ARTICLE
Residents of Western Europe travel increasingly to tropical and sub-tropical
countries for holidays and work. Most of them follow the beaten path,
but an increasing number seeks a more adventurous vacation or actually
work in low-income copuntries.
During their travel and stay they come in contact with micro-organisms,
insects and parasites which are unfamiliar to their immune system and
against which they have not developed proper protection. Notorious are
malaria, parasitic infections and hepatitis. The patients usually consult
specialized physicians and parasitologists for these diseases. However,
the more frequently occurring skin problems are less known. Although most
of these problems are minor and disappear within a short period of time
without causing too much trouble, some last longer and cause discomfort,
thus bringing the patient to seek expert advice.
Most dermatologists are aware of the effect of tropical conditions on
specific skin diseases like psoriasis and atopic eczema. They know that
certain antimalarials may evoke psoriasis and that tropical heat with
accompanying sweating may exacerbate atopic dermatitis. They have expertise
in sun-induced dermatoses like sunburn, pigment changes and also in photoallergic
and phototoxic effects that may occur in patients using drugs like diuretics,
non-steroid anti-inflammatory drugs (NSAIDs) or tetracyclines. However,
their knowledge of tropical "infections" is generally less developed.
This paper aims to fill that gap.
A patient who consults a dermatologist after a tropical holiday usually
has complaints which are centred around two problems: itch and ulceration.
The itch may be localised or generalised, and the ulceration may be
painful or painless.
Itch
Localised itch can be caused by a persistent insect bite or because
of an infestation with insects or worms. The persistent insect bite is
most commonly seen, but myiasis, tungiasis and creeping eruptions are
of more specialised interest. A creeping eruption may be caused by a number
of parasites, most frequently, mine worms or strongyloides presenting
as larva migrans or larva currens, respectively.
Generalised itch may not only be caused by persisting insect bites,
but also by parasites and worms, scabies, onchocerciasis or by urticaria
induced by intestinal parasites or by bacterial or viral infections. A
generalised rash either itchy, burning or painful may also be caused by
intestinal parasites or infections, sometimes it may manifest as erythema
multiforme or erythema nodosum with or without arthralgia.
Ulcerations may be caused by excoriated insect bites, infected with
streptococci, staphylococci or exceptionally with fusobacteria or corynebacteria.
Such ulcerations are usually painful.
However, ulcerations may also be due to leishmania, treponemata, mycobacteria
or deep fungal infections. Such ulcerations are generally indolent. Ulcerations
due to venereal infections like syphilis, chancroid, lymphogranuloma venereum
or donovaniosis are beyond the scope of this paper and are not considered.
A flow chart is shown in Fig.
1. The estimated incidence is shown in Table
I.
Localised itch
The persistent insect bite, usually situated on the extremities or the
face (bare skin), may present as an excoriated prurigo papule. It may
persist for months after the initial bite. It may also disappear and reappear
when the patient comes in contact with insects with similar antigenic
determinants as the causative insect. The histopathology of a persisting
insect bite is the same as that of a recently acquired one and shows a
dense inflammatory infiltrate that may extend into the subcutaneous fat.
The infiltrate consists of mononuclear cells together with some eosinophiles
and plasma cells. The treatment may be difficult and consists of strong
steroid ointments under occlusion, intralesional steroids or sometimes
just simple excision, cryotherapy or electrosurgery.
Prevention is difficult, but covering the skin with clothes and the
use of insect-repellents and impregnated bednets may be helpful. There
are many repellents on the market. The older ones based on citronella-
or eucalyptus-oil are not very active and only short acting. Repellents
based on DEET (n-n-diethyl-m-toluamide) seem most effective, though the
effective high concentration may be irritant and DEET can be absorbed.
In babies, infants and small children this may lead to seizures and
neurological damage. However, newer, safer formulations contain polymers
to diminish the absorption of DEET. New are repellents with dehydroaceton
mono-esters of carboxylic componunts. For the impregnation of bednets,
pyrethroids (permethrin 0.2-0.5 g/m2 or deltamethrin 15-25
mg/m2) are used. These can also effectively be used on clothes.
Pyrethrum-containing scented coils are available for use during the evening
and night. When one has been bitten, immediate application of a class
III or IV steroid is helpful. This may help to prevent sensitisation leading
to a "persistent bite".
Dramatic in a theatrical sense, is myiasis caused by maggots of different
insects like species of dermatobia, cordylobia and chrysoma. The patient,
not accustomed to such an infestation, may show up at a clinic in a state
of panic because he/she feels and sees something moving under the skin.
The condition manifests as a furuncle-like lesion (Fig.
2) which is not very painful but itches and the movements of the
maggot are sometimes felt. There is a pore at the centre through which
the maggot may be seen moving. Different ways are advocated to remove
the maggot. When one seals the pore with vaseline causing asphyxia, the
maggot tries to come up and can be extracted. This cannot easily be done
with the South American dermatobium hominis, because it is covered with
small hooks. Incision with extraction is then the simplest way. The dermatobia
is often found on the arms or on the head. This is because the fly deposits
its eggs on the underside of leaves of a tree or bush. When someone passes
along or underneath, the eggs dislodge and bury themselves in the skin.
In Africa, especially West Africa, the fly (Tumbu fly) may deposit its
eggs on the laundry. When this is not properly hot ironed or pressed,
the eggs survive and may penetrate the skin from the clothes or the bed
sheets. Prevention: covering the skin, but especially in West Africa,
hot ironing of the laundry is essential.
Tungiasis, jiggers, tunga penetrans is caused by female fleas which,
after being fertilised, penetrate into the skin where they hatch with
their body full of eggs. When the eggs mature a terrible itch may start,
usually along the side of the feet or between the toes or in the groove
between the toes and the footsole. Here, a red papule with a central pore,
often black (the backside of the flea) can be seen. The flea with its
eggs can then be pressed out without too much difficulty. Prevention:
wearing socks, closed shoes or sandals with a sole of at least 2-3 cm
(the flea cannot jump higher).
Creeping eruption in its initial phase, just an urticarial lesion, may
be easily missed. However, soon after penetration the larva starts to
migrate seeking a blood vessel to enter. As it has penetrated the wrong
host (the right hosts are cats or dogs), it does not have the proper adherence
molecules and it is doomed to wander and die after a few days, but sometimes
after weeks or even months. Larva migrans, in its classical form, the
creeping mine worm, causes erratic serpentine urticarial lesions, sometimes
obscured by scratch marks. The most frequently involved areas are the
feet, buttocks, lower abdomen (Fig.
3) and breasts. An old treatment is to freeze the parasite with
liquid nitrogen, but this treatment is only effective in the hand of experts
who have the time to observe the worm and know that it takes some time
before an urticarial lesion develops. Thus the parasite may be anywhere
within 1 or 2 cm ahead of the lesion. A 15% thiabendazole cream is more
effective with or without steroid and/or oral antihistamines. Oral thiabendazole
(many side effects) or albendazole (400 mg 2 dd * 5 days, a second course
may be needed) may also be used. Ivermectine (150-200 microg/kg in a single
dose) is also effective. Prevention: avoid contact of the bare skin with
contaminated soil (in endemic countries like The Gambia or Thailand all
beaches frequented by cats and dogs should be regarded as contaminated).
Wet swimming costumes or towels also should not be directly in contact
with the soil. Many patients have been infected via their swimming costumes
(hence involvement of the lower abdomen, buttocks and breasts). Towels
used for lying down should not be turned; the under side may already be
contaminated.
Larva currens, the larva stage of the Strongyloides, enters the skin
of the anal region and then migrates, usually in a more or less straight
line till it finds a vessel to enter (Fig.
4). It is itchy, the lesion is shorter and wider than that of
the larva migrans. It may occur even decades after the initial infection.
Strongyloides larva and sometimes eggs can be demonstrated in the stools,
but frequently concentration methods of the stools are necessary. Serology
may be useful. Treatment: oral albendazole (400 mg 1 dd * 3 days) or ivermectin
(200 microg/kg single dose) (a second course of treatment may be necessary).
Generalised itch
Persistent insect bites (papular urticaria) show numerous papular lesions
with signs of scratching. The lesions may persist or disappear and reappear
again. Histopathologically, the individual lesions show a pattern typical
for insect bites. Treatment may be extremely difficult. Strong topical
steroids and oral antihistamines may have some effect. However, one should
be aware that the lesions may also disappear spontaneously and may reappear
later. Topical 5% doxipin cream may have some beneficial effect. If topical
treatment does not have a lasting effect, acitretin (0.2-0.5 mg/kg) and
dapsone (1-2 mg/kg) have been claimed to be effective but, thalidomide
(50-100 mg) and especially cyclosporin (3-5 mg/kg) for 1-2 months are
more effective in curtailing "an attack". Since the cause is often unknown
an ivermectin trial may be of some use.
Scabies does not warrant further discussion in this article, but schistosomiasis
does. Patients may present with a generalised papular rash a few hours
to a few days after swimming in infected water. The itch is generally
at its worst 3 days after exposure and diminishes over a few weeks. When
infected by zoophilic species, pinpoint erythematous macules may also
develop which may be haemorrhagic and/or ulcerate. The so-called swimmer's-itch
is mostly caused by the cercariae from bird schistosomas and not by the
human zoophilic type. When one is infected with the human-type, urticaria
and/or angioedema may develop after 2 weeks to 3 months. This may be a
part of the Katayama syndrome which consists of fever, headache, coughing,
arthralgia, enlargement of the lymphnodes, liver and spleen, accompanied
by strong eosinophilia in the peripheral blood. This syndrome most frequently
accompanies a S. japonicum infection, but may occur, though usually milder,
with a S. mansoni or S. heamatobium infection. Treatment is with praziquantel
(40 mg/kg single dose), but when the Katayama-syndrome or neurological
involvement occurs oral steroids could be indicated. A late feature of
schistosomiasis may be granulomatous papular lesions, most frequently
in the anogenital region. Prevention: avoid contact with contaminated
sweet water.
Onchocerciasis is caused by a worm (O. volvulus), a filaria introduced
during the bite of the vector, the black fly (a simulium species). The
patient may present years after the initial infection, but at the earliest
after 6 months to 2 years. The patient then presents with an intense generalised
itch. At the start, there are only a few erythematous papules and scratch
marks, later the whole skin becomes dry with lichenification and loss
of elasticity. Skin hyper-, hypo-, and depigmentation may occur in chronic
cases. The latter are hardly ever seen among travellers. Biopsy or skin
snip may show microfilariae. If the history is suspect but microfilariae
have not been demonstrated, a Mazotti test can be performed. Under careful
conditions (be aware: anaphylactic shock) 50-100 mg diethylcarbamazine
(DEC) (Hetrazan®) is given. If the test is positive, it
leads to an intolerable itch within a few hours, probably caused by irritated
microfilariae. Treatment: DEC or better ivermectin (150-200 microg/kg).
When the eye is involved steroids should be prescribed before the ivermectine
is given. However, neither DEC nor ivermectin kills the adult worm which
can sometimes be felt as onchonodules especially above the hipbones. Re-treatment
may be necessary after 3-12 months. Serology may be of help. Adult worms
are only killed by suramin but this has a number of serious side-effects.
Prevention: avoid insect bites.
Two non-itchy filaria-infections, thus not shown in the flow chart,
are discussed here.
Filariasis, more often seen by physicians specialised in Internal Medicine
than by the dermatologist, is caused by Wucheria bancrofti. It presents
after an incubation period of 5-15 months with mild lymphangitis and lymphadenitis
with oedema of one or more extremities or genitalia. Remarkably, the lymphadenitis
is descending and not ascending as is normally the case. These symptoms
are usually accompanied by mild fever and some discomfort. At the beginning,
there may be attacks, but later, the symptoms become chronic. Some patients
may have urticarial lesions during the incubation period and present with
some eosinophilia. Serology may be of some help. The microfilariae can
be demonstrated at night in the peripheral blood when the infection is
full blown. The late effects include lymphoedema of extremities, vulva,
scrotum or breasts. The notorious elephantiasis is then established. However,
these late symptoms are never encountered among tourists and business
travellers.
Loiasis caused by the nematode Loa loa is also occasionally seen. The
patient may present with transient non-pitting oedematous areas of about
10 cm in diameter (Calabar swelling). The swellings are mostly located
above joints or bony prominencis. They are neither itchy nor painful.
It is believed that the swelling is caused by a migrating worm. Sometimes,
the worm passes through the conjunctiva, a passage which lasts 10-30 min.
Such patients generally do not consult a dermatologist, but the dermatologists
are often consulted by the attending physician who is puzzled about the
swelling. Microfilariae may be found in the blood and have a special shape.
The treatment is DEC in increasing doses, from day 1, 3*25 mg to day 5-21
2 mg/kg, which again only kills the microfilariae. Ivermectine and albendazol
may be alternatives, steroids may be needed. Prevention: avoid the bite
of the vector.
Urticaria after a visit to a low-income tropical or sub-tropical country
may be induced by a large number of causes which include intestinal worm
infections and infections due to salmonella, shigella or yersinia or viral
infections (e.g. hepatitis). Sometimes, painful erythematous, erythema
multiforme-like lesions develop, as does erythema nodosum with or without
arthralgia.
Ulcerations
Ulcerations may be painful, itchy or nearly indolent.
Painful ulcerations frequently are infected insect bites or scratches.
The infection is mostly with streptococci or staphylococci. The lesions
are usually situated on the legs and feet but may occur anywhere. The
lesions are generally shallow ulcerations with or without discharge surrounded
by painful erythema and swelling. Sometimes, satellite lesions develop.
Treatment with oral flucloxacillin is often sufficient, topical bacteriostatic
or antiseptic treatment with or without steroids may be helpful as is
a mild non-elastic compression bandage. It must be noted that skin defects
easily infect under humid (sub-)tropical conditions. An ulcus tropicum,
a phagodenic ulcer possibly caused by a necrotic reaction induced by toxins
of anaerobic bacteriae arises in a few patients. Anaerobic fusobacteria
have been seen together with Treponema vincenti. Most of these ulcers
heal spontaneously but some may enlarge quickly. Treatment consists of
necrotomy if necessary and local antiseptics together with oral penicillins
and/or metronidazole. Skin grafting may speed the healing.
In some patients, a diphtheria ulcer develops. These present as a ragged
ulcer with a clearly defined overhanging edge. The exudate from the ulcer
tends to form a tough grey or brownish adherent membrane. Regional lymph
nodes enlarge. The lesions may persist for 2-3 months and then heal with
some scarring. Systemic manifestations are rare because most West Europeans
have been vaccinated. In children, however, the infection may be more
severe with neurological and cardiac manifestations. Treatment, especially
in children, includes, specific antitoxin together with erythromycin and/or
penicillin.
Occasionally, a Buruli ulcer is encountered. This is an indolent ulcer
caused by M. ulcerans. After initial infection, 1-2 months later a nodule
appears with very little inflammatory signs. The nodule is not painful,
but after a few weeks, it starts fluctuating and breaks after about 6
weeks. Then it has a necrotic base with an undermined rim. Later, the
base assumes the aspect of red granulation tissue. The diagnosis is made
on a biopsy from just outside the border where the bacterium can be found.
Treatment consists of total excision and skin grafting since effective
antibacterial treatment is not yet available.
European dermatologists are more familiar with the mycobacterial infections
with M. avium and M. marinum which may also be acquired in Europe.
Other chronic painless ulcerations that similar to the Buruli ulcer
may be acquired by contact with contaminated wood and debris in the bush
are yaws and deep mycotic infections. The primary lesion of yaws is a
wet easily bleeding raspberry-like papule or nodule (Fig.
5) which disappears after a few weeks leaving an atrophic scar
on the skin and a positive VDRL and TPHA in the blood. Secondary yaws
is hardly ever encountered in Europeans. The treatment is with penicillin.
Of the deep mycoses only the sporotrichosis is occasionally seen. Initially,
it is a painless erythematous swelling which starts to ulcerate. The ulceration
shows granulation tissue with crypten and crusts. It is surrounded by
an erythematous wall. The ulcer excudes a purulent sticky fluid. Usually
no fungal elements are found in this material. These can be found in a
biopsy from the rim. The lymph-nodes along the draining lymph-vessel will
enlarge and some may start suppurating. Such spread is now called sporotrichoid
spread. However, this can also be seen in mycobacterial infections, especially
accompanying HIV and in leishmaniasis. Treatment with modern antimycotics
is sometimes disappointing, the old-fashioned potassium iodide usually
suffices.
Recently, the leishmania infections are more frequently seen. The initial
lesion starts after the bite from an infected sand-fly, phlebotomus (Old
World) or lutzomyia or psychodopygus (New World). It is caused by a species
of leishmania. Six major species have been recognized and are L. tropica,
L. major, L. aethiopica and L. donovanii in the Old World and in the New
World the L. brasiliensis and the L. mexicana complex, each complex consisting
of at least 4 subspecies. Though each species can give rise to all known
clinical expressions of the disease from a self-healing nodule to kala
azar and post-kala azar dermal leishmaniasis (PKDL), most species cause
one variant more than the other. So espundia in the Old World is only
seen after infections with L. aethiopica and kala azar is hardly ever
seen in the New World or after a L. tropica or L. major infection. The
clinical symptoms seen in travellers are usually only ulcers with or without
lymphadenitis or local spread (Fig.
6). Multiple bites may occur. In the Americas the leishmania ulcer
is sometimes called bird-watcher's ulcer. This is because such bird-watchers
are present at the right time in the right place (recently cleared woods).
After an incubation period of 2 weeks to 4 months an erythematous papule
may develop which starts to ulcerate. Most lesions are in those areas
which the sand-fly likes to bite, areas which are slightly moist, around
the eyes, ears, nose and mouth, but it may occur anywhere. Most infections
heal spontaneously though it may take quite some time and they may leave
large ugly scars. Beside ulcerations L. d. infantum can be responsible
for kala azar and PKDL, L. aethiopia may cause espundia (mucocutaneous
leishmaniasis which destroys the nose) and diffuse cutaneous leishmaniasis
which is also frequently seen in South America where often multiple verrucous
and nodular lesions occur (L. brasiliensis and L. mexicana).
The diagnosis is based on the history and the clinical aspect, a smear
or tissue fluid obtained by needle and/or biopsy may show Donovan bodies.
A PCR of this material is frequently diagnostic. Culture is often positive.
Serology in localised cutaneous leishmaniasis is usually negative.
Treatment: localised lesions are treated with cryosurgery, laser surgery,
electrosurgery or simple excision, depending on the local expertise and
the localisation. Topical treatment with paromomycin has proved to be
effective in some areas. Intralesional injections with tri- or pentavalent
antimony has also shown to be of value. Some of the leishmania-species
may be sensitive to ketaconazole or itraconazole (tropica and major).
Though in order to kill the South American species, and some of the Old
World species (L.d. infantum, L. aethiopica) pentostam or pentamidine
injections have to be given. However, one should be aware that though
pentamidine isothionate is usually safe, the mesylate may induce diabetes.
In severe cases, amphotericin B may be used; especially, the new liposomal
preparation is effective.
An important disease not fitting in the flow chart (Fig.
1) is leprosy. This is occasionally seen in Europeans who have
spent prolonged periods abroad in a low income tropical country, though
cases after incidental contact during holidays have been documented. An
early diagnosis is important since otherwise irreversible nerve damage
may occur. Patients may present with tingling sensation or loss of sensation
in the extremities or in a skin lesion. They show either hypopigmented
or slightly erythematous patches (tuberculoid leprosy) or infiltrated
plaques and/or papules and nodules (lepromatous leprosy). The macules
show loss of sweating and loss of sensation (especially to light touch).
The patches and nodules after biopsy or smear show acid-fast bacteria
(M. leprae). Histopathologically, involvement of the cutaneous and subcutaneous
nerve branches is pathognomic. Clinically, enlarged peripheral nerves
are palpable and they may be tender. In advanced cases loss of sensation
and strength in hands and feet as well as lagophthalmos may be seen. Ulceration
may develop in anaesthetic areas of hands and feet. Treatment consists
of combinations of rifampicin, dapsone and clofazimine depending on the
classification. During active periods, the so-called reactions, steroids
may be needed.
In conclusion, this paper highlights some memories of tropical holidays,
especially those of an infective nature. One should be aware that every
patient with an unusual skin disease who has ever travelled to low-income
tropical areas may be in danger of having acquired a tropical "gift",
which can usually be treated adequately, provided it has been diagnosed
correctly and in time.
CONCLUSION
Acknowledgement
The English was corrected by Dr. B. Tank.
Figures are from our own archives and from those of the Department of
Dermatology of the Rotterdam University, The Netherlands.
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