Updated: Jun 04, 2019
Author: Kerry O Cleveland, MD; Chief Editor: Michael Stuart Bronze, MD 



Cardiobacterium hominis is a member of the HACEK group (Haemophilus paraphrophilus, Haemophilus parainfluenzae, Aggregatibacter actinomycetemcomitans, Aggregatibacter aphrophilus, C hominis, Eikenella corrodens, and Kingella kingae), which are fastidious, gram-negative, aerobic bacilli that normally reside in the respiratory tract. They have been associated with local infection in the mouth and, collectively, cause 5-10% of cases of native valve endocarditis in persons who do not abuse illicit intravenous drugs.[1, 2, 3]


C hominis can be isolated from the nose or throat of approximately two thirds of healthy individuals. C hominis is a nonmotile organism that requires 5-10% carbon dioxide for growth. It does not grow on selective media such as MacConkey or eosin methylene blue agar.

In animal studies, C hominis has shown low virulence, with injection of large numbers of organisms failing to produce infection. Nearly all Cardiobacterium infections reported in humans have been in the form of bacteremia or endocarditis.[4] Rare instances of other human infections, including endovascular infections, septic arthritis, ocular infections, and neonatal sepsis, have also been attributed to these organisms.[5, 6, 7, 8]



United States

C hominis endocarditis accounts for 0.1% of all cases of endocarditis. Of these cases, 75% occur in individuals with abnormal valves. The mitral and aortic valves are affected most often.


Mycotic aneurysms are an important cause of morbidity and mortality in C hominis endocarditis. Mycotic aneurysm complicates 2.5-10% of cases of C hominis endocarditis. Embolization may occur during the active stages of endocarditis.


Cardiobacterium colonization does not have a race predilection.


Cardiobacterium colonization does not have a sexual predilection. C hominis is occasionally recovered from uterine, cervical, and vaginal cultures in asymptomatic women.


Cardiobacterium colonization does not have an age predilection.




The clinical course of C hominis endocarditis tends to be subacute.[9, 10] In a published series, the mean duration of symptoms was 169 days; however, this may reflect the difficulty in growing C hominis in older blood culture systems. In this same series, 44% of patients had a history of a dental procedure or oral infection.[11]


Common findings in Cardiobacterium infections include the following:

  • Fever (86%)

  • Splenomegaly (59%)

  • Peripheral embolic phenomenon (44%)

  • Petechiae (41%)

  • Clubbing (19%)


Bacteremia with C hominis endocarditis usually occurs in the setting of pre-existing structural heart disease or a prosthetic heart valve. Many patients have a history of a recent dental procedure or poor dentition.


See the list below:

  • Mycotic aneurysm

  • Embolization





Laboratory Studies

Older blood culture systems did not support the growth of HACEK bacteria aerobically or anaerobically; blood cultures needed to be held for up to 2-3 weeks with blind subcultures. Newer blood culture systems support the growth of HACEK bacteria within 5 days. Despite this, some experts continue to recommend holding blood cultures for an extended period (up to 1 mo) when a diagnosis of Cardiobacterium endocarditis is considered.

In one study, anemia was present in 18 of 23 (78%) patients with C hominis endocarditis

The erythrocyte sedimentation rate is usually elevated and may exceed 100 mm/h.

Urinalysis results may show evidence of glomerulonephritis, including hematuria and proteinuria.

Rheumatoid factor test results may be positive, and this finding is one of the minor criteria for endocarditis.

Imaging Studies

Transesophageal echocardiography (TEE) is considerably more sensitive than transthoracic echocardiography (TTE) in helping detect valvular vegetations. TTE is usually performed first; if findings are positive, TEE is probably unnecessary.

Positron emission tomography has been reported to be useful in the diagnosis of infective endocarditis, including cases due to Cardiobacterium infection.[12, 13]



Medical Care

Until recently, the HACEK bacteria were uniformly susceptible to ampicillin. Recently, however, beta-lactamase–producing strains of HACEK have been identified.

A third-generation cephalosporin (ceftriaxone or cefotaxime) should be considered the drug of choice for HACEK endocarditis.

Ampicillin plus an aminoglycoside can be used for susceptible isolates.

In patients unable to take beta-lactams, options include trimethoprim-sulfamethoxazole, fluoroquinolones, or aztreonam.

Native valve endocarditis should be treated for 3-4 weeks. Prosthetic valve endocarditis requires 6 weeks of treatment.

The American Heart Association recommends treatment with ceftriaxone, ampicillin-sulbactam, or ciprofloxacin for 4 weeks.


Antibiotic prophylaxis given prior to dental procedures is primarily directed at Streptococcus viridans but should also help prevent infection due to HACEK bacteria.[14] ​

Further Outpatient Care

Patients with C hominis endocarditis can be treated in an outpatient setting but should remain on intravenous antimicrobial therapy for the duration of treatment.

Risks of embolic complications may arise during therapy.

Patients should be continuously and carefully monitored and should have prompt access to medical care, including cardiac surgery, in the event of complications.

Further Inpatient Care

Native valve endocarditis should be treated for 4 weeks. Prosthetic valve endocarditis requires 6 weeks of treatment.



Medication Summary

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications.


Class Summary

Empiric antimicrobial therapy should cover all likely pathogens in the context of the clinical setting.

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad gram-negative and gram-positive activity.

Mechanism of action is binding to penicillin-binding proteins. Cefotaxime may be used instead.

Ampicillin (Omnipen, Marcillin)

Interferes with bacterial cell wall synthesis during active multiplication, causing bactericidal activity against susceptible organisms.

Gentamicin (Garamycin)

Synergistic activity when used with beta-lactam for gram-negative bacteria. Inhibits protein synthesis by binding to the 30S ribosomal subunits.

Ampicillin and sulbactam (Unasyn)

Drug combination of beta-lactamase inhibitor with ampicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms.

Covers skin, enteric flora, and anaerobes. Not ideal for nosocomial pathogens.

Ciprofloxacin (Cipro)

Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. Has no activity against anaerobes.