Download microorganisms related to cardiac infections

MICROORGANISMS RELATED
TO CARDIAC INFECTIONS
Ramlan Sadeli
CARDIAC INFECTIONS :
Infective endocarditis
Myocarditis
Pericarditis
INFECTIVE ENDOCARDITIS
The proliferation of microorganisms on
to endothelium of the heart. The
prototypic lesion at the site of infection
: the vegetation; is a mass of platelets,
fibrins, micro-colonies of
microorganisms and scant
inflammatory cells.
INFECTIVE ENDOCARDITIS :
Infection most commonly involves
heart valves
May also occur on the ventricular
septum (on the lower pressure site)
Or on the mitral endocardium
CLASSIFICATION BASE ON :
Temporal evolution of disease
Site of infections
The cause of infections
Predisposing risk factor
PORTAL OF ENTRY :
Community-acquired native valve
Endocarditis :
Oral cavity
Skin
Upper respiratory tract
Etiology :
- Viridans streptococci
- Staphylococci
- Haemophilus
- Actinobacillus
- Cardiobacterium
- Eikenella
- Kingella
PORTAL OF ENTRY :
Community-acquired :
Gastrointestinal tract
Genitourinary tract
Etiology :
Streptococcus
Enterococci
PORTAL OF ENTRY :
Nosocomial infection :
Intravascular catheter
Nosocomial wound
Urinary tract infections
Etiology :
Staphylococci (coagulase-negative)
S. aureus
Gram negative bacilli
Diphtheroid
Fungi
Etiology of endocarditis among injection
drug users :
S. aureus
Pseudomonas aeruginosa
Candida
Bacillus
Lactobacillus
Corynebacterium
5-15% of patients with endocarditis have
negative blood culture
1/3 – ½ of these cases, cultures negative
because of prior antibiotic exposure
The remainder of these patients are
infected by fastidious organisms
Pathogenesis :
The normal endothelium is resistant to
infections
Direct infections by virulent organisms
(S. aureus can adhere directly to intact
endothelium or exposed subendothelium tissue)
Development of an uninfected plateletfibrin thrombus  serves as site of
bacterial attachment
Diagnosis :
The diagnosis of infection endocarditis is
Established with certainty only when :
Vegetations obtained at cardiac surgery
At autopsy
Or from an embolus are examined
histologically and microbiologically
Tabel 1. The Duke Criteria for the Clinical Diagnosis of Infective
Endocarditis
Major criteria
1. Positive blood culture :
- Typical microorganisms for infective endocarditis from two separate blood
culture
- Persistently positive blood culture
- Single positive blood culture for Coxiella burnetii or phase I IgG antibody t iter
of 1 : 800
Major Criteria
2. Evidence of endocardial involvement
- positive echocardiogram
- new valvular regurgitation
Minor Criteria
1.
Predisposition
2.
Fever
3.
Vascular phenomena
4.
Immunologic phenomena
5.
Microbiologic evidence
Bacteremic Pattern
Definite infective endocarditis
Two mayor criteria
One mayor criterion and 3 minor
criteria
Five minor criteria
Possible infective endocarditis
One mayor and 1 minor criterion
Three minor criteria
Treatment :
Since all bacteria in the vegetation
must be killed, therapy for endocarditis
must be bactericidal and must be given
for prolonged period
Are given par-enterally
Requires precise knowledge of the
susceptibility of the causative
microorganisms
Myocarditis
Cardiac inflammation is most
commonly the result of an infectious
process
Most commonly caused by viruses,
especially coxsackie virus B
Clinical manifestations :
Asymptomatic
Fulminant condition, with arrhytmia,
heart failure, and death
Most often self-limited and without
sequelae
Or progresses to a chronic form and to
dilated cardiomyopathy
Often a history of flu-like syndrome,
viral nasopharyngitis or tonsillitis
Bacterial myocarditis :
Usually as a complication of
endocarditis
Patients with diphtheria may develop
diphtheritic myocarditis
Diagnosis :
The isolation of virus from the stool,
pharyngeal washing or other body fluid
Changes in specific antibody titers
Endomyocardial biopsy
Myocarditis
Treatment :
Beta interferon
Bed rest
Drug for congestive heart failure
arrythmia
anticoagulation
Myocarditis
Full recovery is usual
Fulminant cases require heart
transplant
Acute pericarditis :
The most common pathologic process
involving pericardium
May be classified both clinically and
etiologically
Clinical manifestations :
Chest pain, pericardial friction rub,
electrocardiographic change,
pericardial effusion with cardiac
tamponade and paradoxal pulse
Pain is often absent in a slowly
developing tuberculosis, postirradiation, neo-plastic, or uremic
pericarditis
Etiology of infective pericarditis :
- Viral :
– Coxsackie virus A and B
– Echovirus
– Mumps
– Adenovirus
– Hepatitis
– HIV
- Pyogenic bacteria :
– Pneumococcus
– Streptococcus
– Staphylococcus
– Neisseria
– Legionella
- M. tuberculosis
- Fungal :
– Candida
– Histoplasma
– Blastomyces
– Coccidioides
Other infections :
– Syphilitic
– Protozoal
– Parasitic
Pericarditis
Diagnosis :
Echocardiography should be performed immediately
- allows assesment of pericardial thickness, pericrdial
fluid and tamponade
- can be used to guide emergency pericariocentesis
electrocardiogram shows diffuse ST and T changes,
depressed PR interval, decreased QRS voltage
Laboratory diagnosis :
Pericardiocenthesis :
Pericardial effusion nearly always has
the physical characteristics of an
exudate
Bloody fluid is commonly due to
tuberculosis
Or post-cardiac injury, post myocardial
infarctions, and neoplasm, and effusion
of rheumatic fever
Microscopic examination :
Gram-stain smear of the centrifuged
sediment of clear or slightly cloudy fluid
should be examined
Purulent material should be smeared
directly
Culture
Culture perform onto a variety of
specialized agar media for identification,
base on microscopic examination
Pericarditis
Pericardial biopsy improves the diagnostic yield
Viral or idiopathic pericarditis is self-limiting
Purulent pericarditis requires emergency surgical
drainage and systemic antibiotic
Mortality is 30 %
Pericarditis
Tuberculous pericarditis is treated with :
- a four-drug antituberculous regimen
= prednison to prevent constriction
- calcific form requires pericardiectomy
Post streptococcal infection :
Following an acute Group A
streptococcal infections (e.g. sore
throat), there is a latent period of 1 – 4
weeks after which rheumatic fever
nephritis occasionally develops
Rheumatic fever :
The most serious sequelae of
hemolytic streptococcal infections
It results in damage to heart muscle
and valves
Antibodies of cell membrane antigen of
staphylococci cross react with the
human tissue antigen
The carditis characteristically leads to
thickened and deformed valve
And to perivascular granulomas in the
myocardium (Aschoff bodies) that are
finally replace by scar tissue
Rheumatic fever has marked tendency
to be reactivated by recurrent
streptococcal infections
The first attack of rheumatic fever
usually produce only slight cardiac
damage
It is therefore important to protect such
patient from recurrent beta-haemolytic
Group A streptococcal infections