Dermatobia homininis is the most common cause of furuncular myiasis in Central and South America. It is diagnosed based on a history of travel to an endemic region and the characteristic cutaneous lesion. We present a 54-year-old patient who presented with both a travel history and cutaneous findings of furuncular myiasis.
Furuncular myiasis is most commonly caused by infestation with Dermatobia hominis (human botfly). (1) It is associated with a history of travel to Central and South America. Cutaneous examination coupled with a history of travel to endemic regions confirms the diagnosis. Multiple therapeutic modalities exist and range from watchful waiting to surgical extirpation. We describe a patient with furuncular myiasis successfully treated with surgical removal of the larva.
A 54-year-old man presented to our clinic with a tender non-healing sore on his scalp. The patient had no significant medical or surgical history; however, he recently returned from a trip to Belize during which time he recalled multiple insect bites on his scalp. The patient was knowledgeable of the diagnosis and reported a larval form that previously removed itself from his scalp prior to presentation to our clinic.
Examination revealed a 1 X 1 cm crusted nodule on his posterior scalp. Surgical exploration and debridement was performed and what appeared to be a mummified first stage larval form of D. hominis was removed (Figure 1). The remaining lesion was surgically removed and sent for routine histology. Histologic examination revealed a mixed dermal inflammatory infiltrate surrounding a well-demarcated space formerly housing the larva (Figure 2). The larval specimen was sent to an entomologist for morphologic identification, which was confirmatory for D. hominis. The larval specimen was also sectioned and stained with hematoxylin/eosin in routine histologic manner (Figure 3 and 4). The patient tolerated surgical debridement well and experienced no complications post-operatively.
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Furuncular myiasis may be the result of infestation by various larvae of the Diptera order, most commonly being Cordylopia anthropophaga (tumbu fly) or D. hominis (human botfly). (1) These organisms represent developing larvae (maggots). D. hominis represents the most common cause of furuncular myiasis in Central and South America. (2-5) Caumes et al reported myiasis to be the fourth most common travel-associated skin disease. (6) D. hominis causes variable cutaneous lesions, most of which appear boil-like and tend to involve exposed areas of the body, such as the scalp, face, forearms, and legs.
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Dermatobia hominis is endemic to Central and South America. (7,8) It favors a warm and moist environment. (8) While D. hominis can parasitize humans, it is a well-known parasite of cattle and other mammals. (8,9)
The life cycle of D. hominis relies on a carrier insect, notably the mosquito to transport the eggs. (5,8) The human botfly attaches her eggs to mosquitos, which serve as mechanical vectors and land on an unsuspecting host. The eggs hatch upon reaching the host as a result of the sudden increase in temperature. (5,8) Now larvae, they penetrate and enter the host skin, either following the tract of a hair follicle or that caused by the bite of the vector mosquito. (5,8,10) An increasing number of potential insect vectors have been identified. (7) Local parasite invasion occurs over a number of weeks as the botfly feeds on local tissue and travels in the dermis. A mixed host inflammatory response induces the evolution of the characteristic furuncular lesion. (8,11,12) The botfly maintains a ventilation hole open to external air for respiration. After 1 to 3 months, the larva undergoes a series of transformations, exits its cavity, and falls to the ground. In the appropriate ambient temperature, an adult fly emerges from the pupa to continue the life cycle. In our case, the botfly was mummified upon discovery although the patient managed to lure a previous botfly via smothering techniques. It is unknown why the second larvae existed in a mummified state--this may have been due to an exuberant host response.
Immunohistologic and ultrastructural studies have identified a mixed inflammatory response to infestation by D. hominis consisting of neutrophils, eosinophils, histiocytes, mast cells, plasma cells, and Langerhans cells. (11,12) Additionally, Grogan et al identified an increased ratio of T-helper versus T-suppressor cells. (11) Routine histologic examination reveals a striking parasite embedded in the dermis.
The differential diagnosis of furuncular myiasis includes a ruptured cyst, abscess, cellulitis, onchocerciasis, leishmaniasis, furunculosis, tungiasis, and arthropod reaction. (3,4)
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Furuncular myiasis is typically self-limited and poses little to no threat to the infected individual. Fatal cerebral myiasis from invasion into the fontanels of infants has been reported but is exceedingly rare. (13) Multiple treatment modalities exist, ranging from conservative monitoring to surgical extirpation. Treatment may include watchful waiting, liquid nitrogen therapy, occlusion via petrolatum or meats (blocks ventilatory hole), suction extraction (early larval forms), ivermectin and surgical debridement/extirpation. (1,5,8,14-17)
The diagnosis of furuncular myiasis is straightforward given a history of travel to an endemic region in conjunction with the cutaneous lesion. Multiple treatment strategies exist and primarily depend on the degree of anxiety and cosmetic concerns of the patient.
Acknowledgement: We thank Dr. Cecil L. Smith (Department of Entomology, The University of Georgia, Athens, Georgia) for assistance with identification of the botfly larva.
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Joshua E. Lane MD, (a) Robert M. Rogers MD, (a) Stephen Mullins MD, (b) Jack L. Lesher Jr. MD (a)
a. Section of Dermatology, Department of Medicine
b. Section of Anatomic Pathology, Department of Pathology
The Medical College of Georgia, Augusta, Georgia
Address for Correspondence
Joshua E. Lane, M.D.
330 Hospital Drive
Building C, Suite 208
Macon, GA 31217
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