Neurovascular Complications of Iatrogenic Fusarium solani Meningitis

Abstract

A multinational outbreak of nosocomial fusarium meningitis occurred among immunocompetent patients who had undergone surgery with epidural anesthesia in Mexico. The pathogen involved had a high predilection for the brain stem and vertebrobasilar arterial system and was associated with high mortality from vessel injury. Effective treatment options remain limited; in vitro susceptibility testing of the organism suggested that it is resistant to all currently approved antifungal medications in the United States. To highlight the severe complications associated with fusarium infection acquired in this manner, we report data, clinical courses, and outcomes from 13 patients in the outbreak who presented with symptoms after a median delay of 39 days.

Figure 1.. Typical Imaging Findings in Patients with Fusarium solani Meningitis.

Imaging from three patients is shown (one patient in Panels A through C, one in Panels D through F, and one in Panels G through I). In Panel A, diffusion-weighted magnetic resonance imaging (MRI) shows acute infarction of right paramedian pons and cerebellum. Panel B shows a computed tomographic (CT) image of the head obtained without the use of contrast material at the time of sudden worsening; diffuse subarachnoid hemorrhage in the prepontine cistern and fourth ventricle can be seen. In Panel C, repeat catheter angiography shows the progression of midbasilar irregularity to complete occlusion. Panel D shows diffusion-weighted MRI, which revealed a small region of restricted diffusion suggestive of infection in the right cerebellar pontine angle. Panel E is a CT image of the head obtained without the use of contrast material, which showed extensive subarachnoid hemorrhage and intraventricular hemorrhage. Panel F shows catheter angiography, which revealed vascular injury in the lateral medullary segment of the right posterior inferior cerebellar artery (circled). In Panel G, T1-weighted MRI with contrast material shows a nodular enhancing lesion in the prepontine cistern (circled). Panel H is a CT angiogram showing segmental stenosis of the vertebral and basilar arteries. Panel I is a CT image of the head obtained without the use of contrast material at the time of clinical deterioration, showing progression to vascular rupture with subarachnoid and intraventricular hemorrhage.

Figure 2.. Pathological Features at Autopsy of a Patient Who Died from F. solani Meningitis.

Panel A shows a gross photograph of the brain at autopsy. The brain-stem base was covered with whitish-yellowish purulent material. Panel B shows a dense granulomatous, lymphoplasmacytic, neutrophilic reaction, with abundant multinucleated giant cells (arrows) and hemosiderin-laden macrophages (arrowheads) in the subarachnoid space. Panels C and D show abundant fungal hyphae (arrows) that are clearly visible within the subarachnoid space and the Virchow–Robin spaces. The hyphae were thin, pauciseptate, dichotomizing, and constricted with areas of dilatation and were occasionally seen to be phagocytized by giant cells. Yeastlike structures were not seen. Panels E and F show intravascular hyphae (arrows) phagocytized by a multinucleated giant cell in the lumen of a necrotic intraparenchymal pontine artery. Panel G shows a midbrain parenchymal microbleed (arrows). Hematoxylin and eosin staining was used in Panels B and G, Grocott’s methenamine silver staining in Panels C and E, and immunohistochemical staining in Panels D and F.