MICROORGANISM ON CARDIOVASCULAR

SY. MIFTAH EL JANNAH

• Endokarditis pertama kali ditemukan oleh Rivera tahun 1946.

• Endokarditis adalah infeksi permukaan endokardial meliputi dinding ventrikel, katup-katup jantung, dinding arteri besar, septum

• The infectious diseases of the cardiovascular system infect the blood, blood vessels, and heart. In many cases, the infections remain in these areas, but in others, the infections are spread to secondary organs.

• most commonly caused by species of oral streptococci (viridans group) :

– Streptococcus sanguis

– Strep. oralis

– Strep. mitis

– Staph. aureus

– Intravenous drug misusers have the added complication of infection due to organisms they

inject into themselves.

– Coagulase-negative staphylococci are common causes of early prosthetic valve endocarditis and

are probably acquired at the time of surgery.

– The species causing late infections-more than 3 months after cardiac surgery-are somewhat

more like those causing native valve endocarditis

Causative agents of endocarditis in

different groups of patients (in rank

order of decreasing importance).

Although almost any organism can

cause endocarditis, the majority of

cases are caused by a relatively

small range of species. The

relative importance of these

species varies depending upon

whether the patient has his/her

own heart valves or a prosthetic

valve.

MIKROORGANISME PENYEBAB

STREPTOCOCCUS

• Streptococcal septicemia Septicemia is a general

expression for microbial infection of the blood and blood

vessels. In previous generations, this condition was known

as blood poisoning.

Streptococcus pyogenes.

Streptococcus pyogenes Physiology and Structure • Gram-positive cocci arranged in pairs and long chains• β-Hemolytic; more viruluent strains with capsule• Facultative anaerobe• Catalase negative; bacitracin susceptible (important

identification tests)• Group-specific carbohydrate (A antigen) and type-specific

antigens (M and T proteins) in cell wall• Produce streptolysin O and DNase B (antibodies against

these antigens [ASO, anti-DNase B] are clinically important)

• An important complication of streptococcal septicemia

is endocarditis, an infection of the heart valves

Kelainan pada sistem immun

Sub akut disebabkan oleh Streptococcus pyogenes,

menyebabkan demam, rasa lemah, dan jantung yang

berdenyut.

Akut disebabkan oleh Staphylococcus aureus,

berhubungan dengan kerusakan pembuluh jantung.

• Most commonly streptococci from the oral flora enter the

bloodstream

During dental procedures or vigorous teeth cleaning or flossing, and

adhere to damaged heart valves.

– fibrin-platelet vegetations are present on damaged valves before the

organisms implant

– Probably associated with the ability of the organisms to produce

dextran as well as adhesins and fibronectin-binding proteins.

– Having attached themselves to the heart valve, the

organisms multiply and attract further fibrin and platelet

deposition protected from the host defenses, and

vegetations can grow to several centimeters in size.

– This is probably quite a slow process and correspondingly

the time period between the initial bacteremia and the

onset of symptoms averages around 5 weeks

Bacteria circulating in the bloodstream adhere to, and establish themselves on, the heart valves. Multiplication of the microbes is associated with destruction of valve tissue and the formation of vegetations, which interfere with, and may severely compromise, the normal function of the valve. These histologic sections show the virtual destruction of the leaflet at the mitral valve by staphylococci. (a) Gram stain. (b) Eosin-Van Geisen stain. (LA, left atrium; LV, left ventricle; MV, remnant of mitral valve; TV, thrombotic vegetation.) (Courtesy of RH Anderson.)

• A patient with infective endocarditis almost always has a fever

and a heart murmur The signs and symptoms of infective

endocarditis are very varied, but relate essentially to four

ongoing processes:

– the infectious process on the valve and local intracardiac complications;

– Septic embolization to virtually any organ;

– bacteremia, often with metastatic foci of infection;

– circulating immune complexes and other factors.

Outward signs of endocarditis may be helpful in suggesting the diagnosis. These result from the host's response to infection in the form of immune complex-mediated vasculitis, focal platelet aggregation and vascular permeability. (a and b, different views) Splinter hemorrhages in the nailbed and petechial lesions in the skin. (c) Osler's nodes. These are tender nodular lesions that tend to affect the palms and fingertips. (Courtesy of H Tubbs.)

• Before the advent of antibiotics infective

endocarditis had a mortality of 100%, and

even today despite treatment with

appropriate antibiotics, the mortality remains

at 20-50%.

• Although the majority of species causing infective

endocarditis are highly susceptible to a range of

antibiotics, complete eradication takes several weeks

to achieve, and relapse is not uncommon. This is

probably due to factors such as: relative

inaccessibility of the organisms within the

vegetations both to antibiotics and to host defenses;

• when the organisms may be hospital-acquired and

consequently often resistant to many antibiotics,

often presents a more difficult therapeutic challenge.

• A β-lactamase stable penicillin such as nafcillin is

often suitable and may be given in combination with

an aminoglycoside or rifampicin.

• Glycopeptide antibiotics (e.g. vancomycin)

should be used for penicillin-allergic patients

and for treating methicillin-resistant

staphylococci.

Rheumatic fever • is an immune reaction taking place in the heart tissues

and is usually stimulated by antigens derived from

Streptococcus pyogenes. Inflammation of the heart

tissues is often accompanied by inflammation and

arthritis of the joints, a condition called rheumatoid

arthritis. A streptococcal sore throat may precede this

condition.

• Arthritis rheumatoid reaksi autoimun, dibentuk IgM

[IgM RF] spesfisik terhadap fraksi Fc dari molekul

IgG komplek RF dan IgG ditimbun di sinovia sendi

dan mengaktifkan komplemen melepas mediator

[sifat kemotaktik terhadap granulosit] respon

inflamasi disertai peningkatan permeabilitas vaskuler

pembengkakan sendi destruksi permukaan sendi

Rheumatic fever• is a nonsuppurative complication of S. pyogenes

disease. It is characterized by inflammatory changes involving the heart, joints, blood vessels, and subcutaneous tissues. Involvement of the heart manifests as a pancarditis (endocarditis, pericarditis, myocarditis) and is often associated with subcutaneous nodules. Chronic, progressive damage to the heart valves may occur.

• carditis (inflammation of the heart), which occurs in 60% of patients is the most severe symptom of ARF and can result in permanent damage to the heart valves, and can be life threatening

How is rheumatic fever treated?• The first step in treating rheumatic fever is to

eradicate the bacteria which initially caused

the immunologic response. This is usually

accomplished with the use of penicillin. For

penicillin-allergic patients, there are other

options such as erytromycin or azithromycin

• Patients with rheumatic fever who develop

carditis may develop long-lasting heart

dysfunction. Often the mitral valve or the

aortic valve is affected, and if patients are not

responsive to medications, surgical valve

replacement may become necessary.

Pemeriksaan :• Kultur darah sangat efektif • Pada kultur darah Ideal diambil 3 kali pd

kurun waktu 24 jam dan sebelum pemberian antibiotik.

• Pemeriksaan microbiologi and cardiologi sangat penting

• Tes serologi Antistreptolisin O [ASO]