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Case Reports
. 2024 Nov 30;16(6):1182-1190.
doi: 10.3390/idr16060093.

Delayed Diagnosis of Disseminated Invasive Aspergillosis with Purulent Myocarditis in an Immunocompromised Host

Affiliations
Case Reports

Delayed Diagnosis of Disseminated Invasive Aspergillosis with Purulent Myocarditis in an Immunocompromised Host

Mark Londema et al. Infect Dis Rep. .

Abstract

Introduction: Invasive aspergillosis (IA) is an opportunistic fungal infection that typically occurs in the immunocompromised host and is associated with severe morbidity and mortality. Myocardial abscess formation is seldomly described. Detailed Case Description: We present a case of IA with purulent myocarditis. The patient was on long-term high-dose corticosteroid and mycophenolate mofetil therapy for severe lupus nephritis. After multiple visits to his general practitioner and nephrologist for general malaise, he was admitted to our hospital with visual complaints. Within several days, he developed atrial fibrillation, respiratory insufficiency, and, finally, a decreased level of consciousness. After admission to the intensive care unit, the broncho alveolar lavage (BAL) fluid galactomannan (GM) index was normal, but the serum GM index was severely elevated. Despite initiation of antifungal therapy, the patient passed away shortly thereafter. Autopsy revealed massive intracranial hemorrhage and disseminated IA affecting the lungs, brain, and myocardium, with macroscopic myocardial abscess formation. Discussion: This classic case of diagnostic uncertainty illustrates how invasive fungal infections can progress to disseminated disease while showing nonspecific symptoms only. It emphasizes the importance of vigilance for opportunistic fungal infections in a growing category of immunocompromised patients. Conclusion: Clinicians should have a low threshold of suspicion for fungal infections in patients on combination immunosuppressive medication, such as high-dose corticosteroid therapy in combination with T-cell inhibitors like MMF.

Keywords: immunocompromised host; invasive aspergillosis; myocarditis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Transverse section through both ventricles, showing multiple myocardial Aspergillus abscesses.
Figure 2
Figure 2
Hematoxylin and eosin staining. Black bar represents 500 μm. Micrograph of the heart, demonstrating heavy intramyocardial inflammation with abscess formation, caused by Aspergillus fumigatus. a: myocardium; b: epicardial fatty tissue; c: lumen of a branch of the coronary arterial system; d: inflammatory infiltrate and abscess wall; e: abscess cavity; rectangle: depicts area that is presented in Figure 3.
Figure 3
Figure 3
Grocott silver staining. Black bar represents 50 μm. Detailed image of the abscess wall, demonstrating the branching Aspergillus hyphae.
Figure 4
Figure 4
Hematoxylin and eosin staining. Black bar represents 2 mm. Micrograph of the lung demonstrating abscess with Aspergillus fumigatus. a: (alveolar) lung parenchyma; b: artery; c: vein; d: inflammatory infiltrate; e: abscess also depicted in Grocott stain in Figure 5.
Figure 5
Figure 5
Grocott silver staining. Black bar represents 50 μm. Detailed image of the lung abscess with abundant branching Aspergillus hyphae.

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