Cardiovascular System Infections

Infections of the Cardiovascular System

• Includes: infective endocarditis, myocarditis, pericarditis, and rheumatic heart disease.

Infective Endocarditis (IE)

• Microbial infection of the heart valves or mural endocardium leading to vegetations.
• Vegetations are friable, bulky, and destructive, containing fibrin, inflammatory cells, and organisms.

Epidemiology/Risk Factors/Affect

• Rare, more common in men, and increasingly found in elderly individuals.

Risk Factors for IE

• Damaged cardiac endothelium + bacteremia = IE.
• Endothelial damage can result from turbulent blood flow, intracardiac catheters, pacemaker leads, rheumatic heart disease, congenital valvular defects like bicuspid aortic valve and VSD(ventricular septal defect), mitral valve prolapse, IV drug use, prosthetic valves, or a previous history of IE, or Marfan’s.

Causes of Bacteremia Leading to IE

• Skin: IV drug use and AV fistula hemodialysis.
• Oro-dental: Extractions, periodontal surgery, and oral irrigation.
• Respiratory tract: Rigid bronchoscopy, intubation, or nasotracheal suction.
• GI tract: Upper GI endoscopy, sigmoidoscopy, colposcopy, barium enema, liver biopsy.
• GU tract: Urethral dilatation, catheterization, cystoscopy, prostatectomy.

IE Can Affect

• Native valves: Inflamed by pathogens.
• Healthy native valves: Affected by virulent organisms.
• Damaged native valves: Affected by normal flora.
• Prosthetic (artificial) valves: Pathogens adhere and grow.
  • Early infection (within 2 months after surgery): Nosocomial pathogens, like Staphylococcus epidermidis, Staphylococcus aureus, Gram-negative aerobic bacilli, and Candida.
  • Late infections (>2 months after surgery): Oro-dental and skin flora, such as S. epidermidis, S. viridans, and HACEK.

Categories of IE

• Subacute: Lower virulence organisms (e.g., Viridans streptococci) cause insidious infections of deformed valves with less destruction.
• Involves smaller lesions on damaged/artificial valves and has an indolent course.
• Native valve endocarditis or prosthetic valve endocarditis.
• Acute - infection of a previously normal heart valve by a highly virulent organism (i.e Staphylococcus aureus) and characterized by large lesions and abscesses formation on previously healthy native native valves.
• Fulminant course

Causative Agents

• Usually grow readily in culture.
• S. aureus (catalase +): Skin abscess, nasopharynx.
• S. epidermidis: Skin, indwelling IV central/peripheral lines.
• S. Viridans (catalase -): Oral cavity (gingiva), pharynx.
• Enterococcus spp: Colon/lower urinary tract.
• S. Gallolyticus/bovis (GDS): Colon/lower urinary tract.
• Pseudomonas aeruginosa: Environment.
• Fungi: Candida (skin/mucous membrane) and Aspergillus (dissemination from respiratory tract).
• Causative agents usually DON'T grow readily in culture
• HAECK (Gram-): Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella oral cavity (gingiva, pharynx).
• Coxiella burnetii (Q fever): Unpasteurized milk/dairy, livestock contact.
• Bartonella:
  • B. Henselae cats/cat fleas.
  • B. Quintana: Louse infestation; homelessness, alcohol abuse.
  • Brucella : Unpasteurized milk/dairy; livestock contact.
• Tropheryma whipplei (whipple's disease): Not clear, GI tract colonizer.

Pathogenesis of IE - Bacterial Factors

• Dextran Production – "Sticky Sugar Coat"
• Pathogen: Viridans Streptococci (e.g., Streptococcus mutans, Streptococcus sanguis).
• Mechanism: Bacteria synthesize dextran (a sticky polysaccharide) from sucrose
  • Dextran binds to fibrin-platelet aggregates at sites of endothelial damage, facilitating attachment.
  • Clinical Correlation: Viridans streptococci commonly cause subacute IE, especially post-dental procedures.
• Surface Adhesins (FimA) – "Sticky Proteins"
  • Pathogen: Viridans Streptococci.
  • Mechanism: FimA is surface adhesin protein, that binds to host cell receptors and facilitates bacterial attachment to the damaged endothelium.
• Clinical Correlation: Facilitates early colonization → bacterial aggregation → vegetation formation.
• Adherence to Non-Bacterial Thrombotic Endocarditis (NBTE)
• Pathogens: -Streptococcus sanguis → binds platelet receptor, fibrin. -Staphylococcus aureus binds fibrinogen & fibronectin.
• Mechanism: NBTE is an initial sterile platelet-fibrin thrombus formed on damaged valves
  • These bacteria bind to fibrin & platelet receptors, making them the first colonizers of the thrombus. Clinical Correlation: Staphylococcus aureus → acute IE, common in IV drug users (tricuspid valve).

Glycocalyx & Slime Layer - "Protective Biofilm"

• Pathogen: Coagulase-negative Staphylococci (e.g., Staphylococcus epidermidis).
  • Mechanism: Glycocalyx & slime layer form a biofilm, that allows bacteria to adhere strongly to prosthetic heart valves and resist immune clearance.
• Protects from antibiotics & host defenses → leads to chronic infections. Clinical Correlation: Common cause of prosthetic valve endocarditis (PVE). Key: -Viridans streptococci adhere via dextran & FimA adhesins → cause subacute IE. -Staphylococcus aureus binds fibrinogen & fibronectin → acute IE (esp. in IV drug users). -Staphylococcus epidermidis forms a biofilm → prosthetic valve infections.

Pathogenesis of IE - (Big Picture)

• Bacterial Entry into the Bloodstream (Bacteremia)
• Sources of Bacteremia: -Dental Procedures (e.g., tooth extractions) → Viridans Streptococci. -Surgery, GI/urinary procedures → Enterococcus species. -IV Drug Use, Skin infections → Staphylococcus aureus. -Prosthetic valves → Coagulase-negative Staphylococci (S. epidermidis). Clinical Correlation:
• If the immune system fails to clear the bacteria, they can reach the heart valves.
• Adherence to the Endothelium and Platelet-Fibrin Clots
• Predisposing Factors: -Valvular Injury: Congenital/acquired heart disease, turbulent blood flow, endothelial damage . -Non-Bacterial Thrombotic Endocarditis (NBTE): Sterile fibrin-platelet deposits form at injured sites.
• Bacterial Adhesion Mechanisms: -Viridans Streptococci → Dextran, FimA adhesins (bind fibrin). -Staphylococcus aureus → Fibronectin-binding proteins (bind endothelium). -S. epidermidis → Biofilm formation on prosthetic valves.
• Clinical Correlation:
• Adherence initiates infection, leading to vegetation formation. Bacterial Proliferation & Vegetation Growth Pathological Progression: -Bacterial proliferation inside vegetations. -Immune evasion: Neutrophils, monocytes, and macrophages infiltrate. Clinical Correlation: -Cytokine Release: Tissue Factor Activation (TFA) promotes fibrin deposition & vegetation expansion. -Staphylococcus aureus: Rapid, aggressive destruction (acute IE). -Viridans Streptococci: Slower-growing, subacute course
• Vegetation Maturation & Systemic Embolization: Consequences of Mature Vegetations. Large friable vegetations can embolize and cause:
• Stroke (CNS emboli).
• Splenic infarcts.
• Septic pulmonary emboli (Right-sided IE).
• Mycotic aneurysms (infected arterial walls).
• Composition of Vegetations in IE -Platelets & Fibrin: Act as a scaffold for bacterial adhesion. -Bacteria: Proliferate within the vegetation, evading the immune system.
• White Blood Cells (WBCs): Attempt to fight the infection but are ineffective due to the dense fibrin matrix. Which Valves Are Most Affected? (Native Valve IE) -Mitral Valve (most common). -Aortic Valve. -Tricuspid Valve (IV drug users). -Pulmonary Valve (least common).
• Left-sided IE (Mitral & Aortic) → More common in non-IV drug users.
• Right-sided IE (Tricuspid) → Seen in IV drug users (S. aureus). Location of Vegetations in Infective Endocarditis. -Aortic Valve - vegetations form on the ventricular side. -Mitral Valve - vegetations form on the atrial side (due to lower pressure). Clinical Manifestation -Seen within 2 weeks in acute IE. Onset of symptoms to diagnosis in Subacute IE is quite long (~ 5 weeks of median interval).
• Clinical features:
• Constitutional symptoms: Fever (+/- chills/rigors), malaise, weight loss, night sweats, myalgias.
• Cardiac: Murmur (new or changing), arrhythmia (conduction block), and heart failure (valve insufficiency).
• Extra cardiac (FROM JANE): -Fever. -Roth spots (immune complex deposition) [Retinal hemorrhages in the eyes]. -Osler nodes: Tender, subcutaneous nodules in the pulp of digits. I- MMurmur. . . . MMurmur. -Janeway lesions: Erythematous or hemorrhagic non-tender lesions on palms or soles . -Anemia, nail bed hemorrhages (splinter hemorrhages),embolic events .
• Complications: -Ring Abscess: Infection spreads into myocardium, forming an abscess. -Septic Embolization: Can lead to stroke, splenic infarcts, mycotic aneurysms, pulmonary emboli. Diagnostic-Includes TTE (Transthoracic echocardiogram) and TEE (Transesophageal echocardiogram). Criteria for diagnosis of infective endocarditis - modified Duke's CRITERIA Subacute Endocarditis
• Stormy onset-fever,chills,anorexia,weight loss,arthralgia,myalgia,back pain.
• Clinical course is related tothe virulence of the infecting organism.
• 2 weeks between colonization and onset of symptoms low grade fever. night sweats,weight loss, malaise . Prosthetic valve endocarditis
• Early onset-< 60 days.
• intermediate onset-60 to >365.
• Late onset - >1 year.
• Vague symptoms within insidious onset chills weight loss myalgia back pain.
• emboli, haematuna,strolk, lesions, splinter hemontage,subcutaneous,nodules, heart murmur, Haelthy Valves. Procedures,dental / oral GIT.Drug user /non-use urinay tracki 6 animal contact damaged, valves Highly Virulent Organisn Antimicrobial therapy:
• Empric 6 targeted Antimicrobial Rx.
• Bactericidal antibiotics are preferred.
• buration of therapy is long (8 weeks 6 relapse is not unusual Surgery is vegetaton too Large: .Prosthetic valve endocardits. Perivalvular abecces. . Fungai enducardi

Empiric antibiotic therapy for infective endocarditis:

• Native valve endocarditis can be:
• Acute bacterial endocarditis (treated for days) with Vancomycin + cefepime or,
• Subacute bacterial endocarditis(treated for weeks) with Vancomycin + ampicilinsuibactam
• Prosthetic valve endocardits can be < year after valve replacement can be trated with Vancomycin + gentamicin + rifampin+ cefepime .>year after valve replacement trated with Vancomycin +eetraxone Who needs ie

Prophylaxis: " Valvular defect. Hirtory of endocarditis. Congenital heait disease

• Prosthestic valve Post. cadac surcey / taraplart

Characteristics of Specific Causative Agents

• S. Viridans (Gram +): -Gram + cocci in chains. -Alpha hemolysis. -Catalase-. -Optochin and Bile solubility- resistant ,oro-dental commensal flora,. synthestze dextrans,Dental periodontal procedure. Causes and causes subacute bactenal endocardts Enterecercas specles. Canbohydate anigen 0 culture charactersties: non-hemolytic and catalase Grows in presence of 6.5% of NaCI Tolerats 40% of bie hydroless esolin
• Staph Aureus Gram+ couc in Clusters (Catalage Positive
• causes acvte endocardits, right side Trinsid endocardit "large Vegetations (Sem)

Details on specific bacteria:

• Staph Aureus Gram+ cocci in Clusters (Catalase Positive)
  • causes acvte endocardts, night side Trmsiddl endocardit
• Gram + Staphylococcus epidermidis:skin flora predletion for prosthetic valve Causes anlective endocardits WOU, exotoxin Oxidas Gram - Bacillus:HACEK
• Causes sublacute endocardits denta procedure is af complexnutitionalreavivements

Acute Rheumatic fever & Rheumatic Heart disease

• The Immune - Strep Pyogenes (OAS) -mmme mediated valwular damage Maaor cnteria and tralment

Molecular Mimicry & Autoimmune Response

• Share structural similarites With human cardiac satcolemma and vasoular tsSues
• Antibodies against GAS cross areact With seir antigens leadirg lo mmme-nedlated

Myocarditis of intectious atology

• Vindes: Coksackie (Pcomavndee, Enterovi SRNA vaked Bactera-Borrelia Burgdorlena (Lyme Staoplo covs Aareus Protozwan:Typanosoma cruzi (chagas disease) Toxoplasma Goriti Helic
• Mode of spread:Vinises Spreads Va contactWith dnoiens from the hrae and throat ofanintected petson
• Children. severe manytsion
• Pethagenezis. acute phase Day 6-a Virasintecth of candeonvocyles. Vitss replcates aside heart muscle inteetons (IENXNBI BNXColls Initiale inrmation

Clinical.recent hastory ok fiuslase svmploms (vinat prodhime) gradwal onset ild dil or plevitic mayreserbia ischenic pain hat posibon bependert

• chronkmanliestations: Dlated candiomyoathy Comestive HL

Cardiac Involvement in Chagas disease

T. cruzi Introduced into the body though ucous menbranes by tubing bug secretion into the are the suelling associated with the chagoma

Myocarditis In Lyme Disease

transmitted bo des tick stage early localiized erychema migrans (typlical bulls-eye rast Is

Diphtheria Myocarditis

• Diontena toxin mhibits eukanatic proten synthess by mhibiting olongation dactors Toxunatteets teopatoy tract opithelium, myocandlunaad CNG ==End of summary==