Invasive fungal infections

Skin breakdown and immunosuppression among the major risk factors for fungal infections.

Acquisition of fungi usually through respiratory tract or via colonization of skin, gastrointestinal tract and mucous membranes.

Highest risk patients have hematologic malignancies, organ and hematopoietic stem cell transplantations.

The risk of fungal infections varies according to the type of leukemia.

Patients with acute lymphocytic leukemia have a lower risk of 5-7%, while the risk in AML is double.

Acute myeloid leukemia has the highest risk of associated fungal infections.

Overall mortality from fungal infections in acute myelogenous leukemia has fallen to 20-30% from 60-70%. in recent years.

Risks for developing fungal infection include neutropenia, mucositis and immunosuppressive therapy.

Comorbid conditions in leukemia such as diabetes, CMV, and other infections increase the risk of fungal infections.

In recent past Candida species was the most common cause of invasive fungal infections in acute leukemia, but Aspergillus, Fusarium, and Mucorales are increasing, due to the adoption of prophylactic azole therapy for high-risk patients.

Incidence of proven or probable mold and yeast infection can reach approximately 24% in leukemia patients.

Studies in leukemia have demonstrated that as many as 2/3 of fungal infections are related to mold, and the rest are form Candida.

Mold infection prevalence has increased in recent years as a result of antifungal prophylaxis with therapies such as fluconazole.

Among patients with leukemia who have received antifungal prophylaxis, Candida infections are frequently caused by resistant Candida species, such as Candida glabrata.

Breakthrough fungal infectiions in patients given antifungal prophylaxis with posaconazole and vorinconazole may also be caused by mucormycosis or zygomycosis.

Mortality from candidiasis or aspergillosis ranges from 40-50% and from fusariosis or zygomycosis 70% or more.

Occur in patients with chronic granulomatous disease with impaired neutrophil function.

Risk of such infections related to intensity of the cytotoxicity of the chemotherapy regimen and duration of neutropenia.

Risk varies from 2-40% depending on degree of neutropenia.

Beta-D-glucan and galactomannan serologic tests have up to 99% predictive value for opportunistic fungal infections.

In North America major agents are Aspergillus and Candida.

Nosocomial infections related to immunosuppression, hospital environmental exposure and parental nutrition can lead to such infections.

The increased use of allogeneic transplants, matched unrelated donors and mismatched family donors have increased risk.

Dissemination of these infections may affect pituitary, thyroid, parathyroid, adrenal, pancreatic and reproductive organ functions.

May lead to electrolyte abnormalities and treatment agents have endocrine and metabolic consequences.

Prophylaxis commonly used since diagnosis is often delayed, difficult to diagnosis and delay in treatment increases mortality.

Prophylaxis commonly used since diagnosis is often delayed, difficult to diagnosis and delay in treatment increases mortality.

Diagnosis difficult because of nonspecific signs, symptoms and rarity of positive blood cultures and difficulty in acquiring histologic tissue diagnosis.

Antifungal prophylaxis with fluconazole reduces morbidity and mortality among allogeneic stem cell transplant recipients.

Invasive aspergillosis is associated with the use of corticosteroids of long duration.

Pituitary involvement rare in patients with central nervous system fungal infections.

Pituitary involvement is related to hematogenous spread seen with disseminated infections in a immunocompromised host, extension from adjacent infected sites such as the sphenoid sinus, cavernous sinus, and skull base, or via iatrogenic inoculation during transphenoidal surgery.

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