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A healthy family who had been living in Brazil presented with crusted plaques on their extremities
Trypanosomatidae
Leishmaniasis is caused by protozoa of the family Trypanosomatidae, called Leishmania. The vector is a sandfly infected with the protozoa.1
The three main forms of leishmaniasis – cutaneous, mucocutaneous, or visceral – varies with the species of organism involved, the geographic distribution, and the immune response of the patient. A majority of the cases seen in the United States are from patients who contracted the disease elsewhere, particularly from Peru and Brazil.2
Lesions can vary from asymptomatic to severe. The initial lesion typically develops within weeks or months, and presents as an erythematous papule that is seen at the bite site.3 The papule evolves into a nodule or plaque that may ulcerate and crust.3 The ulcer can be distinguished by a raised and distinct border. In older stages, atrophic scarring may be seen. In some cases, the lesions may present years after exposure, because of immunosuppression or trauma.
Histology of CL reveals tuberculoid granulomas with parasitized histiocytes present. Amastigotes with distinct nuclei and kinetoplasts characterize Leishmania.2 In addition to histology, the biopsy may be sent for the press-imprint-smear method (PIS). In a study of 75 patients, the PIS method showed a higher sensitivity, as well as being a less costly and more rapid option for diagnosis.5
The treatment depends on the severity of the lesion and the species of the Leishmania genus. Mild lesions may resolve spontaneously. Topical imiquimod, cryotherapy, photodynamic therapy, and heat therapy may aid in the healing process.5 Systemic azole antifungal medications, miltefosine, and amphotericin B, and pentamidine may be used for more persistent lesions. In very severe cases, pentavalent antimonials (sodium stibogluconate, Pentostam) may be administered intravenously, although there is a high occurrence of recorded side effects.2
This case and the photos were submitted by Sabrina Liao, BS, University of California, San Diego; and Brooke Resh Sateesh, MD, San Diego Family Dermatology The case was edited by Donna Bilu Martin, MD.
References
1. Leishmaniasis – Resources for Health Professionals. Centers for Disease Control and Prevention. 2021 Jun 3.
2. Stark CG. Leishmaniasis. Medscape. 2020 Feb 18.
3. Markle WH and Makhoul K. Am Fam Physician. 2004 Mar 15;69(6):1455-604.
4. Ngan V. Leishmaniasis. DermNet NZ. 2017 Jan. 7.
5. Sousa AQ et al. Am J Trop Med Hyg. 2014 Nov;91(5):905-7.
Trypanosomatidae
Leishmaniasis is caused by protozoa of the family Trypanosomatidae, called Leishmania. The vector is a sandfly infected with the protozoa.1
The three main forms of leishmaniasis – cutaneous, mucocutaneous, or visceral – varies with the species of organism involved, the geographic distribution, and the immune response of the patient. A majority of the cases seen in the United States are from patients who contracted the disease elsewhere, particularly from Peru and Brazil.2
Lesions can vary from asymptomatic to severe. The initial lesion typically develops within weeks or months, and presents as an erythematous papule that is seen at the bite site.3 The papule evolves into a nodule or plaque that may ulcerate and crust.3 The ulcer can be distinguished by a raised and distinct border. In older stages, atrophic scarring may be seen. In some cases, the lesions may present years after exposure, because of immunosuppression or trauma.
Histology of CL reveals tuberculoid granulomas with parasitized histiocytes present. Amastigotes with distinct nuclei and kinetoplasts characterize Leishmania.2 In addition to histology, the biopsy may be sent for the press-imprint-smear method (PIS). In a study of 75 patients, the PIS method showed a higher sensitivity, as well as being a less costly and more rapid option for diagnosis.5
The treatment depends on the severity of the lesion and the species of the Leishmania genus. Mild lesions may resolve spontaneously. Topical imiquimod, cryotherapy, photodynamic therapy, and heat therapy may aid in the healing process.5 Systemic azole antifungal medications, miltefosine, and amphotericin B, and pentamidine may be used for more persistent lesions. In very severe cases, pentavalent antimonials (sodium stibogluconate, Pentostam) may be administered intravenously, although there is a high occurrence of recorded side effects.2
This case and the photos were submitted by Sabrina Liao, BS, University of California, San Diego; and Brooke Resh Sateesh, MD, San Diego Family Dermatology The case was edited by Donna Bilu Martin, MD.
References
1. Leishmaniasis – Resources for Health Professionals. Centers for Disease Control and Prevention. 2021 Jun 3.
2. Stark CG. Leishmaniasis. Medscape. 2020 Feb 18.
3. Markle WH and Makhoul K. Am Fam Physician. 2004 Mar 15;69(6):1455-604.
4. Ngan V. Leishmaniasis. DermNet NZ. 2017 Jan. 7.
5. Sousa AQ et al. Am J Trop Med Hyg. 2014 Nov;91(5):905-7.
Trypanosomatidae
Leishmaniasis is caused by protozoa of the family Trypanosomatidae, called Leishmania. The vector is a sandfly infected with the protozoa.1
The three main forms of leishmaniasis – cutaneous, mucocutaneous, or visceral – varies with the species of organism involved, the geographic distribution, and the immune response of the patient. A majority of the cases seen in the United States are from patients who contracted the disease elsewhere, particularly from Peru and Brazil.2
Lesions can vary from asymptomatic to severe. The initial lesion typically develops within weeks or months, and presents as an erythematous papule that is seen at the bite site.3 The papule evolves into a nodule or plaque that may ulcerate and crust.3 The ulcer can be distinguished by a raised and distinct border. In older stages, atrophic scarring may be seen. In some cases, the lesions may present years after exposure, because of immunosuppression or trauma.
Histology of CL reveals tuberculoid granulomas with parasitized histiocytes present. Amastigotes with distinct nuclei and kinetoplasts characterize Leishmania.2 In addition to histology, the biopsy may be sent for the press-imprint-smear method (PIS). In a study of 75 patients, the PIS method showed a higher sensitivity, as well as being a less costly and more rapid option for diagnosis.5
The treatment depends on the severity of the lesion and the species of the Leishmania genus. Mild lesions may resolve spontaneously. Topical imiquimod, cryotherapy, photodynamic therapy, and heat therapy may aid in the healing process.5 Systemic azole antifungal medications, miltefosine, and amphotericin B, and pentamidine may be used for more persistent lesions. In very severe cases, pentavalent antimonials (sodium stibogluconate, Pentostam) may be administered intravenously, although there is a high occurrence of recorded side effects.2
This case and the photos were submitted by Sabrina Liao, BS, University of California, San Diego; and Brooke Resh Sateesh, MD, San Diego Family Dermatology The case was edited by Donna Bilu Martin, MD.
References
1. Leishmaniasis – Resources for Health Professionals. Centers for Disease Control and Prevention. 2021 Jun 3.
2. Stark CG. Leishmaniasis. Medscape. 2020 Feb 18.
3. Markle WH and Makhoul K. Am Fam Physician. 2004 Mar 15;69(6):1455-604.
4. Ngan V. Leishmaniasis. DermNet NZ. 2017 Jan. 7.
5. Sousa AQ et al. Am J Trop Med Hyg. 2014 Nov;91(5):905-7.
