Cardiovascular Infectious Disease Flashcards
What are the most common cardiovascular infections?
Endocarditis
Rheumatic Heart Disease
Myocarditis
Pericarditis
Intravascular Catheter-related Infections
Artificial Valve, Pacemaker and Defibrillator Infections
Rocky Mountain Spotted Fever (Vasculitis)
What are the normal biota of the cardiovascular system?
Nothing, it’s a privileged site. You should NOT have any microorganisms in your bloodstream.
What are the natural host defenses found in the cardiovascular system?
Leukocytes, billions of them
Complement
Immunoglobulins
Cells of immune system, secreted components
Flow of material helps keep heart cleaned out/makes it hard for bacteria to colonize
Where does the damage (which leads to disease) come from?
- Growth of organism: direct cell lysis, apoptosis, and autophagy due to viral and bacterial infection
- Toxins produced by microorganism (bacteria)
- Immune system collateral damage or malfunction
What is infectious endocarditis?
- Inflammation of the inner lining of the heart (endocardium) caused by bacterial infection.
- Most of the time its an infection of the valves of the heart (usually mitral or aortic valve)
What are the signs of subacute infectious endocarditis?
- Symptoms develop more slowly and are less pronounced
- Fever anemia and an abnormal heartbeat
- Abdominal or side pain is sometimes reported
- Patient may look ill, have petechiae, septic emboli, Roth’s spots, and splinter hemorrhages.
- Enlarged spleen may develop
-34 yr old, wakes up with reduced vision
-Dizziness after exercise, Roth spots
-Recent dental procedure
-Murmur upon exam, mitral valve regurgitation
What does this man likely have? Organism?
- Infective endocarditis
- Streptococcus viridans (usually resides in normal mouth flora)
- Patient started on empiric treatment for endocarditis
- Pure culture taken of infection to narrow down organism
What two organisms cause most acute endocarditis?
Largely Staphylococcus aureus
Sometimes Streptococcus pyogenes
What is the progression of acute endocarditis?
- Hectically febrile (fever that comes and goes)
- Rapidly damages cardiac structures
- Seeds infection in distal sites through sepsis
- If untreated, progresses to death in weeks!
What organisms are usually associated with subacute endocarditis?
Streptococcal species (viridians) Enterococcal species
What is the progression of subacute endocarditis?
- Indolent course of infection
- Causes structural cardiac damage slowly
- Rarely seeds infection at distal sites
- Gradually progressive
What is unique about Streptococcus viridians?
Many different species that damage RBC.
Alpha-hemolytic (partial degradation of RBC, turns green on blood agar)
Many oral flora are alpha-hemolytic
Gamma hemolysis
No color change
Doesn’t damage RBC at all
Alpha hemolysis
Viridans, partial degradation of RBC
Leads to color change/oxidation/turns green
Beta hemolysis
Group A strep (streptococcus pyogenes)
Completely destroys RBC
Yellow on blood agar
What are the usual portals of infection for infectious endocarditis?
Oral cavity
Skin
Upper respiratory tract
What do most local infections occur in infective endocarditis?
Mitral valve
Tricuspid valve (injection drug use)
Prosthetic valves
What group has a high rate of infectious endocarditis?
IV drug users
What temperatures are associated with acute vs. subacute infectious endocarditis?
Subacute - fever usually lower
How is initial diagnosis made for infective endocarditis?
Patient presenting with fever and valvular abnormalities
How is more specific diagnosis made for infective endocarditis?
Screening blood cultures for presence of bacteria, unexplained arterial emboli and progressive cardiac valvular incompetence.
What is the Duke Criteria for Infectious Endocarditis?
It gives requirements for a positive diagnosis.
+ result = 2 major criteria are met, 1 major and 3 minor are met, or 5 minor criteria are met
What does the Duke Criteria require for possible infectious endocarditis?
1 major and 1 minor
OR
3 minor criteria are met
When is the Duke Criteria “trumped”?
When alternative diagnosis is established, symptoms resolve and do not recur with less than 5 days of antibiotic therapy, or lack of histological evidence of endocarditis.
What are the two Duke Major Criteria?
- blood culture (many times there can be contamination - brushing teeth, cutting self - all cultures must come back with same microorganism)
- Evidence of endocardial involvement
What are the five Duke Minor Criteria?
- Predisposition (heart condition or injection drug use)
- Fever above 38C (100.3F)
- Vascular phenomena (arterial emboli, Janeway lesions-non-tender, erythematous lesions on hands and soles, etc.)
- Immunological phenomena (Osler node - painful, red raised lesions on hands and feet, Roth’s spots, rheumatic fever, etc.)
- Microbiological evidence (positive blood culture, but not meeting major criteria, etc.)
How should you treat acute endocarditis?
Gear treatment toward staph infection with concern for MRSA or coat-neg. staph
- Nafcillin or Oxacillin +/- gentamicin or tobramycin
- Vancomycin + gentamicin
How should you treat subacute endocarditis?
Gear treatment toward strep infection.
- Ampicillin/sublactam + gentamicin or tobramycin
- Vancomycin + ceftriaxone or gentamicin/tobramycin
What do you give people with endocarditis and penicillin allergy?
- Cephalosporins (3rd to 5th generation) or carbepenems
2. Vancomycin
What virulence factors are associated with staphylococcus aureus?
Biofilm formation, capsule, adhesins, secreted enzymes and hemolysins, and pathogenicity islands which contain information for methicillin resistance.
What is the most common cause of infectious endocarditis?
Staphylococcus aureus –> majority of infective endocarditis in IV drug users
3 things about Staph aureus:
- Gram +
- Facultative anaerobe
- Usually preceded by bacteremia
What is the bacteria tree for S. aureus?
Gram +
Cocci
Catalase +
Coagulase +
What is the MOST COMMON infectious agent of the skin? What lesion scan it cause?
S. aureus
Superficial boils and abscesses
How can staph aureus present on the skin?
Localized skin/subcutaneous infection: impetigo, cellulitis, folliculitis, furuncles, carbuncles.
What is a common infectious agent of surgical wounds?
Staphylococcus aureus
How does S. aureus colonize the skin and evade host defenses?
- Protein A (binds Fc portion of IgG)
- Coagulase (forms fibrin coat around the organism)
- Hemolysins and leukocidins (destroy RBCs and WBCs)
What S. aureus virulence factors help with deep tissue invasion?
-Hyaluronidase (breaks down connective tissue)
-Staphylokinase (lyses formed clots)
-Lipase (breaks down fat)
Overwhelming bloodstream colonization can be fatal
What is the 2nd major cause of endocarditis?
- Streptococcal species (viridians)-several oral species
- Usually involves underlying mitral valve damage (rheumatic fever, etc.) which provides the site for bacterial colonization
What can Viridans produce?
Dextran for glycocalyx formation and surface adhesion proteins that assist colonization
What is the bacteria tree for streptococcus mutans?
Gram + Cocci Catalase - Alpha-hemolytic Bacitracin resistant
What is the 3rd major cause of endocarditis?
Enterococcus species!
What type of patients get enterococcus endocarditis?
- Usually preceded by bacteremia
- Most frequently found following genitourinary procedures in older men and obstetric procedures in younger women
What virulence factors are associated with enterococcus?
Pili, surface proteins, extracellular enzymes (proteases, hyaluronidases)
What is enteroccous usually resistant to?
Penicillin and Carbepenems
What are the usual clinical presentations for Streptococcus pyogenes?
Localized skin/subcutaneous infection = impetigo, erysipelas, cellulitis
Toxin mediated = toxic shock syndrome, necrotizing fasciitis
What is the pathology associated with strep. pyogenes?
- May be normal skin flora
- Can colonize skin following trauma –> inflammation –> pustular lesions and honeycomb-like crusts (impetigo) at site of inoculation.
- Deeper infections lead to erysipelas and cellulitis. Invasion from skin infections can lead to glomerulonephritis but not Rheumatic fever.
What is the bacteria tree associated with S. pyogenes?
Gram + Cocci Catalase - Beta-hemolytic Bacitracin sensitive
What virulence factors are associated with S. pyogenes?
Streptokinase (converts plasminogen to plasmin)
M protein (resists phagocytosis)
Hyaluronidase (breaks down connective tissue)
DNase (digests DNA)
Streptolysin O (destroys RBCs)
Streptolysin S (destroys WBCs)
Streptokinase and hyaluronidase are encoded by a lysogenized prophage.
What two main pathologies are associated with strep. pyogenes?
Toxic shock syndrome
Necrotizing fasciitis
What is the mechanism of TSS?
- Skin infection (cellulitis)
- Systemic release of pyrogenic exotoxins A (super antigen)
- Polyclonal activation of T cells
- Acute fever, shock, multi-organ failure
What is the mechanism of necrotizing fasciitis?
Trauma allows for deep seated infection –> release of exotoxin B (protease) –> rapid necrosis along fascial planes with no damage to muscles
What is a clinical indicator of rheumatic heart disease?
Mitral stenosis following pharyngitis with a RASH
How does Rheumatic Heart Disease work?
- Follows Streptococcus pyogenes pharyngitis in genetically predisposed individuals
- Type II hypersensitivity
- Damage to heart muscle and valves is attributed to autoantibodies (antibodies to bacterial antigens cross-react with meromyosin in the heart).
What risks and symptoms are associated with Rheumatic Heart Disease?
Risk:
-Strep throat infection (prolonged/untreated)
-Prior case of rheumatic fever
-Age 5 to 15 years old
Symptoms
-Appear 2-4 weeks after strep infection
-Fever, weakness, muscle aches, pain swelling in large joints, shortness of breath, chest pain, nausea, vomiting, hacking cough, circular rash, lumps under skin
What are ways to diagnose Rheumatic Heart Disease?
- Blood tests
- Throat culture
- Echocardiogram
- Chest X-rays
- Electrocardiogram
What are the best treatments for RHD?
- Penicillin based antibiotics
- Aspirin
- Corticosteroids
- Rest
How to prevent RHD?
- Treat strep right away with Abx. This prevents the infection from developing into Rheumatic fever.
- Sore throat + fever for more than 24 hrs should go to Dr.
What is myocarditis? What usually causes it? Symptoms?
Inflammation of the myocardium (middle heart wall layer).
Usually caused by viral infection (Coxsackievirus B & Adenovirus (children)).
Chest pain, heart failure, and abnormal heart rhythms possible.
What is the virus tree for Coxsackievirus A & B?
ssRNA (+), Group IV Nonsegmented Icosahedral Nucelocapsid Nonenveloped Picornaviridae Enterovirus Coxsackievirus A & B
What is pericarditis?
Inflammation of the pericardium (sac-like membrane surrounding the heart).
Typically an acute infection.
Usually caused by a viral infection (Coxsackieviruses A and B, Echoviruses, and influenza virus).
Viral pericarditis usually occurs during the summer months, coinciding with a high incidence of enterovirus infect.
What symptom does pericarditis cause?
Chest pain - associated with irritated layers of the pericardium rubbing against each other
What three picornaviruses cause carditis?
- Coxsackie A virus
- Coxsackie B virus
- Echovirus
What bacteria causes Rocky Mountain Spotted Fever?
Rickettsia Rickettsii
What are the symptoms of RMSF?
Fever, headache, abdominal pain, vomiting, muscle pain. A rash (petechiae-like red dots) may develop but often absent first few days and sometimes never develops.
-RMSF can be severe or even fatal illness if not treated in first few days of symptoms
What is first line treatment for all adults and children with RMSF?
Doxycycline
-Most effective if started before fifth day of symptoms
How is RMSF diagnosed?
Initial diagnosis: clinical signs and symptoms - rash, fever, headache, medical history
Later confirmed: specialized laboratory tests
What are the most common areas for RMSF?
Lower midwest to the East Coast
What is the progression/pathology of RMSF?
- Carried in dogs, rodents
- Bite of dermacentor wood tick or dog tick transmits to humans
- Organism infects and proliferates in endothelial cells
- Inflammation of endothelial lining of small blood vessels
- Maculopapular rash on palms and soles spreading to TRUNK
- Widespread vasculitis
- Headache and CNS changes, renal damage
- May lead to death if untreated!
