HACEK Group Infections Clinical Presentation

Updated: Sep 27, 2018
  • Author: Zartash Zafar Khan, MD, FACP; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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Most cases of infective endocarditis (IE) caused by the HACEK organisms are subacute. Patients present with progressive symptoms developing over weeks. Some cases have been present for as long as 18 months before the correct diagnosis is made. [10] This delay is often due to failure to use special culture techniques. [13] (See Lab studies.) HACEK IE should be considered in the differential diagnoses of fever of unknown origin.

Fever is common but may be absent in elderly individuals, immunocompromised patients, or patients taking anti-inflammatory drugs. In some series, it was present in only 50% of cases. [10]

Nonspecific symptoms, such as weight loss, anorexia, nausea and vomiting, fatigue, back pain, and night sweats, are common and may lead to a delay in diagnosis.

Patients may have a history of prior valvular disease.

A history of prior dental, urologic, and other procedures should be elicited.

A history of intravenous drug abuse should be elicited.

A sentinel headache may indicate the impending rupture of a mycotic aneurysm. [14]

Brain abscess can manifest as neurologic symptoms, such as focal weakness or numbness, cranial nerve dysfunction, and/or seizure. Primary brain abscess cases have been associated with canine saliva contamination or head and neck wounds. [7, 15]

Human bite or clenched fist injuries can be infected with HACEK organisms and can present as wound and deeper-tissue infections.

Various other presentations, including orbital cellulitis, necrotizing pneumonia, visceral abscess, bacteremia, and thrombophlebitis, have been reported.



The diagnosis of endocarditis is challenging. The physical findings are often subtle and difficult to identify for many clinicians. Special care should be taken to perform a comprehensive physical examination looking for evidence of endocarditis. Some of the areas to focus on are noted below. [16, 17, 18]


A new or changing heart murmur is the most consistent physical finding, but it may be absent, especially in right-sided endocarditis.


Because of the increased use of healthcare and diagnostic imaging, the peripheral manifestations of endocarditis are not seen as commonly as they once were.

Examine the patient for clubbing (with or without hypertrophic osteoarthropathy), splinter hemorrhages, mucocutaneous petechiae, Osler nodes, Janeway lesions, and Roth spots.

Splenomegaly can be present.

Embolic complications  [19]

A vegetation can embolize to virtually any vessel and can result in various sequelae.

Observe for compromise of circulation to the limbs due to embolization.

Emboli to the central nervous system often presents as a focal neurological deficit or a stroke. Emboli to the frontal lobe may be more subtle, causing personality changes or loss of inhibition. [14]

Emboli to the kidney may cause flank tenderness, hematuria, and/or oliguria.

Embolization to heart vessels can have various manifestations, including acute myocardial infarction and arrhythmia.

A large mesenteric embolus can cause bowel ischemia and thus manifest as abdominal pain and tenderness.

A right-sided vegetation can embolize to the lung and present similarly to a pulmonary embolus or focal pneumonia.

Bone and joint foci can present as osteomyelitis and/or septic arthritis, manifesting as bone or joint tenderness, swelling, or nonhealing wound.

Other clinical manifestations

Other clinical manifestations, such as dental infection, skin and soft tissue infection/abscess, pneumonia/empyema, parotitis, eye infection, and sinus infection, require examination of the involved area, a thorough history, and assessment for underlying comorbidities.



Patients may have a history of a preceding dental, urologic, or gastroenterologic procedure. [19]

Periodontal disease is a known predisposing factor.

A history of intravenous drug use also should be considered because many drug users clean their needles or venipuncture sites with saliva. Among the HACEK organisms, E corrodens is the bacterium that has been most frequently associated with intravenous drug abuse. [20]

A history of heart valve abnormalities or the presence of a prosthetic heart valve or pacemaker device also predisposes to endocarditis.

A review of literature from Mayo Clinic between 1971 and 1976 identified predisposing factors such as trauma with wound infections, malignancies with abscesses, and congenital heart disease with endocarditis. [21]

Rare case reports have linked wound contamination with canine saliva and subsequent invasive infections, particularly of the head and neck, leading to brain abscess. [15, 22]



Many complications can result from IE, regardless of the causative organisms.

CHF is the complication of IE that has the greatest impact on prognosis. It may develop acutely from perforation of a valve leaflet, rupture of an infected chordae, valve obstruction, or because of sudden intracardiac shunts from fistulous tracts. When it appears more insidiously, CHF usually develops during the first month of therapy. Any deterioration in heart function should be taken very seriously because operative mortality increases dramatically after frank ventricular decompensation.

Neurologic complications, whether from emboli, abscess, hemorrhage, or arteritis, are the most frequent causes of death in patients with IE. Mycotic aneurysms are usually clinically silent until they rupture. Consider performing a magnetic resonance angiogram or cerebral CT scan to look for aneurysm in patients with subacute IE.

Splenic infarctions can occur in more than one third of patients but are often clinically silent.

Septic or bland emboli may reach the lung in right-sided endocarditis. These may cause pulmonary infarction, pneumonia, and empyema.