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Fungal and viral infections have emerged as a significant cause of morbidity and mortality in cancer patients. Modern management of infections in cancer requires knowledge of the epidemiology, pathogenesis, treatment, and prevention of such infections. Fungal infections range from nosocomial infections with Candida species to endemic fungi acquired outside the hospital, such as Histoplasma capsulatum. Opportunistic fungi, especially molds, have emerged as a leading cause of death in patients with leukemia or hematopoietic stem cell transplant (HSCT) (1). Viral infections such as varicella-zoster virus (VZV), herpes simplex virus (HSV), or cytomegalovirus (CMV) have been associated with disease and treatment for multiple myeloma and chronic lymphocytic leukemia (CLL) (2-4). Respiratory viruses, such as respiratory syncytial virus (RSV), adenovirus, and influenza, are increasingly recognized as significant pathogens in cancer patients, particularly as molecular diagnostic methods improve. In addition, viruses such as novel influenza H1N1, West Nile virus, bocaviruses, and noroviruses have emerged as newly recognized pathogens in cancer patients.

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Fungal infections remain a challenge for oncology patients. Exposure to fungi is common, with exposure typically occurring in the environment. Cancer patients are susceptible not only to new infection with endemic fungi (such as H capsulatum), but also to reactivation of latent infections. Opportunistic molds, such as Fusarium species, Scedosporium species, and Zygomycetes cause devastating disease in hematologic patients. Cases of nosocomial infection due to molds are reported in the setting of hospital construction, leading to routine air sampling and filtration. In contrast, Candida species are a common component of the patient's and/or health care workers' endogenous microbial flora. Manifestations of infection may not present until the patient receives chemotherapy or undergoes HSCT.

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RISK FACTORS

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Severe neutropenia, particularly prolonged, has long been associated with invasive fungal infections. Chemotherapy resulting in prolonged and severe CD4 lymphocytopenia can also result in infections similar to those seen in untreated HIV/AIDS patients, such as cryptococcosis and reactivation of endemic fungi, including histoplasmosis and coccidioidomycosis. In addition, conditioning regimens for stem cell transplant and immunosuppressives to treat and/or prevent graft-versus-host disease (GVHD) result in deficient cell-mediated immunity increasing risk for invasive fungal infection (4-6). Disruption of mucocutaneous barriers predisposes to invasive candidal infection, exemplified by catheter-related bloodstream infections caused by Candida species (7). Aside from catheter infection, damage from radiation, GVHD, and mucositis are risk factors for invasive infection (8).

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Finally, another aspect of importance is the change in flora that takes place with broad-spectrum antibacterial and antifungal therapy. The latter may result in suppression of normal bacterial flora and candidal overgrowth in the oropharynx and gastrointestinal tract. Antifungal therapy or prophylaxis may result in breakthrough infection with non-Candida albicans species, such as Candida krusei (resistant to fluconazole) (9). Aside from non-C albicans species, prophylaxis with nonmold active antifungals (eg, fluconazole) may predispose to infection with molds, such as aspergillosis.

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Candidiasis

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