Cerebral Invasive Aspergillosis

John D Mackenzie, MD - Case Coordinator
Aaron D Sodickson, MD, PhD - Radiology Discussion
Kirstine Oh, MD - Pathology Discussion
Richard B Schwartz, MD - Attending Radiologist
Steven E Seltzer, MD - Attending Radiologist

April 8, 2002

Presentation

Imaging Findings

There is a large lesion in the left frontal lobe and smaller lesions in the left temporal lobe and left cerebellar hemisphere. On the computed tomogram (CT), the lesion in the frontal lobe is of low attenuation predominantly with a central hemorrhagic focus. On the magnetic resonance (MR) images, these lesions are of low T1-signal and heterogenous, predominantly low T2-signal. These abnormalities are not associated with significant surrounding edema, and they show no evidence of enhancement on T1-weighted images obtained after intravenous gadolinium injection. The lesions are bright on diffusion-weighted images.

Differential Diagnosis

Diagnosis

Discussion

Pathology specimens were obtained post-mortem, approximately two months after the diagnostic images were obtained. The first section of the brain demonstrates both the frontal and temporal lesions. Necrosis and cavitation are evident in both lesions. Severe necrosis and softening are also visible on a second image depicting the cerebellar lesion. Histologic evaluation revealed coagulative necrosis in several areas. Patchy areas of inflammation (inflammatory cells are stained blue) occurred throughout the brain. The second and third microscopic images show the meningeal subarachnoid vessel and meninges. On higher magnification (figure 3), large amount of pus are visible, as is the inflammatory damage to the vessel wall. At the highest magnification, aspergillus organisms are visible. No GMS stains were obtained.

Radiology Discussion

Cerebral invasive aspergillosis is most commonly carried hematogenously from a pulmonary infection, rather than arising as a direct extension of sinonasal disease. Therefore, the risk factors for cerebral infection are the same as for pulmonary infection. Immunosuppression is the primary risk factor, but severe hematologic disease (such as leukemia or lymphoma) or bone marrow transplant involve much higher risk than other sources of immunosuppression, such as solid organ transplant, AIDS, diabetes, steroid use, or chemotherapy.

The pathophysiology of aspergillus sets it apart from other infectious organisms. Because it is angioinvasive, cerebral infection will quickly lead to acute infarcts that may or may not have hemorrhages within them. If the patient survives long enough, these areas of infarct can progress to infectious cerebritis or abscess. The angioinvasive behavior of the organism also results in an atypical infectious distribution. Similar to hematogenous metastases, septic emboli, or other infections, aspergillosis may cause lesions in the corticomedullary junction. Aspergillosis, however, also tends to occlude smaller perforating arteries—so lesions may develop in the basal nuclei, thalami, corpus callosum, and brain stem. These sites are rarely affected by other infectious organisms.

Cerebral invasive aspergillosis can manifest in single or multiple lesions. On CT, the lesions generally have low attenuation and may or may not be accompanied by areas of hemorrhage. The lesions often appear hyperintense on T2-weighted or proton-density MR images, and exhibit restricted diffusion on diffusion-weighted MR images, indicating infarction. The lesions generally exhibit no enhancement, or else only subtle peripheral enhancement, on both CT and MRI. Ring enhancement can occur if abscesses form, but this is uncommon because lesions rarely become "walled off" in severely immunocompromised patients. Despite the fact that leptomeningeal inflammation and ventriculitis are commonly found at autopsy, leptomeningeal and ependymal enhancement are rarely seen on imaging studies. Dural enhancement is often visible, however, if the infection has spread directly from the paranasal sinuses. The infection will demonstrate rapid progression by size and number of lesions on repeat imaging.

References

DeLone DR, Goldstein RA, Petermann G, Salamat MS, Miles JM, Knechtle SJ, Brown WD. Disseminated Aspergillosis Involving the Brain: Distribution and Imaging Characteristics. Am J Neuroradiol. Oct 1999; 20:1597-1604.

Patterson TF, Kirkpatrick WR, White M, Hiemenz JW, Wingard JR, Dupont B, Rinaldi MG, Stevens DA, Graybill JR. Invasive Aspergillosis: Disease Spectrum, Treatment Practices, and Outcomes. Medicine July 2000; 79(4): 250-260.

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