Patient Encounter 3 Invasive Mold Infection

A 40-year-old female with acute myelogenous leukemia at day 115 post matched-al-logeneic donor hematopoietic stem cell transplantation presents to the clinic with increasing complaints of nausea, stomach cramping, and rash on the hands spreading up her arms. She also complains of pain upon deep inspiration. By laboratory examination, she is noted to have an alanine aminotransferase of 85 IU/L (1.42 ^Kat/L), aspartate aminotransferase 75 IU/L (1.25 ^Kat/L) and total bilirubin of 2.1 mg/dL (36 ^mol/L). Her current medications include tacrolimus 5 mg twice daily (most recent level: 8 ng/mL [8 mcg/L]), levofloxacin 500 mg daily, fluconazole 200 mg/day, vala-cyclovir 500 mg twice daily, metoprolol 25 mg twice daily, and benzonatate (tessalon) pearls. She is admitted to the hospital for suspected graft-versus-host disease exacerbation. CT scan of the chest reveals three to four dense pleural base nodules in both lung fields. The primary service wishes to start voriconazole.

What are the patient's risk factors for developing an invasive mold infection?

Is voriconazole an acceptable option in this patient? Are there any drug interaction concerns?

Unlike most opportunistic fungi, true virulence factors have been identified for C. neoformans. The capsules, including the soluble polysaccharides released from the yeast cells during infection, impair phagocytosis and binding of anticryptococcal antibodies. Primary cryptococcal infection begins in the lung, presenting as a mildly symptomatic or asymptomatic infection that resolves spontaneously or results in an encapsulated, usually noncalcified lung nodule. It is common for these isolated nodules to be detected on chest x-rays during routine workup. Diagnosis of primary cryptococcosis is only made ifthe nodule is aspirated or removed because ofconcerns of primary lung cancer.

In the immunocompromised host, infection ofthe lung may present with more diffuse, bilateral, and interstitial disease that mimics the presentation of Pneumocystis jiroveci (carinii) pneumonia (PCP). Dissemination to other organs, particularly the CNS, eye, and possibly the skin, is more likely to occur in patients with severe deficits in cell-mediated immunity. Fever, cough, dyspnea, and pleural pain are common at presentation with accompanying hypoxemia that can rapidly evolve to acute respiratory failure. Because of the features of diffuse pulmonary cryptococcosis overlap with other opportunistic pathogens, early diagnosis requires bronchoalveolar lavage or transbronchial biopsy, which can effectively diagnose 80% to 100% of cases. 1 The clinical course of diffuse cryptococcal pneumonia can be as severe as PCP, with mortality rates approaching 100% in untreated patients by 48 hours.

C. neoformans is strongly neurotropic and readily disseminates from the lung to the CNS, specifically the leptomeninges, and occasionally the parenchyma of the brain. The clinical characteristics of cryptococcal meningitis differ somewhat, however, between patients with and without underlying AIDS. In patients without AIDS, disease presentation is more insidious and symptoms such as dizziness, irritability, decreased comprehension, and unstable gait may present many weeks to months before the diagnosis is established.41 Patients with AIDS generally present much later in the

course of disease with severe meningoencephalitis. The most common signs and symptoms on presentation are fever, headache, meningismus, photophobia, mental status changes, and seizures. CT or more sensitive MRI may reveal cerebral edema, multiple areas of enhanced nodules, or a single mass lesion (cryptococcoma). Examination of the cerebrospinal fluid (CSF) often reveals increased opening pressure upon lumbar puncture, but glucose, protein, and leukocyte levels can be normal.41

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