Introduction to Cardiovascular Infectious Disease Flashcards
Infectious Endocarditis
Inflammation of the inner lining of the heart (endocardium) caused by bacterial infection.
Most of the time this refers to an infection of the valves of the heart (most often the mitral or aortic valve).
Two variations of the infection – acute and subacute – each with distinct groups of microorganisms that cause disease.
signs and symptoms of infectious endocarditis
fever, anemia, and an abnormal heartbeat
Abdominal or side pain is sometimes reported
patient may look very ill and may have petechiae (small red-to-purple discolorations), septic emboli, Roth’s spots, and splinter hemorrhages under the fingernails
In subacute cases, an enlarged spleen may develop.
Septic emboli
Septic emboli with hemorrhage and infarction due to acute Staphylococcus aureus endocarditis
Acute endocarditis
largely Staphylococcus aureus, sometimes Streptococcus pyogenes
Hectically febrile
Rapidly damages cardiac structures
Seeds infection in distal sites through sepsis
If untreated, progresses to death within weeks
103F to 104F fever often seen
Subacute endocarditis
Streptococcal species (viridans), Enterococcal species
Indolent course of infection
Causes structural cardiac damage slowly
Rarely seeds infection at distal sites
Gradually progressive
usually less than 103 fever
Infectious Endocarditis – Clinical Features
Generally nonspecific.
Initial diagnosis can be made through a patient presenting with a fever and valvular abnormalities.
behavior pattern that predisposes the patient to endocarditis (injection drug use).
blood cultures for bacteria that cause endocarditis, otherwise-unexplained arterial emboli, and progressive cardiac valvular incompetence.
The Duke Criteria for infectious endocarditis
Highly sensitive and specific.
Positive result = 2 major criteria met, 1 major and 3 minor criteria met, or 5 minor criteria met.
trumped if 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.
Possible infectious endocarditis is 1 major and 1 minor or 3 minor criteria are met.
The Duke Major Criteria:
Positive blood culture (two separate cultures, or one for Coxiella burnetii)
Evidence of endocardial involvement
The Duke Minor Criteria:
Predisposition (heart condition or injection drug use)
Fever above 38C (100.3F)
Vascular phenomena (arterial emboli, Janeway lesions, etc.)
Immunological phenomena (Osler’s nodes, Roth’s spots, rheumatoid factor, etc)
Microbiological evidence (positive blood culture, but not meeting major criterion, etc)
Infectious Endocarditis – Portals of Entry (Primary Infection Sites):
Oral cavity
Skin
Upper respiratory tract
Infectious Endocarditis - Local infection (in heart):
Mitral valve
Tricuspid valve (injection drug use)
Prosthetic valves
Janeway lesion:
non-tender, small haemorrhagic lesions on the palms and soles.
Osler’s nodes:
painful, red, raised lesions on the hands and feet. –immune complex disposition.
Rheumatiod factor:
autoantibody associated with articular disease. Can be elevated in chronic hepatitis, bacterial endocarditis, leukemia, mono, SLE
Treatment for acute endocarditis
gear towards a staph infections
- Nafcillin or ozacillin +/- gentamicin or tobramycin
- Vancomycin + gentamicin
Treatment for subacute endocarditis
- gear towards a strep infection
1. ampicillin/sublactam + gentamicin or tobramycin
2. Vancomycin+ ceftriazone or tentamicin/tobramycin
Treatment for endocarditis in penicillin allergic patients
- Cephalosporin (3rd and 5th generation or carbapenems
2. vancomycin
Staphylococcus aureus: classification
Gram +
cocci
catalase +
coagulase +
Staphylococcus aureus: virulence factors
protein A (binds Fc portion of IgG)
coagulase (forms fibrin coat around the organism)
hemolysins and leukocidins (destroy RBCs and WBCs)
Hyaluronidase (breaks down connective tissue)
Staphylokinase (lyses formed clots)
Lipase (breaks down fat)
Staphylococcus aureus: clinical presentaton
Most common cause of endocarditis
Localized skin/subcutaneous infection(most common skin infection) = impetigo, cellulitis, folliculitis, furuncles, carbuncles. Common infectious agent of surgical wounds.
Streptococcus mutans: classification
gram + cocci catalase - a-Hemolytic (is a member of strep viridans) Bacitracin resistant
Streptococcal viridans species: Infectious Endocarditis
2nd major cause; several oral species possible
Usually involves underlying mitral valve damage (rheumatic fever) which provides the site for bacterial colonization.
Viridans scan produce dextran for glycocalyx formation and surface adhesion proteins that assist colonization
Enterococcus species: infectious endocarditis
3rd major cause
Usually preceded by bacteremia.
Most frequently found following genitourinary procedures in older men and obstetric procedures in younger women.
Virulence factors include pili, surface proteins, and extracellular enzymes like proteases and hyaluronidases.
Usually resistant to penicillin and carbepenems.
Streptococcus pyogenes: classification
gram + cocci catalase - Beta hemolytic bacitracin sensitive
Streptococcus pyogenes: Clinical Presentation
major cause of bacterial skin infections
Localized skin/subcutaneous infection = impetigo, erysipelas, cellulitis
Toxin-mediated = Toxic shock syndrome, necrotizing fasciitis
Streptococcus pyogenes: mechanism of infection
Can colonize in the skin (following trauma) –> inflammation –> pustular lesions and honeycomb-like crusts (impetigo) at the site of inoculation. Deeper infections lead to erysipelas and cellulitis. Invasion from skin infections can lead not glomerulonephritis but not Rheumatic fever.
Streptococcus pyogenes: virulence factors
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)
Rheumatic Heart Disease
Follows Streptococcus pyogenes pharyngitis in genetically predisposed individuals.
Mitral stenosis following pharyngitis with a rash is a definitive clinical indicator.
The damage to the heart muscle and valves is attributed to autoantibodies (antibodies to bacterial antigens cross-react with meromyosin in the heart). Type II hypersensitivity.
Rheumatic Heart Disease: symptoms
Usually appear 2 to 4 weeks after strep infection Pain swelling in large joints Fever Weakness Muscle aches Shortness of breath Chest pain Nausea and vomiting Hacking cough Circular rash Lumps under the skin
Rheumatic Heart Disease: Risks for aquiring
Strep throat infection (prolonged / untreated)
Prior case of rheumatic fever
Age 5 to 15 years old
Rheumatic Heart Disease - Diagnosis
Blood Tests Throat Culture Echocardiogram Chest x-rays Electrocardiogram
Rheumatic Heart Disease - Treatment
Penicillin based antibiotics
Aspirin
Corticosteroids
Rest
Rheumatic Heart Disease - Prevention
Treat strep throat right away with antibiotics. Prevents the infection from developing into rheumatic fever.
People experiencing a sore throat and a fever lasting more than 24 hours should consult a physician.
Myocarditis: definition
Inflammation of the myocardium (middle layer of the heart wall). Usually caused by a viral infection (Coxsackievirus B and Adenovirus (children)).
Chest pain, heart failure, and abnormal heart rhythms possible.
Coxsackievirus A & B: classification
ssrna (+), group IV nonsegmented Icosahedral Nucleocapsid Nonenveloped Picornaviridae Enterovirus
Pericarditis: definition
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 higher incidence of enterovirus infections.
Chest pain associated with the irritated layers of the pericardium rubbing against each other.
Rocky Mountain Spotted Fever caused by
Rickettsia rickettsii
Rocky Mountain Spotted Fever: Typical symptoms include
fever, headache, abdominal pain, vomiting, and muscle pain. A rash may also develop, but is often absent in the first few days, and in some patients, never develops.
Treatment for Rocky Mountain Spotted Fever
Doxycycline is the first line treatment for adults and children of all ages, and is most effective if started before the fifth day of symptoms
What can cause Palm and Sole Rash:
RMSF
Syphillus
Coxsackievirus
Obligate intracellular parasites that need host ATP to survive:
Chlamydiae and Rickettsiae
don’t know what this has to do with anything, but it’s there
