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THERAPY

    There have been no large trials to evaluate the best therapy for IE caused by HACEK group organisms. Currently available information is in the form of small case series or individual case reports. In the past, ampicillin plus an aminoglycoside was the therapy of choice. This treatment was advocated because synergy between beta-lactams and aminoglycosides was demonstrated in vitro, but such synergy has not been conclusively proved in the clinical setting with HACEK infections. Moreover, a number of case reports have documented therapeutic failures of combined therapy with ampicillin and gentamicin in the treatment of A. actinomycetemcomitans andHaemophilus infections. In addition, a number of recent reports have described beta-lactamase production by numerous strains of HACEK group organisms. Because of their fastidious growth requirements, susceptibility testing is difficult. We and others believe that HACEK group organisms should be considered ampicillin resistant unless proved otherwise. In light of this, we do not advocate ampicillin as therapy for HACEK group organisms.

    Most HACEK organisms, with the notable exceptions of A. actinomycetemcomitans and E. corrodens, are susceptible to first- and second-generation cephalosporins, and virtually all species are susceptible to third-generation cephalosporins. Therefore we believe the best therapy for IE caused by HACEK group bacteria is cefotaxime or ceftriaxone. We advocate using ceftriaxone, 2 g intravenously (IV) or intramuscularly (IM) once daily, because of its convenience and suitability for outpatient parenteral therapy (Table 2). The duration of therapy for native valve endocarditis should be at least 4 weeks; at least 6 weeks of therapy is recommended for prosthetic valve endocarditis.

    HACEK group organisms are also susceptible in vitro to most fluoroquinolones, trimethoprim-sulfamethoxazole, and aztreonam. Thus one of these agents may be used in the beta-lactam–intolerant patient. There is a growing body of evidence to support the use of ciprofloxacin as outpatient therapy for HACEK endocarditis.

    A number of investigators advocate empirical therapy with either ceftriaxone along with an aminoglycoside or ciprofloxacin until sensitivities return. A fluoroquinolone such as ciprofloxacin is the preferred alternative for patients who are allergic to a beta-lactam. Ciprofloxacin is an appropriate choice for the outpatient segment of therapy because of its high bioavailability after oral ingestion and excellent safety profile. However, because of the lack of published data about fluoroquinolone therapy for HACEK group bacterial infections, we prefer to use ceftriaxone as initial therapy. Despite the technical difficulties in obtaining in vitro susceptibility results, we advocate obtaining such results to confirm sensitivity to the agents being used or contemplated for use. Careful follow up of all patients undergoing treatment is also recommended, including periodic assessment of clinical and microbiologic response using careful examinations and follow-up blood cultures. Careful monitoring for compliance is advised for all patients treated with oral therapy.

    HACEK group organisms are usually susceptible to tetracycline and chloramphenicol; however, both of these agents are bacteriostatic and would be poor choices for endovascular infections. Most HACEK group members are resistant to metronidazole, vancomycin, erythromycin, and clindamycin.

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