Cardiovascular system

infections
 Cardiovascular System Infection

Heart infections Intravascular system

infections
Rheumatic Septicemia
Carditis
fever Bacteremia & Atherosclerosis
Septic shock

1-Pericarditis

2-Myocarditis

3-Endocarditis
 Infective Endocarditis

Infective Endocarditis: is an inflammation of the

endocardium, the membrane lining the chambers of the
heart and covering the cusps of the heart valves.

The infection is caused by bacteria or fungi that enter the

bloodstream through the mucous membranes of the mouth,
open wounds, needles.
ENDOCARDITIS
 Subacute bacterial endocarditis (SBE): Acute bacterial endocarditis
it develops slowly;), more rapidly progressive type
caused by alpha-hemolytic streptococci caused by Staphylococcus aureus and
such as are common in the oral cavity,. Streptococcal pyogen.

Preexisting heart lesion organisms find their way from the initial
in people whose heart valves are site of infection to normal or abnormal
abnormal, because of either congenital heart valves;
heart defects or diseases as rheumatic
fever,
the bacteria lodge in the preexisting
lesions.

Left untreated by appropriate antibiotics, the rapid

SBE is fatal within a few months destruction of the heart valves is
frequently fatal within a few days
or weeks if untreated.
 RISK FACTORS

Congenital heart diseases.

An artificial heart valve (hjgh risk)
Previous surgery on your heart valves
A severe case of mitral valve prolapse
History of endocarditis
Recent dental surgery
Using intravenous drugs
 Pathogenesis
The condition probably arises from a focus of infection
elsewhere in the body
Portal of entry:
Dental / Surgical Procedures
◦ Contamination by IV drug use
◦ Obvious infections (RS/Skin(
◦ Occult source from gut, oral cavity)tonsils)
◦ Intravascular catheter infection
◦ Nosocomial wounds
◦ Chronic invasive procedures
 Pathogenesis

 Normally, such bacteria would be quickly cleared from the blood

by the body’s defensive mechanisms. However, in people whose
heart valves are abnormal, because of either congenital heart
defects or such diseases as rheumatic fever, the bacteria lodge in
the preexisting lesions.

 Within the lesions, the bacteria multiply and become entrapped

in blood clots that protect them from phagocytes and antibodies.

 - Once the infection has begun, a combination of organisms and

thrombus form a vegetation
 Sites involved

• Heart valves
• Ventricular septum defects
• Mural endocardium
• Intracardiac devices
 Aetiological Agents

1.Viridans Streptococci) α-haemolytic streptococci)

S. mitis, S. sanguis, S. oralis, S. bovis

2. Staphylococcus aureus : Either healthy or deformed valves, IVdrug abusers

(polymicrobial), devices cause acute endocarditis

3. Coagulase-negative staphylococci
Prosthetic valve endocarditis

4.Enterococci
E. faecalis, E. faecium
 Aetiological Agents
5. Gram-negative rods
 E. coli, Klebsiella (Uncommon)
 Pseudomonas aeruginosa
 Neisseria gonorrhoae
 Chlamydia
 Bartonella
 Legionella
6. Fungi
 Candida species
 Aspergillus species
 Clinical Manifestations

 Symptoms may develop slowly or suddenly

 Fever, most common symptom 80%, sign
 Anorexia, weight-loss, malaise, night sweats
 Heart murmur, short of breath
 Feeling short of breath
 Petechiae on the skin, conjunctivae, oral mucosa
 Investigations
Blood culture, CBC
Echo
ESR/CRP
– Chest X-ray, MRI
Look for multiple focal infiltrates and calcification
of heart valves
– ECG
Rarely diagnostic, Look for evidence of ischemia,
conduction delay, and arrhythmias
 Blood Cultures
• It remains a cornerstone of the diagnosis and should
be taken prior to starting treatment .

• Meticulous aseptic technique is required when taking

blood cultures, to reduce the risk of contamination
with skin commensals, which can lead to misdiagnosis.
 Blood Cultures

• At least 3 sets of samples should be taken from different

venepuncture sites over 24 hours.
Sub-culture & Sensitivity testing
Antibiogram
 Serology
cultures are negative.
organisms will not grow in blood
cultures(Coxiella,Legionella,Bartonella(
 COMPLICATIONS

Congestive heart failure.

Valvular damage
Systemic emboli (Stroke)
 Treatment

1-Antimicrobial therapy
 Empirical therapy should be started as soon as possible
targeting most likely pathogens.

 According to antibiotic sensitivity: penicillin, aminoglycoside,

Ceftriaxone , combination of drugs may be preferred.

 Repeat blood cultures until blood is demonstrated to be

sterile
2-Surgery
 Surgical Therapy
 Indications:
 Congestive cardiac failure
 uncontrolled infection despite maximal antimicrobial
therapy
 Presence of prosthetic valve endocarditis
 Large vegetation
 Major embolus
 Heart block
 Preventions

Patients who are having high risk of endocarditis should

1-Practice good dental hygiene, including regular brushing, flossing

and visits to the dentist.

2- Avoid cosmetic procedures, such as piercing or tattooing, which

can push bacteria from the skin into the bloodstream.

3- See a doctor if they have normal wounds that do not heal quickly.
4- Taken a preventive antibiotics such as amoxicillin before some
medical procedures, including dental work that involves cutting into
the gums or teeth, or certain types of surgery.
 Myocarditis

Definition:
is inflammation of heart muscle (myocardium), that results in myocardium
destruction and/or valvular disease.
This result in decreasing of the strength of the heart to pump blood normally.

The decreased heart function can affect the lungs, liver, and other body
systems.

Causes of Myocarditis:
1-Infectious. 2-Non-Infectious
 Causes of Myocarditis

A. Infectious Myocarditis:
It develops secondary to an underlying infection caused by:
1-Viral: Coxsackieviruse B(common),CMV, EBV, parvovirus B19, Human Herpes virus 6
.

2-Bacterial: Treponema palladium (Syphilis) and Borrelia burgdorferi (Lyme disease)

and Rickettsia.

3-Fungal: Blastomycosis, Coccidiomycosis, Cryptococcosis, and Aspergillosis.

B. Non-Infectious Myocarditis:
1-Autoimmune or systemic disorder:
A-Exogenous Antigen:
Post-Streptococcus pyogenes autoimmune reaction (Acute rheumatic
fever).

B-Endogenous Antigen:
systemic lupus erythematosus , and systemic vasculitis.
2-Cardiotoxins:(Drug-induced Myocarditis)
Myocarditis that associated with an autoimmune
reaction.
-Pharyngitis and tonsillitis caused by Streptococcus
pyogenes (Group A Streptococcus).

Streptococcal M protein and coxsackievirus B virus have regions (epitopes)

that are similar to cardiac protein myosin.
After the virus is gone, the immune system may attack cardiac myosin.

M protein is strongly anti-phagocytic protein and is a major virulence factor.

It binds to serum factor H, destroying C3 convertase and
preventing opsonization by C3b.

Cross-reactivity of anti-M protein antibodies with heart muscle is the basis

for Rheumatic fever.
N

Non-Suppurative Complications of Streptococcus

pyogenes Pharyngitis:
1-Acute rheumatic fever:
-Significant cause of valvular heart
disease.
-Appears 1 to 4 weeks following
Streptococcus throat infection.
-Characterized by:
1-Myocarditis (common).
2-Polyarthritis (common).
3-Subcutanous nodules.
4-Erythema marginatum.
N

2-Recurrent Streptococcus infection :

- It causes ongoing inflammation of cardiac muscle.
- Could result in Chronic form:
-Extensive mitral valve (65-70% of cases) and/or aortic
(25%) valve destruction and Stenosis.

-This manifestation called

rheumatic heart disease:
1-Predisposing for
bacterial endocarditis.
2-Could cause heart
failure and death.
 Clinical Manifestations

Signs and symptoms of heart failure

 Anorexia, weight-loss, malaise, night sweats
 Fever,
 Heart murmur, short of breath
 Feeling short of breath
 Those with associated pericarditis often have chest
pain.
 Diagnosis of Myocarditis

Diagnosis of Myocarditis:
 The most common test is a chest X-ray. Often the heart size is enlarged, the blood
vessels of the lungs are prominent, and fluid may enter the lungs.

 Myocardial inflammation can be suspected on the basis of Electrocardiographic results

(ECG)

 Elevated C-reactive protein (CRP) and/or Erythrocyte sedimentation rate (ESR) and
increased IgM (serology) against viruses known to affect the myocardium.

 Markers of myocardial damage ( Troponin or creatine kinase cardiac isoenzymes) are

elevated.

 A small tissue sample of the endocardium and myocardium is taken, and investigated
by a pathologist by light microscopy and (if necessary) Immunochemistry and special
staining methods.
Post-Streptococcal Sequelae
Acute Rheumatic Fever
Antibodies to M Inflammatory
protein cross-react response
with epitopes on ( C activation)
heart myosin &
sarcolemmal
membrane proteins

Damage of heart valves

Post-Streptococcal Sequelae
In Acute rheumatic fever:
• Recurrence of streptococcal pharyngeal infections is
common.
• Usually associated with an increased probability of
rheumatic fever.
• Repeated recurrences of rheumatic fever may cause
valvular damage.
• Thus following a single attack, life-long antibiotic
(penicillin) prophylaxis is recommended.
 Non-suppurative sequelae:
Begin 1-4 weeks after an acute streptococcal illness.
Pathogensis: autoimmune mechanism.

(1) Acute Rheumatic Fever (ARF)

immune response against Strept. antigens similar to heart antigens lead to
damage of heart valves

(2)Post-Streptococcal glomerulonephritis (AGN)

Deposition of Ag-Ab complexes, activation of complement on the basement
membrane of kidney glomeruli, where they provoke an inflammatory response that
damages the kidney.
Diagnosis of ARF
No single test is pathognomonic .
Diagnosis is based on modified Jones criteria:

(A) Evidence of recent S .pyogenes infection

(B)Two of the five major criteria ,or one major
and two minor criteria .
Post-Streptococcal Sequelae
Diagnosis of ARF:
I. Evidence of recent streptococcal infection:
 History of acute tonsillitis / scarlet fever
+ve throat swab culture for S. pyogenes.
 Elevation of ASO titre(above 200 units).
Post-Streptococcal Sequelae

Diagnosis of ARF
Major Criteria: Minor Criteria:
1. Carditis 1. ↑ ESR
2. Migratory polyarthritis 2. +ve CRP
3. Erythema annulare
3. ↑ WBC
4. SC nodules
5. Chorea
4. Fever
5. Prior history of RF
 Subcutaneous nodules
Erythema annulare
Puerperal fever.

Acute endocarditis.

Necrotizing fasciitis.

Toxic shock syndrome.

 Viridans Streptococci
Alpha hemolytic.

 Normal inhabitants of the

oral cavity, GIT & female
genital tract.

 Most viridans streptococci

do not produce exotoxins
or traditional virulence
factors.
 Viridans
Streptococci
 Have a significant role in dental caries.

 Responsible for nearly 50% of all cases of Subacute

bacterial endocarditis (SBE):
 They adhere to cardiac valves, especially in persons with
underlying valvular disease.
 The organism settles on the prosthetic valve / the deformed heart
valves e.g. rheumatic / congenital heart.
 SBE may occur when dental manipulations / trauma to mucosa of
URT e.g. tonsillectomy, lead to bacteraemia.
Laboratory diagnosis of SBE

 Blood culture technique

followed by identification of the
isolate from the subculture on
sheep blood agar.
 Treatment & Prevention
 Relatively resistant to penicillin.

 Synergistic combination of penicillin & gentamycin in life

threatening conditions (e.g. endocarditis).

 A single large dose of ampicillin / amoxicillin should be given to

patients with abnormal heart valves prior to dental procedures
to prevent endocarditis.
Pericarditis
Definition:
inflammation of the pericardium, which is the sac-like covering around the
heart

Causes of peicarditis:
1-Infection.
2-Autoimmune
3- Trauma
4- Malignancy
 Infectious causes

Pathogens reach the pericardium by either hematogenous spread

or direct from adjacent intrathoracic structures or, rarely,
directly from infected myocardium:
1-Viral: Coxsackieviruse , Echo viruses, CMV and HIV.

2-Bacterial: T.B, , S. aureus and S. pneumoniae

3-Fungal: Cryptococcosis, and Aspergillosis.

 Clinical Manifestations

 Chest pain (the most common manifestation).

Pain often worsens with inspiration or coughing, sitting
up and leaning forward often improve the pain
associated with pericarditis.

 Anorexia, weight-loss, malaise, night sweats

 Fever, of breath
 Investigations

1. Culture of pericardial fluid or pericardial

tissue may reveal causative bacteria.
2. Echo and ECG
3. ESR/CRP, Cardiac enzymes
4. Chest X-ray, MRI
 Treatment

1-Antimicrobial therapy
 For bacterial, mycobacterial, and fungal infections.
 Most viral etiologies are treated with symptomatic
management and supportive care

2-Pericardiocentesis can be life-saving.

 Preventions

Immunization against S. pneumoniae may be effective.

Treatment of early or latent stages of infections (e.g.,
tuberculosis) may prevent development of pericarditis
in some cases.