Bacteremia, septicaemia and endocarditis by Dr. Rakesh Prasad Sah

1. Bacteraemia,
Septicaemia and
Infective
Endocarditis
Dr. Rakesh Prasad Sah
Assistant Professor, Microbiology

2. • Refers to presence of microorganisms in blood  threat to
every organ in the body
• M.Os. Invasion of blood  serious consequences  shock,
multiple organ failure and DIC
• All four categories of microbes (Bacteria, Viruses, fungi and
parasites) can cause BSI.
Introduction

3. • Bacteraemia  +ce of bacteria in blood without any multiplication.
• Septicaemia  bacteria circulate & actively multiply in the bloodstream.
• Pyaemia  septicaemia caused by pyogenic bacteria with multiple
abscesses in internal organs such as spleen, lungs, liver, kidneys, brain,
heart etc.
• Toxaemia  formation of toxic products in the blood
• When bacterial endotoxin circulates in the blood, the condition is called
endotoxaemia.

4. Causative agents of Septicaemia
GNB (Gram negative Bacilli) (60-70%)
1 Salmonella typhi
2 Salmonella paratyphi A
3 Salmonella paratyphi B
4 Salmonella paratyphi C
5 Brucella spp.
6 Haemophilus influenzae
7 Escherichia coli
8 Klebsiella pneumoniae
9 Proteus spp.
10 Enterobacter spp.
11 Bacteroides spp.
12 Pseudomonas spp.
GPC (Gram Positive cocci) (20-40%)
1 Staphylococcus aureus
2 Staph. epidermidis
3 Streptococcus pyogenes
4 Str. pneumoniae
GPB (Gram Positive bacilli)
1 Listeria monocytogenes
GNC (Gram negative cocci)
1 Neisseria meningitidis

5. • Bacteria may entre bloodstream:
– From an infective focus with the help of phagocytic cells carrying
microbes in to capillaries or the lymphatic system
– From breakages of blood vessels adjacent to the skin or mucosal
surfaces.
– By introduction of contaminated material directly into the vascular
system.
Pathogenesis

6. Microorganisms
Blood
Elimination Persistence
Multiply
Signs and Symptoms

7. Clinical Features
• Fever or hypothermia
• Rigors
• Tachycardia
• Tachypnoea
• Hypoxia
• Dyspnoea
• Cynosis
• Hypotension
• Mental Confusion
• Agitation
• Behavioural changes

8. Complications
• Septic
• Endotoxic
• Bacteraemic shock
• DIC
• Acute renal failure
• Shock may lead to multiple organ failure (e.g. heart, lungs,
liver, kidneys)
Most common complication
Complications

9. • Septic Shock  inadequate blood supply to the tissue
(hypotension)  reduces tissue perfusion pressure  tissue
hypoxia  ischemia and organ dysfunction.

10. • Endocarditis is the infection of the endocardium of heart
valves.
• Inf.  inflammation of membrane lining of the heart.
• Bacterial endocarditis  bacterial inf. Of heart valves
• Mortality rate was very high before pre-antibiotic era
• Even now, mortality rate is around 20-50% despite Antibiotics.
Infective Endocarditis

11. Predisposing factors of Endocarditis
Endocarditis
Congenital defects, e.g.
bicuspid aortic valve,
septal defects, patent
ductus, arteriousus,
coarctation of tha aorta
Rheumatic valvular ds,
e.g. stenosis or
incompetence of the
mitral and aortic valves
following rheumatic fever
Intra-cardiac prostheses,
e.g. replacement of
disease heart valves
Intravenous
drug abuse
Degenerative cardiac
diseases, e.g. calcific
aortic stenosis,
syphilitic aortic valve
disease

12. 1. Subacute endocarditis
2. Acute endocarditis
3. Postoperative endocarditis
4. Endocarditis associated with intravenous drug abuse
Clinical Types

13. • 70% of cases
• Chronic course
• Organisms of low virulence
• On damaged or defective valve cusps
• Form large firm vegetation comprising
of dense fibrin, platelets aggregates
with bacterial colonies are formed.
Subacute endocarditis

14. • Bacteria
– Streptococcus sanguis
– Str. Mutans
– Str. Mitis
– Enterococcus faecalis
– Staph. Epidermidis
– Coxiella burnetti
– Chlamydia psittaci
• Fungi
– Candida albicans
– Aspergillus spp.
Causative agents Subacute Endocarditis
Responsible for
60-80% of cases

15. • Rapidly progressive ds  highly virulent pyogenic bacteria
• Tricuspid valve  more commonly affected.
• If not treated  fatal (less than 6 weeks)
Causative agents
• Staphylococcus aureus
• Streptococcus pneumoniae
• Other pyogenic cocci
– Str. Pyogens
– Str. Agalactiae (group B)
Acute endocarditis

16. • Following cardiac surgery in prosthetic valve replacement.
• Causative agents
– Staphylococcus epidermidis (most commonest)
– Stphylococcus aureus
– Candida albicans
– Acinetobacter calcoaceticus
Post-operative endocarditis

17. • Higher risk
• Tricuspid valve (common)
• Skin is the commonest source of infection
• Causative agents
– Staphylococcus aureus (most commonest)
– Others include
• Viridans group of streptococci
• Candida spp.
• Pseudomonas spp.
Endocarditis associated with IV drug abusers

18. • 3-6 samples of blood, 10ml should be collected over 24 hrs.
• Before starting antimicrobial therapy
• From antecubital vein under all aseptic conditions using sterile
disposable syringe.
• Inoculated into 50-100ml of glucose broth
• Large amount of media is required because:
– Number of organisms in the blood may be very few and
– The blood may contains bactericidal substances which are diluted by large
volume of medium.
Lab Diagnosis

19. • Cultures are incubated at 370C for at least 3 weeks and are to be
observed daily for early signs of growth.
• S/c  on B.A. & M.A. (24hrs, 48hrs & 1ce in a week)  incubation
 isolated colony morphology, Gram staining, biochemical rxn
and serological tests.  AST by MIC & MBC  for ensuring the
serum levels  penetrate valves and kills organisms.
Culture

20. • 10-20% cases
• Following resons
– Recent antibiotic therapy
– Inadequate no. of samples
– Infection with Coxiella burnetti or Chlamydia spp.
• OTHER TESTS
– TLC
– ESR
– Echocardiogram
Culture Negative Endocarditis

21. • Good dental hygiene
• Prophylactic antibiotic before dental extraction or other
surgical procedure.
Prevention