonia

  17. Skin and Soft Tissue Infection • Most common manifestation of CA-MRSA, -particularly abscess or furunculosis • Necrotisingpneumonia • Caused by PVL gene-positive CA-MRSA strains • Osteoarticular Infections • Common in children • Other Infections • Infective endocarditis • Sepsis is a complication of CA-MRSA disease

  18. Treatment of CA-MRSA Infections • There is no defined optimum management of CA-MRSA infections. • Current strategies include a combination of pharmacological and non-pharmacological intervention egIn patients with recurrent infections, attempts to decolonize CA-MRSA

  19. Commonly used antibiotic

  20. Thank you

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