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Invasive aspergillosis complicating induction chemotherapy of childhood leukaemia
T Bömelburg1, N Roos, H J von Lengerke
1Kinderklinik, Universität Münster, Federal Republic of Germany.
Insights
Invasive aspergillosis can rapidly affect children with acute leukaemia soon after starting chemotherapy. Early detection is crucial, as infections can manifest in lungs or the abdomen, potentially leading to disseminated disease.
Area of Science:
- Pediatric Oncology
- Infectious Diseases
- Mycology
Background:
- Acute leukaemia treatment often involves intensive polychemotherapy, leading to profound immunosuppression.
- Invasive fungal infections, particularly invasive aspergillosis, are a significant cause of morbidity and mortality in immunocompromised pediatric patients.
- The early phase of induction chemotherapy poses a critical window for opportunistic infections.
Observation:
- Two pediatric patients with acute leukaemia developed invasive aspergillosis within two weeks of initiating polychemotherapy.
- One patient presented with pulmonary aspergillosis (aspergilloma) following upper lobe infiltration.
- The second patient developed caecal aspergillosis, initially mimicking appendicitis, which progressed to disseminated disease.
Findings:
- Histologically confirmed invasive aspergillosis occurred rapidly after chemotherapy initiation in both cases.
- Pulmonary and gastrointestinal tracts are potential sites for early invasive aspergillosis in this population.
- Despite antifungal therapy, disseminated aspergillosis led to a fatal outcome in one patient.
Implications:
- Clinicians must maintain a high index of suspicion for invasive aspergillosis in pediatric leukaemia patients presenting with new symptoms shortly after chemotherapy initiation.
- Diagnostic vigilance is required to identify aspergillosis in atypical presentations, such as abdominal symptoms mimicking appendicitis.
- Prompt diagnosis and management are critical to improve outcomes for invasive aspergillosis in pediatric oncology.
Abstract:
Two children with acute leukaemia developed histologically confirmed invasive aspergillosis within 2 weeks after onset of polychemotherapy. One child had received only prednisone and one pulse of vincristine and daunorubicin before. This child showed classical roentgenographic signs of aspergilloma following an upper pulmonary lobe infiltration. The second patient developed caecal aspergillosis obscured by clinical signs of appendicitis. He died of disseminated aspergillosis several weeks later in spite of systemic antifungal therapy. Both case reports illustrate that the possibility of invasive aspergillosis must also be expected in young patients soon after onset of induction chemotherapy.