Transcript Infective endocarditis

Bacteremia:
Bacteremia is the presence of bacteria in the blood. The blood is
normally a sterile environment, so the detection of bacteria in the
blood (most commonly with blood cultures) is always abnormal.
Bacteria can enter the bloodstream as a severe complication
of infections (like pneumonia ), during surgery (especially when
involving mucous membranes such as the gastrointestinal tract),
or due to catheters and other foreign bodies entering
the arteries or veins (including intravenous drug).
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The immune response to the bacteria can cause sepsis and septic
shock.
Septic shock is a medical emergency caused by decreased
tissue perfusion and oxygen delivery as a result of
severe infection and sepsis.
It can cause multiple organ dysfunction syndrome and death.
The mortality rate from septic shock is approximately 25%-50%.
The Gram negative lipopolysaccharide (Endotoxin) bind to LPSbinding protein which crosslink CD14 in blood.
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Blood monocyte, and neutrophils have CD14 receptors that
discriminate the complexes.
It will initiate cytokines production such as: TNF alpha, and
IL-1 that will induce the following:
1- Decreased synthesis of anticoagulation factors such as tissue
factor pathway inhibitor and thrombomodulin.
2- Systemic vasodilatation , edema, chemotaxis, endothelial
injury and activation of leukocyte adhesion to the endothelial
tissue.
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Bacteremia is different from sepsis (so-called blood poisoning
or toxemia), which is a condition where bacteremia is
associated with an inflammatory response from the body (
characterized by rapid breathing, low blood pressure, fever,
etc.).
Causes:
In the hospital, indwelling catheters are a frequent cause of
bacteremia and subsequent nosocomial infections, because they
provide a means by which bacteria normally found on the skin can
enter the bloodstream.
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Other causes of bacteremia include dental procedures
, herpes , urinary tract infections, peritonitis, Clostridium
difficile colitis, and intravenous drug use.
Sources of Bacteremia:
1-Gastrointestinal infection:
Typhoid fever (Salmonellosis), Malta fever (Brucellosis),
Yersinia infection and Bacteroid fragilis .
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2-Genitourinary tract infection:
Staphylococcus aureus, E.coli, Klebsiella, Citrobacter,
Enterobacter, and Pseudomonus species.
Treponema pallidum, Neisseria gonorrheae,
3-Respiratory tract infection:
Neisseria meningitidis, H. influenza, Streptococcus
pneumoniae, MRSA, and Klebsella pneumonia.
Endocarditis:
Endocarditis is an inflammation of the inner layer of the heart,
the endocardium.
It usually involves the heart valves (native or prosthetic valves).
Other structures which may be involved include the interventricular
septum ,and the chordae tendineae.
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Endocarditis is characterized by a prototypic lesion,
the vegetation, which is a mass of platelets, fibrin,
microcolonies of microorganisms, and inflammatory cells.
In the subacute form of infective endocarditis, the
vegetation also include a center of granulomatous tissue,
which may undergo fibrosis (collagen) or calcification.
Picture of a granuloma
(without necrosis) as seen
through a microscope on
a glass slide. The granuloma
in this picture was found in
a lymph node of a patient
With Mycobacterium avium
infection .
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The simplest classification of endocarditis is based on :
Etiology: infective or non-infective, depending on whether a
microorganism is the source of the inflammation or not.
Diagnosis of endocarditis is based on the clinical features,
investigations such as echocardiogram, as well as any blood
cultures demonstrating the presence of endocarditis-causing
microorganisms.
Infective endocarditis:
Since the valves of the heart do not receive any dedicated
blood supply, defensive immune mechanisms cannot
directly reach the valves via the bloodstream.
If an organism (such as bacteria) attaches to a valve surface
and forms a vegetation, the host immune response is
blunted.
Normally, blood flows smoothly through these valves.
If they have been damaged (from rheumatic fever, for
example) the risk of bacteria attachment is increased.
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The endothelial lining of the chambers of the heart and
blood vessels is resistant to bacterial infection.
Endothelial damage however, for example from a "jet
lesion" caused by involuntary return of blood flow, may
produce a localized, sterile vegetation of platelets and
fibrin.
This may then allow circulating micro-organisms to adhere
to the valve. Once attached, the bacteria may become
enclosed in fibrin and platelets and multiply rapidly.
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Infected vegetations (lesion)occur along the edges of the
heart valves, on the ventricular side for mitral and aortic
valve and on the atrial side in tricuspid valve.
Left sided endocarditis are most common, accounting for
95% of cases.
Right sided endocarditis accounts for 5% of cases and is
most often seen due to IV drug fluid invasion or in the
immunosupressed patients; the tricuspid valve is affected
and the organism is usually a Staphylococcus.
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Prosthetic valve endocarditis results from infection of a
prosthetic valve.
This may occur early, within 60 days of surgery, either
during the operation or due to a perioperative bacteremia
(urinary catheterization).
Types of infective endocarditis:
Infective endocarditis has been classified into two broad
categories according to the pathogenic organism and the clinical
presentation:
1-Acute:
Most often caused by Staphylococcus aureus .
Equally prevalent on normal and abnormal valves.
It is rare.
2-Subacute:
Most often caused by Streptococcus viridans .
Usually affects abnormal valves.
More common.
Incidence of endocarditis:
Acute form:
Incidence of infective endocarditis in Europe and the USA is around
1.7-6.2 per 100,000 person-years.
Twice as common in men than in women.
Average mortality rate is 20%:
Higher in patients over 65 years of age
0.1% of all cardiac deaths.
Subacute infection far more prevalent than acute form.
50% of cases occur on normal valves, 15-30% of cases occur on
prosthetic heart valves.
Left sided endocarditis accounts for 95% of cases, aortic and mitral
valves are effected equally.
Non-infective endocarditis:
This form occurs more often in patients with Lupus
erythematosus and is thought to be due to the deposition of
immune complexes.
These immune complexes precipitate an inflammation
reaction, and it involves small sterile vegetations.
Endocarditis:
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Diagnosis of acute and sub-acute endocarditis:
Blood culture:
A-5-8 ml blood should
be extracted for culture.
B-Specimens should be
extracted during fever
stage.
C-Inoculation of blood
culture bottle, and
incubation under aerobic
and anaerobic conditions.
D- At 37˚C, blood should be
incubated up to 8 days.
Blood culture results:
Growth indicators:
1-Turbidity of blood culture media.
2-Air bubbles formation in the media.
3-Hemolysis of cultivated blood .
Identification of pyogenic Cocci from Blood culture (endocarditis):
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Staphylococcus aureus and Streptococcus viridans:
Staphylococcus aureus species is DNase and Coagulase positive.
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Streptococcus viridans speceis are resistant to Optichin and
insoluble in bile salt.