Tungiasis also known as sand flea disease, is a tropical parasitic skin disease caused by female sand fleas (Tunga penetrans, Siphonaptera: Tungidae, Tunginae) embedded in the skin of the host 1). The Tunga penetrans flea is also referred to as the chigoe, nigua, chica, pico, pique or suthi flea. Tungiasis affects millions of people in South America, the Caribbean and sub-Saharan Africa and predominantly affects children living in impoverished rural communities. In these settings tungiasis is associated with important morbidity.

Children and the elderly bear the highest tunga disease burden 2). In these population groups prevalence may be as high as 65%. Children frequently carry dozens of embedded sand fleas simultaneously 3). In endemic areas 95 to 98% of all tungiasis lesions occur at the feet 4). The toes, the sole and the heel are typical affected sites 5).

The female Tunga penetrans jigger flea penetrates into the skin of its host, undergoes a peculiar hypertrophy, expels several hundred eggs for a period of <3 weeks, and eventually dies. The shriveled carcass is then sloughed from the epidermis by host repair mechanisms 6). Within 10 days, the female Tunga penetrans jigger flea increases its volume by a factor of approximately 2,000, finally reaching the size of a pea 7). Through its hindquarters, which serve for breathing, defecating, and expulsing eggs, the flea remains in contact with the air, leaving a sore (240–500 μm) in the skin; the sore is an entry point for pathogenic microorganisms 8). The preferred localization for female Tunga penetrans jigger fleas is the periungual region of the toes, but lesions may occur on any part of the body 9).

Being a continuously enlarging and biologically active foreign body located in the epidermis, embedded sand fleas cause an intense inflammatory response 10). Bacterial superinfection is common and intensifies the inflammation 11). Intense pain and itching are almost constant 12). Frequent complications are suppuration, ulcers, deep fissures, periungual edema as well as deformation of nails and toes 13).

Tungiasis lesions can range from asymptomatic to pruritic to extremely painful. Note the following history findings:

  • Travel to areas with tunga penetrans, including Central America, South America, India, and tropical Africa 14)
  • Walking along beach areas with bare feet or in sandals
  • Pain or itching and papular or nodular eruptions, usually on the feet (although infection can occur on any area of the body to which the flea has access)

Although an effective and safe treatment exists it is not yet available in endemic countries 15). Therefore, embedded sand fleas are removed by inappropriate sharp and non-sterile instruments such as needles, safety pins or razor blades 16). This further increases the risk of bacterial superinfection and intense inflammation. Constant re-infection–as is the rule in endemic settings—impairs mobility, eventually leads to mutilation of the feet and immobilization of the patient. Anecdotal observations suggest that the restricted mobility may have a detrimental effect on household economics and impair school performance in children, mainly due to high absenteeism 17).

Tungiasis causes

Tungiasis (sand flea disease) is a parasitic skin disease caused by female sand fleas (Tunga penetrans) penetrated into the skin of humans or animals 18). Tungiasis is a zoonosis that affects a broad range of domestic and peridomestic animals, such as dogs, cats, pigs, and rats 19). Where humans live in close contact with these animals and where environmental factors and human behavior favor exposure, the risk for infection is high 20).

Numerous case reports detail the clinical aspects of tungiasis. However, they almost all exclusively describe travelers who have returned from the tropics with a mild disease 21). Having reviewed 14 cases of tungiasis imported to the United States, Sanushi 22) reported that the patients showed only one or two lesions and, that except for itching and local pain, no clinical pathology was observed. In contrast, older observations show that indigenous populations and recent immigrants, as well as deployed military personnel, frequently suffered from severe disease, characterized by deep ulcerations, tissue necrosis leading to denudation of bones, and auto-amputation of digits, resulting in physical disability, such as being unable to work and walk 23). Tungiasis has also been associated with lethal tetanus in nonvaccinated persons 24). In a study in São Paulo State, Brazil, tungiasis was identified as the place of entry in 10% of tetanus cases 25).

Tungiasis life cycle

Tunga penetrans is distributed in tropical and subtropical regions of the world, including Mexico to South America, the West Indies and Africa. The fleas normally occur in sandy climates, including beaches, stables and farms.

Tunga penetrans eggs are shed by the gravid female into the environment (number 1). Eggs hatch into larvae (number 2) in about 3-4 days and feed on organic debris in the environment. Tunga penetrans has two larval stages before forming pupae (number 3). The pupae are in cocoons that are often covered with debris from the environment (sand, pebbles, etc). The larval and pupal stages take about 3-4 weeks to complete. Afterwards, adults hatch from pupae (number 4) and seek out a warm-blooded host for blood meals. Both males and females feed intermittently on their host, but only mated females burrow into the skin (epidermis) of the host, where they cause a nodular swelling (number 5). Females do not have any specialized burrowing organs, and simply claw into the epidermis after attaching with their mouthparts. After penetrating the stratum corneum, they burrow into the stratum granulosum, with only their posterior ends exposed to the environment (number 6). The female fleas continue to feed and their abdomens extend up to about 1 cm. Females shed about 100 eggs over a two-week period, after which they die and are sloughed by the host’s skin. Secondary bacterial infections are not uncommon with tungiasis.

Figure 1. Tungiasis life cycle

tunga penetrans life cycle

Tungiasis prevention

Wearing shoes when travelling in endemic regions can easily prevent infestation. In some areas where the fleas are prevalent, spraying the ground with a insecticide such as malathion can significantly reduce the number of infestations.

Walking barefoot, especially in children, remains the most common reason why tungiasis remains prevalent in poor, rural populations.

Tungiasis symptoms

Due to the limited jumping ability of the tunga flea the most common site of infection is the feet. The lesion forms a punctum or ulceration, and is often described as a white patch with a black dot. The flea breathes through the opening of the lesion. The lesion can range from 4-10mm in diameter.

The lesions can be painful and very itchy, although in some cases there may be no symptoms. In some cases there may also be redness and swelling around the affected site.

The initial burrowing by the gravid tunga penetrans female fleas is usually painless; symptoms, including itching and irritation, usually start to develop as the tunga penetrans female fleas become fully-developed into the engorged state. Inflammation and ulceration may become severe, and multiple lesions in the feet can lead to difficulty in walking. To alleviate the pain patients avoid placing the whole foot on the ground while walking leading to a classical gait which is readily recognized as a tungiasis patient from a long distance 26). Secondary bacterial infections, including tetanus and gangrene, are not uncommon with tungiasis.

Tungiasis lesions were staged according to the Fortaleza classification and counted 27):

  • Stage 1: penetrating sand flea
  • Stage 2: brownish/black dot with a diameter of 1–2 mm
  • Stage 3: circular yellow-white watch glass-like patch with a diameter of 3–10 mm and with a central black dot
  • Stage 4: brownish-black crust with or without surrounding necrosis

Stage 1 to 3 are viable sand fleas; in stage 4 the parasite is dying or already dead 28).

Figure 2. Tungiasis


Footnote: Right foot of a 50-year-old man. All nails have been lost. Embedded fleas have been manipulated by the patient, leaving innumerable sores. Desquamation and ulceration are merged. The skin tends to bleed where the stratum corneum is eroded.

[Source 29) ]

Figure 3. Severe tungiasis

Severe tungiasis

Footnote: Extremely severe tungiasis. The sole is covered with several layers of embedded sand fleas on top of each other.

[Source 30) ]

Figure 4. Tungiasis elbow

Tungiasis elbow

Footnote: A cluster of embedded tunga penetrans fleas at the elbow.

[Source 31) ]

Figure 5. Tungiasis hand

Tungiasis hand

Footnote: Ectopic localization of embedded tunga penetrans sand fleas in the palm of the hand.

[Source 32) ]

Tungiasis complications

Secondary infections, such as bacteremia or septicemia, lymphangitis, tetanus, and gas gangrene, can occur. Among a native population in Brazil, the most common causes of bacterial superinfection included Staphylococcus aureus and various Enterobacteriaceae; anaerobic streptococci and Clostridium species were also found 33). Sores caused by burrowed fleas can be a potential entry point for clostridial and other infections, or these infections may follow attempts to extract the flea. Autoamputation of digits or other extensive soft tissue debridement is also a possibility.

Death from tetanus associated with tungiasis has been reported 34). For example, a case series from Haiti demonstrates a high incidence of tetanus in areas where the prevalence of tungiasis is high. In areas of Northeast Brazil, monthly incidence of tetanus cases has paralleled the seasonal variation of tungiasis. Thus, tetanus prophylaxis should be kept up to date in areas where tungiasis is common 35).

Conditions associated with tungiasis and its complications is depicted in Table 1.

Table 1. Spectrum of morbidity and complications in patients with very severe tungiasis

Deformation of feet (clubfoot-like)Immobility -> malnutrition -> starvation -> cachexia
Mutilation of toesLoss/amputation of toes
Deep fissure, ulcers with extended necrosis of tissue (ulcère phagédénique)Immobility -> malnutrition -> starvation -> cachexia; bacterial superinfection
Abscess, suppuration, phlegmoneLymphangitis, septicemia -> death
Infection with ClostridiaTissue necrosis, gangrene, tetanus -> death
Hyperkeratosis of soleEmbedded sand fleas are located in several layers on top of each other and cannot be removed surgically; immobility due to extreme pain
Inflammation of feetOedema -> pain -> immobility
OsteomyelitisLoss of toes and limbs -> death
AnemiaIncapacity to work and to collect food -> malnutrition -> cachexia; heart failure
[Source 36) ]

Tungiasis diagnosis

Extraction of the gravid tunga penetrans flea using a sterile needle is diagnostic and therapeutic. A skin biopsy of a suspected papule or nodule may be performed.

In general, no laboratory studies are indicated other than a histologic examination of excised tissue to confirm the presence of the flea. No imaging studies are indicated unless there is a secondary infection with a complication such as gas gangrene.


Dermoscopy (direct skin microscopy) may be helpful in identifying typical features, including an irregular, central, brown discoloration with a plugged opening in the middle or a gray-blue discoloration 37). Sometimes, a serosanguineous exudate oozes from the central opening, and eggs may be seen on microscopic examination.

Tungiasis treatment

In many cases tungiasis will heal on its own as the burrowed flea dies within 2 weeks and naturally sloughs off as the skin sheds. Over the 1-2 weeks whilst it feeds on the host’s blood the flea will lay more than 100 eggs that fall to the ground through the opening of the lesion.

Medical interventions include:

  • physical removal of the flea using sterile forceps or needles. The opening needs to be enlarged and often when the flea is engorged it can be difficult to extract. In many cases the entire lesion needs to be cut out.
  • application of topical anti-parasitic medications such as ivermectin, metrifonate, and thiabendazole.
  • suffocation of the flea by applying a thick wax or jelly, and
  • locally freezing the lesion using liquid nitrogen (cryotherapy).

All precautions should be taken to prevent secondary infections such as cellulitis, bacteremia, tetanus and gangrene. A course of oral antibiotics may be instituted if secondary infection is suspected. Ensure that tetanus prophylaxis is up to date.


A two-component dimethicone, available under the brand name NYDA®, has been shown to cause 80%-95% of all embedded sand fleas to lose viability within seven days. It is most effective when applied topically directly to the affected area. Further, dimethicone is considered wholly nontoxic and very safe for extended human use 38).


The insect repellant Zanzarin, a lotion consisting of coconut oil, jojoba oil, and aloe vera, was shown to reduce the number of newly embedded fleas and skin lesions, as well as to almost completely reverse the cutaneous pathology, when applied twice daily 39). In a study in Madagascar, a twice-daily application of Zanzarin was found to be much more effective than the use of closed toed shoes. It is believed that this is because shoes are less financially accessible and often not culturally desired 40). Zanzarin has now been removed from the market but is made of ingredients that could be accessed locally and so manufactured in areas affected by tungiasis.

Topical antibiotics and petroleum jelly

Topical ivermectin, metrifonate, and thiabendazole have been reported as effective. Occlusive petrolatum suffocates the organism. Twenty-percent salicylated petroleum jelly (Vaseline) applied 12-24 hours in profound infestations caused the death of the fleas and facilitated their manual removal 41). However, these treatments do not remove the flea from the skin, and they do not result in quick relief from painful lesions 42). When secondary infection is already present, an oral antibiotic should be considered 43). The primary complicating factor of tungiasis infection is the bacterial superinfections that can result from loss of integrity of the skin structures on the feet and thus a cellulitis and spreading infection. With repeated and extensive infections, pain and difficulty walking are significant contributors to morbidity.

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