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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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Typical histologic features of Tunga penetrans in skin biopsies
From Archives of Pathology & Laboratory Medicine, 6/1/02 by Smith, Marc D

* Context.-Tunga penetrans is a flea that burrows into human skin, causing the disease tungiasis. Although the parasite is not endemic in the United States, patients may present with this disease upon returning from tropical locales. Histologic sections contain a variety of flea parts that may present a diagnostic dilemma for pathologists unfamiliar with this disease.

Objective.-To determine the typical histologic features of T penetrans in biopsies from patients with tungiasis.

Methods.-We reviewed biopsy specimens from 7 patients with tungiasis and sought 8 distinct structures: the exoskeleton, hypodermal layer, respiratory tract (tracheae), digestive tract, striated muscle, head, posterior end, and developing eggs.

Results.-The exoskeleton, hypodermal layer, tracheae,

digestive tract, and developing eggs were present in all biopsy specimens reviewed. Striated muscle, the posterior end, and head, however, were present in 57%, 43%, and 0% of the biopsies, respectively. In addition, we noted a unique, pale-staining layer in the exoskeleton at the posterior end of the organism that, to the best of our knowledge, has not previously been described and that may be of diagnostic value.

Conclusions.-Despite the absence of 3 key morphologic features in many (posterior end and striated muscle) or all (head) of our biopsies, the exoskeleton with a hypodermal layer, tracheae, and developing eggs were uniformly present, and together these features are sufficient for a diagnosis of tungiasis.

(Arch Pathol Lab Med. 2002;126:714-716)

Tunga penetrans is an invasive flea that lodges itself in the epidermis of mammals, producing a painful nodular lesion known as tungiasis. First described in South America by Oviedo in 1526,1 the flea has since spread to the Caribbean, Africa, Pakistan, and the west coast of India, where it has a history of disabling military units and civilians.2,3 Although this flea is not endemic in the United States, patients may present with this disease upon returning from endemic locales. Travelers are usually infested by a single flea, which causes localized discomfort. If multiple fleas infest an individual, physical debilitation and secondary infections, such as tetanus or gas gangrene, may occur.4,5

In endemic areas, tungiasis is readily recognized by experienced physicians during physical examination, and further diagnostic workup is usually not required. In the United States, however, the infrequency of infection and unfamiliarity with this organism may result in a biopsy. These biopsy specimens rarely demonstrate the perfect longitudinal section of the arthropod, which may be presented in textbooks (ie, an attached head with intact body and protruding posterior end). More likely, pathologists encounter a fragmented collection of insect body parts (Figure 1). Although recognizing these structures as parts of a parasite is usually not a problem, the difficulty lies in the definitive diagnosis. The histopathologic differential diagnosis includes ticks, mites, helminths, and fly larvae (myiasis).

We examined 7 biopsies from patients with tungiasis to describe the histologic features that are consistently present. Furthermore, based on a review of the histopathology of ticks, mites, helminths, and fly larvae, we postulate that these features should be sufficient to reliably diagnose T penetrans.


We examined histologic sections from skin biopsies of 7 patients with tungiasis. All cases were obtained in consultation from 1975 to 2000. Clinical data were obtained before or at the time of histologic review and included age, gender, and travel history. All biopsies were fixed, sectioned, and stained with hematoxylin-eosin, and sections were examined independently by both authors. Each pathologist recorded the presence or absence of 8 morphologic structures that may be seen in biopsies containing T penetrans. These structures were the exoskeleton, hypodermal layer, tracheae (a portion of the respiratory tract), digestive tract, striated muscle, head, posterior end, and developing eggs.


All of the patients had a history of recent travel to a tropical climate where T penetrans is endemic and presented with a single nodule without systemic symptoms. The age, gender, and country or continent of travel for each patient are listed in Table 1. Both pathologists agreed regarding the presence or absence of the morphologic features sought in each case. All of the biopsy specimens contained portions of the exoskeleton, hypodermal layer, tracheae, digestive tract, and developing eggs (Figures 2 and 3). Striated muscle was present in 4 (57%) of 7 biopsies, the posterior end was present in 3 (43%) of 7 biopsies, and the head was not identified in any of the biopsies (Figures 2-4). In addition, we noted that a unique pale-staining layer situated between the inner and outer portions of the exoskeleton was associated with the posterior end of the organism (Figure 4).


Clinical data, such as travel history and symptoms, are important clues for the diagnosis of many parasitic infections, including tungiasis. All patients reviewed in this report had a history of recently visiting a tropical climate, and all returned with a single nodular lesion and no systemic symptoms. The nodule produced by T penetrans has a characteristic appearance. It is approximately 6 mm in diameter with a central black dot, representing the hindquarters of the flea.3 Tunga penetrans most frequently attaches to the lower extremities.3,4 Infected patients may have a history of walking barefoot outdoors in endemic regions.

The histopathologic diagnosis of tungiasis may be rendered despite a biopsy that does not contain a perfectly transected flea. In our study, 5 features of T penetrans were present in every case. Of these 5 structures, the developing eggs are likely the most useful for the differentiation of T penetrans from other parasites. The eggs of T penetrans develop while the flea is embedded in the skin; therefore, different stages of development may be seen (Figure 3). Egg production and development are primarily responsible for the enlarged abdomen of the flea and the consequent painful nodule it produces. The other 4 structures that were consistently present-the exoskeleton, hypodermal layer, tracheae, and digestive tract-further support the identification of the organism present as an arthropod. The head (0%), posterior end (43%), and striated muscle (57%) either were not present or were inconsistently present. Tracheae and striated muscle within a parasite are pathognomonic of arthropods; helminths have smooth muscle and do not contain tracheae.6 To our knowledge, the staining characteristics of the posterior end of T penetrans have not been described previously. Although the posterior end of the organism was present in only a few biopsy specimens, the pale staining region, situated between the inner and outer layers of the exoskeleton in the posterior region of the flea, was unequivocally present (Figure 4). The usefulness of this feature for the diagnosis of tungiasis, however, requires further study.

This study suggests that developing eggs, portions of the exoskeleton, hypodermal layer, tracheae, and digestive tract should be present in most biopsy specimens that contain T penetrans, but a more comprehensive study is needed for confirmation. The combination of these features helps differentiate T penetrans from other cutaneous parasites. The hypodermal layer, egg morphology, and exoskeleton morphology exclude Sarcoptes scabei.7,8 The presence of eggs and the distribution of striated muscle exclude myiasis (Table 2).9,11 Although ticks have striated muscle, a hypodermal layer, and tracheae, developing eggs are usually not seen (Figure 5).

We thank Yezid Gutierrez, MD, PhD, for providing 6 cases for review and for helpful insights and comments.


1. De Oviedo y Valdes GF. Cited by: Guyon M. Note accompagnant la presentation d'un ouvrage intitule: histoire naturelle et medicale de la chique, Rhynochoprion penetrans (Oken). C R Acad Sci. 1870;70:785-792.

2. Hoeppli R. Early references to the occurrence of Tunga penetrans in tropical Africa. Acta Trop. 1963;20:143-152.

3. Gordon RM. The jigger flea. Lancet. 1941;2:47-49.

4. Conner DH. Tungiasis. In: Conner DH, Chandler FW, Schwartz DA, Manz HJ, Lack EE, eds. Pathology of Infectious Diseases. Stamford, Conn: Appleton and Lange; 1997:1699-1707.

5. Harmann RRM. Tungiasis. In: Rook A, Wilkinson DS, Ebling FJG, eds. Textbook of Dermatology. 2nd ed. London, England: Blackwell Scientific Publications; 1972:885.

6. Naefie RC, Marty AM. Overview of the pathogenic helminths. In: Meyers WM, Naefie RC, Marty AM, Wear DJ, eds. Helminthiases. Washington, DC: Armed Forces Institute of Pathology; 2000:1-11. Pathology of Infectious Diseases; vol 1.

7. Conner DH. Scabies. In: Conner DH, Chandler FW, Schwartz DA, Manz HJ, Lack EE, eds. Pathology of Infectious Diseases. Stamford, Conn: Appleton and Lange; 1997:1695-1698.

8. Gutierrez Y. Scabies. In: Diagnostic Pathology of Parasitic Infections With Clinical Correlations. 2nd ed. New York, NY: Oxford University Press; 2000:716722.

9. Conner DH. Myiasis. In: Conner DH, Chandler FW, Schwartz DA, Manz HI, Lack EE, eds. Pathology of Infectious Diseases. Stamford, Conn: Appleton and Lange; 1997:1655-1658.

10. Gutierrez Y. Myiasis. In: Diagnostic Pathology of Parasitic Infections With Clinical Correlations. 2nd ed. New York, NY: Oxford University Press; 2000:722728.

Marc D. Smith, MD; Gary W. Procop, MD

Accepted for publication January 24, 2002.

From the Division of Pathology and Laboratory Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio.

Reprints: Gary Procop, MD, Department of Clinical Pathology, L40, Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195 (e-mail:

Copyright College of American Pathologists Jun 2002
Provided by ProQuest Information and Learning Company. All rights Reserved

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