gms | German Medical Science

18th Symposium on Infections in the Immunocompromised Host

International Immunocompromised Host Society

15. to 17.06.2014, Berlin

Proven Invasive Aspergillosis in an ALL Pediatric Patient Under Chemotherapy in ICU

Meeting Abstract

  • C. Lameiras - Instituto Portugues de Oncologia do Porto Francisco Gentil, Porto, Portugal
  • F. Coelho - Portugal
  • V. Costa - Portugal
  • M. Rochas - Portugal
  • M.A. Guimaraes - Portugal
  • F. Faria - Portugal

18th Symposium on Infections in the Immunocompromised Host. Berlin, 15.-17.06.2014. Düsseldorf: German Medical Science GMS Publishing House; 2014. Doc14ichs21

doi: 10.3205/14ichs21, urn:nbn:de:0183-14ichs216

Veröffentlicht: 3. Juni 2014

© 2014 Lameiras et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Invasive Aspergillosis (IA) is a leading cause of mortality and morbidity in onco hematological patients. It is often a presumed diagnostic, but one we can rarely prove it. The difficulty in establishing an early diagnosis remains a challenge for clinicians working in acute care settings.

The aim of this study is to report a proven invasive Aspergillosis case.

A 16-year-old boy was diagnosed with Acute Lymphocytic Leukemia (ALL) Ph+ in 2008, with involvement of bone marrow and central nervous system. He was treated with 1st line chemotherapy (protocol EsPhALL) and corticosteroids until 2010, in Portuguese Oncology Institute of Porto. ALL relapsed two years later (2012) and was admitted for 2nd line chemotherapy with Clofarabina (protocol IntreALL 2010, high risk) and corticosteroids. Due to high risk of fungal infection starts prophylaxis with voriconazol (200 mg oral) in the Pediatric Ward, on July 2012. Chemotherapy is complicated with prolonged aplasia and severe neutropenia (=100 cells/mm3). Due to nosocomial pneumonia (clinical and x-ray diagnosis) he stops voriconazol prophylaxis and starts empirical treatment with liposomal Amphotericin B (350 mg IV). Later he is admitted in the intensive care unit (ICU) with septic shock due to bilateral pneumonia (CT-scan diagnosis) with multiple organ dysfunction syndrome (MODS) (Apache II 20, SAPSII 48) and ARDS. Switches empirical fungal treatment to voriconazol IV. Thorax CT-scan was performed and showed nodular densifications in the periphery of the right lung parenchyma. Bronchoalveolar lavage (BAL) was performed and GM Platelia Aspergillus EIA assay was positive (GMI=13,3), PCR Aspergillus spp was positive with negative Sabouraud Gentamicin Cloranphenicol (SGC) culture. BAL DNA CMV was positive (1,6x105 copies/ml) with 1,1x103 viral load and so Ganciclovir was instituted. Serum GM was strongly positive (GMI=8,7) and remained elevated throughout the entire course of the disease (GMI=15,3). One week later the patient died by MODS refractory to treatment. Necropsy was made from upper and lower lobes of the right and left lungs. After 24h of lung tissue culture at 37ºC, mould colonies were found on SGC from right lower lobe. Aspergillus fumigatus was identified according to macro and micro morphological features. Proven invasive Aspergillosis was diagnosed according to EORTC/MSG criteria. Minimum inhibitory concentrations (MIC) of antifungal agents were evaluated by Etest, according to CLSI procedures, and sensitivity to Amphotericin B (MIC=0,125), Itraconazole (MIC=0,5), Voriconazole (MIC=0,19), Posaconazole (MIC=0,064), Anidulafungin (MIC=0,008) and Caspofungin (MIC=0,008) was detected. A. fumigatus strain isolated didn´t show alterations in cyp51A gene.

Conclusion: Biopsies of tissue lesions are important for the correct diagnosis in these poor outcomes infections. Optimal treatment of invasive aspergillosis involves early diagnosis using the most current diagnostic technologies and antifungal strategies. Detection of Aspergillus GM is an early marker of IA.