Mycotic aneurysm (infectious aneurysm) is a pseudoaneurysm or true aneurysm formed by weakening of the arterial wall through an infectious process. Despite its name 'mycotic,' the vast majority of cases are bacterial in origin (Staphylococcus aureus, Salmonella spp. most common); fungal infections are rare but may occur in immunosuppressed patients. It may originate from infective endocarditis (65-80%), bacteremia, adjacent vertebral osteomyelitis, or penetrating trauma. The aorta is the most commonly affected vessel (50-60%), with suprarenal/infrarenal aorta, iliac, femoral, and intracranial arteries also affected. CT angiography characteristically shows saccular morphology, lobulated irregular contour, periaortic soft tissue/gas, and rapid size increase. Due to high rupture risk (75%), urgent surgical/endovascular treatment is required.
Age Range
40-80
Peak Age
60
Gender
Male predominant
Prevalence
Rare
Four main mechanisms are described for mycotic aneurysm development: (1) Septic embolization — septic emboli from infective endocarditis occlude vasa vasorum of the arterial wall, creating local ischemia and infection → medial necrosis → wall weakening → aneurysm. (2) Bacteremic seeding — bacterial colonization via bloodstream on atherosclerotic plaque or pre-existing aneurysm; Salmonella and Staphylococcus show affinity for atherosclerotic intima. (3) Direct extension — direct invasion of the arterial wall from adjacent infection (vertebral osteomyelitis, paravertebral abscess, spondylitis). (4) Traumatic inoculation — direct contamination following penetrating trauma or intravascular procedure. The infectious process causes release of proteolytic enzymes and inflammatory mediators in the arterial wall → destruction of elastic fibers and collagen → loss of structural integrity → pseudoaneurysm or true aneurysm formation. Periaortic soft tissue on CT reflects perivascular inflammation; gas presence indicates gas-producing organisms or abscess formation.
An aneurysm with saccular morphology arising at a location atypical for atherosclerotic aneurysms (suprarenal aorta, SMA origin, thoracic aorta), especially when accompanied by fever and bacteremia clinical presentation, is highly suspicious for mycotic aneurysm. Periaortic soft tissue/gas and rapid size increase reinforce this suspicion. This triad (atypical location + saccular morphology + clinical signs of infection) is the strongest diagnostic combination for mycotic aneurysm.
Saccular or fusiform aneurysm with lobulated, irregular wall contour on CT angiography. Aneurysm typically located outside typical atherosclerotic aneurysm locations (suprarenal aorta, SMA origin, thoracic aorta). Saccular morphology (80%) is typical for mycotic aneurysm — different from fusiform atherosclerotic aneurysm. Wall contour is irregular and lobulated, may contain focal eccentric outpouchings (blebs) — sign of impending rupture. Aneurysm size is usually <5 cm but grows rapidly (>5 mm increase weekly is significant). Intramural air bubbles may be visible.
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Lobulated, irregularly contoured saccular aneurysm in the suprarenal/infrarenal aorta is observed; in the clinical context (fever, bacteremia), mycotic aneurysm should be primarily considered.
Periaortic/perivascular soft tissue thickening and/or gas bubbles surrounding the aneurysm. Soft tissue represents inflammatory infiltration and abscess formation (30-50 HU). Gas bubbles indicate gas-producing organisms or abscess cavitation — highly specific finding for mycotic aneurysm. Soft tissue may show peripheral rim enhancement on contrast CT (abscess wall). Periaortic lymph node enlargement is an indicator of infectious/inflammatory process. Vertebral body erosion or discitis findings may coexist (spread from adjacent spondylodiscitis).
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Periaortic soft tissue thickening and gas bubbles surrounding the aneurysm are observed, consistent with infectious/mycotic aneurysm; urgent surgical evaluation is recommended.
Rapid increase in aneurysm diameter on serial CT follow-ups — the most dangerous feature of mycotic aneurysm. Weekly >5 mm or >10 mm growth in 2-week period strongly suggests mycotic aneurysm. While annual growth of atherosclerotic AAA is 2-3 mm, mycotic aneurysm can grow centimeters within days. Size increase indicates ongoing infectious process and increased rupture risk. Fresh periaortic hemorrhage (high density 60-80 HU) on non-contrast CT may be a sign of contained rupture.
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Significant increase in aneurysm diameter compared to prior examination on serial CT follow-up, suggesting mycotic aneurysm and high rupture risk; urgent vascular surgery consultation is recommended.
Focal increased FDG uptake in and around the aneurysm wall on FDG PET-CT — metabolic marker of active infectious process. Unlike diffuse vascular uptake in GCA, uptake in mycotic aneurysm is focal and asymmetric. SUVmax is generally >4-5, markedly exceeding liver reference. PET-CT can also be used to evaluate antibiotic treatment response — FDG uptake decreases with successful treatment. Also valuable for investigating the source of infection (endocarditis, spondylitis, other foci).
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Focal high FDG uptake in and around the aneurysm wall on PET-CT, consistent with active infectious/mycotic aneurysm.
Hyperintense periaortic edema on T2/STIR and mural/periaortic enhancement on contrast T1 around the aneurysm on MRI. T2 hyperintensity reflects high water content of active inflammation and edema. Enhancement indicates increased vascular permeability and granulation tissue formation. MRI better evaluates abscess formation and vertebral erosion than CT due to superior soft tissue contrast. Periaortic collection showing diffusion restriction on DWI supports abscess formation.
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Hyperintense periaortic edema on T2/STIR and prominent mural/periaortic enhancement on contrast T1 around the aneurysm on MRI, consistent with active infectious process.
Vertebral body erosion and/or spondylodiscitis findings accompanying mycotic aortic aneurysm. Aneurysm may show direct invasion from the posterior aortic wall into the vertebral body — osteolytic erosions, end-plate irregularity, and disc space destruction. Alternatively, spread from primary spondylodiscitis to the aortic wall may also occur. Psoas abscess or paravertebral abscess may coexist. Vertebral erosions are best evaluated on bone window in CT. MRI may demonstrate early findings of spondylodiscitis (end-plate edema, disc T2 signal increase) before CT.
Report Sentence
Osteolytic erosion and end-plate irregularity in the vertebral body adjacent to the mycotic aneurysm, consistent with vascular spread from infectious spondylodiscitis.
Criteria
Aneurysm developing through septic embolization in the setting of infective endocarditis. More common in peripheral arteries (femoral, popliteal, splenic, intracranial). May be multiple. Most common organism: Staphylococcus aureus, Streptococcus viridans.
Distinct Features
Multiple peripheral pseudoaneurysms strongly suggest septic embolization from endocarditis. Echocardiography confirms vegetations. Intracranial mycotic aneurysm — subarachnoid hemorrhage risk. Requires aggressive antibiotherapy + surgical repair.
Criteria
Bacterial colonization via bloodstream onto atherosclerotic plaque or pre-existing aneurysm. Prefers the aorta (infrarenal>suprarenal). Salmonella spp. and Staphylococcus aureus are most common organisms. Common in elderly, atherosclerotic, immunosuppressed patients.
Distinct Features
Infection developing on existing atherosclerotic AAA — sudden acceleration in size increase rate is a clue. Salmonella aortic infection usually has fulminant course with high mortality. Periaortic gas and abscess may be more prominent.
Criteria
Direct contamination following penetrating trauma, intravascular intervention (catheterization, graft implantation), or intravenous drug use. Pseudoaneurysm development at intervention site. Graft infection may develop after EVAR/surgical graft.
Distinct Features
Intervention history and aneurysm location at intervention site are key clues. Pseudoaneurysm in femoral/brachial arteries typical in intravenous drug abuse. Perigraft fluid, gas, and abscess findings in graft infection. High risk of MRSA and polymicrobial infection.
Distinguishing Feature
Atherosclerotic AAA shows fusiform morphology, calcified wall, and infrarenal predilection; mycotic aneurysm shows saccular morphology, irregular contour, periaortic soft tissue/gas, and atypical location. AAA grows 2-3 mm annually; mycotic aneurysm grows rapidly within days/weeks. Systemic infection signs (fever, leukocytosis) are absent in AAA.
Distinguishing Feature
Penetrating aortic ulcer (PAU) forms through ulceration of atherosclerotic plaque and shows focal crater-like outpouching; mycotic aneurysm has irregular saccular expansion and periaortic soft tissue/gas. Periaortic gas is not seen in PAU and infection signs are absent. PAU usually occurs in the descending aorta in the setting of atherosclerotic changes.
Distinguishing Feature
Aortic rupture shows acute periaortic hematoma and active contrast extravasation; mycotic aneurysm has dominant periaortic gas, soft tissue, and abscess findings. Rupture usually develops acutely in the setting of existing aneurysm or trauma. When mycotic aneurysm ruptures, both findings may coexist — contained rupture with gas/abscess coexistence suggests mycotic etiology.
Distinguishing Feature
IgG4-related periaortitis shows periaortic soft tissue thickening ('mantle sign') but aneurysm morphology is fusiform not saccular, with no gas or abscess findings. IgG4 disease is accompanied by elevated serum IgG4 and multiple organ involvement. Fever and acute infection signs are absent. Periaortic soft tissue is homogeneous and smooth-contoured — different from irregular infiltration in infectious process.
Urgency
emergentManagement
surgicalBiopsy
Not NeededFollow-up
specialist-referralMycotic aneurysm is a vascular emergency — rupture rate reaches 75% and mortality is 50-90% if untreated. Treatment has three components: (1) Aggressive intravenous antibiotherapy — targeted based on blood culture, minimum 6-8 weeks, usually requires lifelong oral suppression. (2) Surgical repair — open surgery (extra-anatomic bypass) or endovascular stent-graft (EVAR). Endovascular approach can be used as bridge therapy in emergencies but carries risk of leaving prosthetic material in infected field. (3) Treatment of infection source — endocarditis, spondylitis, or other foci. Multidisciplinary approach (vascular surgery + infectious disease + radiology) is required. Serial CT angiography during follow-up evaluates aneurysm size, periaortic inflammation, and graft/repair integrity.
Mycotic aneurysm requires urgent treatment due to very high rupture risk. Treatment includes prolonged IV antibiotic therapy + surgical resection (in-situ graft or extra-anatomic bypass) or endovascular stent-graft (bridging). Blood cultures should be obtained before treatment. Endocarditis source should be investigated.