Tungiasis

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Background

Tungiasis is an infestation by the burrowing flea Tunga penetrans or related species.[1] The flea has many common names, being known in various locations as the chigger flea, sand flea, chigoe, jigger, nigua, pigue, or le bicho de pe (see the image below). Painful infections with T penetrans can cause significant morbidity. (See Etiology.)



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Life cycle of the chigoe flea, Tunga penetrans. Courtesy of the CDC.

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. Tungiasis is rarely diagnosed in North America, but it should no longer be obscure to physicians because of increasing international travel to tropical destinations. (See Epidemiology, Clinical, and Workup.)[2]

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 (see the image below). (See Etiology.)[3, 4, 5, 6]



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Life cycle of Tunga penetrans - Fortaleza stages included. Compiled and designed by Fausto Bustos and Lucas Manfield.

See also 7 Bug Bites You Need to Know This Summer, a Critical Images slideshow, for helpful images and information on various bug bites.

The World Health Organization has listed tungiasis as a neglected disease of marginalized populations and has encouraged more significant research of the disease.[7]

Patient Education

Travelers to affected countries, as well as people native to those areas, must be advised to wear shoes (not sandals) when walking along sandy areas in affected regions and to refrain from sitting or lying in the sand.

Etiology

The main habitat for T penetrans is warm, dry soil and sand of beaches, stables, and stock farms. Upon contact, the flea invades unprotected skin. The most common site of involvement is the feet (interdigital skin and subungual area). The flea has limited jumping ability, so infection occurs only on areas of skin that were directly exposed to sand or soil in which the fleas live.

Both the male and the nonfertilized female flea feed intermittently on warm-blooded hosts, but only the female flea can produce the typical skin lesion of tungiasis.[8] . Once impregnated, the female flea anchors herself to the skin by using biting mouthparts and burrows into the epidermis of the host near the plantar surfaces of the foot,[9] in the webbing between the toes, and around the periungual region. 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 (see the images below). The flea breathes through this opening. In many cases, this is described as a white patch with a black dot. Very heavy infestation may cause ulceration and fibrosis that may result in secondary infections, such as bacteremia, tetanus, lymphangitis, and gas gangrene.[10]



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Scanning electron micrograph of flea 6 hours after beginning of penetration. The penetration is almost completed; only the last abdominal segments pro....



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Scanning electron micrograph of flea in stage 2. The rear end, the genital opening, and the 4 pairs of stigmata form a miniature cone, which towers ab....



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Scanning electron micrograph of flea on day 3 after penetration. The hypertrophic zone between abdominal segments 2 and 3 is gaining a bulging shape a....



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Scanning electron micrograph of flea on day 8 after penetration. The hypertrophy zone has taken the shape of a sphere. The 3 parts of abdominal segmen....

Within 2 weeks of penetration, the flea that has burrowed under the skin increases its volume by a factor of 2000.[11] Over 1-2 weeks, more than 100 eggs, which fall to the ground, are individually released from the 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.



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Illustration of Tunga penetrans (sand flea) in its enlarged state. Courtesy of Wikimedia Commons (https://commons.wikimedia.org/wiki/File:ChiggerBMNH.....

The major risk factor for exposure to T penetrans is failure to wear shoes when walking in sand in an area with active infestation. Wearing shoes and not sitting or lying in the sand are the most important steps to reduce infection risk. If available, the repellent Zanzarin has been shown to be effective when applied to the feet once daily.[12]

Epidemiology

Occurrence in the United States

The incidence of tungiasis is unknown because it is not a reportable disease. As of 2000, only 20 cases had been reported in the United States, with 15 of them being reported prior to 1989.[13, 14, 15, 16] Since 2000, sporadic cases have been reported in the United States.[17] All of these cases were imported from outside of the United States.

International occurrence

Tungiasis is potentially endemic in 88 countries worldwide.[18] Tungiasis is especially prevalent in low-resource communities.[11] Estimates on the occurrence of tungiasis rely primarily on community-based studies. Recent prevalence of tungiasis in rural and urban resource-poor communities in Brazil, Nigeria, and Madagascar was up to 60%.[19, 20, 21, 22, 23, 24, 25]

Tungiasis has reemerged to epidemic levels in many countries across sub-Saharan Africa.[26, 27, 28] In April 2012, a community-based cross-sectional study was performed in 2 villages in Western Tanzania. A total of 586 individuals older than 5 years were enrolled, and 249 (42.5%; 95% confidence interval [CI], 38.5-46.5) were diagnosed with tungiasis. Those aged 45 years and older had the highest prevalence of tungiasis at 71.1% and the most severe parasite load (median number of embedded fleas: 17.5; interquartile range: 15-22.5).[29]

In September 2012, an outbreak of tungiasis occurred in a group of Israeli travelers to Ethiopia. The attack rate in the group was 53%, affecting 9 patients, and most skin lesions appeared on the feet, where lesions are most commonly found.[30]

Approximately 45.2% of a Nigerian community in Lagos State was observed to be infected, with most of the cases occurring in children aged 5-14 years.[31] In a traditional fishing village in northeastern Brazil, the overall prevalence was 51%.[32, 33] In a village in rural Haiti, nearly 75% of the population was observed to have tungiasis lesions.[34] Six percent of the patients visiting a travel-associated dermatosis clinic in Paris had tungiasis.[5]

In March 2012, 12 free-ranging jaguars in the Mato Grosso do Sul state of Brazil were captured and examined for the presence of T penetrans. They found the prevalence of tungiasis to be 100% in this group of jaguars. T penetrans presence was based on observations of embedded fleas and morphological identification of free-living fleas. This study was performed during the dry season in Brazil and all of the jaguars were in good health.[35]

Studies have shown that the development of eggs from adult fleas can take place indoors and outdoors. In rural and urban communities in Brazil, tungiasis has been acquired peridomiciliary and intradomiciliary.[36] In many countries with the greatest presence of T penetrans, lack of health education, poor housing (particularly houses with dirt floors), and close proximity to animals are risk factors for tungiasis.[37, 38, 39]

Race-, sex-, and age-related demographics

No racial predisposition is apparent. Infection rates among native inhabitants of developing countries, however, are much higher than among visitors.

In endemic regions, such as Trinidad, males were found to be consistently more likely than females to have an infestation. Males also had higher chigoe flea burdens, with about twice the number of fleas detected per subject.[40]

In Trinidad, tungiasis reaches a peak infestation rate of 54% among males aged 25-35 years. Among females, the peak occurs in those aged 55 years and older.[40] In a village in northeastern Brazil, bimodal prevalence peaks were noted in children aged 5-9 years and in adults older than age 60 years.[32]

Prognosis

The prognosis of tungiasis is excellent if proper sterile methods are followed for the extraction of fleas and if extraction occurs soon after infection. Uncomplicated infestation results in pain, swelling, tenderness, and some limitation in mobility (although sometimes lesions are pruritic or even asymptomatic).

To prevent superinfection, sand fleas should be surgically extracted immediately after penetration and the crater should be treated with topical antibiotic.[41] When secondary infection is already present, an oral antibiotic should be considered.[2]

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.[41] 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.[4] 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.[42]

Pathophysiology

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.

History

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

Physical Examination

Typical areas of involvement include the plantar surface of the foot, the intertriginous regions of the toes, and the periungual regions. However, other ectopic sites of infection have also been reported, including the hands, elbows, thighs, and gluteal region.[44]

Infestation in its simplest form is manifested by the appearance of a white patch with a black dot (see the image below).



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A tungiasis lesion in substage 3a.

Lesions can also occur under the nail, potentially making diagnosis more difficult.

More advanced infestation manifests as crusted, erythematous papules; painful, pruritic nodules; crateriform lesions; and secondary infections, including lymphangitis and septicemia. A case presenting with a large bullous lesion has also been described.[45]



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Example of complicated infection with multiple tungiasis lesions and possible secondary infection. Courtesy of Wikimedia Commons (R Schuster) (https:/....

Approach Considerations

Extraction of the gravid 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

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.[46, 47, 48] Sometimes, a serosanguineous exudate oozes from the central opening, and eggs may be seen on microscopic examination.

Histologic Findings

Microscopically, the flea has a thick cuticle and a band of striated muscle stretching from the head to the abdominal orifice. Also visible are hollow, ring-shaped elements from the flea's tracheal and digestive system and numerous round or oval eggs. A report from a small series of skin biopsies indicated that the exoskeleton, hypodermal layer, trachea, digestive tract, and developing eggs were present in all biopsy specimens; striated muscle and the hindquarters were present in about half of the samples; and the head was found in none of the specimens.[49] Detailed histopathologic findings from 86 cases, including scanning electron microscopy images, elucidated the stages of infestation. (See the images below.)[50]



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A. Tangential cut through a fully developed, gravid flea embedded in the stratum corneum of the epidermis. The flea's head and thorax are enfolded in ....

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 image below). A thick band of striated muscle runs from the head to the terminal orifice. Usually, an inflammatory infiltrate is present in the subjacent dermis.



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Histopathologic findings in tungiasis.

Imaging Studies

Dermoscopy, which is used to examine for the characteristic surface findings (see photos) and to identify tungiasis flea parts and eggs microscopically, is useful in definitively diagnosing tungiasis. High-resolution infrared thermography (HRIT) has also been found to be a useful tool in assessing tungiasis-associated inflammation, particularly in complicated cases of tungiasis in which diagnosis and treatment are more difficult.[51]

Approach Considerations

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. Following surgical extraction of the flea, thoroughly cleanse and cover the remaining crater with a topical antibiotic cream to prevent secondary infection.[2]

A course of oral antibiotics may be instituted if secondary infection is suspected. Ensure that tetanus prophylaxis is up to date.



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Removed parasite shown with needle. Courtesy of Wikimedia Commons (https://commons.wikimedia.org/wiki/File:Puce_chique_(Tonga_penetrans).jpg).

Consultations and follow-up

Consultations are only rarely indicated and are generally for complications of a secondary infection. Follow-up care confirms a complete resolution of all pain and physical findings. Application of an antibiotic ointment several times a day to the wounds after flea extraction is recommended.[1]

Topical Treatments

Dimethicone

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.[52, 53]

Zanzarin

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.[54] 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.[54] 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.[6] However, these treatments do not remove the flea from the skin, and they do not result in quick relief from painful lesions.[55, 56]

Other known treatments

Reported topical treatments for tungiasis include cryotherapy and electrodesiccation of the nodules. Application of formaldehyde, chloroform, or dichlorodiphenyltrichloroethane (DDT) to the infested skin has been used, but such treatments are not recommended and may cause patient morbidity.

Deterrence and Prevention

Prevention of tungiasis centers around using closed shoes in endemic areas. Keeping classroom floors clean and free of organic matter may also be helpful in preventing transmission in crowded endemic areas among vulnerable populations.

However, these two strategies are often more theoretical than practical given the circumstances of transmission in settings of deep poverty. Shoes are rarely worn in areas of potential transmission, indoors or even in classrooms, and shoes may quickly wear out or develop holes, making the wearer vulnerable again.

Studies comparing the use of shoes to twice daily application of the plant-based insect repellant Zanzarin for the prevention of tungiasis show more protective effect with the latter.[12, 57] In areas with a high endemicity of sand fleas, daily application of Zanzarin was found to be very efficacious at preventing tungiasis.[58, 54]

Other control measures include treating infested areas with pesticides and treating infected reservoir hosts. Spraying malathion on the ground in some infested villages was found to significantly reduce the incidence of tungiasis, as was the use of methoprene, an insect growth regulator. A topical aerosol containing chlorfenvinphos 4.8%, dichlorphos 0.75%, and gentian violet 0.145% was found to be highly effective against pig tungiasis. Since pigs are an important reservoir for the fleas, treatment of the domestic pig population could have a large positive effect on tungiasis prevalence.[59]

Medication Summary

See Table 1, below.

Table 1. Medication Summary



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See Table

Niridazole (Ambilhar)

Clinical Context:  This agent is not available in United States. Niridazole has been reported to be completely effective in lysing imbedded fleas in infected children. The response was quicker when a second dose was given 1 week after the first dose.

Class Summary

The biochemical pathways of the parasitic flea are sufficiently different from those of its human host to allow selective interference in the flea’s pathways by relatively small doses of chemotherapeutic agents. A combination of direct toxic action on the flea and anti-inflammatory action on the surrounding tissue is postulated.[60]

Author

Darvin Scott Smith, MD, MSc, DTM&H, Adjunct Associate Clinical Professor, Department of Microbiology and Immunology, Stanford University School of Medicine; Chief of Infectious Diseases and Geographic Medicine, Department of Internal Medicine, Kaiser Permanente Medical Group

Disclosure: Nothing to disclose.

Coauthor(s)

Lisa Manzanete, BS,

Disclosure: Nothing to disclose.

Chief Editor

Mark R Wallace, MD, FACP, FIDSA, Infectious Disease Physician, Skagit Valley Hospital, Skagit Regional Health

Disclosure: Nothing to disclose.

Additional Contributors

Stephanie A Nevins, Research Assistant, Department of Genetics, Snyder Lab, Stanford University School of Medicine

Disclosure: Nothing to disclose.

Zachary S Wettstein, Stanford University

Disclosure: Nothing to disclose.

Acknowledgements

Neil F Gibbs, MD Voluntary Associate Professor, Departments of Pediatrics and Medicine, University of California, San Diego School of Medicine; 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.

William D James, MD Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System

William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Elsevier Royalty Other

Thomas M Kerkering, MD Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Paul McKinney, MD, Associate Dean for Public Health, Professor of Medicine, Department of Health Knowledge and Cognitive Sciences, University of Louisville School of Medicine

Disclosure: Nothing to disclose.

Abdul-Ghani Kibbi, MD Professor and Chair, Department of Dermatology, American University of Beirut Medical Center, Lebanon

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster 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.

Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Head of Infectious Disease Fellowship Program, Orlando Regional Medical Center

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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  48. Bauer J, Forschner A, Garbe C, Röcken M. Dermoscopy of tungiasis. Arch Dermatol. 2004 Jun. 140(6):761-3. [View Abstract]
  49. Smith MD, Procop GW. Typical histologic features of Tunga penetrans in skin biopsies. Arch Pathol Lab Med. 2002 Jun. 126(6):714-6. [View Abstract]
  50. Eisele M, Heukelbach J, Van Marck E, Mehlhorn H, Meckes O, Franck S, et al. Investigations on the biology, epidemiology, pathology and control of Tunga penetrans in Brazil: I. Natural history of tungiasis in man. Parasitol Res. 2003 Jun. 90(2):87-99. [View Abstract]
  51. Thielecke M, Raharimanga V, Rogier C, Stauss-Grabo M, Richard V, Feldmeier H. Prevention of tungiasis and tungiasis-associated morbidity using the plant-based repellent Zanzarin: a randomized, controlled field study in rural Madagascar. PLoS Negl Trop Dis. 2013. 7 (9):e2426. [View Abstract]
  52. Heukelbach J. Revision on tungiasis: treatment options and prevention. Expert Rev Anti Infect Ther. 2006 Feb. 4 (1):151-7. [View Abstract]
  53. Thielecke M, Nordin P, Ngomi N, Feldmeier H. Treatment of Tungiasis with dimeticone: a proof-of-principle study in rural Kenya. PLoS Negl Trop Dis. 2014. 8 (7):e3058. [View Abstract]
  54. Feldmeier H, Kehr JD, Heukelbach J. A plant-based repellent protects against Tunga penetrans infestation and sand flea disease. Acta Trop. 2006 Oct. 99(2-3):126-36. [View Abstract]
  55. Heukelbach J, Eisele M, Jackson A, Feldmeier H. Topical treatment of tungiasis: a randomized, controlled trial. Ann Trop Med Parasitol. 2003 Oct. 97(7):743-9. [View Abstract]
  56. Heukelbach J, Franck S, Feldmeier H. Therapy of tungiasis: a double-blinded randomized controlled trial with oral ivermectin. Mem Inst Oswaldo Cruz. 2004 Dec. 99(8):873-6. [View Abstract]
  57. Feldmeier H, Heukelbach J, Ugbomoiko US, Sentongo E, Mbabazi P, von Samson-Himmelstjerna G, et al. Tungiasis--a neglected disease with many challenges for global public health. PLoS Negl Trop Dis. 2014 Oct. 8 (10):e3133. [View Abstract]
  58. Buckendahl J, Heukelbach J, Ariza L, Kehr JD, Seidenschwang M, Feldmeier H. Control of tungiasis through intermittent application of a plant-based repellent: an intervention study in a resource-poor community in Brazil. PLoS Negl Trop Dis. 2010 Nov 9. 4(11):e879. [View Abstract]
  59. Mutebi F, von Samson-Himmelstjerna G, Feldmeier H, Waiswa C, Bukeka Muhindo J, Krücken J. Successful Treatment of Severe Tungiasis in Pigs Using a Topical Aerosol Containing Chlorfenvinphos, Dichlorphos and Gentian Violet. PLoS Negl Trop Dis. 2016 Oct. 10 (10):e0005056. [View Abstract]
  60. Ade-Serrano MA, Olomolehin OG, Adewunmi A. Treatment of human tungiasis with niridazole (Ambilhar) a double-blind placebo-controlled trial. Ann Trop Med Parasitol. 1982 Feb. 76(1):89-92. [View Abstract]

Life cycle of the chigoe flea, Tunga penetrans. Courtesy of the CDC.

Life cycle of Tunga penetrans - Fortaleza stages included. Compiled and designed by Fausto Bustos and Lucas Manfield.

Scanning electron micrograph of flea 6 hours after beginning of penetration. The penetration is almost completed; only the last abdominal segments protrude through the skin (x240).

Scanning electron micrograph of flea in stage 2. The rear end, the genital opening, and the 4 pairs of stigmata form a miniature cone, which towers above the crater caused by pushing in abdominal segments 7 and 8 (x190).

Scanning electron micrograph of flea on day 3 after penetration. The hypertrophic zone between abdominal segments 2 and 3 is gaining a bulging shape and looks like a life-belt (x100).

Scanning electron micrograph of flea on day 8 after penetration. The hypertrophy zone has taken the shape of a sphere. The 3 parts of abdominal segment 2 are completely bent apart. Together with the newly developed, crescent-shaped chitinous clasps, the anterior part of the flea looks like a 3-leafed clover (x32).

Illustration of Tunga penetrans (sand flea) in its enlarged state. Courtesy of Wikimedia Commons (https://commons.wikimedia.org/wiki/File:ChiggerBMNH.jpg).

A tungiasis lesion in substage 3a.

Example of complicated infection with multiple tungiasis lesions and possible secondary infection. Courtesy of Wikimedia Commons (R Schuster) (https://commons.wikimedia.org/wiki/File:Jigger_infested_foot_(2).jpg).

A. Tangential cut through a fully developed, gravid flea embedded in the stratum corneum of the epidermis. The flea's head and thorax are enfolded in the hypertrophic anterior abdominal segments. The epidermis is hyperplastic and shows papillomatosis, parakeratosis, and hyperkeratosis.B. Tangential cut through the posterior abdominal segments of an embedded sand flea. Next to the chitinous cuticle, a microabscess has formed.C. Dead parasite; the exoskeleton of the posterior abdominal segment has remained intact; the cuticle has disintegrated at the epidermal–dermal interface. The carcass is infiltrated by neutrophils, and pus has formed.D. The head of the flea is located at the epidermal–dermal interface, has penetrated the basal membrane, and is surrounded by many erythrocytes, presumably having leaked from a blood vessel. The abdomen of the parasite is separated from host tissue by a thick, chitinous cuticle.

Histopathologic findings in tungiasis.

Removed parasite shown with needle. Courtesy of Wikimedia Commons (https://commons.wikimedia.org/wiki/File:Puce_chique_(Tonga_penetrans).jpg).

A. Tangential cut through a fully developed, gravid flea embedded in the stratum corneum of the epidermis. The flea's head and thorax are enfolded in the hypertrophic anterior abdominal segments. The epidermis is hyperplastic and shows papillomatosis, parakeratosis, and hyperkeratosis.B. Tangential cut through the posterior abdominal segments of an embedded sand flea. Next to the chitinous cuticle, a microabscess has formed.C. Dead parasite; the exoskeleton of the posterior abdominal segment has remained intact; the cuticle has disintegrated at the epidermal–dermal interface. The carcass is infiltrated by neutrophils, and pus has formed.D. The head of the flea is located at the epidermal–dermal interface, has penetrated the basal membrane, and is surrounded by many erythrocytes, presumably having leaked from a blood vessel. The abdomen of the parasite is separated from host tissue by a thick, chitinous cuticle.

A tungiasis lesion in substage 3a.

Scanning electron micrograph of flea on day 3 after penetration. The hypertrophic zone between abdominal segments 2 and 3 is gaining a bulging shape and looks like a life-belt (x100).

Scanning electron micrograph of flea on day 8 after penetration. The hypertrophy zone has taken the shape of a sphere. The 3 parts of abdominal segment 2 are completely bent apart. Together with the newly developed, crescent-shaped chitinous clasps, the anterior part of the flea looks like a 3-leafed clover (x32).

Scanning electron micrograph of flea 6 hours after beginning of penetration. The penetration is almost completed; only the last abdominal segments protrude through the skin (x240).

Scanning electron micrograph of flea in stage 2. The rear end, the genital opening, and the 4 pairs of stigmata form a miniature cone, which towers above the crater caused by pushing in abdominal segments 7 and 8 (x190).

Life cycle of Tunga penetrans - Fortaleza stages included. Compiled and designed by Fausto Bustos and Lucas Manfield.

Histopathologic findings in tungiasis.

Life cycle of the chigoe flea, Tunga penetrans. Courtesy of the CDC.

Complicated Tungiasis infection. Courtesy of Dermatology Atlas (http://www.atlasdermatologico.com.br/index.jsf) and Samuel Freire da Silva, MD.

Tungiasis lesion under toenail. Courtesy of Dermatology Atlas (http://www.atlasdermatologico.com.br/index.jsf) and Samuel Freire da Silva, MD.

Example of complicated infection with multiple tungiasis lesions and possible secondary infection. Courtesy of Wikimedia Commons (R Schuster) (https://commons.wikimedia.org/wiki/File:Jigger_infested_foot_(2).jpg).

Illustration of Tunga penetrans (sand flea) in its enlarged state. Courtesy of Wikimedia Commons (https://commons.wikimedia.org/wiki/File:ChiggerBMNH.jpg).

Removed parasite shown with needle. Courtesy of Wikimedia Commons (https://commons.wikimedia.org/wiki/File:Puce_chique_(Tonga_penetrans).jpg).

Medication Name

Dosage/Application

Contraindications

Availability

Notes

Dimethicone [53] Apply directly to the affected area once or twice daily.No known contraindications. Shown to be safe for extended use.Available under the brand name NYDA®. 
Topical Antibiotic Lotions [55, 52] 0.8% ivermectin, 0.2% metrifonate and 5% thiabendazole lotions, applied two consecutive days.No contraindications reported.Readily available. 
Zanzarin [54, 12] Apply to all infected areas and areas at risk for tungiasis infection twice daily.No known contraindications.No longer commercially available, but made of ingredients that could be locally manufactured in areas where tungiasis is common. 
Oral Niridazole [60] Single or double dose of niridazole (Ambilhar) at 30 mg kg−1 body weight. If necessary, second dose should be given one week after the first.Abdominal pain, nausea, and vomiting may occur. Has some neurotoxicity and has been known to cause hallucinations, so is not safe for long-term use.This is not available in the United States.Use of systemic therapy for primary treatment has not been advocated for US travelers, particularly if infestation involves only a small number of lesions.