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Infezioni batteriche nel cirrotico



Giovanni Battista Gaeta
Chair of Infectious Diseases
Viral Hepatitis Unit – Second University of Naples
Clinical case history
•69-year-old woman

•Liver transplantation in 1991 for HCV related cirrhosis

•HCV reinfection of the graft and cirrhosis

•First episode of decompensation (ascites) in January 2012

• Type II Diabetes Mellitus treated with Insulin

•Chronic Renal Insufficiency (Cr Clearance ~ 40 mL/m)

• Hypertension treated with calcium antagonists
On Admission (Dec, 9, 2012)
•Body temperature    37.5 °C

•Hypotension (100/60 mmHg)

•Tachycardia (90 b/min)

• Mild jaundice

•Moderate Ascites

•Edema of lower extremities

•Grade II Encephalopathy
December 2012
      2 days prior to admission

•Mild elevation of body temperature

• Mild diarrhea

•Nausea

•Asthenia

• Oliguria

•Confusion and Sleepiness
Infections in cirrhotics: dimension


   20-50% of cirrhotics admitted to hospital
   have an infection

 (Including patients who acquire hospital infection)




Fernandez, Hepatology 2002; Arvaniti, Gastroenterology 2010; Fernandez, Hepatology 2012
Diagnosi di infezione batterica
                  in cirrotici al ricovero
                                             Pazienti con cirrosi:
   N : 536                                   404 ricoveri in 361 pazienti

                                 %                                         %
 Urinary tract                  26.1        Urinary tract                  41
 SBP                            23.9        Ascites                        23
 Bacteremia                     18.5
 Pneumonia                      16.3        Bacteremia                     21
 Soft tissue                     4.3        Pneumonia                      17
 Other                          10.9        Soft tissue                    -
Multicenter Italian Database, unpublished             Borzio et al, 2001
Risk of death in patients with and without infection
(in studies reporting complete information on mortality)




                Arvaniti V. et al. Gastroenterology 2010 ; 139 : 1246-1256
Mortality of patients with cirrhosis after infection

Parameter                   N° of studies   N° of pataients   Median Mortality
Total mortality                  178             11.987             38 %
- 1 mo                           51              2449               30.3%
- 3 mo                           27              1439               44 %
- 12 mo                          40              2154               63 %
1978-1999 total mortality        89              4890              47.4 %
- 1 mo                           21               737              37.3 %
- 3 mo                           18               578               43 %
- 12 mo                          25               758               69.7%
2000-2009 total mortality        89              7132               32.3%
- 1 mo                           29              1621               26 %
- 3 mo                            9               681               44%
- 12 mo                          14               634               60%


                       Arvaniti V. et al. Gastroenterology 2010 ; 139 : 1246-1256
Three-month probability of survival of patients with
  cirrhosis according to the cause of renal failure




                         Martin-Llahi. M. et al. Gastroenterology 2010
Main laboratory data
WBC              8400/ µL      Lipase           28 U/L
Neutrophilis     5300/ µL      GGT              121 U/L
HGB              10.8 g/dL     Uric Acid        10.3 mg/dL
Platelets        129000 µL     Cholinesterase   3876 U/L
PT (INR)         1.1           Glucose          172 mg/dL
Albumin          2.8 g/dL      Alpha            0.7 ng/mL
Tot. Protein     7.0 g/dL      fetoprotein
AST              37 U/L        CRP              6 mg/dL
ALT              27 U/L        ESR (1h)         46 mm
Tot. Bilirubin   3.5 mg/dL     Sodium           128 mEq/L
Alk Phos         523 U/L       Potassium        5.0 mEq/L
LDH              456 U/L       Procalcitonin    3.0 ng/mL


Creatinine       2.5 mg/dL
Cr clearance     20.6 mL/min
Urinalysis

Diuresis 600 ml/24h

Natriuria 38.7 mEq/24h

Cloruria 31.5 mEq/24h

Kaliuria 25.0 mEq /24h

Microalbuminuria (106 mg/24h)

>35 Leukocytes x field

10 RBC x field
Microbiological and Image

 • Cultures of blood, urine, ascites

 • Neutrophil count in ascites

 • Chest Xray

 •Abdominal US
The flow chart of antibiotic treatment


 Infection considered

                   Microbiological investigations


Empirical treatment


                      POS (50%)           NEG (50%)

               Modify tx    Response-based tx
Classification of bacterial infections

Community acquired
the diagnosis of infection is made within 48 hours of hospitalization and the patient did
not fulfill the criteria for HCA infection


Health Care Associated
the diagnosis is made within 48 hours of hospitalization in patients with any of the
following criteria: (1) had attended a hospital or a hemodialysis clinic, or had received
intravenous chemotherapy during the 30 days before infection; or (2) were hospitalized
for at least 2 days, or had undergone surgery during the 180 days before infection; or (3)
had resided in a nursing home or a long-term care
facility.

Hospital Acquired
the diagnosis of infection is made after more than 48 hours of hospital stay
Case discussion

                           Therapy
  • Plasma expansion ( saline, albumin )

  • Antibiotic therapy :


  During the previous six months the patient had received :
  • Quinolones
  • 3rd generation cephalosporins
      given by GP for UTI and upper respiratory infection


  Therapy was started with Meropenem 500mg/12h
  (according to creatinine clearance) and continued for 10
  days
Systemic antibiotic exposure is a risk factor
     for bacterial resistance in cirrhosis

169 infectious episodes in 115 patients

 70 culture positive infections   33 (47%) antibiotic resistant strains

Independent risk factors for resistance

Systemic antibiotics in the previous 30 days
                            OR 13.5 (95% CI = 2.6 – 71.6)

Nosocomial infection
                           OR 4.2 (95% CI = 1.4 -12.5)

Non-adsorbable antibiotics
                             OR 0.4 (95% CI = 0.04 -2.8)

                           Tandon et al. Clin Gastroenterol Hepatol 2012; 10:1291-98
Prevalence of E.coli with resistance
          to quinolones

                   Norfloxacin +     Norfloxacin -     tot

Novella 1997       9/10 (90%)        4/11 (36%)        13/21

Campillo 1998      3/23 (13%)        8/42 (19 %)       11/65

Fernandez 2002    24/37 (65%)        39/135 (29%)      63/172

Cereto 2003       9/13 (69 %)        3/34 (31 %)       12/47




                 3rd generation cephalosporin susceptible
Incidence of 3rd-generation resistant episodes of SBP




                        Ariza et al, J Hepatol 2012; 56 : 825–832
Risk factors for SBP caused by a 3rd-generation
    cephalosporin-resistant microorganism




                      Ariza et al, J Hepatol 2012; 56 : 825–832
Prevalence of resistant strains


Community acquired          7 – 33%


Health care associated      21 – 50%


Hospital acquired           40 – 80%



                         Merli, 2012; Ariza 2012
Prevalence of gram positive/gram negative
                 bacteria

   %




                        Merli, Clin Gastroenterol Hepatol 2010
Prevalence of resistance to ESBL among E. coli isolates from
                 bacteremias (EARSS 2005)




      No data

       < 1%

       1-5%

       5-10%

      10-25%

       >25%
Case discussion

    Microbiology, US and chest Xray

  •Neutrophil count in ascites : 160/µl

  •Ascites culture: sterile

  • E.coli was isolated from blood and urine

  •Chest Xray: no inflammatory images

  •Abdominal US: mild ascites; no nodules
Le infezioni nel cirrotico: aspetti clinici - Gastrolearning®
Quale terapia per le infezioni sostenute da
                ESBL+?

 Antibiotici                          ESBLs
 Cefalosporine di terza generazione     –
 Cefepime                               –
 Fluorochinoloni                       +/–
 Piperacillina/tazobactam              +/–
 Carbapenemici                         +++
 Tigeciclina                           ++
 Colistin                       (for carbapenem resistance)
Risk Factors of Infections by Multiresistant Bacteria in
                        Cirrhosis



                                                      *

                                                      *
                                                      *
                                                      *




                                     Fernandez, Hepatology 2012
ANTIBIOTIC THERAPY STOPPED ON DAY 10
Time course of bilirubin, creatinine, wbc, neutrophil and temperature
   n/µL




                                                  TC°
                           Days                         Days
                   mg/dL




                                        Days

          Diuresis (ml/d)         600 1200 1650
Caratteristiche cliniche delle
       Caratteristiche cliniche delle
     infezioni batteriche nel cirrotico
     infezioni batteriche nel cirrotico
    Deterioramento                                      Segni e sintomi tipici di
    della funzione                                      infezione
    epatica
                                                                  Febbre
            Ittero                                          (assente nel 30-50%)
       Creat. clearance                                    Leucocitosi neutrofila
         Encefalopatia                                          (relativa!)
     Possibile esordio grave: febbre, coagulopatia, coma
Cazzaniga, J Hepatol 2009; 51:475-482; Wong, Gut 2005; 54:718-25; Fasolato, Hepatology 2007; 45:223-2
SIRS criteria: less diagnostic accuracy in cirrhosis ?


        SIRS criteria
                                                  In cirrhosis

                                          • Hyperdynamic circulation
                                          leads to tachycardia

                                          • Beta-blockers cause a
                                          reduced heart rate

                                          • Hypersplenism decreases
                                          white blood cell count




Cazzaniga M,. J Hepatol 2009;51:475–482. Thabut D, Hepatology 2007;46:1872–1882.
Il paziente con cirrosi è immunocompromesso




                  Bonnel, Clinical Gastroenterol Hepatol 2011
Mechanisms of bacterial (and their products)
              translocation
                          Portal hypertension
                          Splancnic vasodilation



    Disruption of                              Increased sympathetic
    intestinal barrier                          nerve activity


                                            Intestinal hypomobility and
       permeability
                                            germ overgrow



                         Translocation
  Transolacation is associated to increased plasma levels of cytokines
  (TNFα, IL-6,), MAP-K,
“Tempesta citochinica” provocata
     da prodotti batterici




                        From: Wong, Gut 2006
Plasma levels of TNFα in patients with cirrhosis
             with and without SBP

                        (pg/ml)
                           * = P < 0.001 vs cirrhosis without SBP
                                                        *




              M. Navasa et al. Hepatology 1998 ; 27 : 1227-1232.
Bacterial translocation becomes clinically significant
    when it produces SBP, bacteremia, post-surgical
    infections



Bacterial peptides (Porins; HSP60;) are present in the
ascites of afebrile patients with increased TNFα and IFN-
gamma concentrations
               Cano et al. J Mol Med, 2010, e-Pub
SBP –     A chronic inflammatory disease with flares?



  bacterial translocation
                              bacterial products which cause:
   cytokine production
                                  inflammatory response
  nitric oxide production




                            SBP                           SBP

                                              time
Acute-on-chronic Liver Failure
    Patients’ features at enrollement




       R. Moreau et al. (Canonic study) Gastroenterology 2013 (in press)
Renal failure in cirrhosis

Leucocyte count in patients with and without ACLF

           ________ Patients with no prior decompensation of cirrhosis
           ___ _ ___ Patients with prior decompensation of cirrhosis




               ACLF




             NO ACLF




                     R. Moreau et al. (Canonic study) Gastroenterology 2013 (in press)
C reactive protein values in patients with and without ACLF


    * = p < 0.01 versus No ACLF                                            *

    # = p < 0.05 versus No ACLF

                       *    *                *           *
                                        #                      *




                       R. Moreau et al. (Canonic study) Gastroenterology 2013 (in press)
Mechanisms for sepsis-induced organ failure

                                                          microorganism-associated
                                                          molecular patterns (MAMPs)

 PRRs, pattern recognition receptors




PAI-1, plasminogen activator inhibitor
APC, activated protein C
TF, tissue factor.                       From: Gustot et al, HEPATOLOGY 2009;50:2022-2033
Summary & Conclusions
Bacterial infection is one of the most frequent cause of
decompensation and death in cirrhosis

Immune defects, mainly acquired but also genetic,
and bacterial translocation are the main mechanisms
involved in its pathogenesis

The prevalence of infections is likelely to be
underestimated in clinical practice due to the reduced
diagnostic capacity of the standard diagnostic criteria

Gram positive and MDR bacteria are increasing
etiologic agents

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Le infezioni nel cirrotico: aspetti clinici - Gastrolearning®

  • 1. Infezioni batteriche nel cirrotico Giovanni Battista Gaeta Chair of Infectious Diseases Viral Hepatitis Unit – Second University of Naples
  • 2. Clinical case history •69-year-old woman •Liver transplantation in 1991 for HCV related cirrhosis •HCV reinfection of the graft and cirrhosis •First episode of decompensation (ascites) in January 2012 • Type II Diabetes Mellitus treated with Insulin •Chronic Renal Insufficiency (Cr Clearance ~ 40 mL/m) • Hypertension treated with calcium antagonists
  • 3. On Admission (Dec, 9, 2012) •Body temperature 37.5 °C •Hypotension (100/60 mmHg) •Tachycardia (90 b/min) • Mild jaundice •Moderate Ascites •Edema of lower extremities •Grade II Encephalopathy
  • 4. December 2012 2 days prior to admission •Mild elevation of body temperature • Mild diarrhea •Nausea •Asthenia • Oliguria •Confusion and Sleepiness
  • 5. Infections in cirrhotics: dimension 20-50% of cirrhotics admitted to hospital have an infection (Including patients who acquire hospital infection) Fernandez, Hepatology 2002; Arvaniti, Gastroenterology 2010; Fernandez, Hepatology 2012
  • 6. Diagnosi di infezione batterica in cirrotici al ricovero Pazienti con cirrosi: N : 536 404 ricoveri in 361 pazienti % % Urinary tract 26.1 Urinary tract 41 SBP 23.9 Ascites 23 Bacteremia 18.5 Pneumonia 16.3 Bacteremia 21 Soft tissue 4.3 Pneumonia 17 Other 10.9 Soft tissue - Multicenter Italian Database, unpublished Borzio et al, 2001
  • 7. Risk of death in patients with and without infection (in studies reporting complete information on mortality) Arvaniti V. et al. Gastroenterology 2010 ; 139 : 1246-1256
  • 8. Mortality of patients with cirrhosis after infection Parameter N° of studies N° of pataients Median Mortality Total mortality 178 11.987 38 % - 1 mo 51 2449 30.3% - 3 mo 27 1439 44 % - 12 mo 40 2154 63 % 1978-1999 total mortality 89 4890 47.4 % - 1 mo 21 737 37.3 % - 3 mo 18 578 43 % - 12 mo 25 758 69.7% 2000-2009 total mortality 89 7132 32.3% - 1 mo 29 1621 26 % - 3 mo 9 681 44% - 12 mo 14 634 60% Arvaniti V. et al. Gastroenterology 2010 ; 139 : 1246-1256
  • 9. Three-month probability of survival of patients with cirrhosis according to the cause of renal failure Martin-Llahi. M. et al. Gastroenterology 2010
  • 10. Main laboratory data WBC 8400/ µL Lipase 28 U/L Neutrophilis 5300/ µL GGT 121 U/L HGB 10.8 g/dL Uric Acid 10.3 mg/dL Platelets 129000 µL Cholinesterase 3876 U/L PT (INR) 1.1 Glucose 172 mg/dL Albumin 2.8 g/dL Alpha 0.7 ng/mL Tot. Protein 7.0 g/dL fetoprotein AST 37 U/L CRP 6 mg/dL ALT 27 U/L ESR (1h) 46 mm Tot. Bilirubin 3.5 mg/dL Sodium 128 mEq/L Alk Phos 523 U/L Potassium 5.0 mEq/L LDH 456 U/L Procalcitonin 3.0 ng/mL Creatinine 2.5 mg/dL Cr clearance 20.6 mL/min
  • 11. Urinalysis Diuresis 600 ml/24h Natriuria 38.7 mEq/24h Cloruria 31.5 mEq/24h Kaliuria 25.0 mEq /24h Microalbuminuria (106 mg/24h) >35 Leukocytes x field 10 RBC x field
  • 12. Microbiological and Image • Cultures of blood, urine, ascites • Neutrophil count in ascites • Chest Xray •Abdominal US
  • 13. The flow chart of antibiotic treatment Infection considered Microbiological investigations Empirical treatment POS (50%) NEG (50%) Modify tx Response-based tx
  • 14. Classification of bacterial infections Community acquired the diagnosis of infection is made within 48 hours of hospitalization and the patient did not fulfill the criteria for HCA infection Health Care Associated the diagnosis is made within 48 hours of hospitalization in patients with any of the following criteria: (1) had attended a hospital or a hemodialysis clinic, or had received intravenous chemotherapy during the 30 days before infection; or (2) were hospitalized for at least 2 days, or had undergone surgery during the 180 days before infection; or (3) had resided in a nursing home or a long-term care facility. Hospital Acquired the diagnosis of infection is made after more than 48 hours of hospital stay
  • 15. Case discussion Therapy • Plasma expansion ( saline, albumin ) • Antibiotic therapy : During the previous six months the patient had received : • Quinolones • 3rd generation cephalosporins given by GP for UTI and upper respiratory infection Therapy was started with Meropenem 500mg/12h (according to creatinine clearance) and continued for 10 days
  • 16. Systemic antibiotic exposure is a risk factor for bacterial resistance in cirrhosis 169 infectious episodes in 115 patients 70 culture positive infections 33 (47%) antibiotic resistant strains Independent risk factors for resistance Systemic antibiotics in the previous 30 days OR 13.5 (95% CI = 2.6 – 71.6) Nosocomial infection OR 4.2 (95% CI = 1.4 -12.5) Non-adsorbable antibiotics OR 0.4 (95% CI = 0.04 -2.8) Tandon et al. Clin Gastroenterol Hepatol 2012; 10:1291-98
  • 17. Prevalence of E.coli with resistance to quinolones Norfloxacin + Norfloxacin - tot Novella 1997 9/10 (90%) 4/11 (36%) 13/21 Campillo 1998 3/23 (13%) 8/42 (19 %) 11/65 Fernandez 2002 24/37 (65%) 39/135 (29%) 63/172 Cereto 2003 9/13 (69 %) 3/34 (31 %) 12/47 3rd generation cephalosporin susceptible
  • 18. Incidence of 3rd-generation resistant episodes of SBP Ariza et al, J Hepatol 2012; 56 : 825–832
  • 19. Risk factors for SBP caused by a 3rd-generation cephalosporin-resistant microorganism Ariza et al, J Hepatol 2012; 56 : 825–832
  • 20. Prevalence of resistant strains Community acquired 7 – 33% Health care associated 21 – 50% Hospital acquired 40 – 80% Merli, 2012; Ariza 2012
  • 21. Prevalence of gram positive/gram negative bacteria % Merli, Clin Gastroenterol Hepatol 2010
  • 22. Prevalence of resistance to ESBL among E. coli isolates from bacteremias (EARSS 2005) No data < 1% 1-5% 5-10% 10-25% >25%
  • 23. Case discussion Microbiology, US and chest Xray •Neutrophil count in ascites : 160/µl •Ascites culture: sterile • E.coli was isolated from blood and urine •Chest Xray: no inflammatory images •Abdominal US: mild ascites; no nodules
  • 25. Quale terapia per le infezioni sostenute da ESBL+? Antibiotici ESBLs Cefalosporine di terza generazione – Cefepime – Fluorochinoloni +/– Piperacillina/tazobactam +/– Carbapenemici +++ Tigeciclina ++ Colistin (for carbapenem resistance)
  • 26. Risk Factors of Infections by Multiresistant Bacteria in Cirrhosis * * * * Fernandez, Hepatology 2012
  • 27. ANTIBIOTIC THERAPY STOPPED ON DAY 10 Time course of bilirubin, creatinine, wbc, neutrophil and temperature n/µL TC° Days Days mg/dL Days Diuresis (ml/d) 600 1200 1650
  • 28. Caratteristiche cliniche delle Caratteristiche cliniche delle infezioni batteriche nel cirrotico infezioni batteriche nel cirrotico Deterioramento Segni e sintomi tipici di della funzione infezione epatica Febbre Ittero (assente nel 30-50%) Creat. clearance Leucocitosi neutrofila Encefalopatia (relativa!) Possibile esordio grave: febbre, coagulopatia, coma Cazzaniga, J Hepatol 2009; 51:475-482; Wong, Gut 2005; 54:718-25; Fasolato, Hepatology 2007; 45:223-2
  • 29. SIRS criteria: less diagnostic accuracy in cirrhosis ? SIRS criteria In cirrhosis • Hyperdynamic circulation leads to tachycardia • Beta-blockers cause a reduced heart rate • Hypersplenism decreases white blood cell count Cazzaniga M,. J Hepatol 2009;51:475–482. Thabut D, Hepatology 2007;46:1872–1882.
  • 30. Il paziente con cirrosi è immunocompromesso Bonnel, Clinical Gastroenterol Hepatol 2011
  • 31. Mechanisms of bacterial (and their products) translocation Portal hypertension Splancnic vasodilation Disruption of Increased sympathetic intestinal barrier nerve activity Intestinal hypomobility and permeability germ overgrow Translocation Transolacation is associated to increased plasma levels of cytokines (TNFα, IL-6,), MAP-K,
  • 32. “Tempesta citochinica” provocata da prodotti batterici From: Wong, Gut 2006
  • 33. Plasma levels of TNFα in patients with cirrhosis with and without SBP (pg/ml) * = P < 0.001 vs cirrhosis without SBP * M. Navasa et al. Hepatology 1998 ; 27 : 1227-1232.
  • 34. Bacterial translocation becomes clinically significant when it produces SBP, bacteremia, post-surgical infections Bacterial peptides (Porins; HSP60;) are present in the ascites of afebrile patients with increased TNFα and IFN- gamma concentrations Cano et al. J Mol Med, 2010, e-Pub
  • 35. SBP – A chronic inflammatory disease with flares? bacterial translocation bacterial products which cause: cytokine production inflammatory response nitric oxide production SBP SBP time
  • 36. Acute-on-chronic Liver Failure Patients’ features at enrollement R. Moreau et al. (Canonic study) Gastroenterology 2013 (in press)
  • 37. Renal failure in cirrhosis Leucocyte count in patients with and without ACLF ________ Patients with no prior decompensation of cirrhosis ___ _ ___ Patients with prior decompensation of cirrhosis ACLF NO ACLF R. Moreau et al. (Canonic study) Gastroenterology 2013 (in press)
  • 38. C reactive protein values in patients with and without ACLF * = p < 0.01 versus No ACLF * # = p < 0.05 versus No ACLF * * * * # * R. Moreau et al. (Canonic study) Gastroenterology 2013 (in press)
  • 39. Mechanisms for sepsis-induced organ failure microorganism-associated molecular patterns (MAMPs) PRRs, pattern recognition receptors PAI-1, plasminogen activator inhibitor APC, activated protein C TF, tissue factor. From: Gustot et al, HEPATOLOGY 2009;50:2022-2033
  • 40. Summary & Conclusions Bacterial infection is one of the most frequent cause of decompensation and death in cirrhosis Immune defects, mainly acquired but also genetic, and bacterial translocation are the main mechanisms involved in its pathogenesis The prevalence of infections is likelely to be underestimated in clinical practice due to the reduced diagnostic capacity of the standard diagnostic criteria Gram positive and MDR bacteria are increasing etiologic agents