Skip to main content

Purpuric Papules in an Immunocompromised Patient: Diagnosis: Fusarium infection

October 2002

Patient Presentation A 57-year-old white male with acute myelogenous leukemia and two allogenic bone marrow transplants was referred for evaluation of tender, non-pruritic skin lesions. The lesions had appeared 2 weeks earlier when he’d undergone chemotherapy. The patient also had a low-grade fever, malaise and myalgias. On examination, we noticed multiple, 1-cm to 2-cm purpuric patches and papules on the man’s trunk and extremities (see above photo). These lesions were tender, necrotic and non-blanchable. The patient’s mucous membranes, hair and nails were uninvolved. A complete blood cell count revealed 200 white blood cells and 20,000 platelets. We obtained biopsies and tissue cultures of the lesions for further analysis. Routine hematoxylin and eosin sections showed a septated fungus with dilated endings and irregular branching patterns. What’s your diagnosis? About this Condition With the increased use of cytotoxic chemotherapy, bone marrow transplantation and immunosuppressive therapy, the incidence of invasive fungal infections has substantially increased. Fusarium species, commonly found in soil and organic debris — and once thought to cause only local infection — has emerged as a deadly human patho-gen in patients who are severely immunocompromised. It’s most commonly seen in acute leukemia (70% to 80% of all fusarium infections) and prolonged neutropenia (in greater than 90% of all reported infections of this type). Infection with fusarium species may result in local, focally invasive, or disseminated disease, and the disease frequently mimics aspergillosis. The skin is the most commonly infected organ, representing the site of infection in 85% of cases. Lesions usually begin as macules with a central pallor and then progress to multiple red papules or painful nodules, which frequently become ulcerated and covered by black eschars. Lesions usually appear on the extremities but have also been reported on the trunk and face. Because these lesions develop at an early stage of the disease, they’re an important clue to an early-stage diagnosis of fusariosis. Disseminated infection with fusarium can rapidly progress to death, making early diagnosis critical. In contrast to aspergillosis, fusariosis is commonly accompanied by positive blood cultures (in 40% to 50% of cases), which reveal sickle-shaped, multiseptate macroconidia. (A serum galactomannan test may help to diagnose aspergillosis.) Biopsy specimens may reveal fungal organisms present within and around dermal blood vessels, resulting in thrombosis and tissue necrosis. The septate hyphae are best visualized when tissue is prepared with methenamine silver or periodic acid-Schiff stains and exhibit both 45-degree and 90-degree branching. Antibodies against fusarium species may be positive in tissue sections, also aiding in the diagnosis. In our patient’s case, routine hematoxylin and eosin sections revealed characteristic patterns of the fusarium species — a septated fungus with dilated endings and irregular branching patterns. In addition, blood and tissue fungal cultures grew fusarium. Therapy and Prevention Disseminated fusariosis in immunocompromised patients is difficult to treat; patients often die from this condition. Because skin is often the primary source of infection, it’s recommended that any patient with a hematologic malignancy who’s scheduled to receive cytotoxic chemotherapy or a bone marrow transplant should undergo a thorough skin examination. The main characteristics to search for include concomitant fungal or yeast infections or any significant break in the integrity of the skin. Normal neutrophil function and count are important for a patient to recover from fusariosis. Amphotericin B is the most commonly prescribed therapy, but it has mixed results. Successful outcomes have been achieved with adjuvant colony-stimulating factors or granulocyte transfusions. In one study, survival was associated with malignancy in remission, adequate neutrophil counts and a lack of significant graft-versus-host disease.

Patient Presentation A 57-year-old white male with acute myelogenous leukemia and two allogenic bone marrow transplants was referred for evaluation of tender, non-pruritic skin lesions. The lesions had appeared 2 weeks earlier when he’d undergone chemotherapy. The patient also had a low-grade fever, malaise and myalgias. On examination, we noticed multiple, 1-cm to 2-cm purpuric patches and papules on the man’s trunk and extremities (see above photo). These lesions were tender, necrotic and non-blanchable. The patient’s mucous membranes, hair and nails were uninvolved. A complete blood cell count revealed 200 white blood cells and 20,000 platelets. We obtained biopsies and tissue cultures of the lesions for further analysis. Routine hematoxylin and eosin sections showed a septated fungus with dilated endings and irregular branching patterns. What’s your diagnosis? About this Condition With the increased use of cytotoxic chemotherapy, bone marrow transplantation and immunosuppressive therapy, the incidence of invasive fungal infections has substantially increased. Fusarium species, commonly found in soil and organic debris — and once thought to cause only local infection — has emerged as a deadly human patho-gen in patients who are severely immunocompromised. It’s most commonly seen in acute leukemia (70% to 80% of all fusarium infections) and prolonged neutropenia (in greater than 90% of all reported infections of this type). Infection with fusarium species may result in local, focally invasive, or disseminated disease, and the disease frequently mimics aspergillosis. The skin is the most commonly infected organ, representing the site of infection in 85% of cases. Lesions usually begin as macules with a central pallor and then progress to multiple red papules or painful nodules, which frequently become ulcerated and covered by black eschars. Lesions usually appear on the extremities but have also been reported on the trunk and face. Because these lesions develop at an early stage of the disease, they’re an important clue to an early-stage diagnosis of fusariosis. Disseminated infection with fusarium can rapidly progress to death, making early diagnosis critical. In contrast to aspergillosis, fusariosis is commonly accompanied by positive blood cultures (in 40% to 50% of cases), which reveal sickle-shaped, multiseptate macroconidia. (A serum galactomannan test may help to diagnose aspergillosis.) Biopsy specimens may reveal fungal organisms present within and around dermal blood vessels, resulting in thrombosis and tissue necrosis. The septate hyphae are best visualized when tissue is prepared with methenamine silver or periodic acid-Schiff stains and exhibit both 45-degree and 90-degree branching. Antibodies against fusarium species may be positive in tissue sections, also aiding in the diagnosis. In our patient’s case, routine hematoxylin and eosin sections revealed characteristic patterns of the fusarium species — a septated fungus with dilated endings and irregular branching patterns. In addition, blood and tissue fungal cultures grew fusarium. Therapy and Prevention Disseminated fusariosis in immunocompromised patients is difficult to treat; patients often die from this condition. Because skin is often the primary source of infection, it’s recommended that any patient with a hematologic malignancy who’s scheduled to receive cytotoxic chemotherapy or a bone marrow transplant should undergo a thorough skin examination. The main characteristics to search for include concomitant fungal or yeast infections or any significant break in the integrity of the skin. Normal neutrophil function and count are important for a patient to recover from fusariosis. Amphotericin B is the most commonly prescribed therapy, but it has mixed results. Successful outcomes have been achieved with adjuvant colony-stimulating factors or granulocyte transfusions. In one study, survival was associated with malignancy in remission, adequate neutrophil counts and a lack of significant graft-versus-host disease.

Patient Presentation A 57-year-old white male with acute myelogenous leukemia and two allogenic bone marrow transplants was referred for evaluation of tender, non-pruritic skin lesions. The lesions had appeared 2 weeks earlier when he’d undergone chemotherapy. The patient also had a low-grade fever, malaise and myalgias. On examination, we noticed multiple, 1-cm to 2-cm purpuric patches and papules on the man’s trunk and extremities (see above photo). These lesions were tender, necrotic and non-blanchable. The patient’s mucous membranes, hair and nails were uninvolved. A complete blood cell count revealed 200 white blood cells and 20,000 platelets. We obtained biopsies and tissue cultures of the lesions for further analysis. Routine hematoxylin and eosin sections showed a septated fungus with dilated endings and irregular branching patterns. What’s your diagnosis? About this Condition With the increased use of cytotoxic chemotherapy, bone marrow transplantation and immunosuppressive therapy, the incidence of invasive fungal infections has substantially increased. Fusarium species, commonly found in soil and organic debris — and once thought to cause only local infection — has emerged as a deadly human patho-gen in patients who are severely immunocompromised. It’s most commonly seen in acute leukemia (70% to 80% of all fusarium infections) and prolonged neutropenia (in greater than 90% of all reported infections of this type). Infection with fusarium species may result in local, focally invasive, or disseminated disease, and the disease frequently mimics aspergillosis. The skin is the most commonly infected organ, representing the site of infection in 85% of cases. Lesions usually begin as macules with a central pallor and then progress to multiple red papules or painful nodules, which frequently become ulcerated and covered by black eschars. Lesions usually appear on the extremities but have also been reported on the trunk and face. Because these lesions develop at an early stage of the disease, they’re an important clue to an early-stage diagnosis of fusariosis. Disseminated infection with fusarium can rapidly progress to death, making early diagnosis critical. In contrast to aspergillosis, fusariosis is commonly accompanied by positive blood cultures (in 40% to 50% of cases), which reveal sickle-shaped, multiseptate macroconidia. (A serum galactomannan test may help to diagnose aspergillosis.) Biopsy specimens may reveal fungal organisms present within and around dermal blood vessels, resulting in thrombosis and tissue necrosis. The septate hyphae are best visualized when tissue is prepared with methenamine silver or periodic acid-Schiff stains and exhibit both 45-degree and 90-degree branching. Antibodies against fusarium species may be positive in tissue sections, also aiding in the diagnosis. In our patient’s case, routine hematoxylin and eosin sections revealed characteristic patterns of the fusarium species — a septated fungus with dilated endings and irregular branching patterns. In addition, blood and tissue fungal cultures grew fusarium. Therapy and Prevention Disseminated fusariosis in immunocompromised patients is difficult to treat; patients often die from this condition. Because skin is often the primary source of infection, it’s recommended that any patient with a hematologic malignancy who’s scheduled to receive cytotoxic chemotherapy or a bone marrow transplant should undergo a thorough skin examination. The main characteristics to search for include concomitant fungal or yeast infections or any significant break in the integrity of the skin. Normal neutrophil function and count are important for a patient to recover from fusariosis. Amphotericin B is the most commonly prescribed therapy, but it has mixed results. Successful outcomes have been achieved with adjuvant colony-stimulating factors or granulocyte transfusions. In one study, survival was associated with malignancy in remission, adequate neutrophil counts and a lack of significant graft-versus-host disease.