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Chest Infections |

Fusariosis Masquerading as Aspergillosis

Laura Hinkle, MD; W. Graham Carlos, MD; Gabriel Bosslet, MD
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Indiana University School of Medicine, Indianapolis, IN


Chest. 2013;144(4_MeetingAbstracts):228A. doi:10.1378/chest.1684102
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Abstract

SESSION TITLE: Infectious Disease Cases III

SESSION TYPE: Medical Student/Resident Case Report

PRESENTED ON: Monday, October 28, 2013 at 04:15 PM - 05:15 PM

INTRODUCTION: Fusarium is an angioinvasive mold recognized as an emerging cause of invasive fungal disease in immunocompromised patients resulting in significant mortality (1).

CASE PRESENTATION: A 42 year-old male with relapsed acute lymphoblastic leukemia presented for salvage chemotherapy. He complained of five days of mild dyspnea, dry cough, and fatigue. He was afebrile and his exam was normal except for decreased breath sounds in the left lower lobe. Pertinent laboratory data included WBC of 1.0x109/L with 68% blasts. A chest CT showed nodular pulmonary opacities and a left pleural effusion; this was exudative with negative bacterial and fungal cultures. Chemotherapy and prophylactic ciprofloxacin and acyclovir were initiated. On day 3, the absolute neutrophil count was zero and fevers developed. Antimicrobial therapy was broadened to cefepime, vancomycin, and acyclovir. The fevers persisted and on day 8 micafungin was added. Repeat cultures were negative. On day 10 new nodular skin lesions with dark centers were biopsied, revealing epidermal necrosis and dermal fungal elements with angioinvasion. Serum galactomannan antigen index was 6.89. A presumptive diagnosis of disseminated aspergillosis was made and voriconazole replaced micafungin. On day 21 hypoxemic respiratory failure requiring mechanical ventilation developed and a chest CT showed bilateral pleural effusions and airspace disease. On day 23 blood cultures were reported positive for mold and liposomal amphotericin B was added. The patient’s neutrophils never recovered and he died on day 27. The mold was subsequently confirmed to be Fusarium.

DISCUSSION: Aspergillus and Fusarium species are causes of severe disseminated infections in immunocompromised patients and are often impossible to distinguish based on clinical presentation or histology. Fusarium is unique in its ability to frequently grow in standard blood culture media (1). Previously, a positive galactomannan antigen was considered sufficient to exclude Fusarium, but this case adds to a growing body of evidence refuting this (2). This distinction is important as several Fusarium species are resistant to voriconazole, and require treatment with amphotericin B (1).

CONCLUSIONS: A positive galactomannan, even when combined with other findings suggesting aspergillosis, does not rule out Fusarium. Awareness of this is critical because of the high mortality associated with disseminated fusariosis and the potential resistance of Fusarium to standard aspergillosis therapy.

Reference #1: Nucci M, Anaissie E. Fusarium infections in immunocompromised patients. Clin Microbiol Rev 2007; 20:695-704

Reference #2: Tortorano AM, Esposto MC, Prigitano A, et al. Cross-reactivity of Fusarium spp. in the Aspergillus Galactomannan enzyme-linked immunosorbent assay. J Clin Microbiol 2012; 50:1051-1053

DISCLOSURE: The following authors have nothing to disclose: Laura Hinkle, W. Graham Carlos, Gabriel Bosslet

No Product/Research Disclosure Information


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