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Tungiasis

  • Author: Darvin Scott Smith, MD, MSc, DTM&H; Chief Editor: Mark R Wallace, MD, FACP, FIDSA  more...
 
Updated: Oct 21, 2015
 

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.)

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

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]

Life cycle of Tunga penetrans - Fortaleza stages i 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]

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Patient Education

Travelers to affected countries 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.

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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.

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]

Scanning electron micrograph of flea 6 hours after 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. T 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 afte 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 afte 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).

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.

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.

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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.[12, 13, 14, 15] Since 2000, sporadic cases have been reported in the United States.[16] All of these cases were imported from outside of the United States.

International occurrence

Tungiasis is potentially endemic in 88 countries worldwide.[17] 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%.[18, 19, 20, 21, 22, 23, 24]

Tungiasis has reemerged to epidemic levels in many countries across sub-Saharan Africa.[25, 26, 27] 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).[28]

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.[29]

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.[30] In a traditional fishing village in northeastern Brazil, the overall prevalence was 51%.[31, 32] In a village in rural Haiti, nearly 75% of the population was observed to have tungiasis lesions.[33] 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.[34]

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.[35] In many countries with the greatest presence of T penetrans, lack of health education, poor housing, and close proximity to animals are risk factors for tungiasis.[36, 37]

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.[38]

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.[38] 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.[31]

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Prognosis

The prognosis in tungiasis is excellent if proper sterile methods are followed for the extraction of fleas. Uncomplicated infestation results in pain, swelling, tenderness, and some limitation in mobility (although sometimes lesions are pruritic or even asymptomatic). As previously mentioned, however, complications can occur, including secondary infections, such as bacteremia or septicemia, lymphangitis, tetanus, and gas gangrene. (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]

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.[39]

To prevent superinfection, sand fleas should be surgically extracted immediately after penetration and the crater should be treated with topical antibiotic.[39]

Complications

Sores caused by burrowed fleas can be a potential entry point for clostridial and other infections.[39] 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.[40]

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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 even difficulty walking are significant contributors to morbidity.

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Contributor Information and Disclosures
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 Redwood City Hospital

Darvin Scott Smith, MD, MSc, DTM&H is a member of the following medical societies: American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society of Travel Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

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

Disclosure: Nothing to disclose.

Chief Editor

Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Clinical Professor of Medicine, University of Central Florida College of Medicine

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, Florida Infectious Diseases Society

Disclosure: Nothing to disclose.

Additional Contributors

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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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.
 
 
 
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