Tungiasis
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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.)
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]
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]
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.
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]
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. If available, the repellent Zanzarin has been shown to be effective when applied to the feet once daily. [12]
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.
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]
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]
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]
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]
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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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. [Medline].
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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.
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.
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
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.
Lisa Manzanete Undergraduate Researcher, Sonnenburg Lab, Stanford University
Disclosure: Nothing to disclose.
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.
Zachary S Wettstein Stanford University
Disclosure: Nothing to disclose.
Stephanie A Nevins Research Assistant, Department of Genetics, Snyder Lab, Stanford University School of Medicine
Disclosure: Nothing to disclose.
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.
Tungiasis
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