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  In this article
    Introduction
    Epidemiology
    Etiopathogenesis
    Clinical features
    Type 2 Human hoo...
    Type 1 Animal ho...
    Type 3 Strongylo...
    Type 4 Animal st...
    Type 5 Gnathostoma
    Type 6 Insect larvae
    Other features a...
    Pathology
    Diagnosis
    Differential dia...
    Treatment
    Prevention
    Significance in ...
    References

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CONTINUING MEDICAL EDUCATION
Year : 2002  |  Volume : 68  |  Issue : 5  |  Page : 252-258

Cutaneous larva migrans


Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry - 605 006, India

Correspondence Address:
Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry - 605 006, India



How to cite this article:
Karthikeyan K, Thappa D. Cutaneous larva migrans. Indian J Dermatol Venereol Leprol 2002;68:252-8


How to cite this URL:
Karthikeyan K, Thappa D. Cutaneous larva migrans. Indian J Dermatol Venereol Leprol [serial online] 2002 [cited 2018 Nov 19];68:252-8. Available from: http://www.ijdvl.com/text.asp?2002/68/5/252/12484



   Introduction Top

Cutaneous larva migrans (CLM) is a dermatitis caused by the invasion and migration of larva of parasites in the skin.[1] These larvae usually have their origin from nematodes and rarely from insects.[2] This entity is also known by various other names such as creeping eruption, sand worm, plumbers itch, duck hunters itch and epidermatitis linearis migrans.[1] It is commonly known as creeping eruption for its distinctive feature that the lesion creep or migrate and is due to the presence of moving parasite in the skin. The credit for the earliest published report of CLM goes to Lee [2], an English physician of 1874. Crocker [3] coined the term "Cutaneous larva' migrans" in 1893. Later in 1896, Hammelstjerna proved its parasitic etiology. Since then many cases have been reported and a variety of organisms are incriminated as the causative agents.

   Epidemiology Top

Though cutaneous larva migrans (creeping eruption) has a world wide distribution, it is common in warmer tropical and sub tropical countries.[1] It is endemic in Caribbean islands, Africa, South America, South East Asia and South eastern United States.[5] This disorder frequently occurs during warm and rainy seasons. People who frequent beaches and the children are at a higher risk of acquiring this disease.[1] The endemic nature of this disease depends on two factors namely poor sanitation and appropriate environmental condition. The environmental factors that are essential for development of the larva include temperature between 23 to 30 C, loose humus soil, shady areas and proper aeration. The factors that influence the occurrence of CLM include the degree of soil contamination and duration of contact with the soil.[6],[7]

   Etiopathogenesis Top

Cutaneous larva migrans can be caused by different parasites. Various organisms causing CLM and their definitive hosts are summarized in [Table - 1]. Mainly, CLM is caused by the larval nematodes, which penetrate into the skin.[1],[8] The normal life cycle of a nematode is described in [Figure - 1]. The embryonated eggs of nematodes are shed in feces by the definitive host and thus reach the soil. Under appropriate temperature and humidity, these eggs hatch and release rhabditiform larvae within 1-2 days. In a week time, these larvae moult, grow and develop into filariform larvae. These infective filariform larvae measure 850 microns in length and have a diameter of 35 microns. They live in the top one half inch of the soil, with their ends projecting upward from the surface, searching for their prey and live within inches of where the eggs are deposited. Under optimal conditions, these larvae may remain infective for several months, though 90% of these larvae die within first 3 weeks. Survival of these larvae is best achieved in the light soil that is protected from flooding and drying.[7] The larvae can migrate vertically through the soil to a potential host in response to contact (thigmotropism), carbon dioxide or warmth. When come in contact with the human skin, the larvae use discontinuities in the epidermis of the host (fissures or hair follicles) to penetrate the skin.[7] The juvenile larvae can penetrate epidermis of any site. The parts most often affected are those which remain in contact with soil such as feet, hands, and buttock.[9] In the skin, the larval migration begins four days after penetration.[10] The movement of the larvae in the epidermis is facilitated by the production of hyaluronidase by them.[11] Within a few days, a typical dermatitis with vesicles, papules and desquamation develops along the track of migration of larva. Since, the larvae are unable to complete their life cycle in human (accidental host), this lead to their death with-in weeks of invasion. These larvae finally degenerate and disease subsides.[12] The sequence of evolution of the lesion in an experimental set up is summarized in the [Table - 2]. All hookworms and Strongyloides that cause CLM in humans are similar morphologically. In contrast, the larvae of Gnathostoma are larger and can be identified by their numerous cuticular spines.[1]

   Clinical features Top

The clinical features of CLM may vary from non-specific dermatitis to typical creeping eruption [Table - 3]. The larva after penetration can lie quiet for weeks or immediately begin creeping activity. The initial lesion is an erythematous, papular itchy lesion. Soon a slightly raised, flesh colored or pink swollen lesion about 2-3 mm thick develops and forms linear, serpentine (serpiginous) or bizarre tracks [Figure - 2], [Figure - 3] & [Figure - 4]. Multiple larvae can be active at the same time with the formation of disorganized loops and tortuous tracks.[13] The larvae migrate about 2-5 cm per day and the visible track moves ahead by 1-2 cm. Multiple vesicles may appear along the lesion. Rarely, folliculitis may be the presenting picture. The eruption is most often located over the feet followed by buttock, anogenital region and upper extremities.[8],[9] Rarely, in severe infections, person may have hundreds of tracks.[9]
The lesions of CLM are intensely itchy, sometimes may produce burning sensation.[13],[14] Itching may be severe enough, to produce insomnia. Since the lesions of CLM are itchy, scratching may lead to secondary changes of dermatitis and bacterial infection.
Cutaneous larva migrans can be grouped into several types depending upon the species responsible for the lesions and their clinical appearance.[15]

   Type 1 Animal hookworms Top

CLM produced by Ancylostoma duodenale and Ancylostoma caninum is characterized by well-defined tracks that extend several centimeters from their point of origin. These juveniles (larvae) migrate at the rate of 3.5 to 5 cm per day. The infection can be chronic, lasting for months.[15]

   Type 2 Human hookworms Top

Ancylostoma duodenale and Necator americanus produce marked blister formation, short tracks and intense itching. This type of larva migrans is also known as "ground itch". They eventually migrate to the lungs and intestine where the parasites mature into adults.[7],[15]

   Type 3 Strongyloides, stercoralis Top

Human strongyloides produce a type of CLM known as "larva currens".[13] The lesion begins in the perineal area and then advances to the extremities and other sites. The track is wide, poorly defined and long. It is called as larva currens as the larvae migrate at a rate of up to 5 cm per hour.[13],[16],[17]

   Type 4 Animal strongyloides Top

CLM produced by strongyloides of animal origin is variable. Some lesions are similar to those seen in Strongyloides stercoralis infection.[18] Infections with Strongyloides myopotomi and Strongyloides procyonis produce lesions resembling erythema multiforme.[19] The typical burrows are seen on examination with indirect light.

   Type 5 Gnathostoma Top

CLM produced by gnathostoma is usually confined to Japan, Thailand and less often in other countries of Southeast Asia.[20] Parasitic infection can occur in two ways. It can occur due to the migration of ingested larva from the intestine to the skin or by direct penetration of the parasite through the skin while handling animal flesh.[21] The lesions are wide tracks that disappear and reappear at a distant location. The rate of migration is variable, in the epidermis the larvae travel at the rate of 4.5 cm per day while in dermis, it is about 3 cm per hour. Gnathostoma larvae can be easily visualized by naked eye because of their size. They can be recovered easily if a small incision is made over the lesion.[11],[20],[22]

   Type 6 Insect larvae Top

Some species of gastrophilus and hypoderma can migrate through the skin producing linear lesions sometimes called as "myiasis linearis". The characteristic lesion consists of single continuous track without blister formation, moving at a rate of 3 to7.5 cm per day.[15] The larvae can be easily visualized by blanching the skin with slight pressure from a magnifying glass or by rubbing the skin with mineral oil.[23] The larva can be extracted intact by excoriating the superficial epidermis.[23]

   Other features associated with CLM Top

Usually, there are few, if any systemic symptoms. CLM produced by Strongyloides can be associated with Loeffler's syndrome as a result of migrating larvae reaching the lungs.[15],[34] In these patients with prominent pulmonary symptoms and signs, the larvae can be recovered from the sputum. Migration of the larvae in the cornea may produce inflammation leading to corneal opacity.[16] CLM produced by Ancylostoma caninum can be associated with myositis as result of the larva invading deep into the muscles.[27]

   Pathology Top

The histopathology of the lesion shows an empty tunnel with polymorphonuclear cell infiltrate consisting mainly of eosinophils and necrotic keratinocytes in the epidermis. The larva is seldom seen in the tissue sections because the clinical lesion develops long after the larva has passed through.[28] If the larva is found, it is located in a burrow or in a hair follicle without inflammation.[15] The site of migration of the larva may vary. All hookworm larva appear to migrate through epidermis in the stratum malpighi while strongyloides larva is found in the upper dermis.[29] The larvae of Gnathostoma, Gastrophilus and Hypoderma are present in both epidermis and dermis.[15] It is impossible to identify various hookworm larvae in the cross section but Gastrophilus, Gnathostoma and Hypoderma are larger and have distinct morphological features.[15]

   Diagnosis Top

Since larvae in the skin are rarely recovered, and they are not readily or easily identified when found, the species involved in individual cases is usually unknown. Laboratory investigations may not be helpful in the diagnosis of CLM.[30],[31],[32] Rarely, patient may have associated eosinophilia or an increase in the immunoglobulin E (IgE) rate. Stool examination is worthless expect for Strongyloides where the larvae may be seen in the stools. Skin biopsy is not recommended as a diagnostic modality.[1] Recently epiluminescent microscopy has been found to be an effective and non-invasive method for detecting a larva to confirm the diagnosis of CLM.[30] Some authors have suggested search for specific IgG with enzyme-linked immunosorbent assay (ELISA) methods.[32] Thus, the diagnosis of CLM is based mainly on clinical features and typical history.

   Differential diagnosis Top

The features of CLM are typical and rarely missed. This dermatosis requires differential diagnosis from other parasitoses e.g., subcutaneous nodules or granulomas due to other species, and different pictures of myiasis, but also from simpler and more common pathologies such as allergic contact dermatitis, urticaria factitia, other types of dermatitis, and pyodermas.[32] The various other differential diagnosis of this condition includes scabies, urticaria, photodermatitis, erythema chronicum migrans and stings of Portuguese man- of-war or jellyfish.[5],[8] In some cases, the diagnosis may be further complicated by superadded bacterial infection and eczematization.[1],[2],[3],[4],[5],[6],[7],[8]

   Treatment Top

Although, CLM normally disappears by itself within anything from 1 to 6 months or rarely, longer, the intense itching, the unpleasant sensation felt by the patient of the larva slowly creeping below the skin, and the possible complications suggest that treatment should be given that can reduce the length of the disease, even if different therapeutic options turn out to be somewhat ineffective or difficult to put into practice.[32] It can be treated by physical modalities (surgery e.g., in creeping eruption due to Gnathostoma sphinigerum), cryotherapy, topical drugs and systemic therapy.[31],[32] Cryotherapy which can be used for limited number of lesions, is obsolete, as it is a painful and imprecise way to kill the migrating larvae which is usually 1-2 cm ahead of the visible track.[5],[8],[33] Further more, the larva can withstand temperature as low as -21 C for more than 5 minutes, resulting in failure of therapy.[34] Surgery often ineffective as the larva is easily missed, being ahead of the visible track. Surgery and cryotherapy may be appropriate in pregnancy.[8] Various topical agents such as 15% thiabendazole, 2% gamrriexane cream, 25% piperazine citrate and metriphonate have also been tried in the treatment of CLM.[10],[11],[12],[13],[14] Among these topical agents, thiabendazole has been found to effective in killing the larvae and. alleviating symptoms.[5],[35] Though topical thiabendazole is effective, it requires repeated application, can result in an irritant reaction and is often followed by recurrences.[36] Oral thiabendazole has been reported to have a very high efficacy and is usually given in the dose of 25-50 mg per kg body weight, once or twice daily for 2-5 days.[5],[32],[37] It is not widely used because of the high incidence of side effects such as nausea, anorexia, headache and gastrointestinal disturbances.[37] Further, it is not available in many countries.[5]
Albendazole, yet another drug was first used to treat CLM in 1982 and subsequently many, reports have substantiated its effectiveness and is now considered to be the drug of choice for this disorder.[38],[39],[40] It is used in the dosage of 400 800mg/day for a period that may vary from 1-7 days.[31],[41] This anti-helminthic is effective against eggs, larvae and adult stage of numerous helminthes. The mechanism of action is not very clear. It may act by reducing or blocking the uptake of glucose, thus depleting glycogen reserves leading to decrease or cessation in production of adenosine triphosphate (ATP). It may also induce degeneration of cytoplasmic microtubules with death of the parasite by autolysis. Some authors believe that it acts by inhibiting microtubule polymerization.[31] Albendazole as such is well tolerated if administered for a short length of time. Its long term use may, lead to elevated liver enzymes, alopecia, allergic reactions, leukopenia and thrombocytopenia.[31],[32] The major advantage with albendazole is thatiit relieves pruritus in 3-5 days and results in resolution of the cutaneous lesions by 5-7 days after treatment.[32] It is teratogenic and embryotoxic in the rot and rabbit, but does not seem to be either mutagenic or, carcinogenic.[31]
Another possible drug for use in, CLM is a single 150-200ig/kg dose of ivermectin, a drug capable of eradicating the parasite with minimum or no side effects, but which still needs more thorough research.[32] In a study, single dose of 12 mg of ivermectin was found to be more effective than single dose of 400mg of albendazole.[41],[42],[43],[44] Flubendazole,(200 mg/day for 5 days), is another anti -helminthic drug, currently under experimental stage, would appear to offer good prospect for the future.[32]

   Prevention Top

Eradication of larvae causing CLM is impractical. The most appropriate preventive measure is to avoid contact of exposed skin with contaminated soil. Wearing shoes and using a beach towel when lying on sand can avoid exposure to the larvae. Periodic deworming of domestic cats and dogs reduces soil contamination. Sand boxes and other similar facilities where children frequently play should be protected from dogs and cats.[1] Thus, CLM can be prevented by adequate precautionary methods, failing which, it can spoil a dream vacation.[45]

   Significance in the context of India Top

Significance in the context of India is its occurrence in the coastal areas of the country where suitable conditions for this entity exist.[42] Children may be advised not to sit, lie, or walk barefoot on wet soil or sand of beaches. The ground should be covered with impenetrable material when sitting or lying on the ground.
To conclude, CLM is a clinical condition with a characteristic presentation that is easily recognizable. Despite the ubiquitous distribution of A. braziliense and A. caninum, CLM seems to restricted mainly to tropical and subtropical countries. The typical patient is a person who has visited a beach or a returning traveler from a tropical or subtropical climate who gives a history of beach exposure. The characteristic skin lesion is a pruritic, erythematous serpiginous or linear raised track. Effective treatment modalities now exist for this entity. 

   References Top

1.Neafie RC, Meyers WM. Cutaneous larva migrans. In: Strickland GT ed. Hunters Tropical Medicine and Emerging Infectious Diseases, 8th edn. Philadelphia: Sounders 2000: 797-799.  Back to cited text no. 1    
2.Nash T. Visceral larva migrans and other unusual helminth infections. In: Mandell G, Douglas R, Bennett J, eds. Principle and Practice of Infectious diseases, 3rd edn. New York, NY: Churchill Livingstone 1990: 2340.  Back to cited text no. 2    
3.Crocker HR. Diseases of the Skin, 2nd edn. Philadelphia 1893: 926-927.  Back to cited text no. 3    
4.Beaver CP, Jung CR, Cupp EN. Strongylida: Hookworms and other bursate nematodes. In: Clinical Parasitology, 9th edn, Philadelphia: Lea & Febiger 1984: 269-301.  Back to cited text no. 4    
5.Davies HD, Sakuls P Keystone JS. Creeping eruption. A review of clinical presentation and management of 60 cases presenting to a tropical disease unit. Arch Dermatol 1993; 129:528-529.  Back to cited text no. 5    
6.Roberts LS, Janovy J. Foundations of Parasitology. 6th edn. San Francisco: McGraw Hill 2000: 405-417.  Back to cited text no. 6    
7.Gilman RH. Intestinal nematodes that migrate through skin and lung. In: Strickland GT ed. Hunter's Tropical Medicine and Emerging Infectious Disease, 8th edn. Philadelphia: Sounders 2000: 730-735.  Back to cited text no. 7    
8.Blackwell V, Vega-Lopez F. Cutaneous larva migrans: Clinical features and management of 44 cases presenting in the returning traveler. Br J Dermatol 2001; 145: 434-437.  Back to cited text no. 8    
9.Jelink T, Maiwald H, Nothdruft HD, et al. Cutaneous larva migrans in travelers: synopsis of histories, symptoms and treatment of 98 patients. Clin Infect Dis 1994; 19:1062-1064.  Back to cited text no. 9    
10.Canizares O. Clinical Tropical Dermatology, Boston: Blackwell Scientific Publications Inc: 1975;210-211.  Back to cited text no. 10    
11.Hotez PJ, Narasimhan S, Haggerty J, et al. Hyaluronidase from infective Ancylostoma hookworm larvae and its possible function as a virulence factor in tissue invasion and in cutaneous larva migrans. Infect Immun 1992; 609(3): 1018-1023.  Back to cited text no. 11    
12.Katz R, Ziegler J, Blank H. The natural course of creeping eruption and treatment with thiabendazole. Arch Dermatol 1965; 91:420-424.  Back to cited text no. 12    
13.Bryceson ADM, Hay RJ. Parasitic worms and protozoa. In: Champion RH, Burton JL, Burns DA, et al eds. Rook/ Wilkinson / Ebling Textbook of Dermatology, 6th edn. Vol 2, Oxford: Blackwell Sciences 1999: 971-972.  Back to cited text no. 13    
14.Gilles HM. Soil transmitted Helminths (geohelminths). Cutaneous larva migrans. In: Cook GC ed. Monsor s Tropical Diseases. London: WB Sounders 1996:1392-1394.  Back to cited text no. 14    
15.Gutierrez Y. Diagnostic Pathology of Parasitic Infections with Clinical Correlations, Second edn, New York: Oxford University Press 2000: 343-353.  Back to cited text no. 15    
16.Arthur RP Shelly WB. Larva currens. A distinctive variant of cutaneous larva migrans due to Strongyloides stercoralis. Arch Dermatol 1958; 78:186-190.  Back to cited text no. 16    
17.Stone OJ, Newell GB, Mullins JF. Cutaneous Strongyloidiasis: larva currens. Arch Dermatol 1972; 106: 734-736.  Back to cited text no. 17    
18.Roeckel IE, Lyons ET. Cutaneous larva migrans, an occupational disease. Ann Clin Lab Sci 1977; 7:405-410.  Back to cited text no. 18    
19.Burks JW, Jung RC. A new type of water dermatitis in Louisiana. South Med J 1960; 53:716-719.  Back to cited text no. 19    
20.Bhaibulaya M, Chareonlarp P. Creeping eruption caused by Gnathostoma spinigerum. Southeast Asian J Trop Med Public Health 1983; 14:266-268.  Back to cited text no. 20    
21.Daengsvang S, Sermswatsri B, Youngyi P, et al. Penetration of skin by Gnathostoma spinigerum larvae. Ann Trop Med Parasitol 1970; 64:399-402.  Back to cited text no. 21    
22.Pinkus H, Fan J, De Giusti D. Creeping eruption due to Gnathostoma spinigerum in a Taiwanese patient. Int J Dermatol 1981; 20: 46-49.  Back to cited text no. 22    
23.Austman KJ. Creeping eruption: report of first case from Manitoba. JAMA 1926; 78: 186-190.  Back to cited text no. 23    
24.Burtland RJA, Coulson IH. Pulmonary eosinophilia associated with cutaneous la+-9 migrans. Thorax 1985; 40:76-77.  Back to cited text no. 24    
25.Gnuill MA, Odom RB. Larva migrons complicated by Loeffler's syndrome. Arch Dermatol 1978; 114:1525-1526.  Back to cited text no. 25    
26.Nabath RP Lowlor PP Nematode (Ancylostoma) in the cornea. A case report. Am J Ophthalmol 1965; 59: 486-490.  Back to cited text no. 26    
27.Little MD, Halsey NA, Cline BL, et al. Ancylostoma larva in a muscle fiber of man following Cutaneous larva migrans. Am J Trop Med Hyg 1983; 32: 1285-1288.  Back to cited text no. 27    
28.Convit J. Protozoan diseases of the skin. In; Elder D, Elenitsas R, Jaworsky C, et al eds. Lever's Histopothology of Skin, 8th edn, Philadelphia: Lippincott Raven 1997: 1392-1394.  Back to cited text no. 28    
29.Nichols RL. Etiology of visceral migrans. II. Comparative larval morphology of Ascaris lumbricoides, Ancylostoma caninum. J Parasitol 1956; 42: 363-369.  Back to cited text no. 29    
30.Elsner E, Thewes M, Worret WI. Cutaneous larva migrans detected by epiluminescent microscopy. Acta Derm Venereal (Stockh) 1997; 77: 487-488.  Back to cited text no. 30    
31.Rizzitelli G, Scarabelli G, Veraldi S. Albendazole: a new therapeutic regimen in cutaneous larva migrans. Int J Dermatol 1997; 36:700-703.  Back to cited text no. 31    
32.Albanese G, Venturi C, Galbiati G. Treatment of larva migrans cutanea (creeping eruption): a comparison between albendazole and traditional therapy. Int J Dermatol 2001; 40:67-71.  Back to cited text no. 32    
33.Pouluzzi P, MagatonRizzi G, Mattighello P. Larva migrans: report of three cases. Therapeutic advice. J EurAcad Dermatol Venereol 1996; 6: 89-91.  Back to cited text no. 33    
34.Elliot DL, Tolle SW, Goldberg L, et al. Pet associated illness. N Eng J Med 1985; 31: 985-995.  Back to cited text no. 34    
35.Whiting D. The successful treatment of creeping eruption with topical thiabendazole. S Afr Med J 1976; 50: 253-254.  Back to cited text no. 35    
36.Goldsmith J, Froese E. A note on cutaneous larva migrans and its treatment with topical thiabendazole. S Afr Med J 1976; 50: 253-255  Back to cited text no. 36    
37.Stone O, Mullins J. Thiabendozole effectiveness in the creeping eruption. Arch Dermatol 1965; 91: 427-429.  Back to cited text no. 37    
38.Coulaud JP Binet D, Voyer C, et al. Treatment of cutaneous larva migrans with albendazole. Bull Soc Fathol Exot 1982; 75:534-537.  Back to cited text no. 38    
39.Williams HC, Monk B. Creeping eruption stopped in its tracks by albendazole. Clin Exp Dermatol 1989; 14:355-356.  Back to cited text no. 39    
40.Jones SK, Reynolds NJ, Oliwiecki S, et al. Oral albendazole for the treatment of cutaneous larvae migrans. Br J Dermatol 1990; 122:99-101.  Back to cited text no. 40    
41.Veraldi S, Rizzitelli G. Effectiveness of new therapeutic regimen with albendazole in cutaneous larva migrans. EurJ Dermatol 1999; 9; 352-353.  Back to cited text no. 41    
42.Thappa DM, Karthikeyan K. Larva migrans eruption in an infant (Images in Clinical Practice). Indian Pediatr 2002 (in press).  Back to cited text no. 42    
43.Caumes E, Carrieri J, Datry A, et al. A randomized trial of ivermectin versus albendazole for the treatment of cutaneous larva migrans. Am J Trop Med Hyg 1993; 49:641-644.  Back to cited text no. 43    
44.Caumes E, Datry A, Paris L, et al. Efficacy of ivermectin in the therapy of cutaneous larva migrans. Arch Dermatol 1992; 128:994-945.  Back to cited text no. 44    
45.Edeglass JW, Douglass MC, Stieffer R, et al. Cutaneous larva migrons in the northern climates: a souvenir of your dream vacation. J Am Acad Dermatol 1982; 7:353-358.  Back to cited text no. 45    

 

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