Gonococcal ascending aortic aneurysm with penetrating ulcer and bovine arch

Introduction

A localized infectious aortitis is termed a mycotic aneurysm; a variety of organisms may invade the arterial wall. The infection may be initiated by a septic embolus or by contiguous spread. The aortic intima is generally highly resistant to bacteria, but certain bacteria have a tendency for this location if this barrier is disrupted. We describe a case of ascending aortic aneurysm with penetrating ulcers caused by Neisseria gonorrhoea in a patient with longstanding fever.

Case report

A 65-year old man with a history of bicuspid aortic valve and smoking was admitted to the emergency department with a high fever. Three months earlier, he had visited the Philippines. Since that trip, he reported several weeks of oscillating fever. His medication included aspirin. Laboratory tests disclosed white blood cells 11.600/µL and C-reactive protein 12 mg·dL⁻¹. A transesophageal echocardiogram revealed a heavily calcified bicuspid aortic valve with a mean transvalvular gradient of 55 mm Hg, and an irregularity of the ascending aorta posterior wall above the sinotubular junction. No vegetations were observed on the aortic valve. Consequently, an aortic computed tomography scan was performed, revealing a bulging saccular aneurysm of more than 3 cm (Figure 1) covering the whole posterior wall of the ascending aorta, with a penetrating aortic ulcer covered by the pulmonary artery. The patient also had a bovine aortic arch, a common trunk for the innominate and left carotid arteries. The coronary arteries were normal. Blood cultures identified Neisseria gonorrhoea, and intravenous administration of gentamicin and penicillin was initiated. On the 2nd hospital day, the patient underwent surgery. After induction of anesthesia, the right femoral artery was exposed and a median sternotomy was performed. The ascending aorta was tightly adherent to the pericardium, and every effort was made to minimize manipulation of the aneurysmatic area prior to cardiac arrest. After initiating femorofemoral cardiopulmonary bypass, the ascending aorta distal to the aneurysm was carefully dissected and crossclamped proximal to the common truncal artery. The heart was arrested using antegrade cold crystalloid cardioplegia, and the aorta was transected above the sinotubular junction. The aneurysm was dissected from the surrounding tissues, and the ascending aorta was resected as a whole. Multiple abscesses with purulent secretion were seen in the posterior aortic wall, with freely mobile vegetations intimately adherent to the penetrating ulcer in the saccular aneurysm (Figure 2). The aortic valve was bicuspid and heavily calcified; it was replaced with a 27-mm St. Jude Medical mechanical prosthesis, according to the patient’s choice. The supracoronary ascending aorta was replaced with a 28-mm low-porosity woven vascular graft. The procedure was uncomplicated and the patient had an uneventful postoperative recovery. A Gram stain of the aortic wall demonstrated multiple polymorphonuclear cells, but no organisms were present. Molecular microbiologic analysis with DNA confirmed the presence of Neisseria gonorrhoea. The patient was treated with antibiotics for 6 weeks postoperatively. He was asymptomatic at the 3-month postoperative follow-up, without any recurrent infection.

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Figure 1.

Computed tomography showing a saccular aneurysm in the posterior wall of ascending aorta against the pulmonary artery.

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Figure 2.

The penetrating ulcer in the saccular aneurysm.

Discussion

The term mycotic aneurysm is a misnomer because the majority of these aneurysms are caused by bacterial rather fungal organisms. The term mycotic aneurysm was first used by Osler. ¹ Infectious aortitis in the pre-antibiotic era was largely a complication of endocarditis caused by group A streptococci, Streptococcus pneumoniae, or Haemophilus influenzae. Aortitis in the antibiotic era is rare but typically appears in older patients with aortic atherosclerosis or cystic medial necrosis. ² Salmonella has been found to have a particular affinity for infecting atherosclerotic aneurysms. The diseased vessel wall is believed to predispose to adherence and growth of pathogenic bacteria. Infection can result from septic embolization to the vasa vasorum, hematogenous seeding of an intimal defect, or extension from a contiguous site of infection.

Although the aortic intima is resistant to bacterial invasion, it is nowadays widely accepted that congenital bicuspid aortic valve is frequently associated with an intrinsic smooth muscle abnormality leading to aneurysmal degeneration of the ascending aorta. This might have been the predisposing factor for the localized infection and formation of the mycotic aneurysm in this case. Furthermore, the patient had a bovine aortic arch, significantly more common in patients with thoracic aortic disease where the aorta tends to expand more rapidly. ³ He was also a heavy smoker, a major risk factor for atherosclerotic disease which might predispose to intimal discontinuity. Symptoms are usually related to primary infection elsewhere in the body, bacteremia or sepsis, or to leakage or rupture of the aneurysm. ⁴ In bacterial thoracic aortitis, symptoms include fever, chest or shoulder pain, or both; 45% of patients present with severe back pain and in 20% with abdominal pains. ⁵ A presentation with bovine aortic arch and penetrating ulcer has not been previously described. Gonorrhoea has been traditionally diagnosed by Gram staining and culture, however, nucleic acid amplification techniques are becoming more common.

Surgical resection of all affected tissue is the treatment of choice for infections aortitis, because overall mortality is high in patients treated with medical therapy alone. For thoracic aortic aneurysm, in-situ reconstruction with a prosthetic graft is recommended, with or without aortic valve replacement, depending on the extent of valvular involvement. Valve replacement with a homograft is also an option. Antibiotic therapy tailored to bacterial sensitivity data should be initiated as soon as possible and continued postoperatively, typically for at least 6 weeks.