Abstract

Aspergillus is a common environmental mold most often recognized as an infectious agent in patients with severe immune compromise. We present a case of an immunocompetent patient presenting with endogenous endophthalmitis in the absence of other infectious symptoms. The search for a systemic source revealed an ascending aortic pseudoaneurysm. Surgical resection and pathology revealed angioinvasive aspergillus aortitis. Recent cardiac surgery has been noted to be a risk factor for angioinvasive aspergillosis. Diagnosis is difficult as symptoms are mild and laboratory studies are often normal. To our knowledge this is the first case of aspergillus aortitis presenting as endogenous endophthalmitis without systemic signs of inflammation. These patients have a high mortality rate therefore early recognition is essential. It is important to consider angioinvasive aspergillus infections in patients with prior cardiac surgery presenting with occult embolic phenomena. Only with early diagnosis and prompt treatment can we improve outcomes of this disease process.

Highlights

  • Systemic and intravitreal Amphotericin-B was administered, and intravenous therapy was continued with voriconazole 350mg twice a day

  • We present a case of an immunocompetent patient presenting with endogenous endophthalmitis in the absence of other infectious symptoms

  • At three months post-op, a CT angiography (CTA) of the chest revealed a recurrent aortic pseudoaneurysm and serum galactomannan EIA had increased from an index of 0.55 to 1.40

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Summary

Introduction

Systemic and intravitreal Amphotericin-B was administered, and intravenous therapy was continued with voriconazole 350mg twice a day (voriconazole trough level 3.40 mg/L). It is important to consider angioinvasive aspergillus infections in patients with m prior cardiac surgery presenting with occult embolic phenomena. At three months post-op, a CTA of the chest revealed a recurrent aortic pseudoaneurysm and serum galactomannan EIA had increased from an index of 0.55 to 1.40.

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Conclusion

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