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					INTRAVASCULAR INFECTION

 INFECTIVE ENDOCARDITIS

                  Dr M Ballal
                     KMC-IC
                   14/2/2011
               INFECTIVE ENDOCARDITIS
   Definition
   Epidemiology
   Patho physiology
   Classification
   Risk groups & pre-disposing conditions
   Microbiology
   Clinical features & complications
   Diagnosis
   Treatment
   Prevention
Anatomy of Normal Heart
   Definition: Inflammation of the membrane
   lining the chambers of the heart & covering
            the cusps of various valves



                      Epidemiology
 2-5 cases/100,000 gen population/year (USA)
 1-2 cases/ 1000 pediatric hospital admissions(USA)
 Male: female ratio – 2:1
 Among the i.v drug users, incidence is
  150-2000/ 100,000 persons
>preantibiotic era-1920s more in people less than30yrs of
  age
> Now common in people > 50 yrs of age
         PREDISPOSING FACTORS
Valvular heart disease
 Rheumatic heart disease
 Congenital heart disease
 Mitral valve prolapse
 Prosthetic devices( valves, pace
 makers)
 Intravenous drug use- current
 epidemic among youngsters
                PATHO PHYSIOLOGY
A high-velocity flow through a stenotic or
 incompetent valve or an abnormal communication
 between systemic and pulmonary circulations


turbulence downstream from the opening.


damages or denudes the endothelium, to which
 platelets and fibrin adhere,


small, sterile thrombus formation(non bacterial thrombotic
 endocarditis – (NBTE))
In addition, indwelling intravascular catheters in the
 right heart may directly traumatize the endocardium or
 valvular endothelium.



Circulating bacteria and inflammatory cells adhere to
 and grow in these thrombi, forming an infected
 vegetation.
   Circulating bacteria/Transient bacteremia
Site               Activity or Procedure     Microorganisms
Oral Cavity        Brushing Teeth, Chewing   α-hemolytic streptococci
                   Dental extraction         (Viridans group),
                   Periodontal surgery       anaerobic streptococci,
                                             dipththeroids
Skin               Intravenous or arterial   Staphylococci (S.
                   catheters; Chronic skin   epidermidis, S. aureus),
                   lesions
                                             Streptococci
Respiratory        Bronchoscopy              Streptococci, aerobic
                                             gram neg rods, S.
                                             epidermidis
Gastrointestinal   Colonoscopy               Streptococci, diptheroids,
                                             Neisseria, S. epidermidis
                                             Aerobic gram negative
                                             rods, streptococci,
                                             Bacteroides species
Urinary Tract      Cystoscopy, Transurethral Aerobic gram negative
                   prostatic resection       rods, diptheroids,
                                             Streptococci
Valvular endothelium                      Mucus membranes



  platelet-fibrin                               Trauma
  deposition

                                               Bacteremia
      NBTE



                          Adherence


                          Colonization


                       Vegetation = Hallmark
Predilection sites for pathogens:
 Non drug abusers: involves previously abnormal aortic
  or Mitral valve
 Injection drug abusers: both previously abnormal left
  heart valves and also normal tricuspid valve
Infective Endocarditis
 Typically involves the valves
    May involve all structures of the heart
      Chordae tendinae
      Sites of shunting

      Mural lesions

    Infection of vascular shunts, by strict definition, is endarteritis,
     but lesion is the same
 Majority of cases caused by streptococcus,
  staphylococcus, enterococcus, or fastidious gram
  negative cocco-bacillary forms
Infective Endocarditis
   Gram negative organisms
      P. aeruginosa most common
      HACEK - slow growing, fastidious organisms that
       may need 3 weeks to grow out of culture
         Haemophilus sp.
         Actinobacillus
         Cardiobacterium
         Eikenella
         Kingella
Major etiological agents of infective
endocarditis:
       Native valve              Oral streptococci
                                   Enterococci
                                  Staph aureus
                                      CONS
                             Gram negative enteric rods
                                 Fungi ( Candida)


 Intravenous drug misusers        Staph aureus
                                 Oral streptococci
                             Gram negative enteric rods
                                      CONS

  PROSTHETIC VALVE                     Cons
                                  Staph aureus
                             Gram negative enteric rods
                                 Oral streptococci
Infective Endocarditis
 Pediatric population
    The vast majority (75-90%) of cases after the neonatal period are
     associated with an underlying congenital abnormality
      Aortic valve

      Tetralogy of Fallot

    Risk of post-op infection in children with IE is 50%
 Microbiology
    Neonates: S. aureus, coag – staph, group B strep
    Older children: 40% strep, S. aureus
Infective Endocarditis
 Adult population
    Rheumatic Heart Disease
        20 – 25% of cases of IE in 1970’s & 80’s
        7 – 18% of cases in recent reported series
        Mitral site more common in women
        Aortic site more common in men
   Congenital Heart Disease
     10 – 20% of cases in young adults
     8% of cases in older adults
     bicuspid aortic valve (esp. in men>60)
Infective Endocarditis
   Intravenous Drug Abuse
      Risk is 2 – 5% per pt./year
      Tendency to involve right-sided valves
          Distribution in clinical series
            46 – 78% tricuspid

            24 – 32% mitral

            8 – 19% aortic

      Underlying valve normal in 75 – 93%
      S. aureus predominant organism (>50%, 60-70% of
       tricuspid cases)
Infective Endocarditis
 Intravenous Drug Abuse
    Increased frequency of gram negative infection such as P.
     aeruginosa & fungal infections
    High concordance of HIV positivity & IE (27-73%)
        HIV status does not in itself modify clinical picture
        Survival is decreased if CD4 count < 200/mm3
Infective Endocarditis
 Prosthetic Valve Endocarditis (PVE)
    10 – 30% of all cases in developed nations
    Cumulative incidence
        1.4 – 3.1% at 12 months
        3.2 – 5.7% at 5 years
    Early PVE – within 60 days
        Nosocomial (s. epi predominates)
    Late PVE – after 60 days
        Community (same organisms as NVE)
Encounter:
    Almost all bacteria and many fungi, when they get into the
       blood stream, can cause infective endocarditis.
      However, 80% of the cases are caused by oral streptococci or
       staphylococci.
      Relatively avirulent microorganisms derived from the normal
       flora of the body cause most cases of infective endocarditis.
      They gain access to the blood intermittently, as a result of
       minor trauma to the mucosa of the oropharynx,
       gastrointestinal tract or genitourinary tract.
      Such transient bacteremia usually occur without ill effects but
       they will lead to endocarditis in patients with an underlying
       cardiovascular lesion or with a suppressed immune system.
 As bacteria colonize the endocardium, they form
  vegetations which vary in size from tiny bodies to masses
  large enough to occlude valve orifices.
 They are soft and friable and only loosely attached to the
  endocardium.
 They break off easily to form arterial emboli.
 Fungal vegetations tend to be bulky, giving rise to large
  emboli.
                        CONSEQUENCES
Consequence of          Complication               Host Consequence
Vegetation

Persistent bacteremia   Seeding of distant sites   Joint, bone, organ
                                                   diseases,
                        Cytokine release           Constitutional
                                                   symptoms
Tissue destruction      Valvular insufficiency     Congestive heart failure
                        AV conduction              Heart blocks (1°, 2°or
                        abnormalities              3°)

Fragmentation           Peripheral emboli          CNS emboli, stroke, MI,
                                                   splenic/kidney infarcts
                                                   emboli to distant
                                                   extremities
Release of bacterial    Immune complex             Glomerulonephritis
antigen                 formation                  Roth spots (deposition
                                                   in choroid plexus)
                                                   Osler’s nodes
Infective endocarditis: Vegetations
 The bulk of the vegetation is an amorphous mass of fibrin and
  platelets containing colonies of microorganisms.

 There may be inflammatory cells attached to the vegetation.

 There are four consequences to the formation of this
  vegetation:

 Organisms within the vegetation are protected from
  antibodies, complement, and leukocytes
 Organisms within the vegetation are metabolically inactive,
    replicating at an unusually slow rate, rendering them relatively
    resistant to the action of many antimicrobials
   Healing is slow because macrophages and fibroblasts must spread
    through the vegetation and endothelial cells must grow over the
    surface.
   Emboli are generated when vegetations break off; these cause
    infarcts.
   Abscesses may develop by direct invasion of the valve rings of the
    heart near the vegetations.
   These are common with pyogenic cocci but rare with other
    organisms
                   Classification
 1. Old classification: based on the course of the
   disease.
Acute bacterial endocarditis (ABE)
  Infection caused by invasive pyogenic bacteria,
   such as Staphylococcus aureus,
  characterized by high fevers and a relatively short
   toxic course of a few days to weeks.
  Structurally normal or abnormal valves may be
   involved.
Subacute bacterial endocarditis (SABE)
  More indolent infection caused by less virulent
   bacteria
  characterized by lower fevers, prolonged
   constitutional symptoms of anorexia, weight loss, and
   night sweats lasting for several weeks.
  This is usually an infection of abnormal valvular
   surfaces.
2. Present classification: based on risk category
 Native-valve infective endocarditis
 Prosthetic-valve infective endocarditis
     Early ( within one year of valve replacement)
     Late ( after 1 year of valve replacement)
 Infective endocarditis in intravenous drug users;
 Nosocomial (or device) related infective endocarditis
  This may be expressed by describing the
  microorganism, type and site of the affected heart
  valve and any predisposing event
 Eg:- “α-hemolytic streptococcal native valve
  endocarditis”
                         or
  “Staphylococcal aureus tricuspid valve infective
  endocarditis in an intravenous drug user”.
             Microbiologic Etiology of IE

Organisms                              %
Staphylococci                          50
S.Aureus                               40
Coagulase negative                     10

Streptococci                           13
(Mostly strept viridans)

Enterococci                            10
Gram negative bacilli                  6
Fastidious GNB – HACEK group           1
Fungi                                  2
No growth                              10
Other including polymicrobial          10
         GRAM POSITIVE BACTERIA
Staphylococcus aureus
 Most common cause of IE
 Manifests as Acute bacterial endocarditis
 Often complicated by
  Myocardial abscesses,Purulent pericarditis,Valve ring
 abscesses
 High mortality due to fulminant infection
 Common cause of right sided IE in IV drug users


CONS (Coagulase negative staphylococci)
 Eg: S. epidermidis
 Most common cause of early prosthetic valve IE
Viridans streptococci
 2nd most common cause of IE
 Includes Steptococcus sanguis
                         bovis
                         mutans
 Manifests as SABE (Subacute bact endocarditis)
 High cure rate, low mortality
 Most common source: oral cavity


 Enterococci (E.faecalis, E.faecium)
 3rd most common cause of IE
 Usually manifests as SABE, but also can be fulminant
 High mortality due to intrinsic antibiotic resistance
            GRAM NEGATIVE BACTERIA
 HACEK group
  (Haemophilus, Actinobacillus, Cardiobacterium,
 Eikenella,Kingella)
 Normal flora of oropharynx
 Fastidious GNB
 Requires upto 2-3 weeks for isolation
 Presents as SABE with
    Large friable vegetations
    Frequent embolism
    Chronic heart failure.
Other Gram negative rods (ex:- Pseudomonas)
 Rare cause of IE
 Most cases in IV drug users
 Requires valve replacement for cure
 High mortality
Fungi
 Candida sp, Aspergillus sp
 Rare cause of IE
 Causes IE in
  i.v drug users
  prosthetic valve endocarditis
  pt receiving prolonged iv. Antibiotics &Total ParenteralNutrition
 Often requires valve replacement for cure.
         CULTURE NEGATIVE ENDOCARDITIS
5-15% of cases
Causes
 Prior antibiotic exposure
 Fastidious organism like
 Pyridoxal requiring Streptococci
 HACEK organism
 Bartonella henselae, Bartonella quintana
 Coxiella burnetti
 Trophyrema whipelli
1.Early prosthetic valve endocarditis is most commonly
    caused by
  Coagulase negative staphylococci
2.Late prosthetic valve endocarditis is commonly caused
    by
  Viridans streptococci & HACEK bacteria
3.Right sided endocarditis in a I.V drug user is
   most commonly caused by
  Staphylococcus aureus
  Also caused by
  Pseudomonas aeruginosa, Candida
4. Most common causative agent of IE
   Staphylococcus aureus
(Streptococci used to be the most common org. in the
    pre antibiotic era)
  Bacterial Factors Involved in the Pathogenesis of
                    Infective Endocarditis
1. Bacterial adhesins mediate binding to the nonbacterial
   thrombus and to endothelial cells:
   Staphylococcus
   fibrinogen-binding proteins(clumping factor),
   fibronectin binding proteins
   Streptococci- dextran, Platelet ActivatingFactor(PAF),
                   Exopolysaccharide-
2. Serum resistance - i.e. complement does not kill Gram
   positive bacteria
   Complements cannot kill capsule producing GNB
3. Invasive potential of bacteria
  Ability to elaborate extracellular proteases
  Capacity for metastatic seeding
4. Phagocytes cannot reach the bacteria hidden in the
   vegetations.
   CLINICAL FEATURES & COMPLICATIONS
 Low grade Fever (85-99% of patients)
 Nonspecific symptoms: fatigue, anorexia, chills,
  myalgia, headache, confusion

 ABE: Acute toxic fever < 2 weeks
     h/o iv drug use may be elicited

 SABE: More of a non specific flu like illness
        Symptoms > 2 weeks
       More often seen in patient with underlying
       congenital heart disease
Clinical Features
     Systemic emboli
           Incidence decreases with effective anti-microbial Rx
     Neurological sequelae
           Embolic stroke 15 – 20% of patients
           Mycotic aneurysm
           Cerebritis
     Renal insufficiency
           Immune complex mediated
           Impaired hemodynamics/drug toxicity
                 OTHER SIGNS
New or changing heart murmur
Neurologic abnormalities (30-40%):
•     Stroke
•     Intracranial hemorhhage        Due to peripheral
•     Subdural hemorrhage                 emboli

Peripheral symptoms(more common in adults)
•     Petechiae (20-40
•     Splinter hemorrhages
•     Osler’s nodes (small painful red subcutaneous
    nodules that develop in finger or toe pads)
•   Janeway lesions(erythematous lesions on palms/soles)
•   Roths spots(retinal lesion)
        Clinical presentations:


 The interval between the colonization of the endocardium and
  the onset of symptoms is two weeks.
 Death can occur about 6 weeks after colonization if the disease
  goes untreated.
 The initial symptoms are those of any infection:

   Low grade fever
   Anorexia
   Fatigue
   Weight loss
   Anemia
   Splenomegaly
Clinical Features
 Interval between index bacteremia & onset of sx’s usually
  < 2 weeks
       May be substantially longer in early PVE
 Fever most common sign
       May be absent in elderly/debilitated pt.
 Murmur present in 80 – 85%
       Generally indication of underlying lesion
       Frequently absent in tricuspid IE
 Changing murmur
The circulating immune complexes give rise to skin
manifestations which include:



a. Osler's nodes
b. Splinter hemorrhages
c. Petechia
d. Janeway's lesions
e. Roth spots

Urinary findings may include:
a. Proteinuria
b. Microscopic hematuria
c. Red blood cell casts
Roth spots
Janeway Lesions(small erythematous lesions on
palms/soles
Splinter Hemorrhage
   Osler’s Nodes(painful raised
lesions on finger and toe pads)
Subconjunctival Hemorrhages
 Acute heart failure due to valve destruction, chordae
                           tendinae rupture
 Chronic heart failure due to progressive valvular
                             insufficiency

 Hepatosplenomegaly (15-20% pts)
 Renal insufficiency (immune complex mediated
 glomerulonephritis

 Neonates – septic embolic phenomena
              osteomyelitis, meningitis, pneumonia
Serologic findings include:
a. Hypergammaglobulinemia
b. High levels of rheumatoid factor
c. High levels of antinuclear
   antibody
d. High levels of circulating
   immune complexes
              IE Work up… Lab studies
Blood culture
 Most important diagnostic test
 Positive in 90% of cases
 5ml for children and 10 ml for adult in 3 separate
 samplings within in 1-24 hours from different
 peripheral site is recommended
 Samples should be taken before initiating antibiotic
 therapy
 Culture should be grown both aerobically &
 anaerobically for at least 3 wks
                  OTHER LAB STUDIES
 Complete blood count
 ESR
 CRP
 Rheumatoid Factor
 Urine analysis
 Imaging study
  Echocardiography
   MRI
             DIAGNOSTIC CRITERIA
          Modified Duke’s diagnostic criteria
Based upon
Clinical evidence
Microbilogy
Pathology &
Echocardiography
A Patient is said to have IE if he meets
A. 2major criteria
      or
B. 1 major criteria & 3 minor criteria
      or
C. 5 minor criteria
      TREATMENT OF INFECTIVE ENDOCARDITIS
 Medical care
 Aim: Complete eradication of organism
 Prolonged parenteral therapy essential
 Therapy tailored according to the etiological agent & the
 type of endocarditis
Etiology                                     Drug


Penicillin Sensitive Streptococcal           Penicillin G I.V 4wks
endocarditis of native valve (PSSE)
Penicillin Resistant Streptococcal           Ampicillin/Ceftriaxone iv- 4 wks+
endocarditis on native valve                 Gentamicin iv- ist 2 wks


PSSE/PRSE on prosthetic valve                Ampicillin/Ceftriaxone iv- 6wks+
                                             Gentamicin for 1st 2 wks


Enterococcal infection of native valves      Ampicillin+Gentamicin iv – 4-6 wks
Enterococcal infection of prosthetic valve   Same as above.. But for > ^ wks
MSSA on native valve                         Nafcillin/oxacillin iv – 6 wks
MSSA on prosthetic valve                     OxacillinRifampicin iv – 6wks+
                                             Gentamicin iv-2 wks
MRSA on native valve                         Vancomycin iv– 6 wks
MRSA on prosthetic valve                     Vancomycin+rRfampicin iv – 6wks+
                                             Gentamicin iv-2 wks



Gram negative endocarditis                   Ceftriaxone/Ampicillin iv+
(HACEK)                                      Gentamicin for 4 wks
                    Surgical Care
Absolute indications for surgery include
Progressive cardiac failure,
Valve obstruction,
Definitive perivalvular abscess,
Noncandidal fungal infection,
Pseudomonal infection.
Relative indications include
Persistent bacteremia despite appropriate antibiotic
 therapy,
Candidal endocarditis,
Very large vegetations >10 mm.
Aortic valve of a patient undergoing emergency valve replacement for acute endocarditis
                   Pt had multiple embolizations & acute heart failure.
        The lower tweezers are holding a valve leaflet covered with vegetations.
                         PREVENTION
 Prevention of bacterial endocarditis with antimicrobial
   prophylaxis in high risk children is key to their long-term
   survival and quality of life.
   American Heart Association (AHA) guidelines for the
    prevention of bacterial endocarditis should be emphasized to
    the family of each patient identified at high risk.
   All children at risk should also be instructed about the
    importance of maintaining the best possible oral health.
   Antibiotics for endocarditis prophylaxis are required for
    patients before performing procedures that may cause
    bacteremia.
Prevention – the procedure
      Dental procedures        Gallbladder surgery
         known to produce       Cystoscopy, urethral
         bleeding                dilation
        Tonsillectomy          Urethral catheter if
        Surgery involving       infection present
         GI, respiratory        Urinary tract
         mucosa                  surgery, including
        Esophageal dilation     prostate
        ERCP for               I&D of infected
         obstruction             tissue
Antibiotic prophylaxis for patients undergoing
dental or upper respiratory procedures include
the following:
Amoxicillin 50 mg/kg by mouth (PO) 1 hour before procedure,
 or Ampicillin 50 mg/kg given IV or intramuscularly (IM) 30
 minutes before the procedure

Patients with a penicillin allergy, clindamycin 20 mg/kg PO 1
 hour before the procedure or azithromycin 15 mg/kg (PO) 1
 hour before the procedure
   THANK YOU

				
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