not to be missed! differential diagnoses of common

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Not to be missed! Differential diagnosesof common dermatological problems inreturning travellers

Andreas Neumayr a,b, Christoph Hatz a,b, Johannes Blum a,b,*

a Swiss Tropical and Public Health Institute, Socinstrasse. 57, 4051 Basel, SwitzerlandbUniversity of Basel, Basel, Switzerland

Received 13 June 2013; received in revised form 20 September 2013; accepted 25 September 2013Available online 6 October 2013

KEYWORDSTravel;Skin;Creeping eruption;Chancre;Eschar

Summary After systemic febrile illnesses and diarrhoea, dermatological disorders are thethird most frequent health problem of returning travellers consulting travel clinics. While mosttravel-related dermatological problems are mild, self-limiting and rather harmless, the chal-lenge is to pick up on dermatological clues to potentially severe or even life-threatening dis-eases. This article provides an overview of the most common and the ‘not to be missed’dermatological diagnoses in international travellers.ª 2013 Elsevier Ltd. All rights reserved.

Introduction

The three most common reasons for returning travellers toseek medical help are systemic febrile illnesses, acute orchronic diarrhoea and dermatological disorders [1]. Variousstudies have recently reviewed the spectrum and the fre-quencies of travel-related dermatological disordersobserved in travel clinics [1e4]. The spectrum of

dermatological diagnoses in travellers is broad and domi-nated by insect bites, bacterial skin infections, creepingeruptions and allergic skin reactions (Table 1).

This article addresses the most frequent dermatologicaldisorders and their differential diagnoses in returningtravellers, and highlights the dermatological clues to severeand potentially life-threatening diseases, which should notbe missed: ‘When you hear hoofbeats, think horses, notzebras’. but make sure not to miss out on zebras.

(Those dermatological disorders that are not confined totravelling d e.g. herpes zoster, pityriasis rosea, syphilisand sun- and heat-related skin pathologies d alsofrequently occur in travellers, but are beyond the scope ofthis review).

* Corresponding author. Swiss Tropical and Public Health Insti-tute, Socinstrasse. 57, 4051 Basel, Switzerland. Tel.: þ41 61 2848111; fax: þ41 61 284 8101.

E-mail address: [email protected] (J. Blum).

1477-8939/$ - see front matter ª 2013 Elsevier Ltd. All rights reserved.http://dx.doi.org/10.1016/j.tmaid.2013.09.005

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Travel Medicine and Infectious Disease (2013) 11, 337e349


Methods

This review is based on the most frequently reported skinpathologies in travellers (see Table 1), on the relevantliterature and on personal experiences from daily practiceat our travel clinic.

Ectoparasites

Insect bites

Consultations for insect bites are frequent and the clinicalpresentations vary widely. One insect may cause differenttypes of skin lesions and each type of skin lesion may becaused by different kinds of insects, thus it is difficult andoften impossible to infer from a skin lesion the causativeinsect. However, in some cases, the clinical aspect and thedistribution of the skin lesions may be suggestive: forexample, pruritic lesions caused by fleas and bed bugs aremore frequently papular and typically clustered or linearlygrouped, which is rarely seen withmosquito bites [5e7]. Thetypical evolution of insect bites is the initial formation ofwheals and flares (with a peak within 20 min), a delayedreaction manifesting as itchy indurated erythematous pap-ules (with a peak at 24e36 h) and the gradual resolution ofthe lesions within days to weeks [8]. However, the clinical

picture may include ecchymoses or vesicles and severelyallergic patientsmay develop haemorrhagic bullae, necrosesor ulcers that heal with residual scarring [7]. In a few cases,insect bites may cause systemic symptoms like generalisedurticaria, angioedema, anaphylaxis or the rare ‘Skeetersyndrome’ (a large local inflammatory reaction accompa-nied by fever, which can be differentiated from cellulitis byits peracute onset within hours) [8e10]. Sequelae of insectbites include bacterial superinfection, post-inflammatorychanges in pigmentation, prurigo simplex-like lesions, pru-rigo nodularis and atrophic scarring [5,7].

DiagnosisDiagnosis is based on the patient’s history and clinicalpicture.

TreatmentInsect bites are primarily treated with topical steroids andoral antihistamines. Patients suffering from agonisingnocturnal pruritus may benefit from the use of older,sedative antihistamines. In severe, disseminated or re-fractory cases, the oral intake of steroids may be required.

Myiasis

The maggots/larvae of various flies (mostly Dermatobiahominis [human bot fly e Central and South America] and

Table 1 Spectrum and frequency of travel-related dermatological disorders.

Setting Herbinger 2011 Lederman 2008 Ansart 2007 Freedman 2006

Travel clinic inMunich, Germany

GeoSentinelsurveillance network(1997e2006)

Travel clinic inParis, France

GeoSentinelsurveillance network(1996e2004)

Number of cases (n Z 4158) % (n Z 4594)% (n Z 165)% (n Z 2947) %

Ectoparasites Arthropod/insect bite 16.8 8.2 9.7 18.7Scabies 2.3 e 10 2.2Myiasis 0.8 e 7.2 3.5Tungiasis 0.6 e 4 e

Tick bites 0.6 e e e

Bacteria Bacterial skin infectionsa 21.6 14.5 21.2 12.4Rickettsial disease 1.3 e 0.6 e

Leprosy e e 2.4 e

Helminths Larva cutanea migrans 7.9 9.8 4.8 12.9Schistosomiasis 0.6 e 0.6 e

Filariasis (Loiasis) 0.7 e 5.5 e

Gnathostomiasis e e 1.8 e

Protozoa Cutaneous leishmaniasis 2.4 3.3 e 3.8Virus infection 5.7 3.4 7.2 e

Fungal infection 4.0 4.0 6.1 5.6Allergic reaction/urticaria 5.4 5.5 4.8 11.3Phototoxic 0.8 e e e

Chemical, toxic 0.5 e 3.6 e

Injuries 1 e e e

Terrestrial animal bites 0.4 4.3 e >4.7Maritime animals 0.7 e e e

Pruritus of unknown origin e e 9.1 e

Unknown skin disorder 16.3 5.5 e 6.6a including skin abscesses, impetigo, erysipelas, superinfected insect bites, etc.

338 A. Neumayr et al.


Cordylobia anthropophaga [tumbu/mango/putzi fly e Sub-saharan Africa]) can cause infection in humans [76]. Africantumbu flies lay their eggs in faecal-contaminated soil or ondamp clothing hanging to dry. Direct contact activates thehatched larvae to penetrate the skin. American human botflies attach their eggs to the body of captured mosquitos, toreach the human host.

DiagnosisDiagnosis is based on the pathognomonic clinical picture,which is characterized by itchy, slowly enlarging (Ø 1e3 cm)subcutaneous furuncular (boil-like) skin lesions. On closeinspection, a central aperture, permitting the maggot tobreathe and to drain waste products, is visible (Fig. 1).

TreatmentThe maggots can be removed by gently squeezing the boil,assisted by first covering the aperture with a layer ofparaffin oil or petroleum jelly to stop the oxygen supply.While mature larvae are easily extracted by these mea-sures, early lesions are best left to develop for a few days,as immature maggots are reluctant to emerge. If surgicalremoval is applied, rupture of the larvae has to be avoided,as this can lead to a severe inflammatory reaction.

Tungiasis (‘Sand flea’, ‘Jigger’)

Tungiasis is endemic in parts of Africa, Central and SouthAmerica, and India. Tunga penetrans is the smallest of allfleas, measuring around 1 mm in length, and lives in the soilnear pigsties and cattle sheds [77]. The female T. penetransflea burrows into the soft skin regions of suitable hosts(humans and various animals) and remains there for up tofive weeks, during which time it feeds on blood, matures,and produces and releases eggs, before finally dying [76].

DiagnosisThe lesions are commonly located at the feet and the clinicalpicture is pathognomonic: the flea’s round whitish abdomenshines through the overlying dermis around a central aper-ture (Fig. 2). The lesions may be pruritic and painful.

TreatmentExtraction of the parasite after removal of the overlayingskin is straightforward.

Scabies

Scabies, caused by the mite Sarcoptes scabiei, is a cosmo-politan ectoparasitic disease, most commonly seen where

hygiene standards are lowandacquiredbydirect contactwithinfected individuals. Scabies mites (�0.5 mm) burrow amostly invisible S-shaped tunnel of up to 4 mm into the su-perficial layer of the epidermis, where they live and lay eggs[77]. The resulting skin lesions (Fig. 3) are most commonlyfound on the fingers, especially in the web spaces, anteriorwrists, upper limbs, axillary lines, the periumbilical region,external genitalia and buttocks [78]. As a result of a hyper-sensitive reaction to mite proteins, patients typicallycomplain about intense itching, typically worst at night whilein thewarmbed.Scratching itchyareasmay result inbacterialsuperinfection. Diagnosis is frequently delayed, as the lesionsare mistaken for eczema, tinea, or atopic dermatitis [79].

DiagnosisDiagnosis is mainly based on the clinical picture. The lesionsare best identified by a handheld dermatoscope.

TreatmentFor practical reasons, although possibly less effective, oralivermectin has largely replaced the cumbersome topicaltreatment with permethrin, benzyl benzoate, crotamitonor lindane as the first-line treatment [78e80]. Thecurrently recommended treatment regimens are two ap-plications (overnight) of topical permethrin 5%, 1e2 weeksapart or oral ivermectin (200 mg/kg body weight) OD on day1 and after 1e2 weeks [78].

Pitfalls/not to be missed� Non-healing or progressively ulcerating insect bitespersisting over weeks or months should raise suspicionsof cutaneous leishmaniasis (see below)

� Consider Myiasis or Tungiasis in lesions showing a cen-tral orification

� Scabies may present a wide range of clinical pictures� Erythema chronicum migrans in Lyme borreliosis� Rickettsioses (see below)� African/South American trypanosomiasis/sleepingsickness (see below)

Bacterial skin infections

Bacterial infections are the most frequent skin disorder intravellers returning from tropical and subtropical countries.The majority of these cases concern superinfected insectbites, with staphylococci and streptococci being the pri-mary causative pathogens. While most cases of ecthyma,erysipelas and cellulitis are caused by streptococci, impe-tigo, folliculitis and abscesses are rather caused by staph-ylococci [11]. While methicillin-resistant Staphylococcus

Figure 1 Myiasis left: South American myiasis; middle: African myiasis; right: removed maggot.

Diagnoses of common dermatological problems in returning travellers 339


aureus (MRSA) infections were formerly considered to be aproblem restricted to healthcare settings (‘hospital ac-quired’ HA-MRSA), ‘community acquired’ MRSA (CA-MRSA)infections have emerged as a global health problem,affecting international travellers [12,13]. Swedish surveil-lance data show that travellers returning from tropical andsubtropical countries have an up to 59-fold higher risk ofbeing colonised or infected with MRSA compared to trav-ellers returning from countries in Western Europe [14].

In cases of skin and soft-tissue infections, linked to therise in medical tourism (cosmetic injections [‘meso-therapy’] or plastic surgery) as well as tattoos acquiredabroad, atypical mycobacteria (e.g. Mycobacterium che-lonae, Mycobacterium fortuitum, Mycobacterium absces-sus) should be considered [24e27].

Cases of cutaneous diphtheria [15,16], cutaneous bar-tonellosis/veruga peruana [17], cutaneous melioidosis[18,19], cutaneous tuberculosis [20], cutaneous atypicalmycobacteriosis (e.g. buruli ulcer [21]), cutaneous anthrax[22] or leprosy [23] are only exceptional diagnoses inreturning travellers.

DiagnosisDiagnosis is based on the clinical picture and the bacterialculture of wound swabs.

TreatmentThe selection of the antibiotic treatment regimen dependson the causative pathogen and should be guided by sus-ceptibility testing.

Pitfalls/not to be missed

� With CA-MRSA emerging as a skin pathogen in travel-lers, microbiological work-up with culture and

sensitivity testing should be performed, if antibiotictreatment of purulent skin lesions is indicated

� Bacterial superinfection of cutaneous leishmaniasis iscommon and should not distract from performing in-vestigations for leishmania (see below)

� When symptoms (esp. pain and fever) and clinicalfindings of skin and soft-tissue infections are dispro-portional, the rare but rapidly life-threatening differ-ential diagnosis of necrotic fasciitis should be ruled outbefore considering other diagnoses

� In skin lesions unresponsive to empirical antibiotictreatment, cutaneous leishmaniasis, cutaneous tuber-culosis, atypical mycobacteria and leprosy should beconsidered

Skin manifestations in febrile patients

Fever D generalised rash

Causes of fever with generalised rash are copious and theirdiscussion is well beyond the scope of this review. Inreturning travellers, arboviral infections like dengue andchikungunya and rickettsial infections (see below) are theprimary infectious causes to consider (Fig. 4). However,cosmopolitan infections like measles, rubella, scarlet feverand acute HIV- and hepatitis B/C infection, as well as drughypersensitivity reactions and connective tissue diseases,should not be forgotten in returning travellers presentingwith fever and rash.

Fever D insect bite: eschars & chancres

In febrile patients returning from endemic regions, rick-ettsioses are common and, even though rare, the

Figure 2 Tungiasis left: tunga lesion with visible shed eggs; middle: multiple tunga lesions; right: removed flea.

Figure 3 Scabies (courtesy of Dr. Martin Pletscher, Binningen, Switzerland).



potentially life-threatening cases of African sleeping sick-ness/African trypanosomiasis must not be missed. There-fore, in febrile patients returning from endemic regions,eschars and chancres should be actively sought after:

Rickettsioses: ‘eschars’

Rickettsial ‘spotted fevers’ are caused by various Rickettsiaspecies worldwide and transmitted by ticks or mites. Mostpatients present with a mild-to-moderately severe flu-likeillness (fever, headache, malaise, myalgia) typicallyaccompanied by a cutaneous rash (maculopapular, vesicu-lar, or petechial), lymphadenopathy and a characteristicinoculation eschar at the site of the tick bite [28,29]. Es-chars are morphologically characterised by a dry, dark(grey, brown, black) scab resembling a cigarette burn(Fig. 5) and lymphadenopathy of the locoregional lymphaticdrainage is common. Most cases are mild, but severecomplications (e.g. vasculitis, meningoencephalitis, pneu-monia, myocarditis/pericarditis, nephritis, pancreatitis)and multi-organ failure can develop. Only a minority ofinfected travellers can recall a preceding tick bite. Eventhough not all rickettsioses show eschars and the absenceof a rash or eschar does not exclude rickettsial infection,the finding of an eschar is often indicative. Among travel-lers, ‘African tick bite fever’ caused by Rickettsia africae isthe most frequent rickettsiosis [30]. Especially amongtravellers to South Africa, the risk of becoming infectedwith ‘African tick bite fever’ is reportedly 4e5 times higherthan the risk of contracting malaria [31]. Other rick-ettsioses regularly seen in travellers are ‘Mediterraneanspotted fever’, caused by Rickettsia conorii, and ‘Scrubtyphus’ (‘Tsutsugamushi fever’), caused by Orientia tsut-sugamushi [30].

DiagnosisIn the absence of suggestive skin manifestations, thediagnosis of a rickettsial disease is often difficult as themost commonly applied serological tests are not usefulbefore the end of the first week of illness and PCR diag-nostic (from blood) is often not available (Note: Lackingsensitivity and specificity, the traditionally-used Weil-Felix [agglutination] test is no longer recommended). Inthese cases, the fast and universal response of rick-ettsioses to doxycycline treatment can help to

corroborate the tentative diagnosis. If available, immu-nohistochemical detection of rickettsia in a biopsy spec-imen is an option, while the culture of rickettsia is wellbeyond routine diagnostics and restricted to specialisedlaboratories.

TreatmentDoxycycline is the drug of choice for all rickettsioses. Ingeneral, a seven-day course is given or until the patient hasbeen afebrile for at least 48 h.

African trypanosomiasis (sleeping sickness):‘chancres’

African trypanosomiasis, a blood protozoal infection, shouldbe considered in safari tourists, hunters and wildlife re-searchers returning from East Africa and that present with asevere febrile illness, once malaria has been ruled out. Todate, approx. 100 cases of African trypanosomiasis have beenreported in travellers, with five cases published in 2012[32e36]. Five to fifteen days after being bitten by an infectedtsetse fly, a painful circumscribed inoculation chancre maydevelop, characterised by an indurated dusky-red papule2e5 cm in diameter (Fig. 6) [37]. Accompanying regionallymphadenopathy may be present. The systemic dissemina-tion of the parasite that follows leads to the ‘hemolymphaticstage’ of the disease, characterised by fever, headache, fa-tigue, malaise, lymphadenopathy, pruritus, skin rash, andgastrointestinal symptoms. Electrocardiography (ECG) mayshow signs of accompanying myopericarditis, which rarelyleads to cardiac insufficiency but can lead to cardiac ar-rhythmias [38]. If diagnosis and treatment is delayed at thisstage, the parasites may invade the central nervous systemand cause the eponymous ‘meningoencephalitic stage’,characterised by neurological (e.g. headache, drowsiness,tremor, seizures) and psychiatric symptoms.With overlappingsymptoms, neither stage can be clinically differentiated andstaging of the disease has to be based on cerebrospinal fluidanalysis. Neuropsychiatric disorders are only rarely seen intravellers and delayed treatment almost always entails multi-organ failure and death [39,40].

South American trypanosomiasis (Chagas disease), whichis transmitted by bloodsucking triatomine insects, is onlyvery rarely seen in travellers [41]. Analogous to Africantrypanosomiasis, a chancre (‘chagoma’) may be seen in

Figure 4 Arboviral rashes left: maculopapular dengue rash middle: confluent dengue rash (‘white islands’) right: chikungunyarash.



acute Chagas disease. This oedematous lesion developswhere the vector’s infective faeces enters (is rubbed) intothe skin, which is mostly at or around the bite site. If theinsect’s infective faeces is deposited close to or acciden-tally rubbed into the eye, a pathognomonic unilateralpainless periorbital oedema with conjunctivitis (‘Romana’ssign’) can be seen. A generalised rash may also occur inacute Chagas disease.

DiagnosisDiagnosis of trypanosomiasis rests on finding the parasite inbody fluid or tissue by microscopy. All patients diagnosedwith African trypanosomiasis must have their cerebrospinalfluid examined to determine whether there is central ner-vous system involvement, since the choice of treatmentwill depend on the disease stage. Serological tests are alsoavailable.

TreatmentDepending on the causative trypanosoma species and stageof the disease, pentamidine, eflornithine/nifurtimox, sur-amin or melarsoprol are the treatment options for Africantrypanosomiasis. In South American trypanosomiasis,benznidazole and nifurtimox are used.

Pitfalls/not to be missed� Fever þ generalised skin rash:- Arboviral infection (dengue, chikungunya)- Acute HIV-, Hepatitis B-, Hepatitis C-infection

� Fever þ insect bite/suspicious skin lesions:- Rickettsioses

- African/South American trypanosomiasis (sleepingsickness)

Cutaneous leishmaniasis

Leishmaniasis is caused by various Leishmania parasitespecies, which are transmitted through Phlebotomus (OldWorld) and Lutzomyia (New World) sandfly bites. The clin-ical manifestations of leishmaniasis vary widely (visceral-,cutaneous-, mucosal disease) and depend on the causativeLeishmania species.

Cutaneous leishmaniasis (CL) manifests one to severalweeks after the bite of an infected sandfly with a slow,progressively growing and ulcerating, granulomatous pla-que (Fig. 7). Due to the high variability of the clinical pic-ture and the overall low awareness of general practitioners,diagnosis is often delayed. In a few patients, mucosalleishmaniasis (ML), characterised by symptoms related tothe progressive infiltration and ulceration of the mucosalmembranes of nose and pharynx, may develop concomi-tantly or months to years after the appearance of the CLlesion(s). ML is mostly seen in patients infected by NewWorld Leishmania species. As the treatment regimens usedin ML differ considerably from the regimens used in CL, anENT examination (inspection of the oral, pharyngeal andnasal mucosa) should be performed in all CL patients to ruleout concomitant ML.

Imported CL cases among travellers returning fromendemic regions have increased in recent years [42]. Forinternational travellers, the risk of contracting CL dependson the region visited and is estimated to be 20 times higher

Figure 5 African tick bite fever eschars.

Figure 6 African trypanosomiasis chancres (courtesy of Prof. Denis Malvy, Bordeaux, France [left, middle] and Prof. JoachimRichter, Dusseldorf, Germany [right]).



in Central and South America, 10 times higher in Africa, and5 times higher in Asia compared to visiting leishmanialendemic regions of Southern Europe [43]. The incidencerates of New World CL in travellers have been estimated tobe between <1/1,000,000 in Mexico and 1/360 in theAmazonas region of Bolivia [44].

DiagnosisDiagnosis is based on epidemiology, the clinical picture anddirect or indirect detection of the parasite in biopsy ma-terial. Polymerase chain reaction (PCR) has a sensitivity of89e100%, is fast, allows species determination and hasbecome the diagnostic method of choice, likely to replacemicroscopy (sensitivity 9e77%) and culture (sensitivity58e62%) [42,45,46].

TreatmentTreatment modality (local cryo- or heat-therapy vs. localdrug therapy [topical or by injection] vs. systemic drugtherapy) and the selection of an anti-leishmanial drugregimen depends on the causative Leishmania species andlocal drug susceptibility, as well as on the number, size andlocalisation of the lesion(s). Treatment is complex andshould be discussed with a specialist or referral centre.Drugs currently in use include pentavalent antimonials(sodium stibogluconate and meglumine antimoniate),amphothericin B formulations, pentamidine, miltefosine,paromomycin, imiquimod, azoles (ketoconazole, itracona-zole, fluconazole), allopurinol and adjunct pentoxyphillinand TNF-inhibitors.

Various recommendations for treating CL in travellershave been published at national level [46e50] and a Euro-pean expert group (‘LeishMan’) is currently working onharmonising diagnostic and treatment recommendationsfor CL.

Pitfalls/not to be missed� CL should be suspected for skin lesions that:- develop one to several weeks after a suspected insectbite

- progress in size over days/weeks/months- persist over weeks/months- do not or only partially* respond to antibiotic treat-ment (* bacterial superinfection of CL lesions iscommon and should not limit investigations forLeishmania)

- worsen under steroid therapy

� Consider mucosal involvement (ML) in CL patients withNew World leishmaniasis

� PCR diagnosis should be enforced, as species determi-nation is crucial for deciding the optimal treatmentmodality

Cutaneous larva migrans syndrome, creepingeruptions and migratory swellings

Various helminth parasites can cause ‘cutaneous larva mi-grans’ syndrome or ‘creeping eruptions’ (demarcated linearor serpiginous tracks beneath the skin) and ‘migratoryswellings’ (less demarcated as the parasite migratesthrough deeper subcutaneous tissues). While Hookworm-related cutaneous larva migrans is always confined to theskin and shows a characteristic clinical picture, it isimportant to highlight that the clinical differentiation ofother parasites (e.g. Strongyloides, Gnathostoma, Loa loa)is often not possible. Some parasites may migrate, unre-stricted, through body tissues and organs, capable ofcausing severe symptoms and sequelae (e.g. CNS invasion ofGnathostoma or Angiostrongylus).

Hookworm-related cutaneous larva migrans(‘ground itch’, ‘sandworm’)

Hookworm-related cutaneous larva migrans is caused byhookworm larvae from various animals (incl. domestic dogsand cats), with Ancylostoma braziliense being the speciesthat most frequently affects humans [51]. Hookworms livein the intestines of animals and shed their eggs with thehost’s faeces; left on the ground the infectious larval stagedevelops. Human infection results from larvae penetratingthe intact skin on contact with contaminated soil (oftensandy beaches). Humans are accidental dead-end hosts andthe parasite lacks the enzymatic provisions to penetratebeyond the human dermis to complete its lifecycle.Therefore, the parasite migrates superficially, exclusivelywithin the dermis, until the parasite eventually dies spon-taneously (within 2e8 weeks). The track is 1e5 mm wide,extends slowly over days to weeks and classically shows awell demarcated linear or serpiginous pattern (Fig. 8).Sensitisation may lead to the formation of papules andvesicles and the (often) intense pruritus tempts patients toscratch, which may in turn cause bacterial superinfection.

Figure 7 Cutaneous leishmaniasis.



DiagnosisHookworm-related cutaneous larva migrans can almost al-ways be differentiated from other creeping eruptions by itsdistinct clinical picture and without the need for additionaldiagnostic investigations [52].

TreatmentOral ivermectin and albendazole are the two first-line drugsfor Hookworm-related cutaneous larva migrans, as thia-bendazole is no longer marketed. Ivermectin is taken as asingle dose (200 mg per kg body weight; usually 12 mg in anadult), is well tolerated and highly efficacious, with curerates of 94%e100% [53]. After ivermectin intake, symptomsdisappear within one week: Ø 3 (1e20) days for pruritus,and Ø 7 (1e30) days for creeping dermatitis [54]. Treatmentfailure or relapse cases usually respond well to 1e2 addi-tional courses of ivermectin [55]. In the absence of aconsensual optimal treatment regimen, oral albendazole ismostly recommended at a dose of 400 mge800 mg/day(according to weight) for 3e5 days [56]. Cryptherapy isobsolete, as the larva is usually located several centimetresbeyond the visible end of the track and larvae are capableof surviving temperatures as low as �21 �C for more than5 min [53]. Additionally, the procedure is painful and maylead to scarring.

Gnathostomiasis

Gnathostoma is a helminthic parasite of dogs, cats andother (mostly fish-eating) mammals, with a complex life-cycle (involving copepods, freshwater fish and a wide rangeof potential paratenic hosts). Humans are accidental dead-end hosts and usually become infected by ingesting raw orinadequately cooked freshwater fish infected with the 3rdstage larva of the parasite. Gnathostomiasis is endemic tosome regions of Asia and South America where raw fish isconsumed as part of the local food tradition (e.g. ‘sushi’ inAsia and ‘ceviche’ in Central and South America). Withincreasing numbers of international travellers, gnathosto-miasis has become recognised as an emerging parasiticdisease in travellers returning from endemic regions[57e59].

Cutaneous gnathostomiasis may manifest as intermittentmigratory swelling or subcutaneous creeping eruption,varying in size and duration (Fig. 9). The migratory tracksare often wider than 5 mm. The larvae are capable ofmigrating with a speed of up to 1 cm per hour and, if left

untreated, for many (up to 10e12) years through the pa-tient’s body [60]. The symptomatic episodes commonly lastseveral days to weeks and the migratory swellings/creepingeruptions may be accompanied by pruritus, local pain and/or inflammation. In most cases, only one single migratorylesion is present at a time. Although most symptomaticinfections are confined to the skin and subcutaneous tissue,severe manifestations due to visceral migration and inva-sion of the central nervous system may occur [61].

DiagnosisDiagnosis is mostly based on the patient’s history (ingestionof raw or undercooked fish dishes), the clinical picture,blood eosinophilia (which is often, but not always, present)and positive serology (Western blot). If the parasite mi-grates very superficially, skin biopsy can be both diagnosticand therapeutic.

TreatmentOral albendazole and ivermectin are the drugs of choice forgnathosotomiasis. Albendazol has shown an efficacy ofaround 94% and is mostly given in a dosage of 400 mg BID for21 days [62]. Ivermectin is given as single dose (200 mg perkg body weight; usually 12 mg in an adult) for two days andshows similar results as albendazole [63e65]. In case ofpersisting symptoms, re-treatment with either drug orsequential treatment with both drugs has been shown to besuccessful. Normalisation of the blood eosinophil count hasproven to be a useful parameter for monitoring effectivetreatment [63]. Gnathostoma larvae tend to migrate out-ward as a result of albendazole treatment, which some-times facilitates excisional biopsy or removing the parasiteby picking with a needle [66].

Strongyloidiasis (‘Larva currens’)

Strongyloidiasis is a human gastrointestinal helminthicparasite with global distribution. The prevalence is highestin tropical and subtropical regions and is related to poorhygienic conditions. Humans become infected by contactwith soil containing infectious larvae. The larvae penetratethe intact skin and symptoms (e.g. pulmonary [‘Loffler’ssyndrome’], gastrointestinal [abdominal pain, diarrhoea])accrue from the parasite’s migration through the host’sbody, including the skin.

There are two types of skin manifestations in strongy-loidiasis. One is a pruritic linear or serpiginous creepingeruption (mostly around the anus and anywhere on thetrunk), which moves rapidly (2e10 cm per hour) and dis-appears within a few hours, hence the name ‘larva currens’(Fig. 10) [67]. In most cases, the skin eruption has alreadycompletely disappeared when the patient is finally seen bythe physician.

The second form is an urticarial rash in an individual whohas already been sensitised. This urticarial rash occurspredominantly in the buttocks and around the waist, lasts1e2 days and may recur at regular intervals [67].

An important feature of Strongyloides stercoralis is theparasite’s unusual ability to complete its lifecycle withinthe human body, leading to continuing cycles of autoin-fection [68]. This is especially important as chronic or

Figure 8 Hookworm-related cutaneous larva migrans left:the classical clinical picture; right: pronounced inflammatory,bullous form.



persistent infection may remain asymptomatic over de-cades and culminate in severe and potentially life-threatening Strongyloides hyperinfection syndrome oncean individual sustains immunosuppression (e.g. chemo-therapy, organ transplantation, high dose steroid- or anyother immunosuppressive therapy) [68,69].

DiagnosisDiagnosis is based on the clinical picture, blood eosinophilia(which is often, but not always, present), positive serology(ELISA), and special stool investigations. Conventional stoolmicroscopy is insufficient for diagnosing strongyloidiasisbecause the parasite load is generally low and the larvaloutput irregular. Therefore, specific stool concentrationmethods (e.g. ‘Baermann’) or stool culture techniques (e.g.HaradaeMori filter paper culture, nutrient agar plate cul-ture) have to be applied [70]. A novel, promising diagnostictool is stool PCR [71].

TreatmentOral ivermectin is the drug of choice for strongyloidiasis,and is more effective than albendazole (400 g BID for 7days) [72]. A single dose of ivermectin may not completelyclear the infection, thus the recommended regimen is200 mg/kg body weight OD for 2 days [72].

Loa loa/loiasis (‘eye worm’)

Loa loa is a filarial disease (helminthic parasite) trans-mitted by bloodsucking flies in West- and Central Africa.The classical symptom of an adult worm (3e7 cm � 0.4 mm)migrating under the conjunctiva of the eye is rarelyobserved, as the visible passage of the worm only lasts10e15 min [73].

The same applies to the fugitive creeping eruptionscaused by superficially migrating adult worms (Fig. 11). Themost frequent symptoms are recurrent subcutaneous soft-tissue swellings (‘Calabar swellings’) and chronic pruritus.Calabar swellings are painless, non-pitting angio-oedemas,most commonly observed on the hands, wrists and forearms(but possibly anywhere on the body), lasting a few hours toseveral days [73].

DiagnosisDiagnosis is based on the epidemiological history, the clin-ical picture, blood eosinophilia (especially common intravellers), positive serology, and the microscopicaldetection of microfilaria in the patient’s blood. Because loa

loa microfilariae exhibit a diurnal periodicity in the pe-ripheral blood, the optimal time for taking a blood sampleis around noon, when the concentration of microfilariae inblood samples is highest [73]. However, the absence ofmicrofilaremia does not rule out the diagnosis; in a studycomparing the clinical symptoms in endemic and non-endemic populations, microfilaremia was present in 90%and Calabar swellings in only 16% of the endemic patients.Conversely, only 10% of the expatriates were micro-filaremic, while 95% complained of Calabar swellings [74].

TreatmentThe drugs used to treat loa loa are diethylcarbamazin(DEC), ivermectin and albendazole, but only DEC is effec-tive against adult worms and microfilariae (ivermectin andalbendazole are microfilaricidal only). Therefore, a defini-tive cure requires DEC therapy. As 20e60% of the adultworms survive the three-week DEC therapy, repeatedcourses of DEC may be necessary [75]. Because treatment iscomplex and may cause severe complications (potentiallyfatal encephalopathy) in patients with high levels ofmicrofilariae in the blood, therapy should be discussed witha specialist or referral centre.

Other parasites causing creeping eruptions

Other parasites able to cause creeping eruptions includedracunculiasis, dirofilariasis, fasciola, paragonimiasis,sparganosis, lagochilascariasis and migratory myiasis.However, these infections are only rarely seen in travellers.

Pitfalls/not to be missed� Diagnosis of Hookworm-related cutaneous larva migransis unlikely, if:- the lesion spontaneously disappears within 2e3 days

Figure 9 Gnathostomiasis left: migratory swelling (thigh); middle: creeping eruption; right: Gnathostoma 3rd stage larva (3 mmlong).

Figure 10 Strongyloidiasis creeping eruption.



- the track is subcutaneously located- the track is wider than 5 mm- peripheral blood eosinophilia is present- the lesion shows almost no migration

� Treatment of gnathostomiasis is mandatory, as severeand potentially fatal neuroinvasive disease may develop

� Treatment of strongyloidiasis is mandatory, as theinfection may cause severe and potentially life-threatening hyperinfection syndrome in cases ofimmunosuppression

� Migrants from regions with high strongyloidiasis preva-lence rates should be screened for asymptomatic chronicinfection before initiating immunosuppressive therapy(e.g. chemotherapy, high dose steroid- or any otherimmunosuppressive therapy, organ transplantation)

Swimmer’s itch

‘Swimmer’s itch’ (also known as ‘lake itch’, ‘duck itch’,‘cercarial dermatitis’, or ‘Schistosome cercarial derma-titis’) is a short-term, self-limiting immune reaction causedby penetration through the skin of various species of zoo-notic schistosomatida larvae (cercariae of e.g. Tricho-bilharzia spp.), and is observed in patients who havebathed in freshwater. These zoonotic schistosomatidaemust not be confused with the Schistosoma spp. that causeinvasive human schistosomiasis/bilharziosis. Zoonoticschistosomatidae are found worldwide and human infectionis well documented in Central Europe and North America.When the parasites’ larvae penetrate the skin, they causesmild itchy spots on the skin. Within hours, these spotsbecome raised papules, which are intensely itchy. Eachpapule corresponds to the penetration site of a single larva(cercaria). As the parasites die off spontaneously, thesymptoms are self-limiting and rarely last longer than a fewdays.

DiagnosisDiagnosis is based on the clinical picture and on the pa-tient’s history of freshwater contact.

TreatmentDepending on the severity, symptomatic treatment withantihistamines or glucocorticosteroids (topical or oral) maybe considered.

Pitfalls/not to be missedThe history of exposure to freshwater is crucial in the dif-ferential diagnosis, as the skin manifestations may other-wise be considered representative of insect bites.

Allergic skin reactions/urticaria

Urticaria is frequently seen in returning travellers and itscauses are copious, ranging from food allergies and jellyfishcontact to parasitic infections. Depending on the travelhistory, parasitic infections should not be excluded as, insome cases, acute or chronic urticaria may be the only in-dicator of infection (e.g. strongyloidiasis, gnathostomiasis,toxocariasis, filariasis, fascioliasis, giardiasis, amoebiasis,Blastocystis hominis) [81]. Other frequently seen travel-related dermal hypersensitivity reactions include contactdermatitis (e.g. poison ivy), phytophotodermatitis (e.g.lime juice), drug induced phototoxic reactions (e.g. bydoxycycline, which is used for malaria chemoprophylaxis)and other drug eruptions (Fig. 12).

DiagnosisDiagnosis is based on the patient’s history, the clinicalpicture and (when indicated) laboratory investigations torule out an underlying parasitic infection.

TreatmentDepending on the severity, symptomatic treatment withantihistamines or glucocorticosteroids (topical or oral) maybe considered. If an underlying parasitic infection has beenidentified, specific treatment is indicated.

Not to be missed/pitfallsIn patients with uriticaria (especially in chronic cases) ruleout a potential underlying parasitosis by stool examination(for intestinal parasites) and serological test (for tissueinvasive parasites), respectively.

Fungal skin infections

Although not confined to travelling, dermatomycoses arefrequently seen in travel clinics but are almost exclusivelylimited to the superficial tinea (ringworm) and pityriasisversicolor infections [1,2]. Tinea pedis (athlete’s foot) is

Figure 11 Loa loa left: Loa loa creeping eruptions in a migrant; right: conjunctival passage of the adult worm.



probably the most common dermatomycosis in travellers,but is rarely seen in travel clinics, as the clinical manifes-tation is well known and most patients will either consulttheir general physician or perform self-treatment with overthe counter products. Dermatomycoses caused by otherfungi endemic to the tropics and subtropics or cutaneousmanifestations of endemic mycoses (e.g. histoplasmosis)are only exceptionally reported in travellers [82].

DiagnosisDiagnosis is based on the clinical picture and on microscopyand culture of skin scrapings.

TreatmentDepending on the severity and causative fungus, topical orsystemic antimycotic drugs are applied.

Pitfalls/not to be missedThe diagnosis of fungal skin infections is mostly straight-forward. However, some lesions may mimic other disorders,e.g. bacterial skin infections or cutaneous leishmaniasis.

Summary

Dermatological disorders in travellers returning from tropicaland subtropical destinations are the daily business of travelclinics. Differential diagnoses largely depend on the pa-tient’s travel history, the geographic background of thejourney (local endemicity of certain diseases) and the clin-ical picture, with a focus on the evolution of skin manifes-tation(s). When evaluating dermatological pathologies intravellers, the main objective is to rule out potentially se-vere or even life-threatening diseases. In this regard, thepresence or development of extra-cutaneous systemicsymptoms (e.g. fever, generalised lymphadenopathy) maybe suggestive (e.g. trypanosomiasis, rickettsiose, etc.). Ifthe pathologies are restricted to the skin, the differentialdiagnoses are best narrowed down by evaluating the pro-gression/evolution of the skin manifestation(s) over time(e.g. cutaneous leishmaniasis, insect bites, etc.).

Conflict of interest

None.

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not to be missed! differential diagnoses of common

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