Description, Causes and Risk Factors:

Tungiasis is a cutaneous infectious disease caused by infestation with the insect, Tunga penetrans (A member of the flea family, Tungidae, commonly known as chigger flea, sand flea, chigoe, or jigger; the minute female penetrates the skin, frequently under the toenails; as she becomes distended with eggs to about pea size, a painful ulcer with inflammation develops at the site), also known as the sand flea or chigoe flea.

Tungiasis is caused by penetration of the flea through an intact epidermis by the pregnant female T. penetrans. The tiny (1 mm in greatest dimension) flea then burrows deep to the epidermal-dermal junction to feed on blood from dermal capillaries. As the parasite becomes engorged, it can enlarge up to 1000-3000 times its original volume, up to a diameter of 1 cm. Subsequently, the invaded local tissues become inflamed and the characteristic pain, tenderness, and swelling ensue. Within 1-3 weeks the flea extrudes hundreds of eggs that disseminate from the wound and into the environment. The exact biohabitat of the early stages of the flea are unknown. Following release of eggs, the adult dies shortly thereafter.

In endemic locales, the disorder may be known as jiggers, nigua, or pico. This flea mainly infests humans, dogs, cats and pigs (although rats and other rodents occasionally become hosts). The earliest well documented records of T. penetrans infections in humans date back to the years of European discovery of the Americas, with the first mention being credited to an author who reported sand flea lesions from Haiti in 1525. It is recorded that this flea caused such rampant disease in some South and Central American countries that inhabitants were forced to leave their infested villages. Although the flea was originally endemic only to South and Central America, it was carried to Africa (Angola) in the 19th century in the ballast sand of an English vessel sailing from Brazil; it was first reported in India in 1899 and in the United States in 1929 in New Orleans.

The gross appearance of the lesion varies according to the progression of the infestation process. This progression is described by the Fortaleza Classification System.

    In stage I (early infestation; 30-120 minutes), the flea that penetrated the epidermis is visible as a reddish spot.

  • In stage II (1-2 days), the hypertrophied flea is visible as a 1-2+ mm opalescent spot with a central dark punctum.

  • In Stage III (2-21 days) is characterized by an indurated white halo, 3-10 mm in diameter, circumscribed around a central dark punctum. Hyperkeratosis is apparent, pain is common, and extruded eggs may be visible.

  • In stage IV (3-5 weeks), a crusty dark ring of necrotic epidermis forms around the lesion, which now contains a dead parasite.

  • Lesional involution with small scar formation characterizes stage V at six weeks to several months following infestation. More severe cases may also present with dystrophy or loss of the toenail, and/or permanently deformed toes.


Patients with this condition most commonly present with a lesion on the plantar, interdigital or periungual regions of the foot, but infestations of the leg, buttocks, hand, and elbow have also been recorded. It is likely that the foot is most often affected, in part, because the flea is a poor jumper.


Differential diagnosis may include fire ant bite, tick bite, scabies, creeping eruption, cercarial dermatitis, myiasis, folliculitis, or dracunculiasis.

Handheld dermoscopy may aid in visualizing the insect's dark exoskeleton and multiple eggs within the hyperkeratotic nodule. A definitive diagnosis depends on demonstration of the flea itself either through a mineral oil preparation or a skin biopsy of the suspected nodule. A histologic examination will reveal the flea's body in the intraepidermal cavity lined with an eosinophilic cuticle. The cavity may also contain the round/oval eggs and hollow, ring-like components of the flea's respiratory and digestive track. Inflammation is usually noted in the underlying dermis.

Sometimes, a fluid will ooze from the central opening of the nodule and T. penetrans eggs may be seen with a microscope.


Treatment consists of the physical removal of the flea by a sharp instrument. The residual cavity should then be surgically cleaned to remove its entire contents. Afterwards, an antibiotic ointment may be applied to prevent secondary infections.

Certain chemicals have also proven to be effective, including 4 percent formaldehyde solution, chlorophenothane (DDT), chloroform, turpentine, and niridazole. These treatments do not physically remove the flea from the skin, however, and therefore don't result in quick relief. They also carry their own risk of morbidity.

Physical removal followed by antibiotic ointment and an anti-tetanus prophylaxis to prevent secondary infection (especially that of tetanus) is most effective.

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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