Download Intravascular Infection

Intravascular Infections:
Endocarditis &
Bacteremia
Microorganisms gain entry to the
intravascular system through:
• The cellular components of blood.
• Structural elements of the circulatory
system.
Examples:
• Plasmodium species, Babesia microti
invades RBCs.
• Hemorrhagic fevers viruses (HFVs) infects
the endothelial cells of cardiovascular
components.
Definitions:
Endarteritis:
intravascular infection of an artery. It is associated
with:
• Congenital arterial anomaly; patent ductus
arteriosus.
• Diseased arterial endothelium; atherosclerotic
plaques.
Phlebitis: inflammation of the vein lumen.
correlated with:
 Direct spread from an adjacent focus of infection.
 Intravascular foreign bodies (catheter) implanted
in the vein.
Endocarditis:
• Inflammation of the endocardial surface
of the heart.
• It can involve the cardiac valves,
the atrial or ventricular wall ,and
the chordae tendineae.
• Can arise as a consequence of cardiac
surgery, intra-cardiac instrumentation or
bacteremia.
Classification of Endocarditis:
• Infective
• Non-Infective
Infective endocarditis is classified to:
• Acute: fever, toxic illness lasting only
days to several weeks.
• Subacute: low grade fever, anorexia,
weakness, weight loss, symptomatic for
longer than several weeks.
Epidemiology:
• Infective endocarditis accounts for 1 in
1000 admissions in developed countries.
• More than 50% of cases involve people
older than 50 years of age.
• Left sided endocarditis are most common,
accounting for ≈ 95% of cases.
• Right sided endocarditis accounts only for
5% of cases (most commonly in drug
users)*.
Predisposing factors for endocarditis:
• Congenital cardiac defects:
bicuspid aortic valves, patent ductus arteriosus,
or ventricular septal defects.
• Degenerative valvular diseases: non
infectious causes, e.g. calcific valvular disease.
• Acute rheumatic fever and rheumatic
disease.
• Prosthetic heart valves.
• Cardiac rhythm management device (CRMD).
• 15-30% are not known to have prior valvular
abnormality.
N
Classification and causes of Infective
endocarditis:
Native valve endocarditis
• Acute
• Subacute
 Injection drug users
 Prosthetic valve endocarditis:
• Nosocomial acquired
• Community acquired

Acute native valve endocarditis:
 Average mortality rate is 20%. Higher
in patients over 65 years of age.
 Staphylococcus aureus accounts for
60% of cases.
 Pneumococci, streptococci and gram
negative bacilli are involved in 40% of
cases
Subacute native valve endocarditis:
 Alpha and non-hemolytic streptococci
accounts for 60%.
 40% are caused by enterococci, coagulase
negative staphylococcus species and
fastidious gram negative bacilli.
Injection drug users (younger persons):
 Right-sided endocarditis: S.aureus 75%
 Left-sided endocarditis: S.aureus,
streptococci and enterococci, fungi and
gram negative bacilli.
N
Prosthetic valve endocarditis:.
Nosocomial acquired endocarditis:
 Acquired perioperative or during admission
(within the 1st year)
 55% of cases are caused by S.aureus.
 Staphylococcus epidermidis (antibiotics resistant),
gram negative, corynebacterium, and fungi.
Community acquired endocarditis:
 It occurs as a consequence of bacteremia.
 It is acquired after the 1st year after valve
replacement.
 Streptococci, S. epidermidis, S.aureus,
enterococci .
N
Pathogenesis:
• Normal endothelium is resistant to infection.
• Valves can be damaged due to:
o Malignancy and some chronic diseases.
o Some cardiac abnormalities e.g.:
▫ Aortic valve regurgitation: vegetation on the
ventricular side of the valve.
▫ Mitral valve regurgitation: vegetation on the
atrial side of the valve.
▫ Ventricular septic defect.
• Damaged valves express integrin.
• Platelets bind integrin and a sterile vegetation will
be formed (non-bacterial thrombotic vegetation).
N
• Only limited types of bacteria can cause
endocarditis. They should be able to resist
complement and phagocytosis and have
adhesion factors (to adhere to the vegetation).
Microbial Adhesion Factors:
 S.aureus: fibrinogen binding protein.
 α hemolytic streptococci : dextran and Fim A
adhesin.
 Enterococci: lipoteichoic acid.
N
• Bacteria reach the heart and adhere to the
thrombotic vegetation on the damaged valve.
• Multiply and increase the size of the vegetation.
• Formation of bacterial vegetation (108 to 109
CFU/gm).
 Microscopically, bacterial vegetation is a mass
of platelets, fibrin, micro-colonies of microbes,
and rarely inflammatory cells.
 In the subacute form of infective endocarditis,
the vegetation also include granulomatous tissue
and may undergo fibrosis or calcification.
N
Host
defense
Abnormal
valve
(plasma
coagulation
factors )
Sterile
thrombotic
vegetation
bacteremia
bacterial
vegetation
Complications:
• continuous bacteremia: Superficial bacteria are
continuously shed into the blood.
N
• In 25-35% of cases, fragmentation of
vegetation into the circulation, causing
peripheral septic emboli:
▫ Visceral organs and brain involvement.
▫ Formation of immune complexes; serum
sickness disease and focal
glomerulonephritis.
Physical Examination
Non specific findings:
• Petechiae: small red or purple spot on
the skin, caused by a minor
hemorrhages.
• Conjunctival hemorrhages.
• Splinter hemorrhages: nonblanching,
reddish-brown lesions found under the
nail bed.
Petechiae on the toe
Splinter hemorrhages
Specific findings:
• Janeway lesions: macular,
nonpainful, erythematous lesions on
the palms and soles.
• Osler's nodes: painful, violaceous
nodules found in the pulp of fingers
and toes
• Roth spots: exudative, hemorrhagic
lesions of the retina.
Janeway lesion (arrow) occurred on the
palm
Osler's nodes: tender pustules on the
pulp of the finger
Roth spots: exudative, hemorrhagic
lesions of the retina.
Diagnosis of infective endocarditis:
• Suggested by clinical presentation and
documented by multiple positive blood
cultures.
• Direct : Microbiology:
Blood culture results have a 95% sensitivity if
done prior to antibiotic therapy.
• Indirect: Serology:
Serologic testing to identify rickettsia species,
coxiella species, and bartonella (infrequent but
important causes of subacute endocarditis).
Treatment
• Antibiotics types should be decided according to
blood culture results.
• For severely ill patients take blood for culture and
start empirical treatment.
• Empirical treatment should cover staphylococci,
enterococci and streptococci e.g. vancomycin and
are usually combined e.g. penicillin &
aminoglycoside.
• Antibiotics are given intravenously for 4-6 weeks.
• Surgical intervention is needed in antibiotic
resistant, fungal infection or if abscess is formed.
Non-infective Endocarditis:
• This form occurs more often in patients
with systemic lupus erythematosus and
is thought to be due to the deposition
of immune complexes.
• These immune complexes form small
sterile vegetation.
Bacteremia &
septicemia
Bacteremia
• Bacteremia is the invasion
of bloodstream by bacteria.
• The blood is normally a sterile, so
detection of bacteria in the blood is
always abnormal.
• Systemic inflammatory response syndrome
(SIRS): Two or more of these: Fever, tachycardia,
tachypnea and high or low WBCs count.
• Septicemia (sepsis) : invasion of bloodstream by
virulent microbes and their toxins (SIRS +
culture-documented infection).
• Sever sepsis: sepsis + hypotension (corrected by
IV fluids)
• Septic shock: A medical emergency caused by
decreased blood & oxygen supply to the organs
and tissues (hypotension; corrected by drugs).
• Multiorgan dysfunction syndrome e.g. renal
failure, DIC…… and death.
Bacteremia, Septicemia, and SIRS:
•
N
Sepsis
SIR
Sever
sepsis
Septic
shock
MODS
•The mortality rate from septic shock is
approximately 25%-50%.
N
• Clinical presentation of SIRS:
 Fever > 38 Cᴼ or ≤ 36 Cᴼ,
 Heart rate > 90 beats/min,
 Rapid breathing (respiratory rate
> 20/min),
 WBCs > 12000 cells/ µl or ≤ 4000
cells/µl .
Microbial virulence and pathogenesis
(Sepsis and septic shock):
• The gram negative lipopolysaccharide and to
a lesser extent peptidoglycan of gram
positives, bind to the soluble CD14 and attract
neutrophil, monocytes & B lymphocytes.
• Cytokines production in bloodstream; (IL-1,
IL-8, IL-12, TNF). These cytokines promotes
fever and capillary vasodilation leading to
edema formation, hypotension and
hypoperfusion, and increased smooth muscle
contraction of respiratory tract.
•
N
Sources of Bacteremia:
• Indwelling catheters, dental procedures,
UTI, respiratory tract infection, GIT
infection, intravenous drug use, endoscopy
or colonoscopy, post-operative infection.
• Why should we know the source of
infection?
Bacterial Causes of Bacteremia & Sepsis:
• Gastrointestinal infection:
Typhoid fever (salmonellosis), Malta fever
(brucellosis), yersinia and Bacteroid fragilis.
• Genitourinary tract infection:
Staphylococcus aureus, E.coli, Klebsiella,
citrobacter, enterobacter, vancomycin resistant
enterococci (VRE), pseudomonas species and
Treponema pallidum.
• Respiratory tract infection:
Neisseria meningitidis, H. influenza, Streptococcus
pneumoniae, MRSA and Klebsiella pneumonia.
• Skin infection: S.aureus
Diagnosis of endocarditis and Bacteremia:
Blood culture:
 Withdraw 5-8 ml of blood for culture under
aseptic conditions.
 Specimens are better withdrawn during fever
stage.
 Inoculate blood culture bottles, and incubate
them under aerobic and anaerobic conditions
at 37Cᴼ for up to 8 days.
 Minimally 2 sets of blood cultures should be
cultured from different venipuncture sites
spaced over 30 - 60 minutes.
N
Blood culture procedure:
Aerobic &
anaerobic
media
bottles
Blood culture growth indicators:
•
•
•
•
Turbidity of blood culture media.
Air bubbles formation in the media.
Hemolysis of cultivated blood.
Visible colonies.
Identification of pyogenic Cocci isolated from Blood culture:
n
Coagulase negative
Staphylococci are catalase +ve
S. aureus is coagulase positive
Novobiocin test
S. Epidermidis is sensitive
S. pneumoniae is sensitive to
optochin and bile soluble