1. Infective Endocarditis

2. Introduction Endocarditis, irrespective of the underlying cardiac condition, Endocarditis, irrespective of the underlying cardiac condition, is a serious, life-threatening disease that was always fatal in the preantibiotic era. is a serious, life-threatening disease that was always fatal in the preantibiotic era. Advances in antimicrobial therapy Advances in antimicrobial therapy Early recognition and management of complications of IE Early recognition and management of complications of IE Improved surgical technology have reduced the morbidity Improved surgical technology have reduced the morbidity and mortality of IE. and mortality of IE. Numerous comorbid factors, may complicate IE such as Numerous comorbid factors, may complicate IE such as older age, diabetes mellitus older age, diabetes mellitus immunosuppressive conditions or therapy immunosuppressive conditions or therapy dialysis. dialysis.

3. DEFINITION Infection or colonization of endocardium, heart valves, congenital defects by bacteria, rickettsiae, fungi Infection or colonization of endocardium, heart valves, congenital defects by bacteria, rickettsiae, fungi. Low grade persistent bacteraemia Low grade persistent bacteraemia

4. IMPORTANCE Serious disease Serious disease mortality : 30 % mortality : 30 % Damage of heart or other organs Damage of heart or other organs Follow dental procedures ( tooth extraction) Follow dental procedures ( tooth extraction) Rheumatic heart disease Rheumatic heart disease Congenital heart disease Congenital heart disease

5. Calssification Classified into four groups: Classified into four groups: Native Valve IE Native Valve IE Prosthetic Valve IE Prosthetic Valve IE Intravenous drug abuse (IVDA) IE Intravenous drug abuse (IVDA) IE Nosocomial IE Nosocomial IE

6. Classification Subacute Often affects damaged heart valves Indolent nature If not treated, usually fatal by one year Acute Acute Affects normal heart valves Affects normal heart valves Rapidly destructive Rapidly destructive Metastatic foci Metastatic foci Commonly Staph. Commonly Staph. If not treated, usually fatal within 6 weeks If not treated, usually fatal within 6 weeks

7. ETIOLOGY SUSCEPTIBLE PATIENT SUSCEPTIBLE PATIENT BACTEREMIA BACTEREMIA

8. FACTORES AFFECTING SEVERITY AND OUTCOME BACTERIAL FACTORS BACTERIAL FACTORS VIRULENCE VIRULENCE No BACTERIA IN THE BLOOD No BACTERIA IN THE BLOOD

9. HOST FACTORS : HOST FACTORS :. FACTORS INCREASING SUSCEPTIBILITY. FACTORS INCREASING SUSCEPTIBILITY LOCAL LOCAL CONGINITALOR RHEUMATIC HEART DISEASE CONGINITALOR RHEUMATIC HEART DISEASE PROSTHETIC HEART VALVES PROSTHETIC HEART VALVES OTHER CARDIOVASCULAR DISEASE OTHER CARDIOVASCULAR DISEASE HEART SURGERY HEART SURGERY GENIRAL GENIRAL UNDERLYING DISEASE ( DIABETES.M ) UNDERLYING DISEASE ( DIABETES.M ) DRUGS DRUGS IATROGENIC: IATROGENIC: IMMUNOSUPPRESSIVE TREATMENT IMMUNOSUPPRESSIVE TREATMENT CYTOTOXIC AGENTS CYTOTOXIC AGENTS SELF- INFLICTED SELF- INFLICTED ALCOHOLISM ALCOHOLISM ADDICTION (INJECTED DRUGS ) ADDICTION (INJECTED DRUGS ) PROTECTIVE FACTORS PROTECTIVE FACTORS ANTIMICROBIAL CHEMOTHERAPY ANTIMICROBIAL CHEMOTHERAPY

10. SOURCES OF INFECTION Dental extraction and other dental procedures Dental extraction and other dental procedures Cardiac surgery ( prosthetic valves) Cardiac surgery ( prosthetic valves) Intravenous medication Intravenous medication Iv. Drug addiction Iv. Drug addiction Intracardiac or intravenous catheters Intracardiac or intravenous catheters Obstetric or gynaecologic procedures Obstetric or gynaecologic procedures

11. PREDISPOSING FACTORS A- cardiac lesions A- cardiac lesions Chronic rheumatic valvular disease Chronic rheumatic valvular disease Congenital heart disease and defects Congenital heart disease and defects Atherosclerosis Atherosclerosis Prosthetic valves Prosthetic valves Immediate Immediate Delayed Delayed Distorted shape causes stasis of blood flow and settee of bacteria on the endocardium Virulent bacteria`, staph. aureus and strept. Pneumoniae can infect normal heart

12. B. systemic factors B. systemic factors Immunosuppressive treatment Immunosuppressive treatment Immune defects ( disease) Immune defects ( disease) Alcoholism Alcoholism Iv. Drug abuse Iv. Drug abuse

13. PORTAL OF ENTRY Dental extraction bleeding bacteraemia Dental extraction bleeding bacteraemia Rocking the tooth in the socket pumping effect on the vessels of periodontal ligament, forces bacteria from gingival pockets into blood stream 40 – 80 % bacteraemia Rocking the tooth in the socket pumping effect on the vessels of periodontal ligament, forces bacteria from gingival pockets into blood stream 40 – 80 % bacteraemia Sensitivity of blood culture techniques Sensitivity of blood culture techniques Severity of gingival infection Severity of gingival infection Oral irrigation device Oral irrigation device

14. NOTE  Bacteraemia may follow scaling, tooth brushing, endodontic therapy.  Lack of clinical effect of many bacteraemia is due to small number or low virulence  They are rapidly cleared by normal body defence ( leucocytes )  Strept. Faecalis may cause endocarditis after genitourinary or gut procedures

15. CAUSATIVE ORGANISMS Viridans streptococci Viridans streptococci Most common cause of sub- acute bacterial endocarditis (SBE) Most common cause of sub- acute bacterial endocarditis (SBE) Produce glucagons adhere to endocardium Produce glucagons adhere to endocardium E.g : E.g : Streptococcus mutans Streptococcus mutans Streptococcus sanguis Streptococcus sanguis

16. Streptococcus faecalis Streptococcus faecalis Streptococcus faecium Streptococcus faecium Streptococcus pneumoniae Streptococcus pneumoniae Staphylococcus aureus Staphylococcus aureus Acute endocarditis Acute endocarditis Staphylococcus epidermidis Staphylococcus epidermidis Prosthetic heart valves Prosthetic heart valves Brucella species Brucella species Actinobacillus actinomycetes comitans Actinobacillus actinomycetes comitans Rickettisae Rickettisae Fungi Fungi Coxiella burneti Coxiella burneti Candida albicans Candida albicans

17. PATHOGENESIS Formation of vegetations Formation of vegetations  Fibrin, platelets (thrombi), bacteria colonies Attached to heart valves  Break off infected emboli distant organs ( kidney, brain )  Immune complex formation causes glomerular damage haematuria  Valves infection destruction heart failure.  Drug addicts tricuspid,pulmonary valves of right side of heart lung emboli pneumonia

18. PATHOLOGICAL CHANGES IN IE

20. CLINICAL FEATURES Onset is insidious ( SBE) – 3 weeks after extraction Fever ( mild and prolonged ) Malaise, weight loss, weakness Changing murmurs Anaemia, leucocytosis Microscopic haematuria PetechiaeSpleenomegaly Splinter haemorrhage Hypergammaglobulinaemia Age young, elderly

21. Petechiae 1.Nonspecific 2.Often located on extremities or mucous membranes

22. Embolic manifestations of endocarditis

23. Splinter hemorrhage

24. Osler’s Nodes 1.More specific 2.Painful and erythematous nodules 3.Located on pulp of fingers and toes 4.More common in subacute IE

25. CNS manifestations of endocarditis

26. MORTALITY With antibiotic treatment 30% 30% High mortality High mortality Virulance of organism or sever infection Virulance of organism or sever infection Presence of underlying disease Presence of underlying disease Elderly Elderly Inadequate treatment Inadequate treatment poor prognosis poor prognosis Candidal Candidal Staphylococcus Staphylococcus Gram-negative Gram-negative

27. LABORATORY DIAGNOSIS A – serial blood culture ( 2-3 sets before antibiotic therapy ) A – serial blood culture ( 2-3 sets before antibiotic therapy ) Aerobic Aerobic Anaerobic Anaerobic Additional tests Additional tests CBC, ESR and CRP, Complement levels (C3, C4, CH50) CBC, ESR and CRP, Complement levels (C3, C4, CH50) RF RF Urinalysis Urinalysis B- serological tests B- serological tests CFT ( coxiella burniti ) CFT ( coxiella burniti ) C- sensitivity test C- sensitivity test

28. Endocarditiis causes: continuous Bacteraemia There are three clinical patterns of bacteremia:  Transient-  lasts minutes to hours: following manipulation of infected tissues(abscess,furuncle,or during a surgical procedure);instrumentation of contaminated mucosal surfaces (dental procedures,cytoscopy,or sigmoidoscopy);and at the onset of bacterial pneumonia,arthritis,osteomylitis,and meningitis.  Intermittent  commonly occurs with undrained abscesses.  Contineous  reflects an endovascular infection such as endocarditis or endarteritis,suppurative thrombophlebitis,or an infected aneurysm. It also occurs in the first two weeks of typhoid fever and brucellosis.

29. Technique for collection of blood for culture Blood for culture contaminated by normal skin flora e.g. Blood for culture contaminated by normal skin flora e.g. A. Staphylococcus epidermidis B. Diphtheriods and C. Propioniobacteria(anaerobic diphtheroides) So first clean the site(mainly anticubital fossa)with alcohol 70%and leave for 1-1 1/2 minutes)or cholorhexidine or iodine

30. Blood culture by automated machines e.g. Bactec or Bactalert- upto 5 days when signal positive, the specimen is gram stained Blood culture by automated machines e.g. Bactec or Bactalert- upto 5 days when signal positive, the specimen is gram stained reported to clinician then cultured identified and tested for antimicrobial susceptibility reported to clinician then cultured identified and tested for antimicrobial susceptibility

31. Imaging Chest x-ray Chest x-ray Look for multiple focal infiltrates and calcification of heart valves Look for multiple focal infiltrates and calcification of heart valves ECG ECG Rarely diagnostic Rarely diagnostic Look for evidence of ischemia, conduction delay, and arrhythmias Look for evidence of ischemia, conduction delay, and arrhythmias Echocardiography Echocardiography

32. Local Spread of Infection Heart failure Heart failure Extensive valvular damage Extensive valvular damage Paravalvular abscess (30-40%) Paravalvular abscess (30-40%) Most common in aortic valve, IVDA, and S. aureus Most common in aortic valve, IVDA, and S. aureus May extend into adjacent conduction tissue causing arrythmias May extend into adjacent conduction tissue causing arrythmias Higher rates of embolization and mortality Higher rates of embolization and mortality Pericarditis Pericarditis Fistulous intracardiac connections Fistulous intracardiac connections

33. Local Spread of Infection Acute S. aureus IE with perforation of the aortic valve and aortic valve vegetations. Acute S. aureus IE with mitral valve ring abscess extending into myocardium.

34. Embolic Complications Stroke Stroke Myocardial Infarction Myocardial Infarction Fragments of valvular vegetation or vegetation- induced stenosis of coronary ostia Fragments of valvular vegetation or vegetation- induced stenosis of coronary ostia Ischemic limbs Ischemic limbs Hypoxia from pulmonary emboli Hypoxia from pulmonary emboli Abdominal pain (splenic or renal infarction) Abdominal pain (splenic or renal infarction)

35. Septic Emboli

36. Metastatic abscess Metastatic abscess Kidneys, spleen, brain, soft tissues Kidneys, spleen, brain, soft tissues Meningitis and/or encephalitis Meningitis and/or encephalitis Vertebral osteomyelitis Vertebral osteomyelitis Septic arthritis Septic arthritis Metastatic Spread of Infection

37. TREATMENT Disk diffusion test ( not sufficient ) Disk diffusion test ( not sufficient ) MIC, MBC MIC, MBC Criteria of antibiotic Criteria of antibiotic Bactericidal Bactericidal Parenteral Parenteral High dose High dose Prolonged Prolonged

38. Viridans streptococci –Benzyl penicillin I.V Viridans streptococci –Benzyl penicillin I.V 4 MU I.V. every 4 hrs for 4 weeks 4 MU I.V. every 4 hrs for 4 weeks or or penicillin + gentamicin penicillin + gentamicin Streptococcus faecalis ampicillin + gentamicin I.V Streptococcus faecalis ampicillin + gentamicin I.V Recurrence after cure is common in: Recurrence after cure is common in:  drug addicts  immunodeficient patients