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Mohd Yazid Bin Idris

NIM: 11616101
Indradevi Kanapa
NIM: 11617761

Definition
In general Endocarditis an inflammation of one or more of the heart valves and lining tissues
of the heart. Having existing congenital defects or damage to the heart valves increases the
risk of developing endocarditis. The most common cause of endocarditis is bacterial
infection, but fungi can also cause the condition.
Once persons get infected it’s called “Infective Endocarditis”(IE). A microbial
infection of a cardiac valve or the endocardium caused by bacteria, fungi, or chlamydia.
Often categorized as acute or subacute based on the rapidity of the clinical course.
Alternatively described by type of risk factor e.g., nosocomial, prosthetic valve, intravenous
drug use associated Pathological findings include the presence of friable valvular vegetations
containing bacteria, fibrin and inflammatory cells. There is often valvular destroy junction
with extension to adjacent structures.

Epidemiology of Endocarditis

There has been an increasing incidence of there has been an increasing incidence of
nosocomial endocarditis, both native and prosthetic valve there is an increased risk of
IE among injecting drug users, patients on long-term hemodialysis, patients with intravenous
catheters, diabetics and HIV infected patients. Among injecting drug users the incidence is as
high as 150-2000/100,000 person years.

Etiology of the diease

Endocarditis is caused by bacteria in the bloodstream multiplying and spreading across the
inner lining of your heart (endocardium). The endocardium becomes inflamed, causing
damage to heart valves. Heart is usually well protected against infection so bacteria can pass
harmlessly by. However, if your heart valves are damaged or you have an artificial valve, it's
easier for bacteria to take root and bypass your normal immune response to infection.Small
clumps of bacteria can develop at the site of the infection. There's a risk of these clumps
acting in a similar way to blood clots, travelling away from the heart and blocking the blood
supply to the organs. This can cause organ failure or trigger a stroke.

Usually, immune system destroys harmful bacteria that make it into bloodstream.
Even if bacteria reach heart, they may pass through without causing an infection. However,
bacteria that live in mouth, throat or other parts of body, such as skin or your gut, can
sometimes cause serious infections like endocarditis under the right circumstances.

Bacteria, fungi or other germs that cause endocarditis might enter bloodstream through:

 Everyday oral activities. Activities such as brushing your teeth, or other activities
that could cause gums to bleed, can allow bacteria to enter bloodstream — especially
if you don't floss or teeth and gums aren't healthy.
 An infection or other medical condition. Bacteria may spread from an infected area,
such as a skin sore. Other medical conditions, such as gum disease, a sexually
transmitted infection or certain intestinal disorders — such as inflammatory bowel
disease — can also give bacteria the opportunity to enter your bloodstream.
  Catheters. Bacteria can enter body through a catheter — a thin tube that doctors
sometimes use to inject or remove fluid from the body. This is more likely to occur if
the catheter is in place for a long period of time.
 Needles used for tattoos and body piercing. The bacteria that can cause endocarditis
can also enter bloodstream through the needles used for tattooing or body piercing.
 Intravenous (IV) illegal drug use. Contaminated needles and syringes are a special
concern for people who use illegal intravenous (IV) drugs, such as heroin or cocaine.
Often, individuals who use these types of drugs don't have access to clean, unused
needles or syringes.
 Certain dental procedures. Some dental procedures that can cut gums may allow
bacteria to enter bloodstream.

Bacteria can more easily attach to the lining of your heart (endocardium), if the lining's
surface is rough. You're also more likely to develop endocarditis if you have faulty, diseased
or damaged heart valves. However, endocarditis does occasionally occur in previously
healthy individuals.

Picture Source: http://medicalnotesonline.blogspot.co.id/2011/01/cardiology-infective-

endocarditis.html

This is a condition caused by infection of the endocardium by bacteria, or rarely, fungus. It

most commonly affects the heart valves (natural or prosthetic), but can occur anywhere along
the lining of the heart or blood vessels.
It will most commonly occur at sites of previous damage, however, particularly virulent
organisms (such as staphylococcus aureus and streptococcus pneumoniae) can infect
previously normal areas of tissue; for example, Staph. Areus will commonly infect the
tricuspid valve in IV drug users.
Sign and symptoms

Endocarditis may develop slowly or suddenly, depending on what germs are causing the
infection and whether persons have any underlying heart problems. Endocarditis signs and
symptoms can vary from person to person.

Common signs and symptoms of endocarditis include:

 Flu-like symptoms, such as fever and chills

 A new or changed heart murmur, which is the heart sounds made by blood rushing
through heart
 Fatigue
 Aching joints and muscles
 Night sweats
 Shortness of breath
 Chest pain when you breathe
 Swelling in your feet, legs or abdomen

Endocarditis can also cause symptoms that are more uncommon. These include:

 Unexplained weight loss

 Blood in your urine, which you might be able to see or that your doctor might see
when he or she views your urine under a microscope
 Tenderness in your spleen, which is an infection-fighting abdominal organ just below
rib cage on the left side of your body
 Janeway lesions, which are red spots on the soles of feet or the palms of hands
 Osler's nodes, which are red, tender spots under the skin of fingers or toes
 Petechiae (puh-TEE-key-e), which are tiny purple or red spots on the skin, whites of
eyes, or inside mouth

Risk factors of Endocarditis

People at highest risk of endocarditis are those who have:

 Artificial heart valves. Germs are more likely to attach to an artificial (prosthetic)
heart valve than to a normal heart valve.
 Congenital heart defects. If you were born with certain types of heart defects, such
as an irregular heart or abnormal heart valves, your heart may be more susceptible to
infection.
  A history of endocarditis. Endocarditis can damage heart tissue and valves,
increasing the risk of a future heart infection.
 Damaged heart valves. Certain medical conditions, such as rheumatic fever or
infection, can damage or scar one or more of your heart valves. This can make them
more prone to endocarditis.
 A history of intravenous (IV) illegal drug use. People who use illegal drugs by
injecting them are at a greater risk of endocarditis. The needles used to inject drugs
can be contaminated with the bacteria that can cause endocarditis.

Pathogenesis of Endocarditis

The pathophysiology of infective endocarditis comprises at least three critical elements:

preparation of the cardiac valve for bacterial adherence, adhesion of circulating bacteria to
the prepared valvular surface, and survival of the adherent bacteria on the surface, with
propagation of the infected vegetation. It appears that circulating bacteria do not readily
adhere to normal endothelial surfaces. Trauma to the valve, however, produces an alteration
in the endothelial cells, leading to either disruption of the surface and deposition of platelets
and fibrin, or other phenomena that render the surface susceptible to colonization by
circulating bacteria. Once the surface is prepared, some bacterial strains appear to adhere to
the fibrin-platelet matrix more avidly than others. The bacterial virulence factors that promote
adherence are complex, but at least one, an extracellular polysaccharide (dextran), has been
identified. Adherence can be blocked by antibodies directed against various surface
structures. The survival of bacteria adherent to the surface of the vegetation appears to be
complex as well, requiring resistance in situ to the bactericidal properties of complement and
phagocytosis by white cells. In addition, vegetation propagation involves activation of the
clotting cascade. For at least some streptococci, this occurs partly through perturbation of the
valvular cells to produce tissue factor (tissue thromboplastin), which results in the deposition
and growth of a fibrin-platelet clot over the rapidly growing bacterial colonies.
Factors Contributing to the Pathogenesis of Endocarditis

Hemodynamic is the blood flow patterns, bacterial properties and host factors.

1) Haemodynamic

The circulatory system is controlled by homeostatic mechanisms, much as hydraulic circuits

are controlled by control systems. Hemodynamic response continuously monitors and adjusts
to conditions in the body and its environment. Thus hemodynamics explains the physical
laws that govern the flow of blood in the blood vessels.Blood flow ensures the transportation
of nutrients, hormones, metabolic wastes, O2 and CO2 throughout the body to maintain cell-
level metabolism, the regulation of the pH, osmotic pressure and temperature of the whole
body, and the protection from microbial and mechanical harms. Blood is a non-Newtonian
fluid, best studied using rheology rather than hydrodynamics. Blood vessels are not rigid
tubes, so classic hydrodynamics and fluids mechanics based on the use of classical
viscometers are not capable of explaining hemodynamics.

Source: Rodbard, Circulation, 1963 Weinstein, Schlesinger NEJM, 1974

2) Bacterial properties
Serum resistance such complement of Gram positives tend to be complement resistant
bacterial adhesins mediate binding to the nonbacterial thrombus and to endothelial cells
Dextran, fibrinogen-binding proteins. Thus, invasive potential of bacteria that ability to
elaborate extracellular proteases and capacity for metastatic seeding. Then Stimulation of
tissue factor activity of the bacteria.

3) Host factors
Valvular surfaces where nonbacterial thrombus forms on damaged valves, direct adherence to
the endovascular surface of normal valves and Suture line, valve surface of prosthetic valves.
Platelets dual role of platelet microbicidal proteins (α-granules). The bacteria induce platelet
aggregation and part of nonbacterial thrombus surface. Leukocytes, complement, cytokines is
more limited role.

Principles of Therapy
Bactericidal antibiotics must be used bactericidal antibiotics must be used and prolonged
therapy is necessary (weeks). Treatment is best started after multiple sets of blood cultures
have been taken. Urgency in the initiation of therapy is required for acute but not subacute
endocarditis. Synergistic combinations of antibiotics are used when available. Antimicrobial
prophylaxis of Endocarditis with potential mechanisms of bactericidal activity, reduce
bacterial adherence and reduce bacterial density in the wound at the time of surgery (for
prosthetic valves)

References:
 The American Journal of Medicine by Paul M. Sullam, M.D., Thomas A. Drake,
M.D., Merle A. Sande, M.D, Volume 78, Issue 6, Supplement 2, Pages 110–115
 http://medicalnotesonline.blogspot.co.id/2011/01/cardiology-infective-
endocarditis.html
 https://www.medicinenet.com/script/main/art.asp?articlekey=165000
 http://www.columbia.edu/itc/hs/medical/pathophys/id/2009/endocarditisColor.pdf
 https://www.nhs.uk/conditions/endocarditis/causes/
 https://www.mayoclinic.org/diseases-conditions/endocarditis/symptoms-causes/syc-
20352576
 http://jaha.ahajournals.org/collection/infectious-endocarditis
 http://circ.ahajournals.org/content/early/2015/09/15/CIR.0000000000000296
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726828/
 https://journals.lww.com/jaapa/Citation/2015/10000/Infective_endocarditis.9.aspx
 http://www.nejm.org/doi/full/10.1056/NEJMcp1206782
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726828/