Hacek endocarditis I33.0

Endocarditis caused by pathogens of the HACEK group.

Haemophilus spp.

Haemophilus parainfluenzae is the most common species isolated in HACEK endocarditis. In 60% of cases, the duration of illness at presentation is less than 2 months, and 19-50% of patients develop cardiac sufficiency. The lethality is less than 5%.

Aggregatibacter spp.

The most common Aggregatibacter species in endocarditis are A. actinomycetemcomitans, A. aphrophilus (formerly Haemophilus), and A. paraphrophilus. Aggregatibacter is more commonly found in endocarditis of artificial heart valves than Haemophilus spp. A. actinomycetemcomitans. Patients who develop endocarditis due to Aggregatibacter typically have periodontitis or, if they have a preexisting valvular defect, have undergone a dental procedure shortly before becoming ill. The disease is insidious and patients may have been ill for several months by the time a diagnosis is confirmed. Embolic events and the development of cardiac and renal insufficiency are common complications. Among other infections, A. actinomycetemcomitans has been isolated in patients with cerebral abscess, meningitis, endophthalmitis, parotitis, osteomyelitis, urinary tract infection, pneumonia, or empyema, whereas A. aphrophilus is often found in bone and joint infections.

Cardiobacterium hominis.

Cardiobacterium hominis primarily causes endocarditis in patients with predisposing valvular defects or prosthetic heart valves. It predominantly affects the aortic valve. At initial clinical presentation, arterial emboli, vasculitis, cerebrovascular events, immune complex glomerulonephritis, or arthritis are often already present. Embolizations, mycotic aneurysms, and the development of cardiac sufficiency are common complications. Meanwhile, another species, C. valvarum, has been described in connection with the occurrence of endocarditis.

Eikenella corrodens:

Eikenella corrodens is usually detected along with other bacterial species in foci of infection. Clinical infections in which E. corrodens may be involved include infected human bite wounds ("clenched-fist injuries"), endocarditis, soft tissue infections, osteomyelitis, head and neck infections, respiratory infections, chorioamnionitis, gynecologic infections in recumbent intrauterine devices, meningitis, cerebral and visceral abscesses.

Kingella kingae.

Isolation of K. kingae is succeeding with increasing frequency due to improved microbiological methods and molecular diagnostic techniques such as real-time PCR. Detection of this organism can be improved by inoculating aerobic blood culture bottles with various clinical materials (for example, synovial fluid). More than half of the cases of K.kingae infection occur in bones and joints, followed by infective endocarditis and bacteremia. Evidence suggests that K. kingae has now replaced Staphylococcus aureus as the leading causative agent of childhood septic arthritis. In 80% of cases, there is an association between upper respiratory tract infections or stomatitis and the invasive form of K. kingae infection with bacteremia. Oropharyngeal colonization is greatest in the first 3 years of life (detectable in approximately 10% of children) and is associated with an increase in the incidence of skeletal infections caused by this organism. Infective endocarditis, unlike other infections caused by K. kingae, occurs in older children and adults. The majority of patients suffer from preexisting valvular heart disease. Complications, such as arterial emboli, cerebrovascular events, tricuspid sufficiency, and cardiac sufficiency with cardiovascular collapse, are very common.

Younger patients

Clinically, HACEK endocarditis is usually subacute, especially in the case of aggregatibacter and cardiobacterium. A K. kingae endocarditis can be aggressive. Systemic embolizations are frequent. In HACEK endocarditis, for example, relevant embolic events occur in 28-71 % of those affected. Echocardiographic valve vegetation can be detected in 85 % of patients. Aggregatibacter spp. and Haemophilus spp. most frequently cause mitral valve vegetation; in cardiobacterium, the aortic valve is the most common. betroffen.

Note: Most cultures containing a HACEK germ become positive within the first week. Furthermore, the diagnosis of a HACEK infection (e.g. on heart valves) can be made by PCR or the MALDI-TOF method (matrix-assisted laser desorption/ionisation in combination with mass spectrometry with time-of-flight analyser) directly on agar plates with pathogen colonies.

The slow growth of the pathogens can also make resistance testing and reliable identification of beta-lactamase-producing strains difficult. Resistance is most common in Haemophilus spp. and Aggregatibacter spp.

HACEK endocarditis is more often associated with embolic, vascular and immunological manifestations, but less often with Herzinsuffizienz.

Antibiogram of the pathogen is essential.

Ceftriaxone (2 g/day) is the therapy of choice in HACEK endocarditis.

Alternatively: Levofloxacin (500-750 mg/day).

Eikenella is resistant to clindamycin, metronidazole and aminoglycosides. Endocarditis of natural heart valves should be treated with antibiotics for 4 weeks, whereas endocarditis of artificial heart valves requires 6 weeks of therapy.

Achromobacter xylosoxidans infection: Antibiogram of the pathogen is essential. Imipenem, piperacillin-tazobactam and trimethoprim-sulfamethoxazole (TMP-SMX) are usually the most effective, but multi-resistant isolates have been described that are only sensitive to colistin. Treatment is based on in vitro sensitivity testing of all clinically relevant isolates, multiple resistance is common. Meropenem, tigecycline and colistin generally show the best activity.

The prognosis for HACEK endocarditis is overall very good and much better than for other endocarditis.

1. Habib G et al (2015) ESC Guidelines for the management of infective endocaditis. Eur Heart J 36:3075-3128