Infections of the

Cardiovascular System
Andani Eka Putra
Cardiovascular infections: Outline
• Viral infections
• acute myocarditis
• acute pericarditis
• Bacterial and fungal infections
• endocarditis
• other intravascular infections
• mycotic aneurysm and aortitis
• septic thrombophlebitis
• indwelling device infections
• tuberculous pericarditis
• spirochetal diseases (syphilis, Lyme disease)
• Parasitic infections
• American trypanosomiasis
• Possible infectious etiology
• endomyocardial fibrosis (EMF)
Viruses associated with acute myocarditis and
Pericarditis

• Most common:
• enteroviruses (particularly coxsackie B)
• Others
• adenoviruses
• herpesviruses
• CMV
• EBV
• HHV-6
• parvovirus B19
• HIV
• influenza (Note: acute or chronic
myocarditis can also be non-
infectious, e.g., allergic, toxic, or
autoimmune in origin)
Endocarditis

• Infective Endocarditis: a microbial infection of the

endocardial surface of the heart
• Common site: heart valve, but may occur at septal
defect, on chordae tendinae or in the mural
endocardium
• Classification:
• acute or subacute-chronic on temporal basis, severity of
presentation and progression
• By organism
• Native valve or prosthetic valve
Bacterial infection

• Bacteraemia
• Bacteraemia occurs when a heavily colonised mucosal
surface is traumatised
• Dental extraction
• Periodontal surgery
• Tonsillectomy
• Operations involving the respiratory, GI or GU tract mucosa
• Oesophageal dilatation
• Biliary tract surgery
• Transient bacteraemia
• Most cases of endocarditis are not preceeded by a specific event
• Tooth brushing, chewing
 ENDOCARDITIS

Characteristic pathological lesion: vegetation,

composed of platelets, fibrin, microorganisms
and inflammatory cells.
Aetiological Agents

1. Streptococci
• Viridans streptococci/α-haemolytic streptococci
• S. mitis, S. sanguis, S. oralis
• S. bovis
• Associated with colonic carcinoma

2. Enterococci
• E. faecalis, E. faecium
• Associated with GU/GI tract procedures
• Approx. 10% of patients with enterococcal bacteraemia develop endocarditis
Aetiological Agents

2. Staphylococci
• Staphylococcci have surpassed
viridans streptococci as the most common cause of
infective endocarditis
• S. aureus
• Native valves
• acute endocarditis
• Coagulase-negative staphylococci
• Prosthetic valve endocarditis
Aetiological Agents

4. Gram-negative rods
• HACEK group
• Haemophilus aphrophilus, Actinobacillus
actinomycetemcomitans, Cardiobacterium hominis, Eikenella
corrodens, Kingella kingae.
• Fastidious oropharyngeal GNBs
• E. coli, Klebsiella etc
• Uncommon
• Pseudomonas aeruginosa
• IVDA
• Neisseria gonorrhoae
• Rare since introduction of penicillin
Aetiological Agents

5. Others
• Fungi
• Candida species, Aspergillus species
• Q fever
• Chlamydia
• Bartonella
• Legionella
 Pathogenesis

• Altered valve surface

• Animal experiments suggest that IE is almost impossible to
establish unless the valve surface is damaged
• Turbulent blood flow
• Bacterial colonisation more likely to occur around lesions with high degrees of tubulence
• eg. small VSD, valvular stenosis
• Large surface areas, low flow and low turbulence are less likely to cause IE
• eg large VSD,
• Scarring – rheumatic fever, sclerosis
• Extrinsic intervention
Pathogenesis

• Deposition of platelets and fibrin – nonbacterial

thrombotic vegetation
• Bacteraemia
• Bacteria attach to platelet-fibrin deposits
• 80% of cases caused by staphylococci, streptococci and
enterococci
• Severeal surface ligands that allow attachment to occur
• Fibrin binding protein, exsopolysaccharides
• Protected from neutrophils
• Multiplication
• Mature vegetation
Pathogenesis

• Bacteraemia
• Bacteraemia occurs when a heavily colonised mucosal
surface is traumatised
• Dental extraction
• Periodontal surgery
• Tonsillectomy
• Operations involving the respiratory, GI or GU tract mucosa
• Oesophageal dilatation
• Biliary tract surgery
• Transient bacteraemia
• Most cases of endocarditis are not preceeded by a specific event
• Tooth brushing, chewing
Site of Infection

• Aortic valve more common than mitral

• Aortic:
• Vegetation usually on ventricular aspect, all 3 cusps usually affected
• Perforation or dysfunction of valve
• Root abscess
• Mitral:
• Dysfunction by rupture of chordae tendinae
Nosocomial Infective Endocarditis

• 7-29% of alll cases seen in tertiary referral hospitals

• At least half linked to intravascular devices
• Other sources GU and GIT procedures or surgical-wound infection
MICROBIOLOGY OF NATIVE VALVE ENDOCARDITIS
Nosocomial Endocarditis

• May present acutely without signs of endocarditis

• Suggested by: Bacteremia persisting for days
before treatment or for 72 hours or more after the
removal of an infected catheter and initiation of
treatment (esp in those with abnormal or
prosthetic valves)
• Risk if prosthetic valve and bacteremia: 11%
• Risk if prosthetic valve and candidaemia: 16%
Investigations

1. Blood culture
2. Echo
• TTE
• TOE
3. FBC/ESR/CRP
4. Rheumatoid Factor
5. MSU
Culture Negative Endocarditis

• 5-7% of patients with endocarditis will have sterile blood

cultures
• 1 Year study from France
• 44 of 88 cases of CNE, negative cultures were associated
with prior administration of antibiotics
• Fasidious or non-culturable organism
• Non-infective endocarditis

• Withhold empirical therapy until cultures drawn

Mortality

• Viridans Streptococci and S. bovis : 4-16%

• Enterococci:15-25%
• S. aureus: 25-47%
• Q fever: 5-37% (17% in Ireland)
• P. aeruginosa, fungi, Enterobacteriaceae > 50%
• Overall mortality 20-25% and for right-sided
endocarditis in IVDA is 10%
Infections of arteries
• Arteries
• Mycotic aneurysms
• almost always a complication of endocarditis
• yhey may rupture in spite of antibiotic treatment
• Aortitis
• rare infection following bacteremia in older persons with extensive atherosclerotic
disease of the aorta
• associated with staphylococci (from contaminated IVs) or with Salmonella (from
bacteremic intestinal infection)
 Infections of veins:
septic thrombophlebitis

Syndrome Veins Predisposition Microbiology Treatment

Lemierre’s Internal Prior exudative Fusobacterium IV Penicillin G
syndrome jugular v. pharyngitis necrophorum

Pylephlebitis Portal v. Diverticulitis; other B. fragilis, other Broad-spectrum

intraabdominal intestinal bacteria IV therapy;
infections heparin
Septic pelvic Ovarian v. Post-partum Intestinal flora Broad-spectrum
thrombophlebitis and others IV therapy;
heparin
Line-related septic Any small Infection indwelling usually Staph. IV anti-staph
phlebitis or great IV catheters antibiotics;
vein excision of
purulent small
veins
Tuberculosis and the heart

• Active TB can present with pericarditis

• Usually associated with concurrent pulmonary
disease
• Treated as pulmonary TB with addition of
corticosteroids (to prevent scarring)
• Constrictive pericarditis is the dreaded long-term
complication
• Causes impaired filling of the ventricles limited in
expansion by the stiff and unyielding pericardium
• Pericardiectomy may be necessary
Spirochetes and the Heart

• Syphilis:
• Heart involvment occurs in the tertiary stage of disease,
many years after acquisition
• Small numbers of spirochetes invade the aortic root and
induce destructive granulomatous inflammation
• Long-standing disease causes enlargement of the aortic
root and aortic valve insufficiency
• Older adults with acquired aortic root dilation and/or
aortic insufficiency should have syphilis serology
performed.
 Cardiovascular syphilis:
syphilitic aortitis

Source unknown

Any adult with aortic root dilation or aortic valve insufficiency should
have serologic testing for syphilis and receive treatment for tertiary
syphilis if confirmed positive.
RHEUMATIC HEART DISEASE

 Rheumatic diseases are defined by the constellation of

results of the physical examination, autoimmune
marker and other serologic tests, tissue pathology, and
imaging.

 Recognition of clinical patterns remains essential for

diagnosis because there is no single diagnostic test
and results may be positive in the absence of disease.
RHEUMATIC HEART DISEASE

• Rheumatic Heart Disease is the permanent heart valve damage

resulting from one or more attacks of ARF.
• It is thought that 40-60% of patients with ARF will go on to
developing RHD.
• The commonest valves affecting are the mitral and aortic, in that
order. However all four valves can be affected
PATHOPHYSIOLOGY

• In 0.3-3% of cases, infection leads to rheumatic

fever several weeks after the sore throat has
resolved.
• The organism spreads by direct contact with oral or
respiratory secretions, and spread is enhanced by
crowded living conditions.
• Patients remain infected for weeks after
symptomatic resolution of pharyngitis and may
serve as a reservoir for infecting others.
• Group A streptococci elaborate the cytolytic toxins streptolysins
S and O.
• Of these, streptolysin O induces persistently high antibody titers
that provide a useful marker of group A streptococcal infection
and its nonsuppurative complications
• Rheumatic fever develops in some children and
adolescents following pharyngitis with group A beta-
hemolytic Streptococcus
• The organisms attach to the epithelial cells of the
upper respiratory tract and produce a battery of
enzymes allowing them to damage and invade human
tissues.
• The presence of the M protein is the most important
virulence factor for group A streptococcal infection in
humans
• Cross-reactive antibodies bind to cardiac tissue facilitating infiltration of
streptococcal-primed CD4+ T cells, which then trigger an autoimmune reaction
releasing inflammatory cytokines (including TNF-alpha and IFN-gamma).
LABORATORY

• Throat culture
• Throat culture findings for group A beta hemolytic Streptococcus are usually negative
by the time symptoms of rheumatic fever or rheumatic heart disease appear.
• Rapid antigen detection test
• This test allows rapid detection of group A streptococcal antigen and allows the
diagnosis of streptococcal pharyngitis