Infections of the

Cardiovascular System
DR M P OKEMWA
PATHOLOGIST

CATEGORIES
Infective Endocarditis
Acute and subacute
Myocarditis
Bacterial, viral and fungal
Pericarditis
Bacterial, viral and fungal

ANATOMY

Endocarditis: Definition

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

ENDOCARDITIS

Characteristic pathological lesion: vegetation,

composed of platelets, fibrin, microorganisms
and inflammatory cells.

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

CLASSIFICATION
Acute
- Affects normal heart due to virulent
organisms making it potentially fatal
Subacute
-Affects damaged valves and is due to less
virulent organisms

ACUTE INFECTIVE
ENDOCARDITIS
Slightly over 50% occur in normal hearts
Often there is a source of infection e.g UTI
Caused by highly virulent organisms
-Staphylococcus aerus-50%
-Strepococcus pyogenes- 35%
-No organisms isolated in 5-10%. Attributed to
difficulty in culturing and previous antibiotic
therapy

Aetiological Agents
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

SUBACUTE I.E.

Much more insidious and less dramatic.

Caused by less virulent organisms
Strepococcus viridans- 50%
Enterococci- 15%
G-ve bacteria-10%
Diptheroids, candida, coxiella burnetti,
actinomyces, ricketsia

Aetiological Agents
Streptococci

Viridans streptococci/-haemolytic streptococci

S. mitis, S. sanguis, S. oralis

S. bovis

Associated with colonic carcinoma

Enterococci

E. faecalis, E. faecium

Associated with GU/GI tract procedures

Approx. 10% of patients with enterococcal
bacteraemia develop endocarditis

Aetiological Agents
Gram-negative rods

HACEK group

E. coli, Klebsiella etc

Uncommon

Pseudomonas aeruginosa

Haemophilus aphrophilus, Actinobacillus

actinomycetemcomitans, Cardiobacterium hominis, Eikenella
corrodens, Kingella kingae.
Fastidious oropharyngeal GNBs

IVDA

Neisseria gonorrhoae

Rare since introduction of penicillin

Aetiological Agents
5.

Others

Fungi

Candida species, Aspergillus species

Q fever
Chlamydia
Bartonella
Legionella

Risk Groups

Native valve

Congenital heart disease

Rheumatic heart disease
Mitral valve prolapse
Degenerative valve lesions

Prosthetic Valve
IVDU
Nosocomial IE

CLINICAL FEATURES

Rapidly progressive high fever and chills

Heart failure sets in with cardiac murmurs
Embolic phenomena from the heart
vegetations- Janeway lesions such splinter
nail hemorrhages, pustular skin lesions,
Anemia, splenomegally
Glomerulonephritis causing hematuria
Death within days to weeks due to infections

Oslers nodes
Tender, s/c
Nodules-immune
complex
Janeway
lesions
Nontender
erythematous,
haemorrhagic,
or pustular
lesions often
on palms or
soles.-infective

MORPHOLOGY

Aortic and mitral valve is involved 80-90%.

Bulky friable masses of thrombi containing
the causative organism are found hanging
on valve leaflets.
Are bulkier some up to 7 cm across more
so in AIE

HISTOLOGY

Irregular, amorphous tangled masses of

fibrin, platelets and masses of
microorganisms are seen on the
vegetations.
In AIE there is an acute inflammatory
exudate with tissue destruction.
Sequlae hence is peforation of valvular
leaflets, erosion of chordae tendinae and
dissemination on microorganisms in
fragments as emboli. Form abscesses
where they lodge

PROSTHETIC VALVES

7-25% of cases of infective endocarditis

The rates of infection are the same at 5 years for
both mechanical and bioprostheses, but higher
for mechanical in first 3 months
Culmulative risk: 3.1% at 12 months and 5.7% at
60 months post surgery
Onset:
within 2 months of surgery early and usually
hospital acquired
12 months post surgery late onset and usually
community acquired

Nosocomial Infective
Endocarditis

7-29% of all cases seen in tertiary referral

hospitals
At least half linked to intravascular devices
Other sources GU and GIT procedures or
surgical-wound infection

CLINICAL FEATURES AND

OUTCOME

Presents with low grade fever, anemia and

debility. Many recover on treatment.
Vegetations develop slowly and cardiac
signs are less obvious.
Right side valves more involved especially
tricuspid in drug addicts.
Vegetations are similar to those in AIE but
usually hanging on valve prosthesis.

Investigations
1.
2.

Blood culture
Echo

3.
4.
5.

TTE
TOE

FBC/ESR/CRP
Rheumatoid Factor
MSU

Modified Duke Criteria for

Diagnosis of IE
(Clin. Inf. Dis. 30:633, 2000)

Definite Infective Endocarditis

- 2 major
- 1 major & 3 minor
- 5 minor
Possible Infective Endocarditis
- 1 major & 1 minor
- 3 minor

Major Criteria

+ Blood cultures for endocarditis

- 2 separate + B.C. with typical organisms including
S. aureus associated with line sepsis (OR)
- Persistent (2 + 12 h apart or 3 + over 1 h)
Evidence of endocardial involvement
+ echo (patients with Possible IE a TEE is
recommended) (OR)
- new regurgitant murmur
Positive Q fever serology or single +BCx for
Coxiella burnetii

Duke Criteria
Definite
: 2 major criteria
: 1 major and 3 minor criteria
: 5 minor criteria
: pathology/histology findings
Possible : 1 major and 1 minor criteria
: 3 minor criteria
Rejected : firm alternate diagnosis
: resolution of manifestations of IE with
antimicrobial therapy or less

4 days

Minor Criteria

Predisposing heart condition or IVDU

Fever > 38C
Vascular phenomenon
Immunologic phenomenon
Single positive BC with typical organism

COMPLICATIONS OF
ENDOCARDITIS

Cardiac :

congestive cardiac failure-valvular damage,

more common with aortic valve endocarditis,
infection beyond valve CCF, higher mortality,
need for surgery, A-V, fascicular or bundle
branch block, pericarditis, tamponade or fistulae

Systemic emboli

Risk depends on valve (mitral>aortic), size of

vegetation, (high risk if >10 mm)
20-40% of patients with endocarditis,
risk decreases once appropriate antimicrobial
therapy started.

..

Deposit in kidneys in upto 1/3 of patients

causing focal embolic glomerulonephritis.
Systemic complications- related to
embolic phenomena Cerebral emboli
-Splenic infarcts and
abscess
-Lung abscess

CAUSES OF DEATH

Cardiac failure- valvular damage, rupture

of chordae tendinae leading to dysfunction
Embolic phenomena to heart-results in MI
Brain infarcts
Uncontrolled sepsis
Arrhythmias
Rupture of mycotic aneurysms

Therapy

Antimicrobial therapy

Use a bactericidal regimen

Use a recommended regimen for the organism
isolated

E.g. American Heart Association JAMA 1995; 274: 1706-13.,

British Society for Antimicrobial Chemotherapy

Repeat blood cultures until blood is demonstrated to

be sterile

Surgery

Get cardiothoracic teams involved early

ANATOMY

Myocarditis

Myocarditis is an inflammation of the

myocardium, the thick muscular
layer making up the major portion of
the heart.
Often follows URTI
May present with chest pain (either
pleuritic or non-specific) or signs of heart
failure when rapid in onset.

Infectious

Noninfectious

Viruses
1. Coxsackie B
2. HIV

Systemic Diseases:
1. SLE
2. Sarcoidosis
3. Vasculitides(Wegene
rs)
4. Celiac disease

Bacterial
1. Corynebacterium
diphtheriae

Neoplastic infiltration

Protozoan
1. Trypanosoma cruzi
(Chagas
disease)

Drugs & toxins:

1. Ethanol
2. Cocaine
3. Radiation
4. Chemotherapeutic
agents - Doxorubicin

Spirochete
1. Borrelia burgdorferi

Signs & Symptoms

Days to weeks after onset of acute febrile

illness with heart failure or without any
known antecedent symptoms.
Onset of heart failure may be abrupt and
fulminant or gradual.
May mimic acute MI with ST elevation,
positive cardiac markers, regional wall
motion abnormalities

Hospital Case
Transvenous myocardial biopsy of right ventricular septum
- myocarditis with intense inflammatory infiltrates,
primarily eosinophils, and myocyte necrosis

PERICARDITIS

May result from bacterial, viral or fungal

infection
Can be associated with systemic diseases
such as autoimmune disorders, rheumatic
fever, renal failure and hypothyroidism
Heart attack
Radiation therapy
Injury to the heart-trauma or surgery

PERICARDITIS

Bacterial- tuberculous
-others include staphylococci,streptococci,
Viral-entero-, echo-, adeno-, cytomegalo-,
Ebstein Barr-, herpes simplex-, influenza,
parvo B19, hepatitis C, HIV, etc
Fungal- mainly due to endemic fungi
(Histoplasma, Coccidioides), or nonendemic
opportunistic fungi (Candida, Aspergillus,
Blastomyces) and semifungi (Nocardia,
Actinomyces).

TUBERCULOUS PERICARDITIS

TBC pericarditis in the developed

countries has been primarily seen in
immunocompromised patients (AIDS)
Usually as an extension from lung
The mortality rate in untreated acute
effusive TBC pericarditis approaches 85%.
Pericardial constriction occurs in 3050%.

CLINICAL FEATURES

Majority of patients with tuberculous

pericarditis include fever, tachycardia,
pleural dullness, increased jugular venous
pressure,
hepatomegaly, ascites, and peripheral edema
Not easy to differentiate tuberclous from non
tuberclous disease
CXR, PERICARDIAL ASPIRATE AND BIOPSY

diagnosis
& control
diagnosis
One Diagnosis,
of
the
main
objectives
for
TB
William Osler

Microbiology

Histology
Clinical suspicion

mcq

A.
B.
C.
D.
E.

Infective endocarditis
The aortic and tricuspid valves are the most
common sites of infection
Involves abnormal valves in most acute cases
Is confirmed by positive blood cultures in less than
50% of cases
May cause splenic infarction
May cause MacCallums plaques to form on
affected valves