cvs infection.......................................

cvs.endocarditid'acute rheumatic fever,blood stream infection

1. Cardiovascular
System Infections
Dr Sara Neha
SIMS

2. Introduction
•Include infection of the heart and blood vessels
–Layers
•Endocardium infective endocarditis
•Myocardium myocarditis
•Pericardium pericarditis & pericardial effusion.
–Infection of blood vessels mycotic aneurysm, infective endocarditis
–Device related infections CRBSI
–Autoimmune-mediated Acute Rheumatic fever

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

4. Predisposing factors of Endocarditis
Endocarditis
Congenital defects, e.g.
bicuspid aortic valve,
septaldefects, patent
ductus, arteriousus,
coarctationof thaaorta
Rheumatic valvulards,
e.g. stenosisor
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

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

6. Feature SubacuteEndocarditis Acute Endocarditis
Progression of disease Slow progressive diseaseRapidlyprogressive disease
Heart valves involved Defective or previously
damaged heart valves
Normal heart valves
Causative agent Lowvirulent organisms e.g.
viridansstreptococci
High virulent organisms e.g.
Staph aureus
Recovery Most patients recoverafter
antibiotic tretment
Causes morbidityand
mortality even after
antibiotic treatment
Occurrence More common Lesscommon

7. •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.
Subacuteendocarditis

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

9. •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

10. Specific types of Endocarditis
Native valve Endocarditis
•Causative organism
–Staph aureus most common
–Viridans streptococci
–HACEK group (Haemophilus aphrophilus, Aggregatibacter
species, Cardiobacterium hominis, Eikenella corrodens, Kingella
kingae)

11. •Following cardiac surgery in prosthetic valve replacement.
•Causative agents
–Staphylococcus epidermidis (most commonest)
–Stphylococcus aureus
–Viridans streptococci
Post-operative endocarditis

12. •Higher risk
•Tricuspid valve (common)
•Skin is the commonest source of infection
•Causative agents
–Staphylococcus aureus (most commonest)
–Others include
•Enterococcus species
•Candida spp.
•Pseudomonas spp.
Endocarditisassociated with IV drug abusers

13. Pathogenesis
Organisms enter the blood stream form the primary site
(mouth, skin, intestine and respiratory system)heart
Mouth Viridansstreptococci
Skin Staphylococci
Intestine Enterococci
Respiratory tract HACEK organisms
Patients at risk are those who have pre-existing cardiac disease,
which include: rhematicfever, congenital valve deformities,
cardiac valve prosthesis, Degenerative cardiac disease, drug
abuse
Tricuspid, aortic and mitral valves. Infection endocardium.
Endothelial injury Friable, bulky vegetations formed 
composed of platelets, fibrin & inflamatorycells
Destruction of underlying cardiac tissue

14. Clinical Features
•Fever and chills
•Fatigue
•Night sweats
•Chest pain while breathing
•Anorexia, weight loss, malaise

15. Lab Diagnosis
•Modified Duke criteria
–Major Criteria
–Minor criteria
Major Criteria :-
1.Positive Blood Culture:-Any of the following
•Typical IE organisms isolated from two separate blood cultures
•Persistent positive blood cultures with organisms other than typical
organisms of IE.
–Blood cutures are taken more than 12hrs apart.
–All three sets or majority of ≥ 4 separate blood cultures, with first and last blood
culture taken at least 1 hr apart.
–Single positive blood culture for C. burnetii or antiphase I IgG Ab titre >1:180
2. Endocardial involvement:-Any of the following
–Postive ECG findings
–New valvular regurgitations

16. •Minor Criteria
–Predisposing heart conditions
–Intravenous drug abuse
–Fever ≥38.0
0
C
–Vascular phenomena :Marorarterial emboli, septic pulmonary infarcts, mycotic
aneurysm, intracranial haemorrhage, conjunctivalhaemorrhagesor Janeway
lesions.
–Immunologic phenomena:Glomerulonephritis, Osler’s nodes, Roth’s spots,
and rheumatoid factor.
–Microbiological evidence: Positive blood culture but not meeting major criteria
as noted earlier or serological evidence of active infection with organism
consistent with infective endocarditis.
•Definitive Endocarditis
–Two major criteria or
–One major criterion and three minor criteria or
–Five minor criteria

17. Specimen
•Two sets of blood cultures collected at interval of ≥12hrs.
•Alternatively three blood cultures collected at interval of 30mins.
•Each blood cultures set has pair of bottles collected from different
sites.
•Sample should be collected before starting of antimicrobial therapy.
•Blood collected antecubital vein 10ml in 50-100ml of BHI.
•Large amount of media is required
–No. of organisms in the blood may be very low
–Blood contains bacteriocidal substances diluted by large volume
•Note:-repeated blood cultures are made bacteremia is intermittent
in I.E.

18. Culture
•Incubated at 37
0
C for 3 weeks.
•And S/C is done on solid media B.A. and M.A. after 24hrs, 48hrs and
once in a week thereafter.
•Biphasic Castaneda’s medium
•Identification
•Automations:-BACTEC and BacT/ALERT.
•Antibiotic sensitivity Tests
•Culture Negative Endocarditis

19. •Culture Negative Endocarditis (10-20% cases, blood cultures are
persistently negative)
–Recent antibiotic therapy
–Inadequate number of specimens
–Infection with HACEK organisms, Coxiellaburnetiior Chlamydia spp
•Other tests for diagnosis
–TLC:-Leucocytosis
–ESR:-Elevated
–Echocardiogram:-demonstrates vegetations and other changes in the valve.

20. Acute Rheumatic Fever
•Occurs in persons who had previously streptococcal (group A) sore
throat and occurs due to autoimmune reaction.
•Is a non-suppurative sequel or complication of Streptococcus
pyogens (Group A streptococci).
•Occurs one to four weeks after the acute infections of streptococcus
pyogens infection.
•Etiological Agent
–Streptococcus pyogens (usually by M-serotypes 3,5,6,14,18,19 and 24).

21. Pathogenesis
•Occurs mainly in children between the age 5-15yrs and rare over
30years of age.
•Recurrent episodes of ARF are common in young adults.
•When cardiac valvulardamage occurs rheumatic heart disease
(RHD).
•Pathogenesis of ARF is not clear but may be due to:-
•Autoimmune
–Abs Streptococcal Ags(M-protein) cross react with myocardial and heart
valve tissue cellular damagedamage of heart valves.
•Cytotoxic
–Streptococcal toxins (SPE streptpyogenicexotoxin) and enzymes (SLO)
cytotoxicfor human cardiac cells.

22. Clinical Features
•ARF invovle heart, joints, nervous system and skin
•Common features
–Fever
–Migrating polyarthritis :-painful, red, hot, swollen and tender joints in the knees,
ankles, elbows and wrists.
–Pancarditis :-endocardium, pericardium or myocardium. Have chest pain. Due to
valvular damage in heart, mitral regurgitation diagnosed by murmur
–Sydenham’s chorea:-jerky involuntary body movements in hands, feets and
face.
–Subcutaneous nodules:-small painless lumps beneath the skin.
–Erythema marginatum

23. Diagnosis
•Diagnosed by modified Jones criteria
Major Criteria
S.No.Low risk population Medium / high risk population
1 Carditis(Clinical and/or subclinical)Carditis(clinincaland/orsubclinical)
2 Arthritis
•Polyarthiritsonly
Arthritis
•Monoarthritsor
•Polyarthritis
•Polyarthralgia
3 Chorea Choera
4 Erythemamarginatum Erythemamarginatum
5 Subcutaneous nodules Subcutaneousnodules

24. Diagnosis
•Diagnosed by modified Jones criteria
Minor Criteria
S.No.Low risk population Medium / high risk population
1 Polyarthralgia Monoarthralgia
2 Fever (≥38.5
0
C) Fever (≥38
0
C)
3 ESR ≥60 mm in the first hour and/or
CRP ≥3.0 mg/dl
ESR ≥30 mm in the first hour and/or
CRP ≥3.0 mg/dl
4 Prolonged PR interval Prolonged PR interval

25. •Diagnosis of ARF is made on the basis of following criteria:
•Evidence of preceding GAS infection
–At least one of the following should be positive
•A positive throat culture for Str. Pyogens
•Rapid Ag test for Str pyogens
•Rise in anti-streptococcus Abs such as elevated ASO titre
•Scarlet fever
1
Initialacute rheumatic fever 1 Two major criteria or one major
criterion plus two minor criteria
2
RecurrentARF 2 Two major criteria or one major
criterion plus two minor criteria or
three minor criteria

26. Lab Diagnosis
•Serology for Ab detection
–Antistreptolysin ‘O’ (ASO) test
•Titre >200 Todd units/ml is significant in rheumatic fever and indicates 
past streptococcal infection
–Antistreptozyme test
•Is a passive slide haemagglutination test
•Positive after nearly all types of Streptococal infection.
–Anti-streptokinase Ab detection
–Anti-hyaluronidase Ab detection
•Detects Abs in patient’s serum

27. Blood Stream Infection
•BSI

28. •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

29. •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.

30. Causative agents of Septicaemia
GNB(Gram negative Bacilli) (60-70%)
1Salmonella typhi
2Salmonella paratyphiA
3SalmonellaparatyphiB
4SalmonellaparatyphiC
5Brucellaspp.
6Haemophilusinfluenzae
7Escherichia coli
8Klebsiella pneumoniae
9Proteus spp.
10Enterobacter spp.
11Bacteroidesspp.
12Pseudomonas spp.
GPC(Gram Positive cocci) (20-40%)
1Staphylococcus aureus
2Staph. epidermidis
3Streptococcus pyogenes
4Str. pneumoniae
GPB(Gram Positive bacilli)
1Listeriamonocytogenes
GNC(Gram negative cocci)
1Neisseriameningitidis

31. •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

32. Microorganisms
Blood
Elimination Persistence
Multiply
Signs and Symptoms

33. Clinical Features
•Fever or hypothermia
•Rigors
•Tachycardia
•Tachypnoea
•Hypoxia
•Dyspnoea
•Cynosis
•Hypotension
•Mental Confusion
•Agitation
•Behaviouralchanges

34. 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

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

36. •Thank YOU