Date: 26 November 2013
Image c. 3 yr old boy with CNS aspergillosis pt TS. MRI scan pre-amphotericin B
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Notes:
A 3 year old boy, quite active and healthy clinically, who has CNS aspergillosis. He was first seen about 4 months ago for a red eye, which turned out to be panophthalmitis; culture yielded Aspergillus spp. He received 2 weeks of iv amphotericin and was sent home by the ophthalmologists. No h/o eye trauma. He returned 2 weeks ago with focal fits, and the MR showed several lesions bilaterally (including ring enhancing lesions) and normal sinuses, and a brain bx showed fungal hyphae (no culture this time). His immune status (normal WCC and neutrophil function so far) was investigated.
He was given conventional amphotericin for 8 weeks, and switched to oral itraconazole. We had to limit the ampho to 0.7 mg/kg owing to toxicity (mainly hypokalaemia).
The MRI scan was repeated at about 6 weeks, and generally showed good improvement (scans e-h). The enhancement/flare were gone but remained in a few lesions, the lesions themselves were all either gone or much smaller. Further investigations revealed the child was immunocompetent.
Patient was switched from amphotericin to oral itraconazole at week 8 essentially on a clinical assessment. Awaiting follow-up.
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Diagnosis: Aspergilloma with invasive aspergillosis evidence of invasion found in the lumbar spine and brain, in addition to heart.
Fungal endocarditis with NO evidence of bacterial endocarditismia.Additional image details:
A. Normal chest X ray:
This (normal) chest X-ray was taken about 6 weeks before endocarditis was diagnosed, and 3 months before death due to disseminated aspergillosis. No CT scan was done (a chest radiograph has a 10% false negative rate in leukaemic patients, compared with CT).B. Aspergillus niger Fungal ball:
Gross section of lung at autopsy showing a discrete, well-demarcated dark/black mass surrounded by a fibrotic capsule. There was no evidence of local invasion, or infarction. The patient had had acute myeloid leukaemia (M1) and responded poorly to chemotherapy. He developed A.niger endocarditis and disseminated disease to the kidneys, lumbar disc and heart, probably arisiong from this lesion. It is unclear whether this lung lesion was a partially cured ‘mycotic lung sequestrum’ following antifungal therapy, or originated as an aspergilloma. The confirmation of genus and species was obtained by PCR on blood and vegetations.C. Endocarditis:
Macroscopic view of the heart at autopsy, showing an infracted lesion on the papillary muscle of the mitral valve in the left ventricle. In addition the patient had large vegetations, which are not shown here. The confirmation of genus and species was obtained by PCR on blood and vegetations; the pericarditis was a manifestation of disseminated aspergillosis.D. Pericarditis due to Aspergillus niger:
Macroscopic view of the pericardium at autopsy, showing gross chronic haemorrhagic pericarditis. The confirmation of genus and species was obtained by PCR on blood and vegetations; the pericarditis was a manifestation of disseminated aspergillosis.E. Lumbar discitis:
Macroscopic lesion of a lumbar intervertebral vertebral at autopsy, showing haemorrhagic necrosis, caused by hyphal invasion and infarction. The confirmation of genus and species was obtained by PCR on blood and vegetations; the discitis was a manifestation of disseminated aspergillosis.
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Secondary metabolites, structure diagram: Trivial name – Folipastatin
