Infections of the

Cardiovascular System
Andani Eka Putra
Diagnostic and Research Centre for Infectious Disease
Microbiology Department, FMAU
Cardiovascular infections
 Viral infections
 acute myocarditis

 acute pericarditis

 Bacterial and fungal infections

 Endocarditis

 Other intravascular infections

 Tuberculous pericarditis

 Spirochetal diseases (syphilis, Lyme disease)

 Parasitic infections
 American trypanosomiasis

 Possible infectious etiology

 Endomyocardial fibrosis (EMF)
Pathomechanism
Viruses associated with acute
Myocarditis and Pericarditis
 Most common:
 Enteroviruses (particularly coxsackie B)

 Others
 adenoviruses

 herpesviruses

 CMV

 EBV

 HHV-6

 Parvovirus B19

 HIV

 influenza
Acute pericarditis: causes

 Infections
 enteroviruses (coxsackievirus, echovirus)
 HIV
 bacteria (S. pneumoniae, S. aureus); note that the
patient with bacterial pericarditis is much more ill,
with shaking chills and high fever
 tuberculosis
 rheumatic fever (rare)
 Non-infectious
 post-MI, post-pericardiotomy, trauma, uremia,
myxedema, radiation therapy, lupus, drugs
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
MICROBIOLOGY OF NATIVE
VALVE ENDOCARDITIS
ENDOCARDITIS

Characteristic pathological lesion: vegetation,

composed of platelets, fibrin, microorganisms
and inflammatory cells.
 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

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
3. 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
4. Gram-negative rods
 HACEK group
 Haemophilus aphrophilus, Actinobacillus
actinomycetemcomitans, Cardiobacterium
hominis, Eikenella corrodens, Kingella kingae.
 E. coli, Klebsiella etc
 Pseudomonas aeruginosa
 Neisseria gonorrhoae
5. Others
 Fungi (Candida species, Aspergillus species
 Q fever
 Chlamydia
 Bartonella
 Legionella
Pathomechanism
 Altered valve surface
 Animal experiments suggest that infection 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
 Large surface areas, low flow and low turbulence are
less likely to cause IE
 Scarring – rheumatic fever, sclerosis

 Extrinsic intervention
 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
 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
 Transient bacteraemia

 Most cases of endocarditis are not preceeded by a

specific event Ex. 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
Investigations

1. Blood culture
2. Echo
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; B. fragilis, other Broad-spectrum

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

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 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
Pathomechanism
 Rheumatic fever develops in some children and
adolescents following pharyngitis with group A
beta haemoliticus 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.
 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
 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