Though Neisseria sicca is part of the normal oral flora, in rare instances it can be a serious pathogen causing endocarditis, meningitis, osteomyelitis, etc. Neisseria sicca endocarditis is characterized by large vegetations and destruction of the valve. Of the various Neisseria species, Neisseria sicca most often results in embolic complications. Since the first report of Neisseria sicca endocarditis in 19181, only 15 other cases have been reported (available upon request) and the last was 6 years ago2. We present a 17th case of endocarditis due to Neisseria sicca, accompanied by multiple embolic complications.
A 39-year-old male without any history of substance use presented with “flu-like” symptoms for one week, mental status changes, and sudden left-sided weakness for one day. He was lethargic and blood pressure was 90/40 mm Hg. Non-blanching, 1cm, purplish macular lesions on the skin, icterus, and conjunctival petechaie were noted. Cardiac examination revealed no murmurs. Left hemiparesis was present. CAT scan of the brain showed multiple non-enhancing parenchymal focal lesions (see Figure). Shortly after admission, he became more lethargic, developed increased respiratory distress, and required intubation. Chest X-ray showed bilateral diffuse alveolar infiltrates. On transesophageal echocardiogram (TEE) left ventricular size was normal and left ventricle function was moderately depressed. There was a sclerotic bicuspid aortic valve with a mobile vegetation on the right cusp prolapsing into the left ventricle (see Figure). Blood cultures grew Neisseria sicca, sensitive to ceftriaxone. He was treated with IV ceftriaxone, and carious teeth were extracted. TEE 8 days later showed a calcified vegetation (whose size had increased) prolapsing in the outflow tract. Severe aortic insufficiency was noted. He improved with intravenous antibiotics and was extubated within 8 days. Three days later, left calf and toes soreness developed, with increasing purpura. Magnetic resonance angiography of the left lower extremity showed significant thrombus in the left distal common iliac artery, left external iliac artery, and left hypogastric artery. Left iliac embolectomy and excision of vegetation were done, and a St. Jude’s mechanical aortic valve was placed. He was discharged home on intravenous ceftriaxone and warfarin. Six weeks later, sharp epigastric pain and vomiting developed. Right upper quadrant abdominal ultrasound showed a hepatic artery mycotic aneurysm with compression of gallbladder, common bile duct, and splenic vein. CAT scan showed an infra-renal abdominal aortic dissection into the left common iliac artery and a hepatic artery mycotic aneurysm with common bile duct obstruction and portal/splenic vein thrombosis from mechanical compression. Under ultrasound guidance, thrombin was injected into the pseudoaneurysm via the celiac artery. The patient was finally discharged home on intravenous antibiotics. He was doing well on outpatient follow-up.
Neisseria species other than Neisseria gonorrhoeae and Neisseria meningitides are generally not considered pathogenic. Endocarditis due to Neisseria sicca may be associated with serious embolic complications including cerebral, hepatic, and peripheral embolism. Treatment should include a 6-week or longer course of intravenous antibiotics and possibly surgical correction of underlying structural heart disease and dental extraction.
Neisseria sicca isolation from blood should be taken seriously rather than attributed to contamination, and should prompt evaluation for possible endocarditis. The index of suspicion should be greater in patients using intravenous drugs and in those with structural heart disease or dental disease. Secondly, if patients with any embolic phenomena or endocarditis have a blood culture that reveals Neisseria sicca, it should be treated as the responsible organism unless proven otherwise.
N. Tripathi, None.