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Opportunistic Fungal Infections, Part 2: Candida and Aspergillus

Opportunistic Fungal Infections, Part 2: Candida and Aspergillus

Candidiasis and aspergillosis are the most common fungal infections in immunocompromised hosts. The spectrum of disease ranges from superficial and mucosal infections to invasive tissue infections. Morbidity and mortality attributed to infections with Candida and Aspergillus can be quite high; therefore, timely identification and treatment are important.

EPIDEMIOLOGY
Candida
is ubiquitous, with more than 200 described species. About 10% of the species are responsible for human disease, with Candida albicans, Candida tropicalis, Candida parapsilosis, and Candida glabrata being the most commonly isolated. Candida krusei and Candida lusitaniae are seen less frequently. Significant risk factors for candidal disease include neutropenia, use of antibiotics, the presence of an indwelling vascular device, and prolonged stay in the ICU.

Infections attributed to Candida species can be divided into 3 categories: hematogenous (eg, candidemia, hepatosplenic candidiasis, and osteomyelitis), nonhematogenous superficial (eg, cutaneous candidiasis, oropharyngeal candidiasis, and vaginitis), and nonhematogenous deepseated (eg, esophageal candidiasis, cystitis, peritonitis, and tracheitis/ bronchitis). It is noteworthy that Candida is the fourth leading cause of nosocomial bloodstream infections in hospitalized patients.1 Immunocompromised patients are at high risk for the development of any of these infections.

In HIV-1-infected patients, oropharyngeal and esophageal candidiasis are common and are recognized as an indicator of immunosuppression. These types of candidiasis are seen most commonly in patients with CD4+ T-lymphocyte counts of less than 200/?L.2 Other types of infections with Candida can certainly occur in this population but are usually associated with other concurrent risk factors. Although C albicans is still the predominant species that is isolated, the emergence of fluconazole- resistant species has been observed, usually in the setting of previous fluconazole exposure.

Patients with hematological malignancies and hematopoietic stem cell transplant (HSCT) recipients are at high risk for development of invasive candidiasis (IC), which is a major cause of morbidity and mortality. The portal of entry is typically the gut mucosa, and less commonly, the integument. Although oral and esophageal infections occur, fungemia is the most serious clinical syndrome observed.3 In addition, although C albicans still accounts for most invasive Candida infections, non-albicans Candida species have emerged with increasing frequency, particularly C glabrata and C krusei. Bloodstream infection with these species has been associated with higher rates of crude mortality.4

Most invasive fungal infections following organ transplant are also due to Candida species. These infections are typically related to complications of surgery and usually appear near the end of the first month posttransplant.5 Liver and pancreas transplant recipients are at especially high risk for invasive Candida infections in the first month following transplant.6

Aspergillus species are also ubiquitous in the environment and are found in soil, water, and decaying vegetation worldwide. Portals of entry include the respiratory tract and damaged skin or operative wounds. Reports suggest that Aspergillus infections occur in 4% to 20% of bone marrow transplant (BMT) recipients, with neutropenia being the most important risk factor for infection.7 A recent prospective trial evaluating the cumulative incidence (CI) in 4261 HSCT recipients during a 22-month period found a CI of 0.5% after autologous HSCT and 2.3% after allogeneic transplant. Mortality following the diagnosis of invasive aspergillosis ranged from 53.8% to 84.6%.8 The incidence of disease in HSCT recipients has a bimodal distribution, occurring in the early engraftment stage (around day 30) and then again after 180 days posttransplant, which probably reflects the presence and treatment of graft versus host disease.

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