Tungiasis is an inflammatory skin disease caused by infection with the female ectoparasitic Tunga penetrans, a flea also known as the chigoe, chigo, chigoe flea, chigo flea, jigger, nigua, sand flea, or burrowing flea (and not to be confused with the chigger, a different arthropod). The flea and the disease that it causes are found in the tropical parts of Africa, the Caribbean, Central and South America, and India. Tunga penetrans is the smallest known flea, measuring 1 mm across. It is also known in Latin America as the nigua and bicho de pie (Spanish) or bicho de pé (Portuguese), literally "foot bug". Tunga penetrans is a member of the genus Tunga, which comprises 13 species.
Tungiasis causes skin inflammation, severe pain, itching, and a lesion at the site of infection that is characterized by a black dot at the center of a swollen red lesion, surrounded by what looks like a white halo. Desquamation of the skin is always seen, especially after the flea expands during hypertrophy.
As of 2009, tungiasis is present worldwide in 88 countries with varying degrees of incidence.http://www.gideononline.com This disease is of special public health concern in highly endemic areas such as Nigeria, Trinidad and Tobago, and Brazil, where its prevalence, especially in poor communities, has been known to approach 50%.Heukelbach, Jorg. "Invited Review—Tungiasis." Revista do Instituto de Medicina Tropical de São Paulo 47.6 (2005): 307–313.
The chigoe flea is properly classified as a member of the order Siphonaptera as it is a flea. Although commonly referred to as chiggers, true chiggers are mites, which are minute arachnids."Chiggers". About.com. 27 Feb. 2009 <http://pediatrics.about.com/od/dermatologytopics/a/06_chiggers.htm> Mites penetrate the skin and feed on skin cells that are broken down by an enzyme they secrete from their mouthparts, but they do not lay eggs in the host as T. penetrans does. Moreover, in mites, the adult and the larval forms both feed on other animals. This is not the case with T. penetrans, as only the adults feed on mammals and it is only the female that stays attached to the host.
Tunga penetrans is also known by the following names: chigoe flea, sand flea, nigua, chigger flea, jigger flea, bicho de pé, pico, sikka, kuti, and piqui, among many others.Heukelbach, Jorg. Tungiasis. Sept. 2004. Orphanet.com. 23 Feb. 2009 <http://www.orpha.net/data/patho/GB/uk-Tungiasis.pdf>
Another species of Tunga, T. trimamillata causes tungiasis in Ecuador and Peru. Signs and symptoms
The symptoms of this disease include: Severe pruritus Pain Inflammation and swelling Lesions and ulcerations, with black dots in the center
If a Tunga infection is left untreated, secondary infections, such as bacteremia, tetanus, necrosis and gangrene, may be expected.
In all cases, tungiasis by itself only caused morbidity, though secondary infection may lead to mortality. The life cycle section presents the Fortaleza stages from the flea's developmental perspective. The discussion is specific to symptoms of human infection. The clinical presentation in humans follows the Fortaleza Classification as the stage of infection will determine the symptoms present. The following discussion will give an overview of the symptoms beginning in stage 2 because patients are not likely to present themselves at the early stages of infection, mostly because the flea's burrowing is usually not felt. This may be due to a keratolytic enzyme secreted during stage 1.
The patient with a single flea may present as early as stage 2 when, though the erythema is barely perceptible, a boring pain and the curious sensation of unpleasant itching occur. This inflammatory reaction is the initial immunological response to the infestation. Heavily infested patients may not notice a stage 2 infection due to the other fleas' causing irritation as well. Feces may be seen, but this is more common in the 3rd stage. Around the third day after penetration, erythema and skin tenderness are felt, accompanied by pruritus (severe itching) and a black furuncular nodule surrounded by a white halo of stretched skin caused by the expansion of the flea. Fecal coils may protrude from the center of the nodule where the flea's anus is facing upward. They should be washed off quickly as the feces may remain in the skin unless removed. During this 3a substage, pain can be severe, especially at night or, if the nodule is on the foot, while walking. Eggs will also begin to be released and a watery secretion can be observed. The radical metamorphosis during the 3rd to 6th day after penetration, or neosomy, precedes the formation of a small caldera-like rim rampart as a result of the increased thickness of the flea's chitin exoskeleton. During the caldera formation, the nodule shrinks a bit and it looks as if it is beginning to dry out; this takes 2 weeks and comprises substage 3b.
At the third week after penetration and substage 4a, the eggs' release will have stopped and the lesion will become smaller and more wrinkled. As the flea is near death, fecal and water secretion will stop altogether. Pain, tenderness, and skin inflammation will still be present. Around the 25th day after penetration, the lesion looks like a black crust and the flea's carcass is removed by host repair mechanisms and the skin begins to heal. With the flea gone, inflammation may still persist for a while.
Although patients would not present within the 5th stage of tungiasis as the flea would be dead and no longer in the body, this stage is characterized by the reorganization of the skin (1–4 weeks) and a circular residue of 5–10 mm in diameter around the site in penetration. An intraepithelial abscess, which developed due to the presence of the flea, will drain and later heal. Although these disease residues would persist for a few months, tungiasis is no longer present.
In severe cases, ulcers are common, as well as complete tissue and nail deformation. A patient may be unable to walk due to severe pain if too many of the lesions are present in the feet. Suppuration (pus formation), tissue death, auto-amputation of digits (via ainhum), and chronic lymphedema may also be seen.
If the patient is not vaccinated, tetanus is often a complication due to secondary infection. Necrosis and gangrene are other common complications of severe infestation and superinfection. Staphylococcus aureus and Wolbachia endobacteria can be transmitted by the chigoe flea, as well as nearly 150 other different pathogens. For these reasons, the chigoe flea should be removed as soon as possible.
Incubation Because of the relatively rapid onset of tungiasis, the incubation period tends to be short. Although some reddening around the site of penetration occurs, the first symptoms are perceived in stage 2 as itching and severe pain, usually a day after penetration.
Cause Tungiasis is caused by chigoe fleas (the term transmission does not apply because Tunga penetrans is itself responsible for the disease.) The preponderance of tungiasis lesions on the toes may be because chigoe flea is a poor jumper, attaining only a height of 20 cm.https://web.archive.org/web/20140407063706/http://www.dermato.med.br/publicacoes/artigos/2007Tungiasis-and-Myiasis.pdf doi= 10.1016/j.clindermatol.2006.05.004 But the reality is more complex; for example, the jumping ability cannot explain why hands are the second-most affected body part. Lesions on the hands are better explained by playing in the sand and noting that hands are often used to remove sand from other parts of the body. The occurrence of tungiasis lesions on the toes, between them, and on the soles can be easily explained because most of the victims are poor, walk barefoot, and live in places where the sand (home to chigoe fleas) constitutes the floor. Rate of incidence therefore is greatly increased in poor communities and populations because of the lack of adequate housing. This occurs in significantly higher proportions during the peak of the dry season in local communities.
Tungiasis in humans and some domestic animals can also be caused by Tunga trimamillata, which is known to exist in Ecuador and Peru. Reservoirs and transmission T. penetrans has been documented to use various warm-blooded animals as reservoir hosts, including humans, pigs, dogs, cats, rats, sheep, cattle, donkeys, monkeys, birds, and elephants. These hosts directly propagate the disease by being the origin of the next generation of fleas. Once the female flea expels 100–200 eggs, the cycle of transmission begins again.
Lifecycle
T. penetrans eggs, on average, are 604 μm long, The larva will hatch from the egg within one to six days, assuming the environmental conditions (e.g., moisture, humidity, etc.) are favorable. After hatching, the flea will progress through two instar phases. This is unique in that most fleas go through three, instead. Over the course of that development, the flea will first decrease in size from its just-hatched size of 1,500 μm to 1,150 μm (first instar) before growing to 2,900 μm (second instar).
About 6 to 8 days after hatching, the larva pupates and builds a cocoon around itself. Because it lives mostly on and below the surface of the sand, sand is used to stabilize the cocoon and help to promote its development. An environmental disturbance such as rain or a lack of sand have been shown to decrease incidence, most likely due to decreasing the environmental factors (i.e., sand) on which the flea depends for overall growth. Barring any disturbances to the cocoon, an adult flea will emerge from the puparium after 9–15 days.
In the adult phase, the flea will occasionally feed on unsuspecting animals. Only once the female burrows into the skin can reproduction occur, as the male and female show no interest in each other in the wild. The male flea dies after copulation. The female flea continues in vivo ectodevelopment, described in stages by the Fortaleza classification of tungiasis.
Fortaleza classification In a seminal paper on the biology and pathology of Tunga penetrans, Eisele et al. (2003) provided and detailed the five stages of tungiasis, thereby detailing the in vivo development of the female chigoe flea for the first time. In dividing the natural history of the disease, the Fortaleza Classification formally describes the last part of the female flea's life cycle where it burrows into its host's skin, expels eggs, and dies. Due to the nature of the discussion, overlap with other sections, particularly the one on symptoms, is unavoidable.
Stage 1 is characterized by the penetration of the skin by the female chigoe flea. Running along the body, the female uses its posterior legs to push its body upward by an angle of 45–90 degrees. Penetration then starts, beginning with the proboscis going through the epidermis.
By stage 2 (day 1–2), penetration is complete and the flea has burrowed most of its body into the skin. Only the anus, the copulatory organs, and four rear air holes in fleas called stigmata remain on the outside of the epidermis. The anus will excrete feces that is thought to attract male fleas for mating, described in a later section. The hypertrophic zone between tergites 2 and 3 in the abdominal region begins to expand a day or two after penetration and takes the appearance of a life belt. During this time, the flea begins to feed on the host's blood.