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• W2077129401 abstract "Opportunistic fungal infections are responsible for severe and life-threatening infections in immunocompromised patients. Fungal pathogens frequently isolated in this population include Candida and Aspergillus. However, as patients experience more profound and prolonged immunosuppression, fungal species such as Fusarium that usually have a low pathogenic potential may emerge as a significant cause of morbidity and mortality.1–5 Additionally patients with severe burns, trauma or instrumentation can develop infections with this organism. Despite treatment with amphotericin B, flucytosine, rifampin, ketoconazole or miconazole (either alone or in combination), there is a high mortality associated with invasive Fusarium spp. infection.1–5 Here we report a child who developed ecthyma gangrenosum with Fusarium solani on the plantar surface of the right foot while undergoing intensive chemotherapy for central nervous system relapsed acute lymphoblastic leukemia. The child was successfully treated with amphotericin B and surgical excision. This case illustrates many of the clinical, pathologic, laboratory and therapeutic aspects of localized F. solani infection and the need to consider multiple organisms in the differential diagnosis of ecthyma gangrenosum. Case report. A 9-year-old girl was admitted for fever and neutropenia to Driscoll Children's Hospital in Corpus Christi, TX, in 1994. She had been diagnosed with acute lymphoblastic leukemia 2 years before this admission and had achieved remission with standard chemotherapy. She had a central nervous system relapse 1 month before this admission. One week before this admission she received high dose cytarabine. On the day of her admission she awoke with a fever of 101.2°F and complained of feeling weak and tired. The initial physical examination was unremarkable. The white blood cell count was 300/mm3 with an absolute neutrophil count (ANC) of 24/mm3. Hemoglobin was 7.4 g/dl, and platelet count was 16 000/mm3. Blood and urine cultures were obtained and she was given iv ceftazidime. Fever continued daily, and on the third day of hospitalization a 1-cm purpuric nontender maculopapular lesion was noted on the lateral plantar surface of her right foot. The lesion subsequently developed a bullous component. At that time her ANC was 0/mm3, and a radiograph of her foot was normal. The lesion was aspirated, and the culture grew a filamentous fungus initially identified as Trichophyton spp. She was given oral fluconazole therapy. Because of the persistence of her fever, tobramycin and vancomycin were added to the ceftazidime regimen. On the eighth day of hospitalization her ANC began to recover and she defervesced. After 10 days in the hospital she was discharged with a white blood cell count count of 4100/mm3 and an ANC of >1000/mm3. Five days later her foot lesion was approximately 3 by 3 cm and erythematous to violaceous in color. At this time the original fungal culture that had been submitted to Dr. Michael Rinaldi at the University of Texas Health Science Center at San Antonio was identified as F. solani susceptible to amphotericin B and itraconazole but resistant to fluconazole. Our patient was then readmitted for treatment. Because of concerns over spread of the Fusarium infection, chemotherapy was placed on hold and amphotericin B was started at 1 mg/kg/day. At the time of this second admission the ANC was >1000/mm3. A magnetic resonance image of her right foot demonstrated a 5 × 5 mm lesion involving the skin and soft tissues of the plantar surface without any associated bone changes. The area was hypointense on T-1 sequences and hyperintense on T-2 images. Additional studies included a chest computerized tomography scan that showed basilar atelectasis and a computerized tomography scan of the paranasal sinuses that revealed left ethmoidal opacification and left maxillary mucosal thickening. A brain magnetic resonance image was normal but demonstrated fluid in the left maxillary sinus. A nuclear bone scan was normal. After having received amphotericin B for 1 week she underwent surgical excision of the mass. An initial resection demonstrated septate hyphae at the margin of resection of the lesion, and a second excision was required. The complete plantar defect was 4 by 3 cm and could not be closed. Pathologic examination revealed focal areas of reactive fibrosis with infiltrations by lymphocytes and macrophages within the fibroadipose tissue containing septate hyphae. Chemotherapy was restarted 4 days after surgery. After 14 days of amphotericin B she was discharged home in good condition receiving no antifungals. There was no subsequent evidence of relapsed Fusarium infection, despite completing chemotherapy treatment for her relapsed central nervous system leukemia. Five years later our patient continues to do well. Discussion. Fusarium spp. are typically plant fungi commonly found on ripening fruit and vegetables, soil organisms and transient components of the fungal aeroflora. These filamentous fungi derive their name from their fusiform spores. In culture they produce purple, yellow or pink fluffy colonies, and microscopically septate hyphae that branch at acute angles can be seen. Fusarium spp. are monomorphic molds that in tissue sections can easily be confused with Aspergillus spp. because both infections have similar histopathology with septate dichotomously branching hyphae. Infections with opportunistic fungal pathogens such as F. solani are seen in severely immunocompromised children and adults.1–5Fusarium spp. can cause superficial and deep infections including endophthalmitis, onychomycosis, cellulitis, keratitis, central venous catheter infections, sinusitis, endocarditis, osteomyelitis, pneumonia and sepsis.6–9 Invasive infections are being reported more frequently as a consequence of the more intensive chemotherapeutic regimens used to treat hematologic malignancies and in preparation for bone marrow transplantation.1–5 Besides profound and prolonged neutropenia, these patients have multiple other risk factors for the development of fungal infections, including the use of broad spectrum antibiotics, ulcerations of their mucous membranes and multiple invasive procedures. Additionally patients with extensive burns have developed invasive infections with F. solani.3, 10 The pathogenesis of Fusarium spp. infection is not well-understood, but the portal of entry may be the respiratory tract as with Aspergillus spp.10 Sinusitis in particular has been reported in several cases.4, 10 Direct inoculation of a wound as happens in burn patients and disruption of the cutaneous barriers with central venous catheters may also be portals of entry. Gastrointestinal colonization and invasion is another possible route of infection.10 In our patient the portal of entry was most likely traumatic inoculation of the skin of the plantar surface of the foot. This is consistent with the presence of only one lesion and a good clinical response. The plantar infection that our patient developed had the clinical characteristics of ecthyma gangrenosum with the appearance of a purpuric maculopapule with a bullous component. Ecthyma gangrenosum is commonly associated with Pseudomonas aeruginosa infection, either disseminated or localized, but it can also be caused by other bacteria such as Staphylococcus aureus or Serratia marcescens. Additionally Aspergillus spp. and Mucor spp. have been reported to cause ecthymic lesions.11 Fusarium infection can present with a variety of skin findings in the immunocompromised host. Merz et al.10 reported four adult patients with necrotic skin lesions, and Venditti et al.5 described one adult and one adolescent patient with leukemia who developed disseminated ecthyma gangrenosum-like skin lesions. Chaulk et al.12 reported a 12-year-old boy with acute lymphoblastic leukemia in relapse who developed multiple necrotic and hemorrhagic lesions. In a review of cutaneous manifestations of saprophytic molds in immunocompromised patients, Weitzman13 discussed the cutaneous manifestations of Fusarium infections, including the development of lesions that progressed from erythematous papules to areas of necrosis with scabs. The description of these lesions is consistent with ecthyma gangrenosum. Other skin findings caused by Fusarium spp. included keratotic masses, painful erythematous nodules and erythematous plaques with pustules. As is the case with other life-threatening infections in immunocompromised patients, the treatment of patients with Fusarium spp. has included different formulations of amphotericin B alone or in combination with 5-fluorocytosine, miconazole, ketoconazole and rifampin.1–5, 10 Surgical excision and drainage have also been used as well as the administration of granulocyte transfusions and granulocyte-macrophage colony-stimulating factor.2, 12, 14, 15 However, despite all of these interventions, most patients with disseminated disease die.1–4 In cancer patients recovery is mainly dependent on the resolution of the neutropenia. In our patient resolution of her neutropenia was associated with defervescence despite initial inadequate antifungal therapy. Often the chemotherapy must be stopped to allow for a faster return of the ANC. This has a detrimental impact on the treatment of the underlying leukemia. Because of this concern, once her foot lesion was completely excised, we decided to restart chemotherapy after only 10 days of amphotericin B treatment. The development of ecthyma gangrenosum is an ominous sign in immunocompromised children and adults. Although most often associated with P. aeruginosa infections, physicians need to be aware that fungal pathogens such as Fusarium spp. can produce this finding. This case demonstrates that localized Fusarium infections in immunocompromised children can be successfully treated with a combination of a short course of amphotericin B and surgical excision." @default.
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• W2077129401 title "SUCCESSFUL TREATMENT OF FUSARIUM SOLANI ECTHYMA GANGRENOSUM IN A CHILD WITH ACUTE LYMPHOBLASTIC LEUKEMIA IN RELAPSE" @default.
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