Case Presentation: A 52-year-old African American woman presented to her local hospital with a 3-week history of headache and diplopia without an inciting event. At that time, she was treated symptomatically and discharged. After persistent symptoms and new onset imbalance, neck stiffness, vomiting, and blurry vision, she reported to a second hospital. Her past medical history is significant for hypertension, chronic kidney disease, and renal transplant. After presentation to the second hospital, she underwent an MRI, which was unremarkable, and an LP and was diagnosed with cryptococcal meningitis (titer 1:320). She began induction therapy with IV amphotericin B liposome and flucytosine and was transferred to Tulane for management due to her previous renal transplant. Here, repeat antigen titer showed 1:160. Her hospital course was complicated by AKI, focal neurologic deficits, and persistently elevated LP opening pressures. Repeat MRI 2 weeks after admission showed findings consistent with meningitis and multiple LPs showed an increased RBC count. As a result of her high fungal burden, persistent neurologic symptoms, and increased ICP, she required a longer length of induction therapy and VP shunt placement. MRI also revealed low-lying cerebellar tonsils, which led to an inability to perform large volume LPs and a lack of significant improvement despite treatment. Three days after VP shunt placement she began maintenance therapy with Fluconazole.
Discussion: The number of solid organ transplant (SOT) recipients acquiring Cryptococcus is steadily increasing. As there is currently no prophylactic therapy, it is imperative we diagnose and begin treatment early. A more acute onset and a higher antigen level, as well as a presentation with less typical clinical manifestations has been noted in patients with T-cell suppression. Most patients are diagnosed within 17-28 months post SOT, however our patient presented 7 years after SOT. With internists normally being the first physicians to engage in a patient’s care, having an advanced organizer for diplopia (specifically CN6 palsy) can assist with correct diagnosis. With this case, we present an advanced organizer for diplopia (CN6 palsy) to assist with the differential diagnosis of CN6 palsy.
Conclusions: Cryptococcus is the third most common invasive fungal infection in SOT recipients, with mortality reaching 50%. Because of this, it is pivotal to have a broad differential diagnosis for patients presenting with focal neurological deficits (i.e. CN palsy) to avoid delay in diagnosis and treatment. With the advent of HAART, there has been an increase of cryptococcal meningitis in non-HIV infected patients, namely SOT recipients who are iatrogenically immunosuppressed. Patients who are HIV-negative or those with non-typical symptoms, may experience a delay in diagnosis and treatment, both of which result in higher morbidity and mortality. As the treatment for HIV becomes more successful and as we increase the use of immunosuppressive agents in patients undergoing SOT, cryptococcal meningitis must be considered in patients presenting with neurologic symptoms (CN6 palsy) with a history of SOT. Furthermore, when patients have an anatomic variant, it is crucial to consider they may require additional therapy or surgical intervention.