itis microbiology of cardiovascular

1. Microbes affecting the
cardiovascular system

2. Endocarditis
•Infection and inflammation of the endocardium (thin
lining inside the heart chambers, covering the valves,
and continuous with the linings of the blood vessels
leaving and entering
•Vegetations: are bulky masses of platelets and clotting
proteins that surround and bury the bacteria
Signs and symptoms
•Subacute
•Acute

3. Signs and Symptoms
• Fever, extreme fatigue, malaise, and breathing difficulty
• Tachycardia and murmurs
• Complications such as blood clots, stroke, and the complete
destruction of the heart valves, leading to heart failure, may
manifest
• Endocarditis most commonly affects the left atrioventricular
(mitral) valve, followed by the aortic semilunar valve

4. I. Infective endocarditis
microbial infection involving the endocardial surface of a natural
(native) heart valve or an artificial (prosthetic) heart valve.
Acute endocarditis: Usually fatal
Subacute endocarditis (SBE): Chronic
Risk factors: Congenital/Acquired disorders in the heart
• Valvular insufficiency/stenosis
• Ventricular septal defect (VSD)
• Prosthetic heart valves
• Patent ductus arteriosis (PDA)
• Coarctation of aorta
• Intracardiac catheters

5. Physical findings often include
 Fever
 a new or changing heart murmur
 Splenomegaly
 various skin lesions
 Petechiae
 splinter hemorrhages (on fingernails and toenails)
 Osler nodes (tender subcutaneous nodules on the fingertips or
palms)
 Janeway lesions (are nontender hemorrhagic lesions on the
palms or soles)
 Rose spot (retinal hemorrhages)

6. Osler’s nodes

7. Petechia

8. Splinter hemorrhages

9. Janeway lesions

10. Increases turbulence blood flow
Intracardiac abnormalities
Damage endothelial surface of the heart valves
Colonization by M.O’s + Fibrin + Inflammatory cells=Vegetation formation
Emboli formation

15. Bacterial Causative Agents
•About half are caused by viridans streptococci are not
highly invasive
•but can enter the blood through
•surgical wounds
•small lesions in the lungs during pneumonia
•lacerations of the gums
•including undetectable cuts produced by dental
procedures
•chewing hard candy
•brushing the teeth

16. Viridans streptococci
Although often alpha-haemolytic on blood agar, the
viridans group of streptococci can also be
nonhaemolytic and occasionally beta-haemolytic
A few species are pathogenic (e.g. S. mutans, S.
sanguis, S. mitis) causing endocarditis, bacteraemia,
and dental caries
Normal human GI tract flora
Nasophrynx
Diseases
Dental Infection
Endocarditis
Abscesses

17. Viridans streptococci
General characteristics
Large group of commensal streptococcal
bacteria species that are either α- hemolytic
or non haemolytic streptococci( from latin viridis
mean green)
Many of the bacteria produce green pigment on
blood agar media
Occurs in chains or pairs
these species are non-group able streptococci
In general their pathogenecity is low
Nutritionally they are fastidious

18. Viridian streptococci includes:
S.anginosus
S.Intermedius
S.constellatus
S.mitis
S.bovis
S.gordonii
S.snguis
S.mutans etc

19. • Viridans strept. Have the unique ability to
synthesize dextrans from glucose, which
allows them to adhere to fibrin –platelete
aggregates at damaged heart valves.
• This ability helps them to cause sub acute
endocarditis following introduction to blood
stream(following dental extraction)
• No enzymatic and toxigenic effect has ever
been documented

20. The viridans streptococci colonize the
oropharynx, gastrointestinal tract and
genito urinary tract.
They are rarely found on the skin
surfaces , because the surface fatty
acids are toxic to them
The most commonly associated infection
are dental carries, sub acute
endocarditis, and suppurative intra
abdominal infection

21.  Specific disease is caused by specific bacteria
 Sub acute bacterial endocarditis is caused by
- S.gordonii - S.mitis
- S.mutans - S.oralis
- S.sanguis
 Dental carries
- S. mutans and S. sobrinus
 Abscess formation- S. anginosus , S. constellatus
and S.intermedius
 Malignancy of GIT- S. bovis

22. Identification
 Optochin sensitivity-sensitive-used to
differentiate from S.pneumonia
 Lacks polysaccharide capsule and Lancefield
antigens
 They are bile insoluble
 S.pneumonia-bile soluble
 Quellung test negative
 Catalase negative
 S.pneumonia almost have >99 % gen
sequence homology with S.mitis and S. oralis

23. Treatment
 In the past , most strains of viridans
streptococci were highly susceptible to
penicillin but now penicillin resistance
virdans become common
 Combination of penicillin with
aminoglycosides are effective for resistance
strains.
 Cephalosporins and vancomycin to treat
serious infections caused by penicillin
resistant strains

24.  Why is it important to differentiate S. pneumoniae from viridans
streptococci?

25. Other pathogens causing endocarditis
Opportunistic bacteria
• Staphylococcus epidermidis
• S. aureus from the skin
• Streptococcus pneumoniae
• Escherichia
Both opportunistic and pathogenic
• Neisseria, Pseudomonas, Bartonella , Mycobacterium
• “Culture negative” endocarditis is a condition in which the
causative agent either has not or cannot be cultured and
often remains unknown.

26. Pathogenesis
• Most patients with endocarditis have obvious sources of infection
such as an infected tooth, skin lesion, or intravascular catheter
• Intravenous drug users: at high risk of
• Patients with abnormal hearts
• birth defects
• scarring from previous bacterial infections
• heart valve replacements
Embolus: fragments of vegetation and blood clots, can break off and
travel via the blood to lodge in small blood vessels of the brain,
kidneys, lungs, or abdominal organs, interrupting the flow of blood
and causing severe damage.
• A stroke is such an interruption of blood flow through the brain

27. Genus Enterococci
 Previously they were classified as group D
streptococci(group D glycerol teichoic acid )
 Later it was recognized separately from non
enterococcal group D streptococci known as
S.bovis
 The enterococci and non enterococcal groups
were differentiated on the basis of their
physiologic properties and with nucleic acid
analysis.
 In 1984 , they reclassified in to new genera,
Enterococcus, currently 29 species are present

28.  The most commonly isolated ,clinically important
species are Enterococcus faecalis and
Enterococcus faecium
 Are gram positive cocci in short chains/pairs
 It resembles S.pneumonia in microscopic
morphology
 Facultative anaerobes
 Grow at optimum temperature of 35 oC
 Requires complex nutritional needs(B-vit, nucleic
acid bases, and glucose
 Enriched sheep blood agar- large white colonies
 Colonies can appear non-hemolytic, α-hemolytic,
or rarely β-hemolytic.

29.  Grow in the presence of 6.5% NaCl and 40 % bile
salts , helps to distinguish from other catalase
negative gram-positive cocci
 Enterococci are commensal organisms that don
not have a potent toxin or other well –defined
virulence factors
 These bacteria have surface adhesin proteins that
allow them to bind to the cells lining the human
intestine and vagina host tissues,
 secrete extracellular proteins with hemolytic
activity(cytolysin) and proteolytic activities
 Enterococci can also produce can also produce
bacteriocins that inhibit competitive bacteria

30. • Enterococci are commonly recovered from
in feces collected from humans and fro a
variety of animals.
• E.faecalis are found in large intestine in
large numbers per gram of stool and in the
genitourinary tract
• Most infections are from patient’s bacteria
flora flora, some person to person spread.
• Hospitalization and broad spectrum
antibiotics increases the risk

31. Enterococcal human diseases
• Bacteremia
• Endocarditis
• UTI
• Wound infections
• peritonitis

32. Laboratory diagnosis
• Enterococci grow on non selective media,
blood agar and chocolate agar
• In gram stain it resembles with S.pneumonia
• Differentiated by biochemical
reaction(resistant to optochin, not soluble
by bile)

33. Treatment and prevention
• Enterococci developed inherent resistance to
many commonly used antibiotics (e.g. Oxacilline
and cephalosporins) or have acquired
resistance genes (e.g. To aminoglycosides and
vancomycin)
• Series infections requires combination of
aminoglycosides with cell wall active
antibiotics(P, AM and vancomycin)
• Avoiding broad spectrum drugs and infectious
control measures reduce the prevalence