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Galati V. Quali sono i principali tipi di infezione? E come si manifestano? ASMaD 2013

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  • 1. Quali sono i principali tipi di infezione? E come si manifestano? Dr Vincenzo Galati INMI L. Spallanzani
  • 2. PRINCIPALI LOCALIZZAZIONI DELLE INFEZIONI NOSOCOMIALI varie 18% vie urinarie 30%cute 6% app. sito chirurgico app.digerente 14% respiratorio 8% 24%Fonte: NNIS
  • 3. HAI IN ICUUS NHSN 2006-2007 EUROPE EPIC 2 - 2007 • lungs 64% • abdomen 20% • bloodstream 15% • renal tract/genitourinary system 14% JAMA, December 2, 2009—Vol 302, No. 21
  • 4. HAI IN ICU
  • 5. HAI IN ICU
  • 6. Pneumonia classification CAP
  • 7. Pneumonia classification CAP HAP
  • 8. Pneumonia classification CAP non-VAP HAP VAP
  • 9. Pneumonia classification CAP HCAP non-VAP HAP VAP
  • 10. Pneumonia classification CAP HCAP NHAP non-VAP HAP VAP
  • 11. PATOGENESI DELLA VAP ENDOGENA ESOGENA Colonizzazione del Colonizzazione del circuito ventilatorio, tratto aereo-digestivo contaminazione superiore (EGNB) luminale (crociata) Aspirazione Inalazione Colonizzazione del tratto respiratorio inferiore POLMONITE
  • 12. POLMONITE - Diagnosi microbiologica Coltura dell’espettorato: può riflettere una colonizzazionedell’orofaringe, più che la presenza di microrganismi nelle basse vierespiratorie. CRITERI DI BARTLETT per giudicare l’adeguatezza delcampione: >25 leucociti e <10 cellule epiteliali per campo. Coltura da sangue o liquido pleurico (in casi piuttosto rari). Da aspirato endotracheale, BAL (bronchoalveolar lavage), o PSB(protected specimen brush) (effettuati più spesso su pazienti intubati); Colture quantitative (da aspirato endotracheale, BAL o PSB) :vengono utilizzate per distinguere la colonizzazione/contaminazioneall’infezione.
  • 13. N Engl J Med 362;19 may13, 2010
  • 14. VAP - FATTORI DI RISCHIOChastre J, Fagon JY. Am J Resp Crit Care Med, 2002
  • 15. Timing e microbiologia •VAP precoce (Early onset): durante i primi 4 giorni- MSSA, H. influenzae, S. pneumoniae, Enterobacteriaceae •VAP tardiva (late onset): dal 5° (7°) giorno- P. aeruginosa, Acinetobacter spp, MRSA, bacilli gram-negativi antibiotico- multiresistenti •HAP ad insorgenza precoce (entro 3-5gg): S. pneumoniae, H. influenzae, M. catarrhalis •HAP ad insorgenza tardiva (dopo 5 gg): Enterobacteriaceae (K.pneumoniae, Enterobacter spp, E. coli), P. aeruginosaAm J Infect Contr 24:380, 1996; Crit Care Clin 14:119,1998; Am J Respir Crit Care Med 165:867-903, 2002
  • 16. CAP Incidence: 3-40 cases /1,000population per year- 80 % outpatient: low risk of mortality- 18% non-ICU inpatient: 5-8% mortality- 2% ICU inpatient: 10-20% mortality Hospitalization rate is increasing in recent years up to40-60%, mainly among elderly patients and those withmultiple comorbidities Fry AM et al. JAMA 2005, Torres and Rello Am J Resp Crit Care Med 2010 Ruuskanen O et al. Lancet 2011
  • 17. CAPExpected CAP pathogen distribution, by site of careOutpatient Non-ICU inpatient ICU inpatientS. pneumoniae S. pneumoniae S. pneumoniaeM. pneumoniae M. pneumoniae S. aureus (CA-MRSA)H. influenzae C. pneumoniae Legionella sp.C. pneumoniae H. influenzae Gram-negative bacilliResp. viruses Legionella sp. H. Influenzae Aspiration pneumonia Resp. viruses File TM. Lancet 2003 Vardakas KZ Eur Respir J 2009
  • 18. HAP-VAP Incidence: 5-10 cases/1,000 admitted patients - increasing 6-20 folds in mechanically ventilated pts - VAP incidence: 20%, 10-15 cases/1,000 days of MV Prolonged LOS,increased healthcarecosts, and a 15–45%attributable mortality Hortal J, Giannella M, and Bouza E Intensive Care Med 2009 Esperatti E et al. Am J Respir Crit Care Med 2010 Torres and Rello Am J Respir Crit Care Med 2010
  • 19. HAP-VAPCausative pathogens of HAP and VAP in the SENTRYAntimicrobial Surveillance Programme, 2004-2008 (NorthAmerica, Europe, Latin America) N=7,496 HAP VAP S. aureus 26.6% (MRSA 59%) 19.5% (MRSA 51%) P. aeruginosa 22.4% 26.6% Enterobacter spp. 7.5% 7% Klebsiella spp. 10.5% 10.2% Serratia spp. 4.1% 4.1% A. baumannii 8.3% 14.3% CAP pathogens* 2.6% 4.1%*S. pneumoniae, H. influenzae, M. catarrhalis Jones RN Clin Infect Dis 2010
  • 20. Origins of HCAP CAP ATS 1996 HAP, VAPMorin and Hadler Community onset MRSA bacteremiaJ Infect Dis 2001Friedman et al. MDR bloodstream infectionsAnn Intern Med 2002Tacconelli et al. Community onset MRSA bacteremiaJAC 2004 HCAP ATS guidelines 2005
  • 21. Definition of HCAP Contact with the health systemPrior Residence in a Chronic IV/wound care athospitalization nursing home or hemodialysis homeand/or surgery LTCF Chemotherapy
  • 22. Epidemiology of HCAP patients Median age 64-81 years High rate of comorbidities (CHF, COPD,cerebrovascular disease) Poor functional status Risk factors for aspiration pneumonia Treatment restrictions CAP << HCAP = HAP Kollef et al. Chest 2005; Carratala et al. Arch Intern Med 2007; Shindo et al Chest 2009; Venditti et al. Ann Intern Med 2009; Chalmers et al Clin Infect Dis 2011; Jung et al. BMC Infect Dis 2011
  • 23. The concept of HCAP HCAP presents an etiologicalpattern similar to that of HAP Failure to cover MDR pathogens leads to inadequateinitial antimicrobial coverage and accounts for excessmortality HCAP patients should be identified and treated withinitial broad-spectrum antibiotic therapy
  • 24. NHAP Pneumonia is the second most common infection innursing home residents High mortality (15-60%) and common cause forhospital transfer Functional status may play a role in: -Risk of drug resistant pathogen -Mortality Mylotte JM Drugs Aging 2006 El-Solh et al. AA Clin Infect Dis 2004
  • 25. Infezioni correlate a catetere vascolare
  • 26. CVC-related blodstream infections
  • 27. CVC-related blodstream infections
  • 28. DEFINIZIONI di BATTERIEMIA correlata a CVC (CDC 2002) FEBBRE + SEGNI e SINTOMI di SIRS + in ASSENZA di ALTRE FONTI d’INFEZIONE ISOLAMENTO dello STESSO MICRORGANISMO in EMOCOLTURA da VASO PERIFERICO e in COLTURA SEMI-QUANTITATIVA del CATETERE IN ASSENZA di DATI MICROBIOLOGICI: DEFERVESCENZA /SCOMPARSA DEI SINTOMI ENTRO 24 h dalla RIMOZIONE del CATETERE VENOSO EMOCOLTURE QUANTITATIVE (eseguite in contemporanea) POSITIVE sia da CATETERE VASCOLARE che da VASO PERIFERICO, con CRESCITA da 5 a 10 VOLTE SUPERIORE nel SANGUE PRELEVATO da CATETERE ovvero con CRESCITA SIGNIFICATIVAMENTE PIU’ RAPIDA da CVC rispetto a VP.
  • 29. LCBI - Laboratory-confirmed bloodstream infectionLCBI must meet at least 1 of the following criteria:1. Patient has a recognized pathogen cultured from 1 or more blood culturesandorganism cultured from blood is not related to an infection at another site.2. Patient has at least 1 of the following signs or symptoms: fever (>38°C),chills, or hypotensionandsigns and symptoms and positive laboratory results are not related to aninfection at another siteandcommon skin contaminant (ie, diphtheroids [Corynebacterium spp], Bacillus[not B anthracis] spp, Propionibacterium spp, coagulase-negativestaphylococci [including S epidermidis], viridans group streptococci,Aerococcus spp, Micrococcus spp) is cultured from 2 or more blood culturesdrawn on separate occasions.
  • 30. BATTERIEMIA CORRELATA A CATETERE VENOSO- DIAGNOSITempo differenziale di positività della coltura da catetere rispetto alla coltura da vena periferica ≥120 min.: - sensibilità 81% e specificità 92% per cateteri a breve termine - sensibilità 93% e specificità 75% per cateteri a lungo termine Ann Intern Med 2004; 140: 18-25
  • 31.  Most CRBSIs emanate from the insertion site, hub, or both. Forlong-term catheters—particularly tunneled catheters— the catheterhub is a prominent source of microbes causing bloodstreaminfection. the 4 groups of microbes that most commonly cause CRBSIassociated with percutaneously inserted, noncuffed cathetersare: coagulase- negative staphylococci, S. aureus, Candida species,and enteric gram-negative bacilli.For surgically implanted catheters and peripherally insertedCVCs, they are coagulase-negative staphylococci, enteric gram-negative bacilli, S. aureus, and P. aeruginosa [8].
  • 32.  Semiquantitative (roll plate) or quantitative catheter culturetechniques (luminal flushing or sonication methods) are the mostreliable diagnostic methodologies and have much greater specificitythan qualitative broth cultures. A recently inserted catheter (i.e., one that had been indwelling for<14 days) is most commonly colonized from a skin microorganismalong the external surface of the catheter. Thus, the roll-plate methodhas high sensitivity. Intraluminal spread of microbes from the catheter hub into thebloodstream is increasingly important for long-term catheters (i.e.,those that have been indwelling ≥14 days).
  • 33.  Blood cultures that are positive for S. aureus, coagulase-negative staphylococci, or Candida species, in the absenceof other identifiable sources of infection, should increase thesuspicion for CRBSI. Improved symptomatology within 24 h after catheterremoval suggests but does not prove that the catheter is thesource of infection.
  • 34. Although catheter colonization withaccompanying systemic signs of infection suggestscatheter- related infection, adefinitive diagnosis of CRBSI requires positivepercutaneous blood culture results with concordantmicrobial growth from the catheter tip or catheter-drawn cultures that meet the quantitative culture orDTP criteria.
  • 35. Definizioni di Sepsi, Sepsi Grave e Shock SetticoDa Consensus Conference ACCP/SCCM Bone RC, Balk RA, Cerra FB e al. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: Definitions for sepsis and organ failure and gudelines for the use of innovative therapies in sepsis. Chest 101: 1644-1655, 1992
  • 36. Infezione Sepsi ShockSepsi grave Settico Gravità in aumento della risposta sistemica allinfezione
  • 37. SIRS = sindrome della risposta infiammatoria sistemica Infezione/ Sepsi Shock SIRS Sepsi Settico Trauma Grave Risposta infiammatoria sistemica ad una moltitudine di insulti clinici severi manifestata da due o più delle seguenti condizioni: 1. Temperatura >38°C o <36°C. 2. Frequenza Cardiaca >90 battiti/min. 3. Frequenza respiratoria >20/min o PaCO2 <32 mm Hg. 4. Conta dei leucociti >12.000/mm3 o <4.000/mm3 o neutrofili immaturi (cellule "a bande") >10%.Bone RC, Chest 101: 1644-1655, 1992
  • 38. Sepsi. Risposta infiammatoria sistemica Infezione/ Sepsi Shock SIRS Sepsi Settico Trauma Grave La risposta infiammatoria sistemica ad una infezione documentata. Le manifestazioni della sepsi associate allinfezione sono le stesse definite per la SIRS (due o più). Deve essere accertato se tali manifestazioni sono una risposta sistemica diretta alla presenza di un processo infettivo e rappresentano unalterazione acuta rispetto alle condizioni di base in assenza di altre ragioni conosciute responsabili di queste anomalie.Bone RC, Chest 101: 1644-1655, 1992
  • 39. Batteriemia Altro Fungemia TraumaInfezione Sepsi SIRS Viremia Ustioni Altro Pancreatite
  • 40. Sepsi Grave Infezione/ Sepsi Shock SIRS Sepsi Settico Trauma Grave Sepsi (SIRS) associata a disfunzione d’organo, ipoperfusione o ipotensione. L’ipoperfusione e le alterazioni della perfusione possono includere acidosi lattica, oliguria e alterazioni acute dello stato mentale.Bone RC Chest 101: 1644-1655, 1992
  • 41. Ipotensione Sepsi (SIRS) – Indotta. Pressione sistolica < 90 mmHg o una riduzione  40 mmHg rispetto al basale in assenza di altre cause di ipotensione.Bone RC, Balk RA, Cerra FB e al. American College of Chest Physicians/Society of Critical Care Medicine ConsensusConference: Definitions for sepsis and organ failure and gudelines for the use of innovative therapies in sepsis.Chest 101: 1644-1655, 1992
  • 42. Shock settico Infezione/ Sepsi Shock SIRS Sepsi Settico Trauma GraveSottogruppo delle Sepsi Gravi e delle ipotensioni Sepsi (SIRS)- indotteche, malgrado adeguata reintegrazione di liquidi mostrano segni diipoperfusione che può includere acidosi lattica, oliguria o alterazioneacuta dello stato mentale.I pazienti che ricevono agenti inotropi o vasopressori possono nonessere più ipotesi al momento in cui manifestano alterazioni delleperfusione o disfunzione dorgano, tuttavia dovrebbero ancora essereclassificati come Shock Settico (SIRS).Bone RC, Balk RA, Cerra FB e al. American College of Chest Physicians/Society of Critical Care MedicineConsensus Conference: Definitions for sepsis and organ failure and gudelines for the use of innovative therapiesin sepsis. Chest 101: 1644-1655, 1992
  • 43. Sindrome da Disfunzione dOrgano Multipla (MODS) Presenza di alterazione della funzione dorgano in un paziente acuto tale che lomeostasi non possa essere mantenuta senza intervento.Bone RC, Balk RA, Cerra FB e al. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: Definitionsfor sepsis and organ failure and gudelines for the use of innovative therapies in sepsis. Chest 101: 1644-1655, 1992
  • 44. Levy et al, Crit Care Med 2003
  • 45. Levy et al, Crit Care Med 2003
  • 46. Objective: To define the frequency and prognosticimplications of SIRS criteria in critically ill patientshospitalized in European ICUsDesign and setting: Cohort, multicentre, observationalstudy of 198 ICUs in 24 European countries.Patients and interventions: All 3,147 new adult admissionsto participating ICUs between 1 and 15 May 2002 wereincluded. Data were collected prospectively, with commonSIRS criteria.
  • 47. DiscussionICU outcome did not differ according to individual SIRS criteria at admission,and the maximum number of SIRS criteria did not differ according to the site ofinfection or stage of sepsisThere was, however, a higher frequency of three or four SIRS criteria vs. twoSIRS criteria in infected then in non-infected patients. All infected patients had at least two SIRS criteriaAs the number of SIRS criteria at the time of admission increased, mortalityincreased in patients without infections and also for those patients withinfections at the various grades of sepsis.It is clear from this study and others that SIRS has a great prognosticimportance in predicting infections, length of stay, severity of disease, organfailure and outcome.
  • 48. GRAZIE PER L’ATTENZIONE