Updated: Jan 6, 2009
Tungiasis is an infestation by the burrowing flea Tunga penetrans or related species.1 The flea has many common names as listed above. Tungiasis was first reported in crewmen who sailed with Christopher Columbus. The flea is indigenous to the West Indies/Caribbean/Central America region, but it has spread to Africa, India, Pakistan, and South America. Travelers to endemic areas may import cases to other countries, including the United States. These painful infections can cause significant morbidity in groups, such as soldiers.
To reproduce, the flea requires a warm-blooded host. In addition to humans, reservoir hosts include pigs, dogs, cats, cattle, sheep, horses, mules, rats, mice, and other wild animals.2,3,4,5
The main habitat is warm, dry soil and sand of beaches, stables, and stock farms. Upon contact, the fleas invade unprotected skin. The most common site of involvement is the feet (interdigital skin and subungual area). The flea has limited jumping ability.
Both the male and the nonfertilized female flea feed intermittently on warm-blooded hosts. Once impregnated, however, the female flea anchors herself to the skin by using biting mouthparts and burrows into the epidermis. Because the process is painless, a keratolytic enzyme may be involved. The flea expands, often reaching 1 cm in diameter. The head is down into the upper dermis feeding from blood vessels, while the caudal tip of the abdomen is at the skin surface, often forming a punctum or an ulceration. The flea breathes through this opening. In many cases, this is described as a white patch with a black dot.
Over 1-2 weeks, more than 100 eggs, which fall to the ground, are individually released from this exposed orifice. Afterwards, the flea dies and is slowly sloughed by the host. The eggs hatch on the ground in 3-4 days, go through larval and pupal stages and become adults in 2-3 weeks. The complete life cycle lasts approximately 1 month.
Imported cases rarely occur in the United States.6,7
In the endemic areas, the prevalence ranges from 15-40%, but cases in other areas are sporadic. Six percent of the patients visiting a travel-associated dermatosis clinic in Paris had tungiasis.5
Individual lesions may be painful, although sometimes they are pruritic or even asymptomatic. In most cases, tungiasis resolves without complications. However, heavy infestations may lead to severe inflammation, ulceration, and fibrosis. The risk of secondary infection is high. Lymphangitis, gangrene, and ainhum may occur. Death from tetanus associated with tungiasis has been reported.4
Lesions can range from asymptomatic to pruritic to extremely painful.
The typical presentation is a nodule (usually on the foot) that slowly enlarges over a few weeks in a patient who has recently been in an endemic area. The nodule can range from 4-10 mm in diameter.
Tungiasis is caused by an infestation with the burrowing flea T penetrans.
Insect Bites
Dracunculiasis
Histologic examination reveals an intraepidermal cavity lined by an eosinophilic cuticle, which represents the body of the flea. In the cavity are round to oval eggs, hollow ringlike components of the tracheal system, and the digestive tract (see Media File 1). A thick band of striated muscle runs from the head to the terminal orifice. Usually, an inflammatory infiltrate is present in the subjacent dermis.
Reported topical treatments include cryotherapy or electrodesiccation of the nodules. Application of formaldehyde, chloroform, or dichlorodiphenyltrichloroethane (DDT) to the infested skin has been used, but it may cause a person's own morbidity. Topical ivermectin, metrifonate, and thiabendazole have also been reported as effective. Occlusive petrolatum suffocates the organism. Twenty-percent salicylated petroleum jelly (Vaseline) applied 12-24 h in profound infestations caused the death of the fleas and facilitated their manual removal.9 These treatments do not remove the flea from the skin, and they do not result in quick relief from painful lesions. The flea may also be gently removed with a needle or a forceps.10,11
A number of surgical treatment methods are available. The flea can be removed from its cavity with sterile instruments, but this is more difficult when the flea is engorged. The orifice needs to be enlarged, and the entire nodule should be curetted or excised. An antibiotic ointment may be applied, along with systemic antibiotic therapy when indicated. Aggressive treatment of secondary infection and tetanus prophylaxis are important.
Usually, topical and/or surgical modalities are used to treat tungiasis; however, a report relates oral niridazole clearing cases in patients who were infested. Oral ivermectin was found to be ineffective in at least one study.
Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses. A combination of direct toxic action on the flea and anti-inflammatory action on the surrounding tissue is postulated.12
Not available in United States. Has been reported to be completely effective in lysing imbedded fleas in children who are infected. Response was quicker when a second dose was given 1 wk after the first dose.
30 mg/kg PO in juice
Administer as in adults
May elevate theophylline serum levels increasing toxicity (monitor serum levels and reduce dose prn)
Documented hypersensitivity; known G-6-P deficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause nausea, vomiting, and abdominal pain
Veraldi S, Valsecchi M. Imported tungiasis: a report of 19 cases and review of the literature. Int J Dermatol. Oct 2007;46(10):1061-6. [Medline].
Chadee DD. Tungiasis among five communities in south-western Trinidad, West Indies. Ann Trop Med Parasitol. Jan 1998;92(1):107-13. [Medline].
Feldmeier H, Eisele M, Van Marck E, Mehlhorn H, Ribeiro R, Heukelbach J. Investigations on the biology, epidemiology, pathology and control of Tunga penetrans in Brazil: IV. Clinical and histopathology. Parasitol Res. Oct 2004;94(4):275-282. [Medline].
Pilger D, Schwalfenberg S, Heukelbach J, Witt L, Mehlhorn H, Mencke N, et al. Investigations on the biology, epidemiology, pathology, and control of Tunga penetrans in Brazil: VII. The importance of animal reservoirs for human infestation. Parasitol Res. Apr 2008;102(5):875-80. [Medline].
Caumes E, Carriere J, Guermonprez G, Bricaire F, Danis M, Gentilini M. 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. Mar 1995;20(3):542-8. [Medline].
Mashek H, Licznerski B, Pincus S. Tungiasis in New York. Int J Dermatol. Apr 1997;36(4):276-8. [Medline].
Sanusi ID, Brown EB, Shepard TG, Grafton WD. Tungiasis: report of one case and review of the 14 reported cases in the United States. J Am Acad Dermatol. May 1989;20(5 Pt 2):941-4. [Medline].
Bauer J, Forschner A, Garbe C, Rocken M. Dermoscopy of tungiasis. Arch Dermatol. Jun 2004;140(6):761-3. [Medline].
Clyti E, Couppie P, Deligny C, Jouary T, Sainte-Marie D, Pradinaud R. [Effectiveness of 20% salicylated vaseline in the treatment of profuse tungiasis. Report of 8 cases in French Guiana]. Bull Soc Pathol Exot. Jan 2003;96(5):412-4. [Medline].
Heukelbach J, Eisele M, Jackson A, Feldmeier H. Topical treatment of tungiasis: a randomized, controlled trial. Ann Trop Med Parasitol. Oct 2003;97(7):743-9. [Medline].
Heukelbach J, Franck S, Feldmeier H. Therapy of tungiasis: a double-blinded randomized controlled trial with oral ivermectin. Mem Inst Oswaldo Cruz. Dec 2004;99(8):873-6. [Medline].
Ade-Serrano MA, Olomolehin OG, Adewunmi A. Treatment of human tungiasis with niridazole (Ambilhar) a double-blind placebo-controlled trial. Ann Trop Med Parasitol. Feb 1982;76(1):89-92. [Medline].
tungiasis, chigoe flea, chica, chigga, jiga, jigger, pigue, nigua, pico, bicho de pie, bug of the foot, suthi, puce chique, piroque, pique, moukardam, Tunga penetrans, T penetrans
Neil F Gibbs, MD, Voluntary Associate Professor, Departments of Pediatrics and Medicine, University of California, San Diego School of Medicine; Assistant Chair, Program Director, Pediatric Dermatologist, Department of Dermatology, Naval Medical Center, San Diego
Neil F Gibbs, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, and Society for Pediatric Dermatology
Disclosure: Nothing to disclose.
Abdul-Ghani Kibbi, MD, Chairman and Professor, Department of Dermatology, American University of Beirut Medical Center, Lebanon
Disclosure: none None None
Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.
Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
Disclosure: Nothing to disclose.
Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.