Case Presentation: The patient is a 20-year-old male who is an immigrant from Egypt with no significant medical history. He presented with recurrent fevers, chills, and dysuria for one week. He was prescribed cephalexin for a urinary tract infection at an urgent care clinic. The patient continued to have fevers and developed a dry cough associated with chest pain, intermittent headaches, lightheadedness, and vomiting. The patient came to the hospital with a temperature of 39.5 °C. Blood cultures were drawn and returned positive two days later; gram stain showed gram negative rods. White cell count was 11,700/mcL on admission. Physical exam revealed a new systolic murmur and tenderness in the left upper quadrant. The patient also had dental plaques. Chest x-ray showed a left lower lobe consolidation. Transthoracic echocardiogram revealed a thickened posterior mitral leaflet prolapsing into the left atrium with a 0.5 cm x 0.6 cm mobile echodensity. There was significant mitral regurgitation. CT abdomen revealed a splenic infarct. The patient was started on ceftriaxone. The organism was identified as H. parainfluenza on day four and was revealed to be resistant to ceftriaxone and cefepime but sensitive to ampicillin-sulbactam on day seven. Antibiotics were adjusted accordingly. Repeat sensitivities at another laboratory revealed that the strain was sensitive to ceftriaxone and cefepime. He was placed on ceftriaxone again. The patient underwent surgical repair of his mitral valve (annuloplasty). He was treated with levofloxacin on discharge. A repeat echocardiogram one month later showed no residual vegetation.
Discussion: The majority of native valve-infective endocarditis cases are caused by Staphylococcus, Streptococcus, or Enterococcus species. Endocarditis due to HACEK organisms is rare. HACEK organisms, zoonoses, and fungi collectively account for <5% of infective endocarditis cases. Haemophilus species cause only 0.8-1.3% of cases of infective endocarditis. H. parainfluenzae is part of the human genitourinary and oropharyngeal microbiota. H. parainfluenzae is indigenous to the mouth or nasopharynx in 5 to 25% of healthy individuals. Risk factors for the development of endocarditis include dental work, nasopharyngeal infection, and tongue piercing. Furthermore, H. parainfluenzae is commonly isolated in patients with chronic obstructive pulmonary disease and bronchiectasis. The patient’s diagnosis and treatment were delayed by the slow growth of H. parainfluenzae. It took four days for the blood cultures to reveal the organism, which is not uncommon in HACEK organisms. The patient had three potential risk factors for H. parainfluenzae; he had poor dentition, pneumonia and a recent urinary tract infection. This patient experienced splenic infarct from embolization, the second most common consequence of endocarditis. Echocardiogram also revealed severe mitral regurgitation, which can be an indication for surgery, even without heart failure. The H. parainfluenzae present was initially reported as resistant to cephalosporins. However, repeat sensitivities showed a more sensitive bacterium.
Conclusions: Infective endocarditis due to H. parainfluenzae has a high mortality rate, approaching 30% after one year. HACEK organisms are notoriously difficult to culture, which leads to delayed or missed diagnoses of endocarditis. In this case, the discrepancy in the antibiotic sensitivities highlights the significance of questioning blood culture results if they are unusual.