Introduction

HIV-infected patients, like others with impaired T-cell function, are at increased risk for developing fungal infections [1]. Other HIV-associated conditions, such as depletion of gut-associated lymphoid tissue, decreased gastric acidity, viral esophagitis, depressed mucosal immunity, and possibly altered epithelial attachment sites also may increase the susceptibility of these patients to mycoses [2–3].

Fungal infections represent an important cause of morbidity and mortality in HIV-infected children. Most children with low CD4+ lymphocyte counts develop mucosal candidiasis that increases in severity with worsening immunosuppression [2–4]. Invasive fungal infections due to pathogens such as Cryptococcus neoformans, Coccidioides immitis, Histoplasma capsulatum, Penicillium marneffei and others occur less frequently in pediatric than in adult patients with the acquired immunodeficiency syndrome (AIDS), but carry similar high morbidity and mortality. The basis for such differences in susceptibility between pediatric and adult AIDS populations is probably related to lower exposure to the sources of these fungal pathogens at younger ages. More recently, invasive pulmonary aspergillosis has emerged as an HIV-associated complication.

Fungal infections may present with atypical clinical manifestations, making their recognition a true challenge (Table 40.1). Thus, when fungal cultures or serologic or antigenic markers are negative, biopsies of affected sites are often important in making a diagnosis [5].

In the past decade, the therapeutic options for invasive fungal infections have broadened with the introduction of the triazole compounds fluconazole and itraconazole, the lipid formulations of amphotericin B, the allilamine terbinafine, and the echinocandin caspofungin [6–11].