1 / 57

Acinetobacter Infections in a Hospital Setting

Acinetobacter Infections in a Hospital Setting. University Medical Center-Medical Grand Rounds Las Vegas, Nevada February 17, 2006. Gonzalo Bearman MD, MPH Assistant Professor of Medicine, Epidemiology and Community Health Associate Hospital Epidemiologist Virginia Commonwealth University.

lotus
Download Presentation

Acinetobacter Infections in a Hospital Setting

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Acinetobacter Infections in a Hospital Setting University Medical Center-Medical Grand Rounds Las Vegas, Nevada February 17, 2006 Gonzalo Bearman MD, MPHAssistant Professor of Medicine, Epidemiology and Community HealthAssociate Hospital EpidemiologistVirginia Commonwealth University

  2. Epidemiology & Prevention of Acinetobacter Infections • Microbiology • Infections: • Scope of the problem • Impact • Outbreaks • Reservoirs of Acinetobacter in the hospital • Colonization • HCWs, patients, environment • Cross transmission • Treatment of Acinetobacter infections • Limiting cross transmission of Acinetobacter • Infection control • Summary

  3. Acinetobacter • Akinetos, Greek adjective, unable to move • Bakterion, Greek noun, rod • Nonmotile rod Brisou and Prévot, 1954

  4. Microbiology • Oxidase negative • Nitrate negative • Catalase positive • Nonfermentative • Nonmotile • Strictly aerobic • Gram negative coccobacillus • Sometimes difficult to decolorize • Frequently arranged in pairs Bergogne-Bérézin E, Towner KJ. Clin Microbiol Rev 1996;9:148-165.

  5. Microbiology • Ubiquitous: • Widely distributed in nature (soil, water, food, sewage) & the hospital environment • Survive on moist & dry surfaces • 32 species • >2/3 of Acinetobacter infections are due to A. baumanii • Highly antibiotic resistant • Numerous mechanisms of resistance to β-lactams described in A. baumanii • 15 aminoglycoside-modifying enzymes described • Quinolone resistance due to mutations in DNA gyrase

  6. Hospital acquired Acinetobacter infections

  7. Major infections due to Acinetobacter • Ventilator-associated pneumonia • Urinary tract • Bloodstream infection infection • Secondary meningitis • Skin/wound infections • Endocarditis • CAPD-associated peritonitis • Ventriculitis

  8. Acinetobacter Ventilator-Associated Pneumonia • Acinetobacter accounts for 5-25% of all cases of VAP • Risk factors: • Advanced age • Chronic lung disease • Immunosuppression • Surgery • Use of antimicrobial agents • Invasive devices • Prolonged ICU stay

  9. Acinetobacter Bloodstream Infection • Most common source is respiratory tract infection • Predisposing factors: • Malignancy • Trauma • Burns • Surgical wound infections • Neonates • Low birth weight • Need for mechanical ventilation

  10. Nosocomial Bloodstream Infections 49 US centers 1995-2002 N= 24,179 Wisplinghoff H, Edmond MB et al. Clin Infect Dis. 2004 Aug 1;39(3):309-17

  11. SCOPEAcinetobacter Nosocomial BSI • Incidence = 0.6/10,000 admissions • Accounts for 1.3% of all nosocomial BSI • Accounts for 1.6% of all nosocomial BSI in the ICU setting • Crude mortality: • Overall 34% • ICU 43% Despite the low incidence, the mortality is high Wisplinghoff H, Edmond MB et al. Clin Infect Dis. 2004 Aug 1;39(3):309-17

  12. Time to Nosocomial BSI Acinetobacter BSI tends to be a late onset, hospital acquired phenomenon Wisplinghoff H, Edmond MB et al. Clin Infect Dis. 2004 Aug 1;39(3):309-17

  13. Source of A. baumanii Nosocomial Bloodstream Infection Abdominal infection 19% The respiratory tract is an important reservoir for Acinetobacter bloodstream infections Central venous line 8% Respiratory tract 71% N=37 Garcia-Garmendia J-L et al. Clin Infect Dis 2001;33:939-946.

  14. Inflammatory Response to A. baumanii Nosocomial Bloodstream Infection Severe sepsis 21% Septic shock 24% Sepsis 55% N=42 Garcia-Garmendia J-L et al. Clin Infect Dis 2001;33:939-946.

  15. Independent Predictors of A. baumanii Nosocomial Bloodstream Infection No. of invasive procedure-days/number of days in ICU prior to BSI Garcia-Garmendia J-L et al. Clin Infect Dis 2001;33:939-946.

  16. Acinetobacter Meningitis • Most cases are hospital-acquired • Often associated with neurosurgical procedures • Risk factors: • Ventriculostomy • Heavy use of antibiotics in the neurosurgical ICU

  17. Impact of Acinetobacter Infection in the ICU

  18. Impact of Acinetobacter Infection in the ICU: historical cohort study 48 patients with Acinetobacter infection matched 1:1 to patients without infection Controls were matched to cases on: age (+6yrs), APACHE II (+ 4 points), admission date, principal diagnosis at ICU admission, LOS at least as long as case until isolation of AB, requirement for mechanical ventilation Garcia-Garmendia JL et al. Crit Care Med 1999;27:1794-1799.

  19. Impact of Acinetobacter Bloodstream Infection in the ICU • Historical cohort study of 45 patients with Acinetobacter bloodstream infection matched 1:2 to patients without infection • Controls were matched to cases on: APACHE II (+ 2 points), principal diagnosis at ICU admission, LOS at least as long as case until bacteremia Blot S. Intensive Care Med 2003;29:471-475.

  20. Impact of A. baumanii Ventilator-Associated Pneumonia in the ICU Historical cohort study of 60 patients with A. baumanii VAP matched 1:1 to patients without A. baumanii infection Controls were matched to cases on: age, APACHE II score, admission date, principal diagnosis, LOS at least as long as case until onset of pneumonia, chronic health status Garnacho J et al. Crit Care Med 2003;10:2478-2482.

  21. Acinetobacter outbreaks Detection of Acinetobacter Infections Consider: organ site, genetic typing, hospital location Common source outbreak with respiratory site predominance Common source outbreak without respiratory site predominance Respiratory site outbreaks without an identified common source Non- respiratory site outbreaks without an identified common source Villegas M, Hartstein A. Infect Control Hosp Epidemiol. 2003;24:284-295

  22. Acinetobacter outbreaks 1977-2000 Extensive Literature review and summary of 51 Acinetobacter outbreaks Villegas M, Hartstein A. Infect Control Hosp Epidemiol. 2003;24:284-295

  23. Acinetobacter outbreaks 1977-2000 Villegas M, Hartstein A. Infect Control Hosp Epidemiol. 2003;24:284-295

  24. Acinetobacter outbreaks 1977-2000 Villegas M, Hartstein A. Infect Control Hosp Epidemiol. 2003;24:284-295

  25. Acinetobacter outbreaks 1977-2000 Villegas M, Hartstein A. Infect Control Hosp Epidemiol. 2003;24:284-295

  26. Acinetobacter outbreaks 1977-2000 Villegas M, Hartstein A. Infect Control Hosp Epidemiol. 2003;24:284-295

  27. Reservoirs of Acinetobacter:Where do these organisms reside?

  28. Bed rails Bedside tables Ventilators Infusion pumps Mattresses Pillows Air humidifers Patient monitors X-ray view boxes Curtain rails Curtains Equipment carts Sinks Ventilator circuits Floor mops Environmental Contamination with Acinetobacter

  29. Factors Promoting Transmission of of Acinetobacter in the ICU • Long survival time on inanimate surfaces • In vitro survival time 329 days(Wagenvoort JHT, Joosten EJAJ. J Hosp Infect 2002;52:226-229) • 11 days survival on Formica, 12 days on stainless steel(Webster C et al. Infect Control Hosp Epidemiol 2000;21:246) • Up to 4 months on dry surfaces(Wendt C et al. J Clin Microbiol 1997;35:1394-1397) • Extensive environmental contamination • Highly antibiotic resistant • High proportion of colonized patients • Frequent contamination of the hands of healthcare workers

  30. Acinetobacter Transmission in the Hospital Setting • Direct or indirect contact • Contaminated hands of healthcare workers • Airborne transmission via aerosol production (e.g., hydrotherapy) may occur Simor AE et al. Infect Control Hosp Epidemiol 2002;23:261-267.

  31. Evidence for Airborne Transmission of Acinetobacter • Sedimentation plates placed in 7 patients’ rooms with respiratory infection or colonization % of plates growing Acinetobacter Brooks SE et al. Infect Control Hosp Epidemiol 2000;21:304.

  32. Acinetobacter spp Skin Colonization Seifert H et al. J Clin Microbiol 1997;35:2819-2825. A. baumanii isolated from 2 patients & 1 control only

  33. Acinetobacter Transmission in the Hospital SettingColonization of Healthcare Workers • Outbreak of multidrug resistant A. baumanii in a Dutch ICU involving 66 patients with an epidemic strain • Nursing staff were cultured (nares & axilla, same swab) • 15 nurses found to harbor epidemic strain • All were culture negative when re-cultured (nose, throat, axilla, perineum) Wagenvoort JHT et al. Eur J Clin Microbiol Infect Dis 2002;21:326-327.

  34. Hand Contamination in HCWs % of HCWs (n=328) with hand contamination Bauer TM et al. J Hosp Infect 1990;15:301-309.

  35. Opportunities for cross transmission are multiple

  36. Treatment of Acinetobacter infections

  37. Acinetobacter Susceptibility, US, 2002-2003 % susceptible Increasing rate of antibiotic resistance TSN Database. http://www.geis.ha.osd.mil/GEIS/SurveillanceActivities/AntimicrobialResistance/AcinetobacterGraphs.htm

  38. Antibiotic ResistanceCommunity vs. Hospital Acquisition • Comparison of A. baumanii isolates obtained from the hands of homemakers to isolates obtained from 2 US hospitals • 23/222 (10.4%) homemakers had A.baumanii isolated from hands *3rd gen. cephalosporins + carbapenem + aminoglycoside Zeana C. Infect Control Hosp Epidemiol 2003;24:275-279.

  39. Polymyxin antibiotics • A group of polypeptide antibioticsthat consists of 5chemically different compounds (polymyxinsA E). • Only polymyxinB and polymyxin E(colistin) have been usedin clinically. • Intravenous colistin should beconsidered for the treatmentof infections caused bygram-negative bacteria resistant toother available antimicrobial agents,confirmed by appropriate invitro susceptibility testing

  40. Polymyxin antibiotics: • History • Used extensivelyworldwide in topical oticand ophthalmic solutions fordecades • Intravenous Colistin wasinitially used inJapan and in Europeduring the 1950s, andin the United Statesin the form ofcolistimethate sodium in 1959 • The intravenousformulations of colistin andpolymyxin B were graduallyabandoned in most partsof the world inthe early 1980s becauseof the reported highincidence of nephrotoxicity • Colistin was mainlyrestricted during the past2 decades for thetreatment of lung infectionsdue to multidrug-resistant (MDR),gram-negative bacteria in patientswith cystic fibrosis

  41. Polymyxin antibiotics colistin sulfate: oral, used for bowel decontamination colistimethatesodium: (also called colistinmethanesulfate, pentasodium colistimethanesulfate, andcolistin sulfonyl methate)- Intravenous formulation Clinical Infectious Diseases 2005;40:1333-1341

  42. Polymyxin antibiotics • Mechanism of action: • Target: • Bacterial cellmembrane • Colistin binding with thebacterial membrane occurs throughelectrostatic interactions between thecationic polypeptide (colistin) andanionic lipopolysaccharide (LPS) moleculesin the outer membraneof the gram-negative bacteria • leads to a derangement ofthe cell membrane • The resultof this isan increase in thepermeability of the cellenvelope, leakage of cellcontents, and, subsequently, celldeath.

  43. Polymyxin antibiotics Sectionsof a Pseudomonas aeruginosa strainshowing the alterations inthe cell following theadministration of polymyxin B(25 g/mL for 30min) and colistin methanesulfate(250 g/mL for 30min). A: untreatedcell; B: cell treatedwith polymyxin C:cell treated with colistinmethanesulfate; D: cell treatedwith polymyxin B at highermagnification.= 0.1 m Clinical Infectious Diseases 2005;40:1333-1341

  44. Polymyxin antibiotics • Development of Resistance • Resistanceto colistin occurs through mutationor adaptation mechanisms • Almost complete cross-resistanceexists between colistin andpolymyxin B

  45. Polymyxin antibiotics • Important pharmacokinetic parameters • Colistinsulfate and colistimethate sodiumare not absorbed bythe gastrointestinal tract withoral administration • Primary routeof excretion is throughglomerular filtration • Experimental studieshave shown that colistinis tightly bound tomembrane lipids of tissues,including liver, lung, kidney,brain, heart, and muscles • Concentration of colistinin the CSF is 25% of the serumconcentration

  46. Polymyxin antibiotics • Spectrum of activity • Mostgram-negative aerobic bacilli: • Acinetobacter species, P. aeruginosa, Klebsiella species,Enterobacter species, Escherichia coli, Salmonella species,Shigella species, Citrobacter species,Yersinia pseudotuberculosis, Morganella morganii, and Haemophilus influenzae • No activity against: • Pseudomonas mallei, Burkholderia cepacia, Proteus species,Providencia species, Serratia species,Edwardsiella species, and Brucella

  47. Polymyxin antibiotics • Susceptibility testing: • Disk diffusion- Colistin • Disk diffusion method thatuses a 10-ug colistinsulfate disk • Isolatesis susceptible ifthe zone of inhibitionis >11 mm • Dilution method- colistimethate sodium • TheMIC break pointfor susceptibility is <4 mg/L • If the MIC is >8 mg/L, the isolateshould be considered resistant

  48. Polymyxin antibiotics

  49. Polymixin adverse effects

  50. Polymixin adverse effects

More Related