Other strains of streptococci can cause subacute endocarditis as well. These include streptococcus intermedius, which can cause
acute or subacute infection (about 15% of cases pertaining to infective endocarditis).[7]
The mechanism of subacute bacterial endocarditis could be due to malformed stenotic valves which in the company of bacteremia, become infected, via adhesion and subsequent colonization of the surface area. This causes an inflammatory response, with recruitment of matrix metalloproteinases, and destruction of collagen.[8]
Underlying structural valve disease is usually present in patients before developing subacute endocarditis, and is less likely to lead to septicemboli than is acute endocarditis, but subacute endocarditis has a relatively slow process of infection and, if left untreated, can worsen for up to one year before it is fatal.[medical citation needed] In cases of subacute bacterial endocarditis, the causative organism (streptococcus viridans) needs a previous heart valve disease to colonize.[9] On the other hand, in cases of acute bacterial endocarditis, the organism can colonize on the healthy heart valve, causing the disease.[10]
Subacute bacterial endocarditis can be diagnosed by collecting three blood culture specimens over a 24-hour period for analysis,[4] also it can usually be indicated by the existence of:
The standard treatment is with a minimum of four weeks of high-dose intravenous penicillin with an aminoglycoside such as gentamicin.
The use of high-dose antibiotics is largely based upon animal models.[2]
Leo Loewe of Brooklyn Jewish Hospital was the first to successfully treat subacute bacterial endocarditis with penicillin. Loewe reported at the time seven cases of subacute bacterial endocarditis in 1944.[14]
^ abcdVerhagen, DW; Vedder, AC; Speelman, P; van der Meer, JT (2006). "Antimicrobial treatment of infective endocarditis caused by viridans streptococci highly susceptible to penicillin: historic overview and future considerations". The Journal of Antimicrobial Chemotherapy. 57 (5): 819–24. doi:10.1093/jac/dkl087. PMID16549513.
