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

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Not to be missed! Differential diagnoses

of common dermatological problems in
returning travellers
Andreas Neumayr a,b, Christoph Hatz a,b, Johannes Blum a,b,*

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

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

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

Introduction dermatological diagnoses in travellers is broad and domi-

The three most common reasons for returning travellers to
seek medical help are systemic febrile illnesses, acute or
chronic diarrhoea and dermatological disorders [1]. Various
studies have recently reviewed the spectrum and the fre-
quencies of travel-related dermatological disorders
observed in travel clinics [1e4]. The spectrum of
* Corresponding author. Swiss Tropical and Public Health Insti-
tute, Socinstrasse. 57, 4051 Basel, Switzerland. Tel.: þ41 61 284
8111; fax: þ41 61 284 8101.
E-mail address: johannes.blum@unibas.ch (J. Blum).
nated by insect bites, bacterial skin infections, creeping
eruptions and allergic skin reactions (Table 1).
This article addresses the most frequent dermatological
disorders and their differential diagnoses in returning
travellers, and highlights the dermatological clues to severe
and potentially life-threatening diseases, which should not
be missed: ‘When you hear hoofbeats, think horses, not
zebras’. but make sure not to miss out on zebras.
(Those dermatological disorders that are not confined to
travelling d e.g. herpes zoster, pityriasis rosea, syphilis
and sun- and heat-related skin pathologies d also
frequently occur in travellers, but are beyond the scope of
this review).

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

338 A. Neumayr et al.

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

Setting Herbinger 2011 Lederman 2008 Ansart 2007 Freedman 2006
Travel clinic in GeoSentinel Travel clinic in GeoSentinel
Munich, Germany surveillance network Paris, France surveillance network
(1997e2006) (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 18.7
Scabies 2.3 e 10 2.2
Myiasis 0.8 e 7.2 3.5
Tungiasis 0.6 e 4 e
Tick bites 0.6 e e e
Bacteria Bacterial skin infectionsa 21.6 14.5 21.2 12.4
Rickettsial disease 1.3 e 0.6 e
Leprosy e e 2.4 e
Helminths Larva cutanea migrans 7.9 9.8 4.8 12.9
Schistosomiasis 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 3.8
Virus infection 5.7 3.4 7.2 e
Fungal infection 4.0 4.0 6.1 5.6
Allergic reaction/urticaria 5.4 5.5 4.8 11.3
Phototoxic 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 >4.7
Maritime animals 0.7 e e e
Pruritus of unknown origin e e 9.1 e
Unknown skin disorder 16.3 5.5 e 6.6
a
including skin abscesses, impetigo, erysipelas, superinfected insect bites, etc.

Methods picture may include ecchymoses or vesicles and severely

This review is based on the most frequently reported skin
pathologies in travellers (see Table 1), on the relevant
literature and on personal experiences from daily practice
at our travel clinic.
Ectoparasites
Insect bites
allergic patients may develop haemorrhagic bullae, necroses
or ulcers that heal with residual scarring [7]. In a few cases,
insect bites may cause systemic symptoms like generalised
urticaria, angioedema, anaphylaxis or the rare ‘Skeeter
syndrome’ (a large local inflammatory reaction accompa-
nied by fever, which can be differentiated from cellulitis by
its peracute onset within hours) [8e10]. Sequelae of insect
bites include bacterial superinfection, post-inflammatory
changes in pigmentation, prurigo simplex-like lesions, pru-
rigo nodularis and atrophic scarring [5,7].

Diagnosis
Consultations for insect bites are frequent and the clinical
Diagnosis is based on the patient’s history and clinical
presentations vary widely. One insect may cause different
picture.
types of skin lesions and each type of skin lesion may be
caused by different kinds of insects, thus it is difficult and
Treatment
often impossible to infer from a skin lesion the causative
Insect bites are primarily treated with topical steroids and
insect. However, in some cases, the clinical aspect and the
oral antihistamines. Patients suffering from agonising
distribution of the skin lesions may be suggestive: for
nocturnal pruritus may benefit from the use of older,
example, pruritic lesions caused by fleas and bed bugs are
sedative antihistamines. In severe, disseminated or re-
more frequently papular and typically clustered or linearly
fractory cases, the oral intake of steroids may be required.
grouped, which is rarely seen with mosquito bites [5e7]. The
typical evolution of insect bites is the initial formation of
wheals and flares (with a peak within 20 min), a delayed Myiasis
reaction manifesting as itchy indurated erythematous pap-
ules (with a peak at 24e36 h) and the gradual resolution of The maggots/larvae of various flies (mostly Dermatobia
the lesions within days to weeks [8]. However, the clinical hominis [human bot fly e Central and South America] and
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Diagnoses of common dermatological problems in returning travellers
Cordylobia anthropophaga [tumbu/mango/putzi fly e Sub-
saharan Africa]) can cause infection in humans [76]. African
tumbu flies lay their eggs in faecal-contaminated soil or on
damp clothing hanging to dry. Direct contact activates the
hatched larvae to penetrate the skin. American human bot
flies attach their eggs to the body of captured mosquitos, to
reach the human host.
Diagnosis
Diagnosis is based on the pathognomonic clinical picture,
which is characterized by itchy, slowly enlarging (Ø 1e3 cm)
subcutaneous furuncular (boil-like) skin lesions. On close
inspection, a central aperture, permitting the maggot to
breathe and to drain waste products, is visible (Fig. 1).
Treatment
The maggots can be removed by gently squeezing the boil,
assisted by first covering the aperture with a layer of
paraffin 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 surgical
removal 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 South
America, and India. Tunga penetrans is the smallest of all
fleas, measuring around 1 mm in length, and lives in the soil
near pigsties and cattle sheds [77]. The female T. penetrans
flea burrows into the soft skin regions of suitable hosts
(humans and various animals) and remains there for up to
five weeks, during which time it feeds on blood, matures,
and produces and releases eggs, before finally dying [76].
Diagnosis
The lesions are commonly located at the feet and the clinical
picture is pathognomonic: the flea’s round whitish abdomen
shines through the overlying dermis around a central aper-
ture (Fig. 2). The lesions may be pruritic and painful.
Treatment
Extraction of the parasite after removal of the overlaying
skin is straightforward.
Scabies
Scabies, caused by the mite Sarcoptes scabiei, is a cosmo-
politan ectoparasitic disease, most commonly seen where
Figure 1 Myiasis left: South American myiasis; middle: African myiasis; right: removed maggot.
339
hygiene standards are low and acquired by direct contact with
infected individuals. Scabies mites (0.5 mm) burrow a
mostly 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 commonly
found on the fingers, especially in the web spaces, anterior
wrists, upper limbs, axillary lines, the periumbilical region,
external genitalia and buttocks [78]. As a result of a hyper-
sensitive reaction to mite proteins, patients typically
complain about intense itching, typically worst at night while
in the warm bed. Scratching itchy areas may result in bacterial
superinfection. Diagnosis is frequently delayed, as the lesions
are mistaken for eczema, tinea, or atopic dermatitis [79].
Diagnosis
Diagnosis is mainly based on the clinical picture. The lesions
are best identified by a handheld dermatoscope.
Treatment
For practical reasons, although possibly less effective, oral
ivermectin has largely replaced the cumbersome topical
treatment with permethrin, benzyl benzoate, crotamiton
or lindane as the first-line treatment [78e80]. The
currently recommended treatment regimens are two ap-
plications (overnight) of topical permethrin 5%, 1e2 weeks
apart or oral ivermectin (200 mg/kg body weight) OD on day
1 and after 1e2 weeks [78].
Pitfalls/not to be missed
 Non-healing or progressively ulcerating insect bites
persisting over weeks or months should raise suspicions
of 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/sleeping
sickness (see below)
Bacterial skin infections
Bacterial infections are the most frequent skin disorder in
travellers returning from tropical and subtropical countries.
The majority of these cases concern superinfected insect
bites, 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
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340
Figure 2 Tungiasis left: tunga lesion with visible shed eggs; middle: multiple tunga lesions; right: removed flea.
aureus (MRSA) infections were formerly considered to be a
problem 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 and
subtropical countries have an up to 59-fold higher risk of
being 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 the
rise in medical tourism (cosmetic injections [‘meso-
therapy’] or plastic surgery) as well as tattoos acquired
abroad, 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 atypical
mycobacteriosis (e.g. buruli ulcer [21]), cutaneous anthrax
[22] or leprosy [23] are only exceptional diagnoses in
returning travellers.
Diagnosis
Diagnosis is based on the clinical picture and the bacterial
culture of wound swabs.
Treatment
The selection of the antibiotic treatment regimen depends
on 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
Figure 3 Scabies (courtesy of Dr. Martin Pletscher, Binningen, Switzerland).
A. Neumayr et al.
sensitivity testing should be performed, if antibiotic
treatment of purulent skin lesions is indicated
 Bacterial superinfection of cutaneous leishmaniasis is
common and should not distract from performing in-
vestigations for leishmania (see below)
 When symptoms (esp. pain and fever) and clinical
findings of skin and soft-tissue infections are dispro-
portional, the rare but rapidly life-threatening differ-
ential diagnosis of necrotic fasciitis should be ruled out
before considering other diagnoses
 In skin lesions unresponsive to empirical antibiotic
treatment, cutaneous leishmaniasis, cutaneous tuber-
culosis, atypical mycobacteria and leprosy should be
considered
Skin manifestations in febrile patients
Fever D generalised rash
Causes of fever with generalised rash are copious and their
discussion is well beyond the scope of this review. In
returning travellers, arboviral infections like dengue and
chikungunya and rickettsial infections (see below) are the
primary infectious causes to consider (Fig. 4). However,
cosmopolitan infections like measles, rubella, scarlet fever
and acute HIV- and hepatitis B/C infection, as well as drug
hypersensitivity reactions and connective tissue diseases,
should not be forgotten in returning travellers presenting
with 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
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Diagnoses of common dermatological problems in returning travellers
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 Rickettsia
species worldwide and transmitted by ticks or mites. Most
patients present with a mild-to-moderately severe flu-like
illness (fever, headache, malaise, myalgia) typically
accompanied by a cutaneous rash (maculopapular, vesicu-
lar, or petechial), lymphadenopathy and a characteristic
inoculation 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 lymphatic
drainage is common. Most cases are mild, but severe
complications (e.g. vasculitis, meningoencephalitis, pneu-
monia, myocarditis/pericarditis, nephritis, pancreatitis)
and multi-organ failure can develop. Only a minority of
infected travellers can recall a preceding tick bite. Even
though not all rickettsioses show eschars and the absence
of 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 is
the most frequent rickettsiosis [30]. Especially among
travellers to South Africa, the risk of becoming infected
with ‘African tick bite fever’ is reportedly 4e5 times higher
than the risk of contracting malaria [31]. Other rick-
ettsioses regularly seen in travellers are ‘Mediterranean
spotted fever’, caused by Rickettsia conorii, and ‘Scrub
typhus’ (‘Tsutsugamushi fever’), caused by Orientia tsut-
sugamushi [30].
Diagnosis
In the absence of suggestive skin manifestations, the
diagnosis of a rickettsial disease is often difficult as the
most commonly applied serological tests are not useful
before the end of the first week of illness and PCR diag-
nostic (from blood) is often not available (Note: Lacking
sensitivity and specificity, the traditionally-used Weil-
Felix [agglutination] test is no longer recommended). In
these cases, the fast and universal response of rick-
ettsioses to doxycycline treatment can help to
Figure 4 Arboviral rashes left: maculopapular dengue rash middle: confluent dengue rash (‘white islands’) right: chikungunya
rash.
341
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 well
beyond routine diagnostics and restricted to specialised
laboratories.
Treatment
Doxycycline is the drug of choice for all rickettsioses. In
general, a seven-day course is given or until the patient has
been afebrile for at least 48 h.
African trypanosomiasis (sleeping sickness):
‘chancres’
African trypanosomiasis, a blood protozoal infection, should
be considered in safari tourists, hunters and wildlife re-
searchers returning from East Africa and that present with a
severe febrile illness, once malaria has been ruled out. To
date, approx. 100 cases of African trypanosomiasis have been
reported in travellers, with five cases published in 2012
[32e36]. Five to fifteen days after being bitten by an infected
tsetse fly, a painful circumscribed inoculation chancre may
develop, characterised by an indurated dusky-red papule
2e5 cm in diameter (Fig. 6) [37]. Accompanying regional
lymphadenopathy may be present. The systemic dissemina-
tion of the parasite that follows leads to the ‘hemolymphatic
stage’ of the disease, characterised by fever, headache, fa-
tigue, malaise, lymphadenopathy, pruritus, skin rash, and
gastrointestinal symptoms. Electrocardiography (ECG) may
show signs of accompanying myopericarditis, which rarely
leads to cardiac insufficiency but can lead to cardiac ar-
rhythmias [38]. If diagnosis and treatment is delayed at this
stage, the parasites may invade the central nervous system
and cause the eponymous ‘meningoencephalitic stage’,
characterised by neurological (e.g. headache, drowsiness,
tremor, seizures) and psychiatric symptoms. With overlapping
symptoms, neither stage can be clinically differentiated and
staging of the disease has to be based on cerebrospinal fluid
analysis. Neuropsychiatric disorders are only rarely seen in
travellers and delayed treatment almost always entails multi-
organ failure and death [39,40].
South American trypanosomiasis (Chagas disease), which
is transmitted by bloodsucking triatomine insects, is only
very rarely seen in travellers [41]. Analogous to African
trypanosomiasis, a chancre (‘chagoma’) may be seen in
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342
Figure 5 African tick bite fever eschars.
acute Chagas disease. This oedematous lesion develops
where the vector’s infective faeces enters (is rubbed) into
the skin, which is mostly at or around the bite site. If the
insect’s infective faeces is deposited close to or acciden-
tally rubbed into the eye, a pathognomonic unilateral
painless periorbital oedema with conjunctivitis (‘Romaña’s
sign’) can be seen. A generalised rash may also occur in
acute Chagas disease.
Diagnosis
Diagnosis of trypanosomiasis rests on finding the parasite in
body fluid or tissue by microscopy. All patients diagnosed
with African trypanosomiasis must have their cerebrospinal
fluid examined to determine whether there is central ner-
vous system involvement, since the choice of treatment
will depend on the disease stage. Serological tests are also
available.
Treatment
Depending on the causative trypanosoma species and stage
of the disease, pentamidine, eflornithine/nifurtimox, sur-
amin or melarsoprol are the treatment options for African
trypanosomiasis. 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
Figure 6 African trypanosomiasis chancres (courtesy of Prof. Denis Malvy, Bordeaux, France [left, middle] and Prof. Joachim
Richter, Düsseldorf, Germany [right]).
A. Neumayr et al.
- African/South American trypanosomiasis (sleeping
sickness)
Cutaneous leishmaniasis
Leishmaniasis is caused by various Leishmania parasite
species, which are transmitted through Phlebotomus (Old
World) and Lutzomyia (New World) sandfly bites. The clin-
ical manifestations of leishmaniasis vary widely (visceral-,
cutaneous-, mucosal disease) and depend on the causative
Leishmania species.
Cutaneous leishmaniasis (CL) manifests one to several
weeks 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, mucosal
leishmaniasis (ML), characterised by symptoms related to
the progressive infiltration and ulceration of the mucosal
membranes of nose and pharynx, may develop concomi-
tantly or months to years after the appearance of the CL
lesion(s). ML is mostly seen in patients infected by New
World Leishmania species. As the treatment regimens used
in ML differ considerably from the regimens used in CL, an
ENT examination (inspection of the oral, pharyngeal and
nasal mucosa) should be performed in all CL patients to rule
out concomitant ML.
Imported CL cases among travellers returning from
endemic regions have increased in recent years [42]. For
international travellers, the risk of contracting CL depends
on the region visited and is estimated to be 20 times higher
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Diagnoses of common dermatological problems in returning travellers
in Central and South America, 10 times higher in Africa, and
5 times higher in Asia compared to visiting leishmanial
endemic regions of Southern Europe [43]. The incidence
rates of New World CL in travellers have been estimated to
be between <1/1,000,000 in Mexico and 1/360 in the
Amazonas region of Bolivia [44].
Diagnosis
Diagnosis is based on epidemiology, the clinical picture and
direct or indirect detection of the parasite in biopsy ma-
terial. Polymerase chain reaction (PCR) has a sensitivity of
89e100%, is fast, allows species determination and has
become the diagnostic method of choice, likely to replace
microscopy (sensitivity 9e77%) and culture (sensitivity
58e62%) [42,45,46].
Treatment
Treatment modality (local cryo- or heat-therapy vs. local
drug therapy [topical or by injection] vs. systemic drug
therapy) and the selection of an anti-leishmanial drug
regimen depends on the causative Leishmania species and
local drug susceptibility, as well as on the number, size and
localisation of the lesion(s). Treatment is complex and
should 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 pentoxyphillin
and TNF-inhibitors.
Various recommendations for treating CL in travellers
have been published at national level [46e50] and a Euro-
pean expert group (‘LeishMan’) is currently working on
harmonising diagnostic and treatment recommendations
for CL.
Pitfalls/not to be missed
 CL should be suspected for skin lesions that:
- develop one to several weeks after a suspected insect
bite
- 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 is
common and should not limit investigations for
Leishmania)
- worsen under steroid therapy
Figure 7 Cutaneous leishmaniasis.
343
 Consider mucosal involvement (ML) in CL patients with
New World leishmaniasis
 PCR diagnosis should be enforced, as species determi-
nation is crucial for deciding the optimal treatment
modality
Cutaneous larva migrans syndrome, creeping
eruptions and migratory swellings
Various helminth parasites can cause ‘cutaneous larva mi-
grans’ syndrome or ‘creeping eruptions’ (demarcated linear
or serpiginous tracks beneath the skin) and ‘migratory
swellings’ (less demarcated as the parasite migrates
through deeper subcutaneous tissues). While Hookworm-
related cutaneous larva migrans is always confined to the
skin and shows a characteristic clinical picture, it is
important to highlight that the clinical differentiation of
other parasites (e.g. Strongyloides, Gnathostoma, Loa loa)
is often not possible. Some parasites may migrate, unre-
stricted, through body tissues and organs, capable of
causing severe symptoms and sequelae (e.g. CNS invasion of
Gnathostoma or Angiostrongylus).
Hookworm-related cutaneous larva migrans
(‘ground itch’, ‘sandworm’)
Hookworm-related cutaneous larva migrans is caused by
hookworm larvae from various animals (incl. domestic dogs
and cats), with Ancylostoma braziliense being the species
that most frequently affects humans [51]. Hookworms live
in the intestines of animals and shed their eggs with the
host’s faeces; left on the ground the infectious larval stage
develops. Human infection results from larvae penetrating
the intact skin on contact with contaminated soil (often
sandy beaches). Humans are accidental dead-end hosts and
the parasite lacks the enzymatic provisions to penetrate
beyond the human dermis to complete its lifecycle.
Therefore, the parasite migrates superficially, exclusively
within 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 a
well demarcated linear or serpiginous pattern (Fig. 8).
Sensitisation may lead to the formation of papules and
vesicles and the (often) intense pruritus tempts patients to
scratch, which may in turn cause bacterial superinfection.
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344
Diagnosis
Hookworm-related cutaneous larva migrans can almost al-
ways be differentiated from other creeping eruptions by its
distinct clinical picture and without the need for additional
diagnostic investigations [52].
Treatment
Oral ivermectin and albendazole are the two first-line drugs
for Hookworm-related cutaneous larva migrans, as thia-
bendazole is no longer marketed. Ivermectin is taken as a
single dose (200 mg per kg body weight; usually 12 mg in an
adult), is well tolerated and highly efficacious, with cure
rates of 94%e100% [53]. After ivermectin intake, symptoms
disappear within one week: Ø 3 (1e20) days for pruritus,
and Ø 7 (1e30) days for creeping dermatitis [54]. Treatment
failure or relapse cases usually respond well to 1e2 addi-
tional courses of ivermectin [55]. In the absence of a
consensual optimal treatment regimen, oral albendazole is
mostly recommended at a dose of 400 mge800 mg/day
(according to weight) for 3e5 days [56]. Cryptherapy is
obsolete, as the larva is usually located several centimetres
beyond the visible end of the track and larvae are capable
of surviving temperatures as low as 21  C for more than
5 min [53]. Additionally, the procedure is painful and may
lead to scarring.
Gnathostomiasis
Gnathostoma is a helminthic parasite of dogs, cats and
other (mostly fish-eating) mammals, with a complex life-
cycle (involving copepods, freshwater fish and a wide range
of potential paratenic hosts). Humans are accidental dead-
end hosts and usually become infected by ingesting raw or
inadequately cooked freshwater fish infected with the 3rd
stage larva of the parasite. Gnathostomiasis is endemic to
some regions of Asia and South America where raw fish is
consumed as part of the local food tradition (e.g. ‘sushi’ in
Asia and ‘ceviche’ in Central and South America). With
increasing numbers of international travellers, gnathosto-
miasis has become recognised as an emerging parasitic
disease in travellers returning from endemic regions
[57e59].
Cutaneous gnathostomiasis may manifest as intermittent
migratory swelling or subcutaneous creeping eruption,
varying in size and duration (Fig. 9). The migratory tracks
are often wider than 5 mm. The larvae are capable of
migrating with a speed of up to 1 cm per hour and, if left
Figure 8 Hookworm-related cutaneous larva migrans left:
the classical clinical picture; right: pronounced inflammatory,
bullous form.
A. Neumayr et al.
untreated, for many (up to 10e12) years through the pa-
tient’s body [60]. The symptomatic episodes commonly last
several days to weeks and the migratory swellings/creeping
eruptions may be accompanied by pruritus, local pain and/
or inflammation. In most cases, only one single migratory
lesion is present at a time. Although most symptomatic
infections 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].
Diagnosis
Diagnosis is mostly based on the patient’s history (ingestion
of 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 diagnostic
and therapeutic.
Treatment
Oral albendazole and ivermectin are the drugs of choice for
gnathosotomiasis. Albendazol has shown an efficacy of
around 94% and is mostly given in a dosage of 400 mg BID for
21 days [62]. Ivermectin is given as single dose (200 mg per
kg body weight; usually 12 mg in an adult) for two days and
shows similar results as albendazole [63e65]. In case of
persisting symptoms, re-treatment with either drug or
sequential treatment with both drugs has been shown to be
successful. Normalisation of the blood eosinophil count has
proven to be a useful parameter for monitoring effective
treatment [63]. Gnathostoma larvae tend to migrate out-
ward as a result of albendazole treatment, which some-
times facilitates excisional biopsy or removing the parasite
by picking with a needle [66].
Strongyloidiasis (‘Larva currens’)
Strongyloidiasis is a human gastrointestinal helminthic
parasite with global distribution. The prevalence is highest
in tropical and subtropical regions and is related to poor
hygienic conditions. Humans become infected by contact
with soil containing infectious larvae. The larvae penetrate
the intact skin and symptoms (e.g. pulmonary [‘Löffler’s
syndrome’], gastrointestinal [abdominal pain, diarrhoea])
accrue from the parasite’s migration through the host’s
body, including the skin.
There are two types of skin manifestations in strongy-
loidiasis. One is a pruritic linear or serpiginous creeping
eruption (mostly around the anus and anywhere on the
trunk), 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 already
completely disappeared when the patient is finally seen by
the physician.
The second form is an urticarial rash in an individual who
has already been sensitised. This urticarial rash occurs
predominantly in the buttocks and around the waist, lasts
1e2 days and may recur at regular intervals [67].
An important feature of Strongyloides stercoralis is the
parasite’s unusual ability to complete its lifecycle within
the human body, leading to continuing cycles of autoin-
fection [68]. This is especially important as chronic or
 Author's personal copy
Diagnoses of common dermatological problems in returning travellers
Figure 9 Gnathostomiasis left: migratory swelling (thigh); middle: creeping eruption; right: Gnathostoma 3rd stage larva (3 mm
long).
persistent infection may remain asymptomatic over de-
cades and culminate in severe and potentially life-
threatening Strongyloides hyperinfection syndrome once
an individual sustains immunosuppression (e.g. chemo-
therapy, organ transplantation, high dose steroid- or any
other immunosuppressive therapy) [68,69].
Diagnosis
Diagnosis is based on the clinical picture, blood eosinophilia
(which is often, but not always, present), positive serology
(ELISA), and special stool investigations. Conventional stool
microscopy is insufficient for diagnosing strongyloidiasis
because the parasite load is generally low and the larval
output irregular. Therefore, specific stool concentration
methods (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 diagnostic
tool is stool PCR [71].
Treatment
Oral ivermectin is the drug of choice for strongyloidiasis,
and is more effective than albendazole (400 g BID for 7
days) [72]. A single dose of ivermectin may not completely
clear the infection, thus the recommended regimen is
200 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 rarely
observed, as the visible passage of the worm only lasts
10e15 min [73].
The same applies to the fugitive creeping eruptions
caused by superficially migrating adult worms (Fig. 11). The
most 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 to
several days [73].
Diagnosis
Diagnosis is based on the epidemiological history, the clin-
ical picture, blood eosinophilia (especially common in
travellers), positive serology, and the microscopical
detection of microfilaria in the patient’s blood. Because loa
345
loa microfilariae exhibit a diurnal periodicity in the pe-
ripheral blood, the optimal time for taking a blood sample
is around noon, when the concentration of microfilariae in
blood samples is highest [73]. However, the absence of
microfilaremia does not rule out the diagnosis; in a study
comparing 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].
Treatment
The drugs used to treat loa loa are diethylcarbamazin
(DEC), ivermectin and albendazole, but only DEC is effec-
tive against adult worms and microfilariae (ivermectin and
albendazole are microfilaricidal only). Therefore, a defini-
tive cure requires DEC therapy. As 20e60% of the adult
worms survive the three-week DEC therapy, repeated
courses of DEC may be necessary [75]. Because treatment is
complex and may cause severe complications (potentially
fatal encephalopathy) in patients with high levels of
microfilariae in the blood, therapy should be discussed with
a specialist or referral centre.
Other parasites causing creeping eruptions
Other parasites able to cause creeping eruptions include
dracunculiasis, 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 migrans
is unlikely, if:
- the lesion spontaneously disappears within 2e3 days
Figure 10 Strongyloidiasis creeping eruption.
 Author's personal copy
346
- 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 severe
and potentially fatal neuroinvasive disease may develop
 Treatment of strongyloidiasis is mandatory, as the
infection may cause severe and potentially life-
threatening hyperinfection syndrome in cases of
immunosuppression
 Migrants from regions with high strongyloidiasis preva-
lence rates should be screened for asymptomatic chronic
infection before initiating immunosuppressive therapy
(e.g. chemotherapy, high dose steroid- or any other
immunosuppressive 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 caused
by 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 have
bathed in freshwater. These zoonotic schistosomatidae
must not be confused with the Schistosoma spp. that cause
invasive human schistosomiasis/bilharziosis. Zoonotic
schistosomatidae are found worldwide and human infection
is well documented in Central Europe and North America.
When the parasites’ larvae penetrate the skin, they causes
mild itchy spots on the skin. Within hours, these spots
become raised papules, which are intensely itchy. Each
papule corresponds to the penetration site of a single larva
(cercaria). As the parasites die off spontaneously, the
symptoms are self-limiting and rarely last longer than a few
days.
Diagnosis
Diagnosis is based on the clinical picture and on the pa-
tient’s history of freshwater contact.
Treatment
Depending on the severity, symptomatic treatment with
antihistamines or glucocorticosteroids (topical or oral) may
be considered.
Figure 11 Loa loa left: Loa loa creeping eruptions in a migrant; right: conjunctival passage of the adult worm.
A. Neumayr et al.
Pitfalls/not to be missed
The 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 its
causes are copious, ranging from food allergies and jellyfish
contact to parasitic infections. Depending on the travel
history, parasitic infections should not be excluded as, in
some 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 contact
dermatitis (e.g. poison ivy), phytophotodermatitis (e.g.
lime juice), drug induced phototoxic reactions (e.g. by
doxycycline, which is used for malaria chemoprophylaxis)
and other drug eruptions (Fig. 12).
Diagnosis
Diagnosis is based on the patient’s history, the clinical
picture and (when indicated) laboratory investigations to
rule out an underlying parasitic infection.
Treatment
Depending on the severity, symptomatic treatment with
antihistamines or glucocorticosteroids (topical or oral) may
be considered. If an underlying parasitic infection has been
identified, specific treatment is indicated.
Not to be missed/pitfalls
In patients with uriticaria (especially in chronic cases) rule
out a potential underlying parasitosis by stool examination
(for intestinal parasites) and serological test (for tissue
invasive parasites), respectively.
Fungal skin infections
Although not confined to travelling, dermatomycoses are
frequently seen in travel clinics but are almost exclusively
limited to the superficial tinea (ringworm) and pityriasis
versicolor infections [1,2]. Tinea pedis (athlete’s foot) is
 Author's personal copy
Diagnoses of common dermatological problems in returning travellers
Figure 12 Non-infectious skin disorders left: phytotoxic reaction to lime juice; middle: drug rash to atovaquone-proguanil
[Malarone] (malaria chemoprophylaxis); right: phototoxic reaction to doxycycline (malaria chemoprophylaxis).
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 consult [2]
their general physician or perform self-treatment with over
the counter products. Dermatomycoses caused by other
fungi endemic to the tropics and subtropics or cutaneous [3]
manifestations of endemic mycoses (e.g. histoplasmosis)
are only exceptionally reported in travellers [82].
Diagnosis [4]
Diagnosis is based on the clinical picture and on microscopy
and culture of skin scrapings.
Treatment [5]
Depending on the severity and causative fungus, topical or
systemic antimycotic drugs are applied.
Pitfalls/not to be missed [6]
The diagnosis of fungal skin infections is mostly straight-
forward. However, some lesions may mimic other disorders, [7]
e.g. bacterial skin infections or cutaneous leishmaniasis.
Summary [8]
Dermatological disorders in travellers returning from tropical [9]
and subtropical destinations are the daily business of travel
clinics. Differential diagnoses largely depend on the pa-
tient’s travel history, the geographic background of the
journey (local endemicity of certain diseases) and the clin- [10]
ical picture, with a focus on the evolution of skin manifes-
tation(s). When evaluating dermatological pathologies in [11]
travellers, the main objective is to rule out potentially se-
vere or even life-threatening diseases. In this regard, the
[12]
presence or development of extra-cutaneous systemic
symptoms (e.g. fever, generalised lymphadenopathy) may
be suggestive (e.g. trypanosomiasis, rickettsiose, etc.). If [13]
the pathologies are restricted to the skin, the differential
diagnoses are best narrowed down by evaluating the pro-
gression/evolution of the skin manifestation(s) over time
(e.g. cutaneous leishmaniasis, insect bites, etc.).
[14]
Conflict of interest
None.
[15]
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