Structure:
· Gram (+) cocci
· Not encapsulated
· Non-sporulating
· No Lancefield carbohydrate antigen in cell wall
· Biofilm former
Pathobiology:
S. sanguinis:
· NORMALLY inhabits oropharynx epithelium
· Can seep into bloodstream (i.e. flossing)
· Can adhere to platelet-fibrin clumps on PREVIOUSLY damaged heart valves that were damaged from group A Strep (i.e. from Rheumatic fever affecting mitral valve)
· This can lead to subacute bacterial endocarditis (SBE)
S. mutans
· Can attach to teeth via extracellular dextran
· Converts sugars to lactic acid via fermentation →decrease in pH → destruction of tooth enamel → dental caries
S. intermedius
· A member of normally GI flora
· Can progress to abscesses in low-O2 environment of brain/abdomen
Epidemiology:
· Neutropenic patients have been shown to be at increased risk of susceptibility to S. viridians (Tunkel, et. al)
· Incidence of SBE: 11-15 per 100,000 patients
Laboratory diagnosis:
· Catalase (-)
· Alpha hemolytic (appear green on blood agar plate due to partial hemolysis) *note “viridis” in Latin means “green”
· Bile-esculin insoluble (solution will appear cloudy)
· Optochin resistant (no halo will form around optochin disc)
· Quellung reaction (-)
Disease Manifestations:
· Systemic: Subacute Bacteria Endocarditis (SBE) (S. sanguinis/S. bovis)
o Patients can present with fever, general malaise
o Osler’s nodes on hands and feet (due to deposition of immune complexes): tender, erythematous lesions on hands and feet
o Janeway lesions (non-tender, erythematous lesions on hands and feet)
o Can cause Bacteremia which can progress to Endocarditis
· Local: Biofilm formation can lead to dental caries (S. mutans). Infection of anaerobic strain can form brain/abdominal abscesses (S. intermedius)
Treatment:
Penicillin