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New Issues in bacteria we thought we knew so well. Meet the new Staphylococcus aureus

New Issues in bacteria we thought we knew so well. Meet the new Staphylococcus aureus. Donna Holton, Infectious Diseases, CHR Oct 23, 2008. HARBOUR BRETON NEWFOUNDLAND. Who am I. ID specialist with training in epidemiology GP who worked in outport NFLD 1981-1983

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New Issues in bacteria we thought we knew so well. Meet the new Staphylococcus aureus

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  1. New Issues in bacteria we thought we knew so well.Meet the new Staphylococcus aureus Donna Holton, Infectious Diseases, CHR Oct 23, 2008

  2. HARBOUR BRETON NEWFOUNDLAND

  3. Who am I • ID specialist with training in epidemiology • GP who worked in outport NFLD 1981-1983 • Worked in Kenya doing HIV in the late ’80s • Worked for Health Canada as epidemiologist (created the TB Guidelines for Canadian Hospitals) • Self employed epidemiologist (organized the 1997 Canadian Antimicrobial Resistance Conference) • Worked in Regina as Infectious Diseases doctor • Work in Calgary as ID and do HIV and Infection Control

  4. Who am I • I have done talks for all the companies re: antibiotics and HIV • Abbott, BMS, Wyeth-Ayerst, GSK • Interested in biofilm infections and hospital building design • HIV trials with a wide variety of companies Tibotec, GSK, Abbott, Boehringer-Ingelheim, NeurogesX, Argos Therapeutics, Gilead, Pzifer, Merck • I sit on three boards for new HIV drugs (Abbott, Kaletra: Merck, Raltegrevir: Pzifer, Maraviroc) • I am part of the committee writing Canadian HIV treatment guidelines

  5. Learning Objectives Methicillin resistant Staphylococcus aureus MRSA • How have Staphylococcus aureus infections changed? • What is the prevalence of MRSA in the CHR • Infection vs colonization • Treatment- who, what , and when? • What will the future look like?

  6. With Many Thanks • To all the IPCs who collect the bloodstream infections and to Stephanie who enters the data • To CLS and Provincial Lab especially Drs. Dan Gregson, Deirdre Church and Marie Louie • To all IPCs who took part in the Mark of Zoro study

  7. Staphylococcus aureus • Very successful bacteria: can infect anyone bacteria • Ubiquitous • In the days before antibiotics whole wings of hospitals were filled with people who had chronic S. aureus infections • 2% of lactating women died of S. aureus mastitis

  8. S. aureus causes • Soft tissue infections • Basically any, impetigo, cellulitis, muscle abscess • Joint infections • Surgery site infections • Endocarditis • Osteomyelitis • Prosthetic device infections • Others: pneumonia, organ abscesses Produces toxins that cause different diseases • food poisoning, toxic shock

  9. My Jan 28th caseWhy is my patient not improving? • 40 yr female with abscess in her left thigh • WBC 22 with 20 neutrophils • Blood cultures negative • Not toxic, just not getting better

  10. Clinical issues • the usual bacterial suspects that cause uncomplicated soft tissue infection are • Group A Streptococcus • S. aureus Cultures rarely done • Because this lady has a large abscess, the pathogen is more likely to be S. aureus rather than Group A Streptococcus

  11. Staphylococcus aureus is a common cause of infectionName five drugs from five different antibiotics classes that are a) Oral S. aureus antibiotics b) IV S. aureus antibiotics

  12. 15 Classes of anti-S. aureus drugs *CIPRO has an MIC that just works but that also means it often fails against S. aureus. Spain has a > 30% resistance rate **Rifamycins work but not alone

  13. My Jan 28th caseWhy is my patient not improving? • 40 yr female with abscess in her left thigh • WBC 22 with 20 neutrophils • Blood cultures negative • Nasal and rectal cultures negative for MRSA • Superficial wound (skin intact) swab grew Cloxacillin susceptible S. aureus

  14. In your practice, what kind of soft tissues infections are you seeing? If you are aware of several patients have MRSA, do they have the same spectrum of disease?

  15. In HPTP we are seeing a new spectrum of disease 90% are variations of soft tissue themes • Story of the Spider bite • Large often complex abscesses • Multiple skin lesions • Co-infection with Group A Streptococcus • Patients have multiple infections despite good treatment • Patients come from the community

  16. Carbuncle Furuncle (boil) Folliculitis Abscess Courtesy Melissa Tobin-D’Angelo, Georgia DHR

  17. We are seeing a new spectrum of disease ~10% infections creating critical illnesses • Necrotizing pneumonia -Vayalumkal (new ped ID staff) article CJEM 2007:9(4):300-3.. Pt died -CDC is investigating 2 deaths (11 yr old and 13 year children) who died when MRSA complicated a viral “flu” like illness (2008) 22/73 kids who died of influenza in 2006-7 had Staphylococcus 2nd bacterial infection • Rare cases where it caused necrotizing fasciitis, purpura fulmanans This type of MRSA seems to have acquired new abilities to cause critically serious disease

  18. Courtesy of M. Farley BMJ 2006;332;838-841

  19. My Jan 28th caseWhy is my patient not improving? • 40 yr female with abscess in her left thigh • WBC 22 with 20 neutrophils • Blood cultures negative • Nasal and rectal cultures negative for MRSA • Superficial wound swab grew Cloxacillin susceptible S. aureus • Smart hospitalists are concerned this patient has an antibiotic resistant S. aureus

  20. Hospitalist was concerned patient had Methicillin resistant Staphylococcus aureus (MRSA) Which of the 15 class(es) of Staphylococcal Drugs can not be used if a patient has MRSA?

  21. MRSA has developed resistance to ALL current Beta Lactams Name the three beta lactam classes

  22. MRSA = resistance to all of current beta lactam antibiotics • All of the penicillin class regardless of generation or complexity i.e., can not use Cloxacillin, Clavulin or Tazocin • All of the current cephalosporins regardless of generation • All of the current carbapenum (meropenum, imipenum, ertapenum) And MRSA usually comes with even MORE resistance than this!!!

  23. 12 non-Beta lactam S. aureus drugs *CIPRO has an MIC that just works but that also means it often fails against S. aureus. Spain has a > 30% resistance rate **Rifamycins work but not alone

  24. Why is this resistance so important that the Alberta Government has declared war on it?

  25. Because the loss of the Betalactam = the loss of bactercidal antibiotics If the Betalactms are gone so are the Fluroquinolones

  26. What is an Antibiotic Resistant Organism? An organism that We can no longer use our first string (bactercidal) antibiotics We still have antibiotics but we are sending in the second string (bacteriostatic)

  27. 12 non-Beta lactam S. aureus drugs **Rifamycins work but not alone

  28. Betalactam antibiotics work by interfering with the penicillin binding proteins (PBP). This prevents the bacteria cell wall from being built

  29. Think Cement Retaining Wall • S. aureus builds cross links in the bacteria cell wall that strengthen the wall (think rebar) • If beta lactams can bind to the cell wall, the beta lactams prevent the cross links • The cell wall has no “ribar” and collapses • The bacteria die MRSA means that S. aureus has worked out how to prevent Beta lactams from binding

  30. Mechanism of Staphylococcus aureus Methicillin Resistance • Beta lactam antibiotics bind to penicillin binding protein 2 (PBP 2) • When S. aureus changes PBP 2 to PBP 2’ (also called PBP 2a) all currently licensed for use in Alberta beta lactam antibiotics become useless. -Change occurs via the Mec A gene. In the presence of the Mec A gene, the beta lactam antibiotics can not attach to the PBP and so the bacteria grow because the bacteria cells walls are cross linked and strong

  31. A short history of S. aureus Resistance Penicillin (the drug not the class) • 1928 - Penicillin discovered • 1939 - Penicillin first used as treatment • 1945 - Resistance to penicillin identified • 1980’s < 1% susceptible to penicillin

  32. A short history of S. aureus Resistance: Solving Penicillin Resistance • 1959 Vancomycin created and looked like drug of choice • 1959 Methicillin introduced followed by many “copycat” semi synthetic penicillins (i.e., cloxacillin, oxacillin, nafcillin) • 1964 first cephalosporins introduced (Ancef)

  33. A Short History of S. aureus resistance:Develops Resistance to Semi-synthetic penicillins and cephalosporins • 1961 - First identified MRSA (UK) • 1981 - MRSA appears in Canada • 1995 - MRSA begins to escalate in Canada • 1999 – 6% of S. aureus are MRSA in Canada

  34. Antimicrobial Resistance among NosocomialInfections with Gram-Positive Pathogens, Canada (yellow) & US (green) and by ICU Status (pink) United States Canada Source: NNIS Data:Fridkin and Gaynes Clinics in Chest Medicine June ‘99 303-16 CNISP 2000 (colonization/infection)

  35. Figure 1. Incidence and rate per 1,000 patient admissions for MRSA (infections and colonizations) from 1995 to 2006 in Canadian hospitals participating in CNISP Rate is blue line # of cases = red bars Data from CNISP Jan 2008

  36. To all organisms Resistance is not futile, Resistance is survival S. aureus has 4 different alphabet soup names to describe resistance MRSA, hVISA, GISA (not VISA), VRSA Look up Staphylococcus aureus in Infection Control manual

  37. S. Aureus resistance to “methicillin” and Vancomycin 1st use methicillin 1959   1st MRSA 1961  1st MRSA US Outbreak  Vancomycin intermediate resistance 1997 Europe, UK Aus, India  Vancomycin Resistance2002   USA ,Aus Ireland Worldwide

  38. What is happening to S. aureus Calgary?

  39. Odd year

  40. Calgary Health Region, Adult Nosocomial Blood Stream Infections SA Total BSI Stable rate of BSI per 1000 patient days (0.8)

  41. Comparison of Organisms Having Multiple Drug Resistances 2004 to 2007 (Fiscal Year) 2004 fiscal year (n=41) 2005 fiscal year (n=43) 2006 fiscal year (n=56) 2007 fiscal year (n=82)

  42. S. aureus in CHR Emergency Room: prior to 2004 slow but steady increase in per cent

  43. From 2004 to Dec 2007, MRSA took off

  44. MRSA seems to have changed

  45. Before 2004, MRSA wasacquired in Acute Care Hospitals 75% of cases Specific clones Long term care 10% of cases Community 8%

  46. As a resident at FMC I meet my first “Hospital MRSA” • This MRSA was the one in the journals • Was associated with Thames, Australia, U.S. Burn Units • Only available antibiotic was Vancomycin • Occurred in • elderly, frail hospital patients • burn, ICU and dialysis units • Caused infection (bacteremias) but a lot of people just seemed to be colonized • This organism plus VRE were the basis of creating increased isolation in acute care settings • Private room • Standard + contact

  47. After that first patient my MRSA experience changed “Prairie” MRSA • caused simple skin infections • had an effective oral agents (TMP-SMX, clindamycin) • occurred in an isolated population (First Nations) • was found on the Prairies • Was not a research project, no one was able to get any traction for research on this type of MRSA So we treated the kids and young people with Septra and they got better.

  48. 2005 • Until 2005, the majority of MRSA isolates came from the hospital environment • Since mid 2005, most of the MRSA isolates came from the community

  49. Clinical Syndromes – Invasive MRSA †Difference tested by Chi Square with p value <0.0001 Ray SM et al. IDSA 2005

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