Disseminated Aspergillus fumigatus Presenting as a Tri-Cavitary Infection with Fungal Pericarditis, Pleuritis, and Peritonitis in a Patient with CLL

Presenting Author(s)

• 

  Ankush Ankush, MD

  Cardiothoracic Imaging Fellow
  Atrium Wake Forest Baptist Medical Center
  Winston Salem, North Carolina, United States

Primary Author(s)

• MS

  Muthu Sakthivel, MD, FSCMR

  Assistant Professor/Cardiothoracic Imaging Fellowship Program Director
  UNC School of Medicine
  Chapel Hill, North Carolina, United States

Co-Author(s)

• ES

  Eswara Sellamuthu, MD

  Assistant Professor
  Atrium Health Wake Forest Baptist Medical Center, United States
• UJ

  Usha Jayagurunathan, MD

  Assistant Professor
  Atrium Health Wake Forest Baptist Medical Center, United States
• HG

  HARISH GUDI, MD

  Assistant Professor
  University of Arizona College of Medicine, United States

Description of Clinical Presentation: A 66-year-old immunocompromised male with chronic lymphoid leukemia presented with acute respiratory failure secondary to recurrent effusions. His condition was critical, with examinations revealing concurrent pleural effusions, ascites, and a new pericardial effusion. This presentation of tri-cavitary serosal effusions in a severely immunocompromised host suggested a complex systemic process. Initial fluid analysis of samples from the pleural, peritoneal, and pericardial fluids all revealed the presence of fungal elements. This suspicion was strongly supported by a markedly elevated serum (1,3)-β-D-glucan (Fungitell) level of >500 pg/mL, indicating an invasive fungal infection. Subsequent fungal cultures from the pleural fluid speciated the causative pathogen as Aspergillus fumigatus, confirming disseminated aspergillosis.

Diagnostic Techniques and Their Most Important Findings: To definitively characterize the extent of cardiac involvement, CMR was performed. The study revealed a large, complex pericardial mass-like collection that demonstrated direct invasion into the posterior mid-left ventricular myocardial wall on cine imaging (Figure 1A). Post-contrast sequences were critical, showing avid peripheral rim enhancement with a centrally nonenhancing core, confirming the collection to be a large pericardial abscess (Figure 1B). Late gadolinium enhancement (LGE) imaging further delineated the pathology, identifying multifocal, multiloculated pericardial abscesses and, crucially, a distinct intramyocardial abscess within the inferior wall (Figure 2). These findings established a life-threatening diagnosis of fungal purulent pericarditis with myocardial abscess formation. Following four weeks of aggressive antifungal therapy, a follow-up CMR demonstrated a dramatic therapeutic response, with a marked interval reduction in the size and enhancement of both the pericardial and myocardial abscesses (Figure 3).

Learning Points from this Case: This case highlights a lethal presentation of disseminated aspergillosis as a tri-cavitary infection with direct cardiac invasion. It powerfully demonstrates the indispensable role of CMR in the diagnosis and management of suspected fungal pericarditis. While other modalities may identify a pericardial effusion, CMR provided unique tissue characterization that was pivotal in differentiating a simple effusion from complex, multiloculated abscesses and, most critically, in identifying direct myocardial extension. This distinction has profound prognostic and therapeutic implications. Furthermore, the utility of follow-up CMR to objectively monitor treatment response was clearly established, providing clinicians with invaluable, non-invasive evidence to guide ongoing therapy. In complex pericardial disease, CMR is an essential tool for definitive diagnosis, risk stratification, and therapeutic monitoring.

Figure 1. Cardiac MRI—cine and delayed post-contrast characterization of pericardial abscess with myocardial extension. (A) Real-time spiral cine balanced SSFP (non-Cartesian) images show an intermediate-signal pericardial mass-like collection (yellow arrow) with invasion of the posterior mid–left ventricular myocardial wall (red arrow). (B) Delayed post-contrast T1-weighted fat-suppressed 2-chamber images demonstrate avid peripheral rim enhancement with a centrally nonenhancing fluid core, consistent with a pericardial abscess (yellow arrow), with adjacent myocardial extension (red arrow).
Figure 2. Cardiac MRI—LGE delineation of pericardial abscesses with myocardial involvement. (A) Short-axis phase-sensitive inversion recovery (SA PSIR) late gadolinium enhancement (LGE) images show multifocal pericardial collections with avid rim enhancement and centrally nonenhancing fluid, consistent with pericardial abscesses (white arrows). (B) SA PSIR LGE images again demonstrate pericardial rim enhancement with central nonenhancing fluid (blue arrows) and a similar focus within the inferior mid–left ventricular myocardium, compatible with a myocardial abscess (red arrow). (C) Axial post-contrast T1-weighted fat-suppressed images demonstrate multifocal, multiloculated pericardial collections with avid peripheral rim enhancement (green arrows) surrounding centrally nonenhancing fluid components (red arrows), in keeping with pericardial abscesses.
Figure 3. Cardiac MRI—post-treatment response of pericardial abscess with myocardial extension. (A) Two-chamber localizer cine images obtained 4 weeks after initiation of antifungal therapy (amphotericin) show interval decrease with only trace residual pericardial collection (yellow arrow) and marked reduction of the prior myocardial extension. (B) Two-chamber PSIR late gadolinium enhancement (LGE) images at 4 weeks demonstrate decreased avid rim enhancement of the pericardial abscess (yellow arrow) with only a minimal residual myocardial component (red arrow). (C) Short-axis magnitude-reconstructed LGE images at 4 weeks show decreased extent of pericardial enhancement and reduction in the size of the multifocal, multiloculated, centrally nonenhancing fluid components.