13 minute read
Dermatology Clinic
CASE #1 Cutaneous Leishmaniasis
Leishmaniasis is a disease caused by intracellular protozoan parasites predominantly found in tropical areas of the world. Leishmania-like species have been discovered in amber dating back more than 100 million years. 1 Archeologists discovered evidence of leishmaniasis in samples from Egyptian mummies as well as tablets from ancient Arabic societies. 1
William Boog Leishman, a Scottish pathologist, discovered ovoid bodies in smears taken from the spleen of a soldier who died from emaciation and splenomegaly while in Calcutta, India, in 1900. 1 Around the same time, Charles Donovan, a physician and professor of physiology, discovered similar ovoid bodies in splenic smears from Indian patients who had fever and splenomegaly. 1 These 2 physicians are credited with the discovery of the parasite that causes visceral leishmaniasis. 1
Leishmaniasis is categorized into 3 types: cutaneous, mucocutaneous, and visceral. Cutaneous leishmaniasis can be found in many places around the world, specifically in Latin America, Africa, Asia, and southern Europe. An estimated 350 million people are at risk for the disease; the worldwide prevalence is 12 million, with an annual incidence of cutaneous leishmaniasis of 1.5 million cases. 2 The condition is particularly prevalent in the Middle East and North African countries, such as Afghanistan, Iran, Iraq, Morocco, Pakistan, Saudi Arabia, Sudan, Syria, and Yemen. 3
Transmitted via an insect bite of infected female phlebotomine sand flies, leishmaniasis is caused by intracellular protozoan parasites of the genus Leishmania. 4 Specifically, when a sand fly bites a host, it transmits the parasite in the promastigote form through its proboscis. These promastigotes are then phagocytosed by the host macrophages, transformed into amastigotes and multiply, and then spread to different tissues of the body. Sandflies can then have a blood meal on an infected host and become infected with amastigotes, which migrate to the gut of the sand fly to multiply. These amastigotes develop into promastigotes and then migrate to the sand fly’s proboscis to repeat the process when having a blood meal on the next host. 4
The amastigotes within the macrophages are termed Leishman-Donovan bodies and can be visualized histologically. 2 Initially, a wide variety of inflammatory cells are present at the site of infection. Histologic appearance of chronic lesions is characterized based on the strength of the immune response of the host. If the immune response is sufficient, then epithelioid granulomata with few parasites are seen. If the immune response is poor, then a diffuse macrophage infiltrate with many parasites is seen. The immune response is T-cell-mediated, but the outcome differs in Th 1 lymphocyte vs Th 2 lymphocyte responses. Generally, the Th 1 lymphocyte response leads to better outcomes. 2,5
The cutaneous form of leishmaniasis is caused by approximately 14 different species of protozoa within the genus Leishmania, including L mexicana, L brasiliensis, L donovani, among others. 2 Knowing the species of Leishmania that infected a patient can be useful because certain species are associated with prolonged, more severe courses of disease.
Risk factors for cutaneous leishmaniasis include living in or visiting endemic regions or urban areas, warmer climate, environmental factors such as proximity of housing to dams and cowsheds, cracks in the walls of houses that encourage sand fly aggregation, and a suppressed immune system such as in individuals with HIV. 6 Additionally, travelers and military personnel are at risk. 7
Clinically, leishmaniasis appears initially as a small papule. If the lesion enlarges and develops an area of central necrosis, resembling the appearance of a volcano, then the lesion is termed a “wet” lesion. 2,7 However, if the initial small papule either remains smooth or becomes hyperkeratotic, then the lesion is called a “dry” lesion. 2,7 The outcome associated with a wet or a dry lesion can vary with different species of Leishmania. The edge of the lesion is thickened, and ulceration rarely extends into the subcutaneous tissue. Lesions develop on exposed areas of the skin where the sand fly can get access for a blood meal; however, satellite lesions may also develop due to the local spread of parasites. The size of the lesion is typically <5 cm in diameter but can reach up to 10 cm. 2
The differential diagnosis of leishmaniasis can be broad, primarily due to considerable variation in presentation of the lesions. Several conditions that may mimic leishmaniasis include infected insect bites, ulceroglandular tularemia, cutaneous anthrax, cutaneous tuberculosis, and leprosy. 2,7 It is also important to include noninfectious conditions such as basal cell carcinoma, squamous cell carcinoma, cutaneous lymphoma, and pyoderma gangrenosum within the differential. 2,7
A diagnosis is made by performing a 4-mm punch biopsy at the edge of the lesion and histologic examination. Classically, the presence of amastigotes within macrophages is specific for a diagnosis of leishmaniasis. 7 The amastigotes may also be visualized in skin scrapings or smears. Polymerase chain reaction is being used increasingly as a method to detect Leishmania DNA and make the diagnosis, as it is the most sensitive technique. 7
Prevention is essential for controlling leishmaniasis. This can be accomplished by the use of nets and insecticide, especially while sleeping. 7 Once an individual has developed cutaneous leishmaniasis, treatment methods include pentavalent antimonials (meglumine antimoniate and sodium stibogluconate), paromomycin, miltefosine, and pentamidine. 2,7 The size of the lesion should decrease after several weeks of treatment. If left untreated, it may take several months to a year for the ulcers to self-heal. Disfiguring scars can often appear. Therefore, the goals of treatment are to prevent local dissemination of parasites, decrease the size of the scar, and accelerate the healing process. 7,8
The patient in this case underwent a punch biopsy of his lesion, and histologic examination revealed Leishman-Donovan bodies. The Centers for Disease Control and Prevention was notified, and the patient was referred to an infectious disease specialist for treatment.
Yelena Dokic, BSA, and Eleanor Johnson, BS, are medical students at Baylor College of Medicine, and Christopher Rizk, MD, is a dermatologist affiliated with Elite Dermatology in Houston, Texas.
References
1. Steverding D. The history of leishmaniasis. Parasit Vectors. 2017;10(1):82. 2. Bailey MS, Lockwood DN. Cutaneous leishmaniasis. Clin Dermatol. 2007;25(2):203-211. 3. Postigo JAR. Leishmaniasis in the World Health Organization Eastern Mediterranean region. Int J Antimicrob Agents. 2010;36(Suppl 1): S62-S65. 4. Gossage SM, Rogers ME, Bates PA. Two separate growth phases during the development of Leishmania in sand flies: implications for understanding the life cycle. Int J Parasitol. 2003;33(10):1027-1034. 5. Ghersetich I, Menchini G, Teofoli P, Lotti T. Immune response to Leishmania infection in human skin. Clin Dermatol. 1999;17(3):333-338. 6. Desjeux P. The increase in risk factors for leishmaniasis worldwide. Trans R Soc Trop Med Hyg. 2001;95(3):239-243. 7. Murray HW, Berman JD, Davies CR, Saravia NG. Advances in leishmaniasis. Lancet. 2005;366(9496):1561-1577. 8. Shin JY, Lee YB, Cho BK, Park HJ. New world cutaneous leishmaniasis treated with intralesional injection of pentavalent antimony. Ann Dermatol. 2013;25(1):80-83.
CASE #2 Tinea Nigra
Tinea nigra is an uncommon superficial fungal infection. It is strictly limited to the stratum corneum and is caused by dematiaceous fungi. The characteristic causative organism of tinea nigra is Hortaea werneckii, a fungus that grows as a black yeast and can transform into a mold. 1,2 The fungus is halophilic and favors hypersaline environments up to 30% NaCl, such as coastal regions. 3 Other fungi that have been considered to cause tinea nigra are Cladosporium castellanii, Cladophialophora saturnica, and Phoma hibernica. 4-7
The condition was first described in 1973 in Venezuela. 4 Although tinea nigra is generally not associated with other manifestations in the body, H werneckii was reportedly isolated from a splenic abscess in 2 patients in 2005. 8 Most cases of tinea nigra have been reported in Latin America, Asia, Africa, and the Pacific Islands. 2,9-13 Tinea nigra has less commonly been reported in Europe and the United States. 2 The condition is more commonly seen in children and adolescents.
The most important predisposing factor for tinea nigra is hyperhidrosis, and it is most commonly found in the palmoplantar regions of the body. 2 Initially, the organism most likely attaches to its host through minor trauma. The incubation time of H werneckii is unknown but may vary from weeks to years. 12 It is seen less commonly on the arms, legs, neck, trunk, and dorsal aspects of the hands. 1,2,9,10,14
Typically, tinea nigra is unilateral and appears as a brown to gray macule or plaque that is hyperpigmented and circumscribed. The lesion can become darker at the borders with an irregular outline. Some patients have observed that the macules change color throughout the day. 2 Patients are typically asymptomatic, but occasionally patients report pruritus. 1,2
Diagnosis of tinea nigra is based on clinical physical findings and confirmed with a laboratory diagnosis of fungal infection. This can be performed by direct mycological examination with 10% to 20% KOH preparation. KOH prep testing of the affected skin scraping reveals dematiaceous, septate hyphae with colors that vary from brown to black on microscopic examination. 1,2,9,10,15 Dermoscopy is also useful for distinguishing tinea nigra from a melanocytic lesion. Tinea nigra will show a nonmelanocytic-pattern macule with superficial brown pigmentation in specks. Seeing the characteristic fungal growth pattern can help differentiate the infection from nevi, particularly melanoma. 1
Dermatology Clinic
Culturing of the affected skin on Sabouraud glucose agar with or without antibiotics, incubated at 28 °C, usually reveals fungal growth within 5 to 6 days. 1 The fungus grows in 2 phases: the initial yeast-like phase shows smooth colonies that can be creamy in appearance and dark green to black in color, and the mold phase shows fungus as filaments with wooly or smooth appearance and filamentous hyphae. 1
The differential diagnosis for tinea nigra should include melanocytic nevi, lentigines, palmar lichen planus, fixed drug eruptions, and melanoma. 16,17 These can be distinguished from tinea nigra by fungal culture, KOH prep, or skin biopsy. Light brown, wavy, and thick hyphae with occasional dark hyphae differentiate tinea nigra from other fungal infections, particularly those caused by conidia, which appear more uniformly heavily pigmented. 2 On
Tinea nigra appears as a hyperpigmented brown to gray macule or plaque that is circumscribed, often darker on the edges.
hematoxylin and eosin stain, hyphae and spores are seen at the stratum corneum. 1 Due to the irregular borders, pigmentation, and growth of the lesion, tinea nigra may be mistaken for melanoma. 13 An accurate diagnosis is important in order to prevent unnecessary diagnostic and excisional surgery as well as scarring.
Treatment of tinea nigra include topical antifungals bifonazole, clotrimazole, ketoconazole, terbinafine, and ciclopirox olamine gel. 2,18-21 Oral itraconazole was first reported to be effective in a case correspondence. 22 Topical keratolytic agents such as 3% salicylic acid or Whitfield ointment (6% benzoic acid and 3% salicylic acid) may also be beneficial. 2 Oral griseofulvin has not been found to be effective. 1 No randomized controlled clinical trials have evaluated treatments for tinea nigra. Overall, tinea nigra is found to clear quickly and effectively with these treatments.
The patient in this case was prescribed topical ketoconazole cream for 4 weeks, and the lesion regressed. ■
Yasmin Khalfe, BA, and Emily Burns, BA, are medical students at Baylor College of Medicine, and Christopher Rizk, MD, is a dermatologist at Elite Dermatology in Houston, Texas.
References
1. Bonifaz A, Badali H, de Hoog GS, et al. Tinea nigra by Hortaea werneckii, a report of 22 cases from Mexico. Stud Mycol. 2008;61:77-82. 2. Bonifaz A, Gómez-Daza F, Paredes V, Ponce RM. Tinea versicolor, tinea nigra, white piedra, and black piedra. Clin Dermatol. 2010;28(2):140-145. 3. Kogej T, Stein M, Volkmann M, Gorbushina AA, Galinski EA, GundeCimerman N. Osmotic adaptation of the halophilic fungus Hortaea werneckii: role of osmolytes and melanization. Microbiology. 2007;153(12):4261-4273. 4. Borelli D, Marcano C. Cladosporium castellanii nova espécie agente de tinea nigra. Castellania. 1973;1:151-154. 5. Crous PW, Braun U, Schubert K, Groenewald JZ. Delimiting Cladosporium from morphologically similar genera. Stud Mycol. 2007;58:33-56. 6. Bakerspigel A. The isolation of Phoma hibernica from a lesion on a leg. Sabouraudia. 1969;7(3):261-264. 7. Badali H, Carvalho VO, Vicente V, et al. Cladophialophora saturnica sp. nov., a new opportunistic species of Chaetothyriales revealed using molecular data. Med Mycol. 2009;47(1):51-62. 8. Ng KP, Soo-Hoo TS, Na SL, et al. The mycological and molecular study of Hortaea werneckii isolated from blood and splenic abscess. Mycopathologia. 2005;159(4):495-500. 9. Perez C, Colella MT, Olaizola C, Hartung de Capriles C, Magaldi S, MataEssayag S. Tinea nigra: report of twelve cases in Venezuela. Mycopathologia. 2005;160(3):235-238. 10. Severo LC, Bassanesi MC, Londero AT. Tinea nigra: report of four cases observed in Rio Grande do Sul (Brazil) and a review of Brazilian literature. Mycopathologia. 1994;126(3):157-162. 11. Cabrera R, Sabatini N, Urrutia M, Sepúlveda R. [Tinea nigra: a allochthonous case report in Chile]. Rev Chilena Infectol. 2013;30(1):90-93. 12. Pegas JR, Criado PR, Lucena SK, de Oliveira MA. Tinea nigra: report of two cases in infants. Pediatr Dermatol. 2003;20(4):315-317. 13. Uezato H, Gushi M, Hagiwara K, Kayo S, Hosokawa A, Nonaka S. A case of tinea nigra palmaris in Okinawa, Japan. J Dermatol. 2006;33(1):23-29. 14. Gupta AK, Chaudhry M, Elewski B. Tinea corporis, tinea cruris, tinea nigra, and piedra. Dermatol Clin. 2003;21(3):395-400. 15. Veasey JV, Avila RB, Miguel BAF, Muramatu LH. White piedra, black piedra, tinea versicolor, and tinea nigra: contribution to the diagnosis of superficial mycosis. An Bras Dermatol. 2017;92(3):413-416. 16. Tseng SS, Whittier S, Miller SR, Zalar GL. Bilateral tinea nigra plantaris and tinea nigra plantaris mimicking melanoma. Cutis. 1999;64(4):265-268. 17. Hall J, Perry VE. Tinea nigra palmaris: differentiation from malignant melanoma or junctional nevi. Cutis. 1998;62(1):45-46. 18. Sarangi G, Dash D, Chayani N, Patjoshi SK, Jena S. Bilateral tinea nigra of palm: a rare case report from Eastern India. Indian J Med Microbiol. 2014;32(1):86-88. 19. Burke WA. Tinea nigra: treatment with topical ketoconazole. Cutis. 1993;52(4):209-211. 20. Rossetto AL, Cruz RC, Haddad Junior V. [Double-blind study with topical isoconazole and terbinafine for the treatment of one patient with bilateral tinea nigra plantaris and suggestions for new differential diagnosis.] Rev Inst Med Trop Sao Paulo. 2013;55(2):125-128. 21. Rosen T, Lingappan A. Rapid treatment of tinea nigra palmaris with ciclopirox olamine gel, 0.77%. Skinmed. 2006;5(4):201-203. 22. Gupta G, Burden AD, Shankland GS, Fallowfield ME, Richardson MD. Tinea nigra secondary to Exophiala werneckii responding to itraconazole. Br J Dermatol. 1997;137(3):483-484.
Dermatologic Look-Alikes
Multiple Pustular Eruptions
ALEXANDRIA BROWN, BSA; SHRAVYA POTHULA, BS; EMILY BURNS, BA; CHRISTOPHER RIZK, MD
CASE #1
CASE #2
A 50-year-old man presents with a 2-day history of fever, malaise, and erythematous skin with widespread pustules. He reports a history of psoriasis and is concerned about the recent development of skin pustules. The patient is also febrile and has an upper respiratory tract infection. Biopsy of a pustular lesion is performed. On histopathologic examination, the lesion displays neutrophilic infiltration and psoriasiform changes of the epidermis. Laboratory testing reveals leukocytosis and an elevated erythrocyte sedimentation rate (ESR).
A 21-year-old woman presents to the dermatology clinic with fever and a generalized pustular rash on her torso that developed 2 days ago. The rash is pruritic and has sterile, nonfollicular, pinhead-sized pustules over an erythematous, edematous base. She reports the rash first appeared in the axillary folds and then spread to her arms and trunk. Last week, she was prescribed amoxicillin for a urinary tract infection and has been taking ibuprofen as needed for symptomatic relief. She states that she has not had a similar rash before.
