Rapidly progressive multiple ischemic lesions caused by Cryptococcus neoformans infection presenting with meningoencephalitis and cerebral infarction as the initial manifestations: A case report

Introduction: Cryptococcus neoformans is an opportunistic pathogenic fungus that primarily infects individuals with compromised immune systems. Cryptococcosis caused by this fungus commonly affects the central nervous system and the lungs. This report describes a rare case of a patient who was negative for human immunodeficiency virus (HIV) and developed rapidly progressive multiple ischemic lesions secondary to infection with C. neoformans, initially presenting with meningoencephalitis and cerebral infarction. Case Presentation: A 62-year-old male patient with a history of hypertension was admitted to the hospital because of altered mental status, behavioral changes, dizziness, and urinary retention. Laboratory tests revealed an HIV-negative result, leukocytosis, elevated inflammatory markers, and hyperglycemia. Magnetic resonance imaging of the head showed multiple scattered abnormal signals within the cranial cavity. Diffusion-weighted imaging, T2-weighted imaging, and fluid-attenuated inversion recovery sequences demonstrated high signal intensity, whereas T1-weighted imaging and the apparent diffusion coefficient sequence showed low signal intensity. These findings suggested multiple cerebral infarctions. The patient underwent lumbar puncture, which revealed elevated protein levels in the cerebrospinal fluid, decreased glucose and chloride levels, and a positive result for Cryptococcus capsular antigen in the cerebrospinal fluid. Cryptococcus was also detected by India ink staining of the cerebrospinal fluid. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry identified the isolate as C. neoformans. Based on these findings, the patient was diagnosed with cryptococcal meningoencephalitis caused by the Cryptococcus neoformans, complicated by cerebral infarction. Despite receiving anti-infective treatments, anticoagulant, and glucocorticoid intervention, the patient’s condition continued to deteriorate rapidly. The patient developed progressively worsening cerebral edema and pneumonia, accompanied by suspected subarachnoid hemorrhage, suspected venous sinus thrombosis, and subcutaneous/muscular edema of the abdominal wall. These findings suggested the presence of multiple ischemic lesions. After 16 days of treatment, the patient’s family decided to discontinue medical care, and the patient was discharged voluntarily. Conclusion: In HIV-negative patients, C. neoformans infection may lead to rapidly progressive multiple ischemic lesions, initially presenting with meningoencephalitis and multiple cerebral infarctions. The disease progresses rapidly and carries an extremely poor prognosis. Early recognition, prompt antifungal and antithrombotic therapy, and further investigation of optimal glucocorticoid administration are critical for diagnosis and management.