PMC5457932_01
Timeline of the clinical course. The patient was treated for fungal meningitis. Antituberculous drugs and antibiotics were also administered, but not continuously. His condition gradually deteriorated and death from transtentorial hernia occurred on day 99. CTM: cefotiam, CTRX: ceftriaxone, EB: ethambutol, INH: isoniazid, L-AMB: liposomal amphotericin-B, MEPM: meropenem, MINO: minocycline, PAMP/BP: panipenem/betamipron, PIPC: piperacillin, RFP: rifampicin, VCM: vancomycin
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The first cerebrospinal fluid (CSF) analysis, on day 4, revealed: cell count, 1,244 /muL (polymorphonuclear cells, 90%; monomorphonuclear cells, 10%); protein, 273 mg/dL; and glucose, 47 mg/dL (simultaneous blood glucose, 135 mg/dL) (Table 1 and Fig. 1). On day 4, bacterial meningitis was suspected and treatment with vancomycin (VCM), ceftriaxone (CTRX) and piperacillin (PIPC) was initiated (Fig. 1). High fever had not resolved (Fig. 1). Although negative results were obtained for the CSF culture for fungi, fever resolved several days after beginning L-AMB (Fig. 1) and findings from the third CSF analysis on day 18 had improved: cell count, 128 /muL (polymorphonuclear cells, 83%; monomorphonuclear cells, 17%); protein, 117 mg/dL; and glucose, 38 mg/dL (simultaneous blood glucose, not determined) (Table 1, Fig. 1). Fever of 37-38C reappeared around day 35 (Fig. 1), and oral fluconazole (FCZ) was started on day 36. A fifth CSF analysis on day 50 revealed worsened findings: cell count, 1,311 /muL (polymorphonuclear cells, 85%; monomorphonuclear cells, 15%); protein, 732 mg/dL; and glucose, 44 mg/dL (simultaneous blood glucose, not determined) (Table 1 and Fig. 1). Disturbance of consciousness slowly worsened (Fig. 1), and aphasia and left hemispatial neglect gradually appeared around day 60. On days 71 and 84, pneumonia complicated the hospital course, resulting in administration of CTM for 9 days and MEPM for 11 days, respectively (Fig. 1). Fig. 1). FCZ was continued because of improvements in cell counts.
MRI on days 14, 50 and 71. A) MRI on day 14 shows a DWI hyperintense spot in the posterior horn of the left lateral ventricle (arrow). B) The lesion is iso-intense on ADC. C) On FLAIR, a hyperintense lesion is apparent in the white matter adjacent to the posterior horn of the left lateral ventricle (arrow). D, G) DWI on days 50 and 71 reveals gradual deterioration of ventriculitis (arrows). E, H) ADC mapping, the area of the DWI-hyperintense lesion appears partially hypointense (arrows). F, I) Spread of the FLAIR-hyperintense lesion in the white matter adjacent to the ventricles (arrows).
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On magnetic resonance imaging (MRI) performed on day 14, diffusion-weighted imaging (DWI) revealed a high-intensity spot in the posterior horn of the left lateral ventricle of the brain (Fig. 2A), implying ventriculitis. However, this region appeared iso-intense on apparent diffusion coefficient (ADC) mapping (Fig. 2B). On fluid-attenuated inversion recovery (FLAIR) imaging, a high-intensity lesion was detected in the white matter adjacent to the posterior horn of the left lateral ventricle (Fig. 2C). DWI on days 50 and 71 revealed exacerbation of the ventriculitis (Fig. 2D and G) and partial ADC hypointensity (Fig. 2E and H). Spread of a hyperintense region was evident in the white matter adjacent to both lateral ventricles on FLAIR imaging (Fig. 2F and I). MRI on day 71 showed the ventriculitis and hyperintense lesion in the white matter adjacent to both lateral ventricles on FLAIR imaging had become more severe (Fig. 2D-F).
Autopsy findings. A) Yellowish pus is seen flowing from a ventricle (arrow). B) Gram staining of pus from the ventricle reveals a delicate, branching, filamentous organism. C) Pus is scattered throughout the basal cistern and pontomedullary cistern (arrows). D) In formalin-fixed brain sections, both lateral ventricles are full of pus (arrows). E) Magnification of the outlined square in D shows some small abscesses in the cerebral white matter (arrows).
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On opening the cranium, yellowish pus flowed from the left ventricle (Fig. 3A). This pus was not malodorous, and Gram staining revealed a delicate, branching, filamentous organism (Fig. 3B). Pus was observed throughout the basal cistern and pontomedullary cistern (Fig. 3C). In formalin-fixed sections of brain, both lateral ventricles were filled with pus (Fig. 3D) and some small abscesses that had remained undetectable on MRI were seen in the cerebral white matter (Fig. 3E).