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Tungiasis is a skin infestation of the Tunga penetrans flea (also known as chigoe flea, jigger, nigua or sand flea), found in the tropical parts of Africa, Caribbean, Central and South America, and India. This disease is endemic in Nigeria and Trinidad and Tobago where in the 1980s the prevalance of tungiasis among children approached 40%. It is rarely found outside these areas. more...

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The parasitic flea lives in soil and sand, and feeds intermittently on warm-blooded hosts such as humans, cattle, sheep, dogs, mice, and other animals. In order to reproduce, the female flea burrows head-first into the hosts' skin, often leaving the caudal tip of its abdomen visible through an orifice in a skin lesion. This orifice allows the chigoe flea to breathe while feeding on blood vessels in the cutaneous and subcutaneous dermal layer. In the next two weeks, the flea releases about 100 eggs through the orifice, which fall to the ground. The flea then dies and is sloughed by the host's skin. Within the next three to four days, the eggs hatch and mature into adult fleas within three to four weeks.


The first reported case of tungiasis was noted in the 1500s by Gonzalez Fernandez De Oviedo y Valdes, when sailors from the Santa Maria who sailed with Christopher Columbus were shipwrecked on Haiti and became infected. Tungiasis also infected many of the soldiers of the Spanish conquistadores, who also reported that an entire village in Colombia was abandoned because of this disease. The first clinical account of tungiasis was provided by the Portuguese doctor Aleixo de Abreu.


The symptoms of this disease include:

  • Severe pruritus
  • Pain
  • Inflammation and swelling
  • Lesions and ulcerations, with black dots in the center

Left untreated, secondary infections such as bacteremia, tetanus, and gangrene can occur.


Because of their limited jumping ability, the most common sites of infection are the soles of the feet, the toe web and toenails. Preventing infection by chigoe flea is easily achieved by wearing shoes when traveling in endemic regions and spraying insecticides on infested soil. Walking barefoot, especially in children, remains the most common reason why tungiasis remains prevalent in poor, illiterate, rural populations.


Treatment for tungiasis include physical removal of the flea by use of forceps or needles, application of topical anti-parasitic medicine, and surgery to completely remove the nodules.

Other successful reported treatment include applying a thick wax, nail polish, or petroleum solution to suffocate the flea and locally freezing the lesion by using liquid nitrogen. Local application of formaldehyde, chloroform and DDT have also been reported although their use is discouraged due to potential side effects.

Even without treatment, the burrowed fleas will die within two weeks and are naturally sloughed off as the skin sheds.


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Furuncular myiasis secondary to Dermatobia hominis
From Journal of Drugs in Dermatology, 5/1/05 by Joshua E. Lane


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.

Case Report

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.



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.



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)


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.


1. Jelinek T, Nothdurft HD, Rieder N, et al. Cutaneous myiasis: review of 13 cases in travelers returning from tropical countries. Int J Dermatol. 1995;34:624-626.

2. White GB. Flies causing myiasis. In: Cok GC, ed. Manson's Tropical Diseases. London: WB Saunders; 1996:1661-1663.

3. Gewirtzman A, Rabinovitz H. Botfly infestation (myiasis) masquerading as furunculosis. Cutis. 1999;63;63:71-72.

4. Harbin LJ, Khan M, Thompson EM, et al. A sebaceous cyst with a difference: Dermatobia hominis. J Clin Pathol. 2002;55:798-799.

5. Tamir J, Haik J, Orenstein A, et al. Dermatobia hominis myiasis among travelers returning from South America. J Am Acad Dermatol. 2003;48:630-632.

6. Caumes E, Carriere J, Guermonprez G, et al. Dermatoses associated with travel to tropical countries: a prospective study of the diagnosis and management of 269 patients presenting to a tropical disease unit. Clin Infect Dis. 1995;20:542-548.

7. Marinho CR, Barbosa LS, de Azevedo ACG, et al. Hemilucilia segmentaria (Fabricius, 1805) (Diptera: Calliphoridae) as new biologic vector for eggs of Dermatobia hominis (Linnaeus Jr, 1781) (Diptera: Oestridae) in Researva Biologica do Tingua, Rio de Janeiro, Brazil. Mem Inst Oswaldo Cruz. 2003;98:937-938.

8. Maier H, Honigsmann H. Furuncular myiasis caused by Dermatobia hominis, the human botfly. J Am Acad Dermatol. 2004;50:S26-S30.

9. Hall M, Wall R. Myiasis of humans and domestic animals. Adv Parasitol. 1995;35:257-334.

10. Powers NR, Yorgensen ML, Rumm PD, et al. Myiasis in humans: an overview and a report of two cases in the Republic of Panama. Mil Med. 1996;161:495-497.

11. Grogan TM, Payne CM, Payne TB, et al. Cutaneous myiasis. Immunohistologic and ultrastructural morphometric features of a human botfly lesion. Am J Dermatopathol. 1987;9:232-239.

12. Baker DJ, Kantor GR, Stierstorfer MB, et al. Furuncular myiasis from Dermatobia hominis infestation. Diagnosis by light microscopy. Am J Dermatopathol. 1995;17:389-394.

13. Loong PT, Lui H, Buck HW. Cutaneous myiasis: a simple and effective technique for extraction of Dermatobia hominis larvae. Int J Dermatol. 1992;31:657-659.

14. Brewer TF, Wilson ME, Gonzalez E, et al. Bacon therapy and furuncular myiasis. JAMA. 1993;270:2087-2088.

15. Richards KA, Brieva J. Myaisis in a pregnant woman and an effective, sterile method of surgical extraction. Dermatol Surg. 2000;26:955-957.

16. Boggild AK, Keystone JS, Kain KC. Furuncular myiasis: a simple and rapid method for extraction of intact Dermatobia hominis larvae. Clin Infect Dis. 2002;35:336-338.

17. Rossi MA, Zucoloto S. Fatal cerebral myiasis caused by the tropical warble fly, Dermatobia hominis. Am J Trop Med Hyg. 1973;34:22-31.

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

Phone: 478-742-2180

Fax: 478-745-2623


COPYRIGHT 2005 Journal of Drugs in Dermatology, Inc.
COPYRIGHT 2005 Gale Group

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