10.2.

CHAPTER 10.2

Parasitic infections of the skin

John M. Goldsmid and Wayne Melrose

10.2.1 INTRODUCTION

A wide range of parasitic infections can involve the skin and subcutaneous tissues.
Depending on the species of parasite, this involvement may be transient, the parasite
passing through the skin on its migration to the blood stream and so to a specific target
organ, or the infection may be localised to the skin. In the latter infections, the skin may
be the primary site of infection or there may be a secondary invasion of the skin. All
parasitic groups (protozoa, trematodes, cestodes, nematodes and arthropods) have species
which can involve the skin or subcutaneous tissues:

10.2.2 PROTOZOAN INFECTIONS

Protozoan infections, in which there may be a transient skin phase following infection
through the cutaneous route, include African trypanosomiasis (sleeping sickness due to
Trypanosoma brucei rhodesiense and T. b. gambiense) and South American
trypanosomiasis (Chagas’ disease, due to T. cruzi). In the former disease, a vesicular
lesion develops about five days after an infected tsetse fly bite and is known as a Sleeping
Sickness Chancre. In Chagas’ disease the lesion is similar and is termed a chagoma. In
Chagas’ disease too, there may be a marked, often unilateral, periorbital oedema termed
Romana’s Sign and which is due to the irritation of the conjunctiva by the infected
assassin bug faeces and the penetration of the infecting trypanosomes.

Protozoan infections, which cause localised skin lesions, include various forms of
cutaneous leishmaniasis. Commonly recognised species include Leishmania tropica
(Oriental Sore); L. braziliensis (Espundia) and L. mexicana (Chiclero Ulcer) but there are
many species and subspecies of the genus Leishmania causing regional variations of
cutaneous leishmaniasis 1. The geographical distribution of cutaneous leishmaniasis is
wide, encompassing Africa, the Middle East, the Mediterranean, SE Asia, Asia and Latin
America1,2.

The clinical picture is also variable. In Old World cutaneous leishmaniasis, the lesions
are typically single or few in number, while in some of the New World forms of the
disease, lesions tend to be diffuse or mucosal in distribution1. In cutaneous leishmaniasis,
the lesions tend to eventually heal but leave extensive and, disfiguring scarring.
Leishmania donovani and L. infantum are the causes of visceral leishmaniasis, which
involves the liver and spleen. However, L donovani can cause secondary skin lesions,
especially post treatment.

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 10.2.2

Entamoeba histolytica, the cause of amoebiasis, can also involve the skin in the form of
amoebiasis cutis. These lesions develop as secondary lesions from direct extension of an
amoebic liver abscess or from the rectum3. Balamuthia mandrillaris , one of the free-
living limax amoebae, while usually recognised as involving the CNS4, may also invade
the skin causing extensive skin lesions3

Diagnosis of protozoan skin infections usually involves a biopsy from the edge of the
lesion with histological identification of the protozoa. Cutaneous leishmaniasis can also
be diagnosed by culture on media such as NNN Medium1.

In the treatment of severe cutaneous leishmaniasis, stibogluconate sodium 20mg

antimony/kg/day iv or im as a single dose or in two divided doses for 20 - 28 days can be
used, but serious side effects are common 5,6. Alternative treatments include meglumine
antimonite, itraconizole, ketoconazole or liposomal amphotericin B 1,5,6.

Amoebiasis cutis is treated with metronidazole as for invasive amoebiasis (Chapter 7) but
there is no known and accepted, effective treatment for Balamuthia mandrillaris
infections, which, fortunately, are extremely rare.

10.2.2 TREMATODE INFECTIONS

Trematode infections involving the skin are few. Thus in schistosomiasis invading
cercariae may cause a transient allergic rash lasting 1-5 days while penetrating the skin
(known as cercarial dermatitis) en route to the blood stream. This tends to occur most
frequently with Schistosoma japonicum, less frequently with S. mansoni and rarely with
S. haematobium.. It is more often seen in previously unexposed people who acquire a
heavy infection while swimming. The non-human schistosome species (mostly avian
species) can also cause a cercarial dermatitis – known as swimmer’s itch or pelican itch.
These latter infections are diagnosed clinically, including a history of exposure to
infected water. They are self-limiting and never develop beyond the skin itching stage.
They can thus be treated symptomatically with antihistamines to relieve the itch.

10.2.3 CESTODE INFECTIONS

A number of tapeworm species may cause subcutaneous lesions in their larval stages.
Thus tapeworm cysticerci (Taenia solium), hydatid cysts (Echinococcus granulosus) and
sparganum larvae (Spirometra spp) may all be seen as forming cysts under the skin.

Cysticercosis: This occurs when humans swallow the eggs of the pork tapeworm, Taenia
solium. The eggs may be on salad plants contaminated with infected human faeces
(heteroinfection); they may be ingested from the patient’s own contaminated fingers
(external autoinfection) or the eggs may be regurgitated up in a proglottid from a worm in
the patient’s intestine and then re-swallowed from the stomach (internal autoinfection)7,8.

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 10.2.3

The eggs hatch and the onchosphere larvae migrate through the intestinal wall to settle at
various locations through the body where they develop into cysticerci. In some cases,
cysticerci may settle in the subcutaneous tissues, appearing as small lumps under the
skin. Diagnosis can be made by identifying the larva (known as Cyticercus cellulosae)
microscopically after biopsy or on histological section7. Once they have calcified,
cysticerci can be seen on x-ray, CT scan or MRI. Diagnosis can also be confirmed
serologically (eg EIA). Treatment for subcutaneous cyticercosis is usually unnecessary
but where cysticerci lodge in a vital organ (eg the CNS) then treatment with albendazole
(15mg/kg/day in three doses for 8-15 days) or praziquantel (20mg/kg tid for 14 days) can
be used5,6. Corticosteroids are often recommended to be used in conjunction with
anthelmintic treatment5.

Hydatid: Humans acquire hydatid cysts (the larval stage of the tapeworm, Echinococcus
granulosus) when they ingest eggs passed by dogs and other canids such as the dingo in
Australia. The common sites for hydatid cysts in humans are the liver and the lungs but
the CNS, the spleen and other organs may be involved7. Subcutaneous cysts may
occasionally be encountered. These cysts may grow to a large size and so impair the
function of the organ (or even destroy it) in which they are sited. Under the skin they
cause little clinical discomfort but if ruptured (eg in a fall), anaphylaxis and the formation
of metastatic cysts may occur. Diagnosis is clinical, radiological or using ultrasound and
confirmed by antibody serology. Suspected hydatid cysts should never be aspirated or
biopsied due to the danger of metastatic spread. Treatment is surgical removal or, if
inoperable, the use of albendazole (400mg bd by mouth for 28 days or longer). Repeat
treatments may be necessary, with 14 days rest periods between each course)5,6.

Sparganosis: This is infection with the sparganum (plerocercoid) larva of one of the
pseudophyllidean tapeworm species. The larvae may occur in the eye, the CNS, muscle
or in the subcutaneous tissues, presenting as nodules or a mass in the organ involved.
While sparganosis has been recorded sporadically from many parts of the world, the
commonest species is Spirometra mansonoides in Asia with infection resulting when
humans accidently ingest the minute crustacean, Cyclops, with water. The cyclops
contains the procercoid larva of the cestode. Infection may also be acquired from
ingestion of infected fish, amphibians, reptiles, birds or even pigs9,10. The most severe
form of sparganosis is that caused by Sparganum proliferatum. The life cycle of this
parasite, as is the case of most species causing human sparganosis, is unknown. The latter
species is unusual in that the sparganum proliferates in human tissues. Diagnosis is
clinical with a definitive diagnosis of sparganosis relying on parasite identification. No
effective drug therapy is known and treatment relies on surgical removal 5,9,10.

10.2.4 NEMATODE INFECTIONS

Various nematode species, often zoonotic species infecting humans accidentally, can
cause subcutaneous lesions. Nematode species infecting the skin include Gnathostoma
and the filarial species, Loa loa, Onchocerca volvulus, Mansonella streptocerca and

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 10.2.4

Dirofilaria spp. Additionally, many nematode species, which infect through the skin,
may cause skin lesions at the point of entry.

Thus the human hookworm species, Ancylostoma duodenale and Necator americanus,
may cause a transient itchy papular rash (ground itch/dew itch) at the site of penetration.
Although they mostly never mature to adults in the human host, the dog and cat
hookworms (Ancylostoma braziliense, A. caninum etc), may cause serpiginous itchy
tunnel-like lesions in the skin (sandworm/cutaneous larva migrans/creeping eruption)
lasting for weeks or months. So too, Strongyloides stercoralis larvae can cause similar
lesions (larva currens rash) while penetrating the skin when autoinfection occurs. In the
latter case, the rash lasts a few days before disappearing as the infective larvae of the
Strongyloides enter the circulation to perpetuate the infection. Such larva currens rashes
may occur at irregular intervals for months or years after leaving an endemic region,
sometimes for 20 –50 years or longer.

Gnathostomiasis is caused by various species of nematode belonging to the genus

Gnathostoma. Transmission usually occurs after ingestion of fresh water fish or
sometimes snakes8. Clinically, gnathostomiasis presents as swellings, which might be
migratory, in the tissues including subcutaneous tissues5.

10.2.4.1 Filarial infections

10.2.4.1.1 Onchocerciasis (“river blindness”)

Onchocerciasis is caused by infection with the filaroid Onchocerca volvulus. It is

endemic in 37 countries in West, East and Central Africa, the Arabian peninsular, and
parts of Central and South America. The global burden is estimated to be around 126
million, mostly in Africa 11. Onchocerciasis is the second most common infectious cause
of blindness after trachoma and causes immense misery and socio-economic loss in
infected communities, especially in areas of heavy transmission where infection occurs
early in life. The fear of blindness drives people away from the best arable land near the
rivers and streams where the vector black flies, (Simulium spp.), breed. Work output is
reduced because of the number of sight-impaired people in the community. O. volvulus
follows the general life cycle of filarial nematodes but there are important differences
between it and the life cycle of W. bancrofti and Brugia species: Onchocerca volvulus
microfilariae are found in the skin not the blood and they do not do not have sheaths. The
adult worms live in the subcutaneous tissue and not the lymphatics. The vectors are black
flies (Simulium spp.) not mosquitoes.

The main clinical features of onchocerciasis are: dermatitis (onchodermatitis), skin

nodules, and eye lesions 11:

Dermatitis: Various combinations of rashes, hyper-pigmentation, atrophic changes and

micro-abscesses are seen. There is intense itching and secondary bacterial infection may
occur during scratching. Some patients may suffer from hyperreactive onchodermatitis
or “sowda” where itching is so intense that daily activities are impaired and normal sleep

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 10.2.5

patterns are disrupted12. Chronic dermatitis causes premature aging of the skin and
patches of de-pigmentation (a condition called "leopard skin"). Atrophy of subcutaneous
tissue in the groin area may lead to sagging of the skin, the so called "hanging groin".
The skin lesions of onchocerciasis are sometimes confused with contagious skin diseases
by local populations and sufferers may be stigmatised by their community.

Nodules: Nodules are subcutaneous granulomas resulting from tissue reactions around
adult worms. They are usually less than 2cm in diameter, firm to the touch, mobile and
neither tender nor painful. They tend to be commoner on the head in Latin America and
around the groin (‘hanging groin’) in Africa.

Eye lesions: The exact cause of the eye lesions has yet to be determined but a number of
factors are known to be involved: tissue reaction to microfilariae migrating through the
eye, allergic reactions to parasite secretions, and the impact of other irritating agents such
as ultraviolet light, dust and smoke. There is progressive loss of vision that can lead to
irreversible blindness.

As is the case in lymphatic filariasis, cellular immune responses against a range of

antigens are reduced and IgG4 dominates the isotype pattern in classical onchocerciasis
13,14
. Tetanus vaccine response is impaired but not enough to prevent the production of a
protective response 15. By contrast, the immunological profile in the sowdah variant is
analogous with the hyperreactivity seen in the TPE variant of lymphatic filariasis with a
marked increase in antibody levels and increased cellular responses to filarial antigens16.

The most common method of diagnosis is by the use of skin snips. These should be
obtained from the iliac crests and lower legs of African patients and from the shoulders of
patients from the Americas. The classic method is to clean the skin with an alcohol swab,
leave to dry, and then elevate a portion of the skin with the point of a needle and cut out a
portion 2-3 mm in diameter with a scalpel or razor blade. The biopsy should be blood-
free. The biopsy is placed into a drop of water/saline on a microscope slide, covered with
a cover glass, and examined microscopically after around two hours. If the person has
onchocerciasis motile microfilariae will emerge from the skin. The number of
microfilariae per gram of skin can be determined by weighing the biopsy and counting
the number of microfilariae 11. Antigen and antibody assays, rapid card tests and PCR
techniques for the diagnosis of onchocerciasis are under development but are not
routinely available as yet 17-19.

The first drug to be successfully used for the treatment of onchocerciasis was suramin
which was introduced in the late 1940’s. It kills both adult worms and microfilariae, but
is extremely toxic and severe side effects, including some deaths, were seen in up to 30%
of treated patients. Diethyl-carbamazine (DEC) was also introduced in the 1940’s. It is
very effective in killing microfilariae but again, severe side effects are a problem and it
increases the risk of eye damage. Ivermectin is now the drug of choice. It is given orally
as a single dose of 150-200µg/kg body weight at 3 - 12 monthly intervals5,6. Adverse
reactions still occur in about 20% of treated patients but they are usually mild and self-
limiting and confined to transient increase in skin rash and itching, soft tissue swelling,

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 10.2.6

arthralgia, fever, and lymphadenitis. Some patients may experience peri-orbital oedema
and rarely, hypotension, bronchospasm, and bullous eruptions. Adverse reactions are
more common during the first round of treatment and reduce in prevalence and
seriousness with later rounds because of the reduced number of microfilariae 11. It is
recommended that where infection involves the eye, oral corticosteroids (1mg/kg/day)
should be given for several days before ivermectin is started5. Over the last two decades a
control programme for onchocerciasis has been underway in Africa and the Americas,
based on the community-wide, mass administration of ivermectin and vector control
measures. As a result, onchocerciasis has been eliminated as a health problem in 11 West
African countries, and the rest of the endemic areas of that continent, and those in the
Americas are being progressively brought under control11, 20-22. Nodules on the head are
associated with an increased risk of eye damage and extensive nodulectomy campaigns
have been carried out for many years in the Americas and have been effective in reducing
the prevalence of blindness. In Africa, the nodules tend to occur on the trunk, pelvic areas
and upper legs rather than the head and nodulectomy is not an effective means of
control11,22.

10.2.4.1.2 Loasis

Loiasis, caused by infection with Loa loa infects 3 to 13 million people in Western and
Central Africa. It is also the most common filaroid parasite seen in travellers and other
expatriates. It is transmitted by the bite of female flies of the genus Chrysops and has a
typical filaroid life cycle. The adult worms actively migrate through subcutaneous tissue
and sheathed microfilariae appear in the blood during the day. Many of the infected
individuals are asymptomatic despite having circulating microfilariae. Expatriates seldom
develop microfilaraemia but they can suffer from a range of allergic symptoms such as
pruritis, urticaria, and transient angiodema or “Calabar swellings. Calabar swellings can
occur anywhere on the body but are most common on the face, arms and hands. Loiasis is
often accompanied by marked eosinophilia and high serum IgE. Eosinophilia and a
history of travel to a Loa loa-endemic area is often the first indication that someone may
have the disease. Sometimes a migrating worm may be observed crossing the conjunctiva
giving rise to the common name “eyeworm”. Patients may be alarmed, but apart from
mild transient local inflammation the worm causes no long-term damage to the eye 23.
Renal involvement, as revealed by haematuria and/or proteinuria may occur in up to 30%
of loiasis cases and may be exacerbated by treatment 24. The most serious complication is
encephalitis. It is most commonly precipitated by treatment of individuals with
microfilarial counts >5000 per ml of blood and is caused by a rapid increase in antigen
shed from the dying microfilariae.

A definitive diagnosis is obtained if an adult worm is removed from the eye by surgery or
if characteristic microfilariae are obtained from blood collected during the day23,25.
Microfilarial density can be low and it is advisable to use concentration tests as per
diagnosis of lymphatic filariasis. PCR-based tests have been developed but are only
available at a few specialised centres25,26. Testing for antifilarial antibody is of little value
in endemic populations but is of value in expatriate cases were the absence of such
antibody makes loiasis unlikely 25.

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 10.2.7

Medical practitioners are urged to obtain up to date information from a tropical medicine
specialist or the Centers for Disease Control in the USA before treating a case of loiasis
because there is a risk of severe and even fatal complications and drug treatment regimes
are under review. DEC is effective against both adult worms and microfilariae and is the
drug of choice in amicrofilaraemic cases or when microfilaria density is light, including
expatriate cases. It is given at a dose building up to 9 mg/kg of body weight for 21
days5,6. Multiple courses may be required and recrudescence may occur years later. Mild
side effects are common and include Calabar swellings, pruritis, nausea and fever. The
treatment irritates the worms and the may be observed moving around under the skin. It
must be stressed that treating Loa loa in patients with microfilaraemia carries some risk,
and if the microfilaraemia density is over 5000 per ml the risk of severe or even fatal
shock, renal failure and encephalitis is very high. “Graduated doses” of DEC and pre-
treatment with antihistamines and steroids are recommended5,6 to try and reduce the
incidence of severe adverse reactions but experience shows that they do not prevent
encephalitis 27. The removal of microfilariae by apheresis has been used to lower the risk
but the technology is not available in many Loa loa-endemic areas 28. Ivermectin (200
ug/kg stat, repeated every 6 – 12 months)5 kills microfilariae effectively but it too has
been reported to cause adverse effects 24. Trials with albendazole are underway and the
early results look promising. Adverse effects do not occur because the microfilariae
decrease slowly over several months rather than rapidly as is the case with DEC and
Ivermectin but there is still work to been done on defining the dose and treatment regime
29,30
.

10.2.4.1.3 Mansonellosis

Mansonellosis is caused by filarial nematodes belonging to the genus Mansonella.

Mansonella perstans (formerly Dipetalonema/Acanthocheilonema perstans), is
transmitted by a number of species of midges belonging to the genus Culicoides, and
infects monkeys and apes as well as man. The parasite is endemic across Central Africa,
Tunisia, Algeria, the Northern Coast of South America, and parts of Brazil and
Argentina. It is often considered a commensal but is better regarded as a low-grade
pathogen. This species of the genus does not infect the skin, but can cause an allergic
response from the host and can be associated with angioedema (similar to the Calabar
swelling in loiasis), pruritis, fever, headache, arthralgia and right upper quadrant pain.
Eosinophilia and elevated serum IgE are common. The unsheathed microfilariae, which
show no periodicity, are found in the blood but concentration techniques may be required
to find them. Antifilarial antibodies are elevated. The standard treatment is DEC at 8-
10mg/kg body weight for 21 days but there is little evidence that it effective and multiple
courses may be required 99. Mebendazole given at 100mg per day for 30 days is effective
but ivermectin and albendazole are not 23.

Mansonellosis can also be caused by two other species of the genus. Mansonella ozzardi
is confined to the New World with a wide distribution in Northern South America, the
West Indies, and the Caribbean. It is transmitted by either Culicoides spp midges or
simuliid blackflies while Mansonella streptocerca (formerly Dipetalonema streptocerca)

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 10.2.8

is found in both humans and monkeys in Central Africa. Adult worms live in the thoracic
and peritoneal cavities and the sheathless, aperiodic microfilariae are found in blood and
skin. Most cases are asymptomatic but there are reliable reports of marked eosinophilia,
urticaria, pruritis, lymphadenopathy, headache, joint pains and asthma-like symptoms,
especially with M. ozzardi 23. DEC and albendazole are ineffective but ivermectin
reduces the microfilarial load and symptoms 32.

10.2.4.1.4 Dracontiasis

Dracontiasis is infection with the Guineaworm, Dracunculus medinensis, a filarial

nematode which is unlike the other worms of this group in that it is transmitted through
the ingestion with water, of the intermediate host, a small freshwater crustacean, Cyclops.
The infection has been widespread, but often localised, in Asia and the Middle East in the
past, but the WHO has hopes that it will be eradicated in the near future.

The long, thin adult worms settle under the skin and muscular tissues (often on the leg)
and the female worm extrudes her posterior end through a blister/ulcer when the limb is
immersed in water. The worm liberates larvae into the water where they are taken up by
the Cyclops.

The lesions can be extremely painful and diagnosis is clinical, noting of the end of the
female worm emerging from the skin or by x-ray. Treatment involves the use of
metronidazole 250mg td for 10 days for adults or thiabendazole 25-37.5 mg/kg bd for 3
days5,6.

10.2.4.1.5 Miscellaneous Zoonotic filariases involving the skin

A number of animal, mosquito-borne filaroids cause occasional infections in humans, the

most common being species of Dirofilaria, especially the dog heartworm D. immitis.
Their life cycle cannot be completed in humans and the parasites in incorporated in a
granuloma or a calcified lesion. They can be associated with skin lesions but if they occur
in the lung they can be mistaken for tuberculosis or the “coin lesions” of malignancy.
Occasional patients may present with eosinophilia and allergic symptoms. Diagnosis is
usually made microscopically after excision and histology. Antifilarial serology results
are variable 33.

10.2.5 ARTHROPOD INFECTIONS/INFESTATIONS OF THE SKIN:

Arthropods are hard bodied animals with jointed legs. They comprise insects, mites,
ticks, spiders and crustaceans. The medical significance of various species relates to their
blood-sucking habit; their ability to serve as vectors to transmit other microorganisms;
their role as intermediate hosts in the life cycles of other parasites and in some cases, the
fact that they are venomous/toxic34.

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 10.2.9

Arthropods can thus be either temporary or permanent ectoparasites and infest the host
(i.e. live on the surface of the skin of the host) or they can infect the host (live within the
skin of the host). Some might be better described as micropredators as they actively hunt
their host (eg mosquitoes; tsetse flies).

Where they transmit a disease-causing organism, the transmission may be mechanical, as

when the microorganisms contaminate the feet or mouthparts of the arthropod, or
biological, where the microorganisms pass through a biological cycle in the vector.

10.2.5.1 Insect infections/infestations

Many insect species can infest/infect the skin34,35. This can vary from a simple accidental
bite (eg from a thrips or collembolan34,36) to a more severe infection (eg from a fly
maggot, jigger flea or a louse infestation). Thrips and collembolans are free-living, plant
feeding insects which occasionally bite humans, become encapsulated in small nodules in
the skin or cause a pruritic rash. Insects which suck human blood include the sucking lice
(Anoplura); blood-feeding bugs (Hemiptera); fleas (Siphonaptera) and the blood-sucking
flies (Diptera). Some lepidopteran species (caterpillars of moths) have irritating hairs
which can cause an allergic rash on contact with the skin and some beetles such as the
meloids and staphylinids (blister beetles), Paederus spp. (containing paederin), Lytta
spp.(the Spanish fly, containing cantharidin) and Epicauta spp. can also cause blistering
on contact with the skin34.

10.2.5.1.1 Louse (Anoplura) infestations

Three species of lice infest humans - the bodylouse (Pediculus humanus corporis), the
head louse (P. h. capitis) and the pubic or crab louse (Pthirus pubis)34,35. Animal lice do
not attack humans, these insects being very host specific. Transmission is by close head
contact (headlice); close contact and sharing of blankets and clothing (bodylice) and
sexual contact (crablice).

Lice feed on the blood of the host and their feeding can cause itching, inflammation and
skin discoloration (Vagabond’s Disease). Of the three species of human louse, only the
body louse is a significant vector of disease, transmitting epidemic relapsing fever
(Borrelia recurrentis), epidemic typhus (Rickettsia prowazekii) and trench fever due to
Bartonella (= Rochalimaea) quintana.

Diagnosis of pediculosis and phthiriasis is by direct observation – detecting the lice or

their eggs (nits) on the hairs of the head (headlice) or the pubic, under arm, chest, and
beard hairs or on the eyelashes (crablice). In the case of the bodylice, which are
morphologically identical to the headlice, the adult lice can be found on the body or the
clothing of the victim. Eggs of bodylice are laid in the seams of clothing.

Treatment and control of headlice involves the use of specially formulated, low
concentrations of insecticides such as 0.5%malathion (Maldison) or pyrethroids (eg 1%
permethrin)35,37,38 for cases and close contacts (especially family members). Ivermectin

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 10.2.10

200ug/kg orally as a single does is also reported to be effective6.. Alternatively, repeated

use of standard hair conditioners can be used combined with rigorous inspection and
combing of the hair with a fine tooth comb to remove adult lice and eggs38. Careful and
repeated examination of the hair is an integral part for successful treatment and control as
is treatment of close contacts. For pubic lice, treatment of the patient and all sexual
partners with 1% permethrin is the usual approach, although 1% lindane is still suggested
as an alternative by some authorities6. For bodylice, treatment of the body with pyrethrin
or benzyl benzoate is suggested but for control5, fumigation of clothing, blankets etc is
required.

10.2.5.1.2 Blood-feeding bugs (Hemiptera)

Blood-feeding bugs include the assassin (cone-nosed) bugs belonging to the genera
Rhodnius, Triatoma or Panstrongylus and the bedbugs (Cimex spp)34. The cone-nosed
bugs of Latin America are vectors of Trypanosoma cruzi, the cause of Chagas’ disease.
They transmit the protozoan to the human host through their faeces, contaminating the
bite wound, often on/near the conjunctiva. The bugs often feed around the eye and the
infected faeces are irritant, resulting in the diagnostic sign for early South American
Trypanosoamiasis, Romana’s Sign.

Bedbugs inhabit houses, feeding on the sleeping inhabitants. Their bites can be itchy but
they are not known to be significant vectors of any disease.

10.2.5.1.3 Fleas (Siphonaptera)

Many flea species bite humans, suck blood and may cause allergic reactions of varying
degrees of severity34. The common fleas attacking humans are the dog and cat fleas
(Ctenocephalides canis and Ct. felis); the human flea (Pulex irritans) and rat fleas of the
genus Xenopsylla. The bite of these insects is irritating but not of much clinical
significance. Of great importance, however, is the fact that fleas of the genus Xenopsylla
can serve as vectors of Yersinia pestis, the causative agent of Bubonic Plague, and
Rickettsia typhi, the cause of murine typhus.

Another flea worthy of consideration in tropical areas is the Jigger (Chigoe) flea, Tunga
penetrans34,35. This flea differs from other fleas attacking humans in that the female flea
burrows into the skin and lives there as a permanent parasite within an ulcer-like lesion.
The female of this flea lives in skin lesions in pigs, rodents and other animal hosts in
tropical South America, and it has been introduced into Africa and India as a result
human movements. Eggs laid by the female flea fall onto the ground and develop into
free living larvae which pupate and emerge as adults. Mating occurs and the females find
a host, burrow into the skin, often on the foot and between the toes. The life cycle then
repeats itself. Diagnosis is by finding the embedded female flea and treatment consists of
removal of the flea taking care to avoid the risk of secondary bacterial infection including
tetanus.

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 10.2.11

10.2.5.1.4 Blood-feeding flies and myiasis (Diptera)

Blood-feeding flies comprise the biting midges (Culicoides spp. vectors of perstans
filariasis); black flies (Simulium spp, vectors of onchocerciasis); tsetse flies (Glossina
spp, vectors of African trypanosomiasis); horseflies (Chrysops spp., vectors of loiasis)
and the mosquitoes, belonging to the dipterous family, Culicidae)34. One can classify
these insects as temporary ectoparasites (such as mosquitoes, blackflies, biting midges
and tsetse flies or.alternatively, mosquitoes and tsetse flies are sometimes classified as
micropredators as they actively seek out their hosts.

Myiasis is infection of the human host with fly larvae (maggots)35,39,40. A range of
blowflies (Calliphoridae) have maggots that can, if the opportunity arises, attack human
flesh. Most of these derive from eggs or maggots deposited in open wounds on the skin –
especially septic wounds. The maggots then live in the wound until mature, drop off and
pupate on the ground. Most of these flies attack putrid flesh only, and in fact these
specific species of fly maggots have been used in the past (and are being used once more
today) in the treatment of such wounds because they attack only dead tissue and thus
clean up the wound. Additionally, their secretions contain antibacterials which help
resolve and prevent infection of the wound. Other species, such as the screw worm flies
(eg Callitroga spp), however, are invasive and can attack healthy skin or wounds and
destroy healthy skin often causing severe invasive damage.

Of particular interest in relation to human myiasis, however, are the Putsi (or Tumbu) fly
of tropical Africa and the Human Botfly (Dermatobia hominis) of Central and tropical
South America. Of these, the Putsi fly lays its eggs on clothing laid out to dry on the
ground while Dermatobia hominis lays its eggs on female mosquitoes or ticks. The eggs
hatch as a result of the warmth from the human body when the clothes are worn or when
the tick or mosquito feeds. The maggots develop in pustular, boil-like skin lesions for
about 7-10 days, after which the fully developed larva emerges, drops to the ground and
pupates, eventually emerging as the adult fly. Mostly these skin lesions are benign,
although scarring can result when the maggot drops out of the skin. Sometimes, however
serious complications or even death may result when a maggot on the head penetrates the
skull and invades the brain. Heavy maggot fly infections have been misdiagnosed as
chickenpox or even, in the past, as smallpox.

Various forms of myiasis are recognised39:

• Cutaneous myiasis – calliphorid blowflies; putsi flies, human botflies

• Gastrointestinal myiasis – calliphorid blowflies
• Ophthalmomyiasis – sheep nasal bot fly, Oestrus ovis41; screw worms
• Genitourinary myiasis – calliphorid blowflies.
• Sanguinivorous myiasis – the Congo Floor Maggot

Sanguinivorous myiasis due to Auchmeromyia luteola (The Congo Floor maggot) in

Central Africa is different from the others in that the maggots behave rather like bedbugs.
They inhabit rodent burrows and occasionally houses with mud floors and come out at

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 10.2.12

night while the host sleeps to take a blood meal before retreating back into the floor
cracks to moult39,40.

Diagnosis of myiasis is clinical, with the species identification being based on the
morphology of the posterior spiracular plate. Treatment is removal of the maggot – for
skin lesions, smearing with Vaseline prior to squeezing out the maggot may be used.

20.5.2 Arachnid infections/infestations

The arachnids are 8-legged arthropods. The group includes spiders, scorpions, ticks and
the mites. The first two are medically important as some species are venomous, while the
latter two groups can be ectoparasitic blood-suckers and in some cases important disease
vectors34.

10.2.5.2.1 Mites

A number of animal parasitic mites can at times attack humans, often causing unpleasant
allergic reactions which may be severe in some patients34. These mite species vary from
the ubiquitous, non-parasitic housedust mite (Dermatophagoides spp.), allergy to which
is widespread and an important cause of asthma-like attacks, to the wide range of animal
parasitic mites that bite humans - trombiculid mites and bird or rodent mites, such as the
genera Cheyletiella (dogs; cats; rabbits), Ornithonyssus (birds) , Liponyssoides (mice),
Dermanyssus (birds) and Leptotrombidium (rodents) 34. The latter species is the vector of
Scrub typhus (Tsutsugamushi Fever) due to Orientia tsutsugamushi. Grain workers may
also sometimes be attacked by free-living, mites of the genus Pyemotes which are
universally present in barley, wheat, cotton seed, grasses and hay and stored tobacco34.
These people often present with a mild to severe skin eruption which in some cases can
even superficially resemble chickenpox34.

Demodex folliculorum is the hair follicle mite of humans. It is a common parasite of

humans and while mostly of no or little clinical significance, it can block hair follicles
causing a ‘blackhead-like’ condition or a roseaceous skin rash34.

The scabies mites are by far the most important parasitic mites of humans and scabies is
the most important mite infection of humans. The cause is the human scabies mite,
Sarcoptes scabiei. The animal scabies mites can sometimes infect humans, but most cases
and outbreaks of scabies are due to the human strain. Clinical features of scabies involve
two components – the tunnels in which the mites live (which occur predominantly on the
wrists, the elbows, the ankles and around the thigh and genital region) and an allergic
rash. The mite lesions itch unbearably and the rash tends to cover the body, but spare the
face. Thus as a diagnostic rule of thumb, any person presenting with an itchy rash which
covers the body but spares the face, can be considered to have scabies until proven
otherwise. A problem which can arise from scabies is secondary infection of the lesions
with Streptococcus pyogenes and the development of glomerular nephritis.

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 10.2.13

Transmission of scabies is by close personal bodily contact (hand holding; sexual contact
etc) and blankets and clothing are not important in transmission. Scabies is worldwide
and epidemics and pandemics seem to occur every few years.

While diagnosis can be confirmed by isolation of the mites from the burrows42, this is not
a practical procedure in most cases and diagnosis is usually clinical.

Treatment for scabies usually relies on 25%benzyl benzoate but alternatives include
permethrin 5%, lindane 1% (contraindicated in pregnancy and during lactation), and 10%
crotomiton5,6,35. Usually a single application is adequate, but sometimes a second
treatment is needed after about 4-6 weeks if the infestation is not cleared. Care must be
taken to avoid over-treatment as the rash, which is a hypersensitivity reaction to the mite
and its waste products in the skin, may well remain after successful killing of the mites.
This often convinces the patient (and the doctor!) that the treatment has failed. A good
strategy to overcome this, is to treat with benzyl benzoate by covering the whole body
except the face with the medication, and then giving the patient crotomiton (Eurax) cream
to apply to spots where itching persists over the next few weeks. The crotomiton will
relieve the itch and has some miticidal activity. All contacts also need to be treated if the
infestation is to be controlled. Ivermectin 200ug/kg as a single oral dose has also been
used for the treatment of scabies, but should be used with caution in the elderly because
of increased toxicity5 Mass treatments may be necessary to control scabies outbreaks in
institutions.

10.2.5.2.2 Ticks

Ticks can be separated from the mites by their complex mouthparts, with a characteristic
many-hooked hypostome. Two major families of ticks can be recognised, the Argasidae
(soft ticks or tampans) and the hard ticks, the Ixodidae.

10.2.5.2.2.1 Argasid ticks

The argasids or tampans are blood-sucking ectoparasites of animals. They are known as
soft ticks because the body is covered by a soft, leathery integument. They live in sand or
the burrow of their usual animal host and feed intermittently. When humans intrude into
their environment, they will attack the human host. Important species include
Ornithodoros moubata and other species of the genus, which are the vectors of Borrelia
duttonii, a spirochaete harboured by rats and which causes endemic relapsing fever in
humans. The bat tampan of Africa, Argas brumpti, is found in caves inhabited by bats.
When humans are bitten by this species, extensive bruising of the skin results from the
powerful anticoagualant in the tick saliva. Such bites can cause an itchy rash, often
lasting for weeks or even months43.

10.2.5.2.2.2 Ixodid ticks

These are known as the hard ticks as they have a hard shield on the dorsal surface. There
are many genera and species, the best known of which are the genera Amblyomma,

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 10.2.14

Aponomma, Boophilus, Dermacentor, Haemaphysalis, Hyalomma, Ixodes, and

Rhipicephalis34. Tick bites are more of a nuisance that a hazard, but the complex
mouthparts including the hypostome, anchor the tick firmly to the skin while it feeds and
this makes removal a matter of care to avoid leaving the mouthparts embedded in the skin
when the tick is removed. Removal of a tick is usually easily achieved by grabbing the
tick as close to the skin as possible and removing it with a gentle pull. The applicationm
of vaseline to the attached tick can help in the process of removal. For removal of small
ticks (including the minute immature larval ticks), a pair of forceps can be of great help.

Tick bites can be irritating and can itch due to injected saliva. Mostly, however they are
of minor clinical significance unless they become secondarily infected, which tends to
happen especially if the mouthpart are detached during removal in which case a localised
ulceration may develop. The engorging females of some species, however, may produce
a salivary toxin which can paralyse the host and death will result unless the tick is
removed. In humans, the patient develops a localised or ascending paralysis reminiscent
of poliomyelitis from which it must be differentiated by finding the tick – which may be
embedded in such obscure locations as the ear canal or eardrum, in the hair, under the
armpit etc. Recovery commences with the removal of the tick. Such tick paralysis is
recorded from Europe (Ixodes spp., Rhipicephalis spp., Hyalomma spp., Boophilus spp.,
Haemaphysalis spp.); the USA (Dermacentor spp., Ixodes spp.); Africa (Ixodes spp.;
Hyalomma spp.) and Australia (Ixodes holocyclis)34. In Australia, antivenom is available,

Various species of these hard ticks are important vectors of viral illnesses such as Congo-
Crimean Haemorrhagic Fever, several viral encephalitides; rickettsial diseases such as
Rocky Mountain Spotted fever34, the Australian Spotted Fevers44, Boutonneuse Fever;
the spirochaetal Lyme disease and the protozoan disease of babesiosis34.

10.2.6 REFERENCES

1. Pearson, R.D., Jeronimo, S.M.B., Sousa, A. de Q. Leishmaniasis. In: Essentials of

Tropical Infectious Diseases. Guerrant, R.L., Walker, D.H. and Weller, P.F. (Eds)
Philadelphia; Churchill Livingstone. 2001. pp 372- 379.

2. Sturchler, D. Epidemic Areas of Tropical Infections. Basle; Roche, 1988.

3. Mills, A. and Goldsmid, J.M. Intestinal protozoa. In: Doerr, W. and Siefriet, G.
Tropical Pathology. 2nd ed. Berlin; Springer-Verlag, 1995. pp 477-556

4. Martinez, A.J. and Visvesara, G.S. Free-living amoebae: Naegleria,

Acanthasmoeba and Balamuthia infections. In: Essentials of Tropical Infectious
Diseases. Guerrant, R.L., Walker, D.H. and Weller, P.F. (Eds). Philadelphia;
Churchill Livingstone, 2001. pp 379-384.

5. Shorey, H., Walker, J., Biggs, B.-A. Clinical Parasitology. Melbourne; University
Press, 2000.

PARASITIC INFECTIONS OF THE SKIN

 10.2.15

6. Bartlett, J.G. Pocket Book of Infectious Disease Therapy. Philadelphia; Lippincott,

Williams and Wilkins, 2000.

7. Goldsmid, J.M., Mills, A. and Kibel, M. Helminth infections In: Textbook of

Pediatrics. 6th ed. McIntosh, N., Helms, P. and Smyth, R. (Eds) Edinburgh;
Churchill-Livingstone, 2003 pp 1475 - 1504

8. Goldsmid, J.M., Speare, R. and Bettiol, S The parasitology of foods. In: Foodborne
Microorganisms of Public Health Significance. 6th ed. Hocking, A.D. (Ed.)
Waterloo; AIFST, 2003. pp 705-722.

9. Beaver, P.C., Jung, R.C. and Cupp, E.W. Clinical Parasitology. 9th edit.,
Philadelphia; Lea and Febiger, 1984

10. Wittner, M. and Tanowitz, H.B. Other cestode infections. In: Essentials of Tropical
Infectious Diseases. Guerrant, R.L., Walker, D.H. and Weller, P.F. (Eds). N.Y.;
Churchill Livingstone, 2001. pp 490-491

11. Whitworth J. Onchocerciasis. In: Principles and Practice of Clinical Parasitology,

Gillespie S. and Pearson RD. (Eds) New York: John Wiley and Sons, 2001.

12. Darge K, Buttner DW. Ivermectin treatment of hyperreactive onchodermatitis

(sowda) in Liberia. Trop Med Parasitol 1995; 46: 206-212.

13. Greene BM, Gbaklima AA, Albiez EJ, Taylor HR. Humoral and cellular immune
responses to Onchocerca volvulus infection in humans. Rev Inf Dis 1985; 789-794.

14. Elkhalifa MY, Ghalib HW, Dafa’Alla T, Williams JF. Suppression of human
lymphocyte responses to specific and non-specifc stimuli in human onchocerciasis.
Clin Exp Immunol. 1991; 86: 433-439.

15. Cooper P, Espinel I, Wieseman M, Paredes W, Espinel M, Guderian RH, Nutman

TB. Human onchocerciasis and tetanus vaccination: impact on the post-vaccination
anti-tetanus antibody response. Infect Immunity 1999; 67: 5951-5957.

16. Brattig NW, Krawietz I, Abakar AZ, Erttmann KD, Kruppa TP, Massougbodji A.
Strong IgG isotypic antibody response in sowdah type onchocerciasis. J Inf Dis
1994; 170: 955-961.

17. Vincent JA, Lustigman S, Zhang S, Weil GJ. A comparison of the newer tests for
the diagnosis of onchocerciasis. Ann Trop Med Parasitol. 2000; 94: 253-258.

18. Weil GJ, Steel C, Liftis F, Li BW, Mearns G, Lobos E, Nutman TB. A rapid-format
antibody card test for diagnosis of onchocerciasis. J Inf Dis. 2000; 182: 1796-1799.

PARASITIC INFECTIONS OF THE SKIN

 10.2.16

19. Rodriguez-Perez MA, Dominguez-Vazquez A, Mendez-Galvan J, Sifuentes-Rincon

AM, Larralde-Cprona P, Barrera-Saldana HA, Bradley JE. Antibody tests for
Onchocerca volvulus: comparison of the sensitivity of a cocktail of recombinant
antigens used in the indirect enzyme-linked immunosorbent assay with a rapid-
format antibody test. Trans R Soc Trop Med Hyg. 2003; 97: 539-541.

20. Remme JH. Research for control: the onchocerciasis experience. Trop Med Int
Health. 2004; 9: 243-254.

21. Davies JB. Sixty years of onchocerciasis vector control: a chronological summary
with comments on eradication, re-invasion, and insecticide resistance. Ann Rev
Entomol. 1994; 39: 23-45.

22. World Health Organisation, Onchocerciasis and its control. Technical report series
852. Geneva; WHO. 1995.

23. Nutman TB. Blood-borne filarial infections. In: Principles and Practice of Clinical
Parasitology, Gillespie S. and Pearson RD. (Eds) New York; John Wiley and Sons,
2001.

24. Chippaux JP, Boussinesq M, Gardon J, Gardon-Wendel N, Ernould JC. Severe

adverse reaction risks during mass treatment with ivermectin in Loasis-endemic
areas. Parasitol Today. 1996; 12: 448-50.

25. Eberhard Ml, Lammie PJ. Laboratory Diagnosis of Filariasis. Clin Lab Med 1991;
4: 977-1010.

26. Nutman TB, Zimmerman PA, Kubofcik J, Kostyu DD. A universally applicable
diagnostic approach to filaroid and other infections. Parasitol Today 1994; 10: 239-
243.

27. Carme B, Boulesteiz J, Boutes H, Puruehnce MF. Five cases of encephalitis during
treatment of Loasis with diethylcarbamazine. Am J Trop Med Hyg 1991; 44: 684-
690.

28. Abel L, Ioly V, Jeni P, Carbon C, Bussel A. Apheresis in the management of

Loasis with high microfilaraemia and renal disease. Br. Med. J. (Clin. Res Ed.)
1986; 292: 24.

29. Klion AD, Massougbodji A, Horton J. Albendazole in human Loasis: results of a

double-blind placebo-controlled trial. J Inf Dis 1993; 168: 202-206.

30. Tabi TE, Befidi-Mengue R, Nutman TB, Horton J, Folefack A, Pensia E, Fualen R,
Fogako J, Gwanmesia P, Quakyi I, Leke R. Human loasis in a Cameroonian

PARASITIC INFECTIONS OF THE SKIN

 10.2.17

village: a double-blind, placebo-controlled, crossover clinical trial of a three-day

albendazole regime. Am J Trop. Med Hyg 2004; 71: 211-215.

31. Goldsmid JM, Rogers S. Studies on the diagnosis and treatment of human filariasis
in Rhodesia. S Afr Med J. 1979; 50: 1129-1132.

32. Nutman TB, Nash TE, Ottesen EA, Ivermectin in the successful trial of a patient
with Mansonella ozzardi infection. J. Inf. Dis 1987; 156: 662-665.

33. Orihel TC, Eberhard ML. Zoonotic filariasis. Clin Microbiol Rev 1998; 36:381.

34. Alexander, J.O’D. Arthropods and Human Skin. .Berlin; Springer-Verlag, 1984.

35. Goldsmid, J.M.., Mills, A. and Kibel, M. Flies, fleas, lice and mites In: Textbook of
Pediatrics. 6th ed. Arneil, G (Ed) Edinburgh. Churchill Livingstone, 2003. pp 1504-
1508

36. Dasgupta, R. and Dasgupta, B. Collembolan insects as potential parasites. Trans. R.

Soc. Trop. Med. Hyg. 1990; 84: 438.

37. Donaldson, R.J. (Ed.) Parasites and Western Man. Lancaster. MTP. 1979.

38. Spicer, J. (Chairman) Therapeutic Guidelines. Version 12. Melbourne; Therapeutic

Guidelines Ltd., 2003.

39. Zumpt, F. Myiasis in Man and Animals in the Old World. London.
Butterworth, 1965.

40. Goldsmid, J.M. and Phelps, R.J. A review of myiasis of man in Rhodesia. C. Afr. J.
Med. 1977; 23: 174-179.

41. Hoffman, B.L. and Goldsmid, J.M. Ophthalmomyiasis caused by Oestrus ovis L.
(Diptera: Oestridae) in Rhodesia. S. Afr. Med. J. 1970; 44: 644-645.

42. Chin, J. (Ed.) Control of Communicable Diseases Manual. 17th ed. Washington.
APHA, 2000.

43. Condy, J.R., Norval, R.A.I., Blackburn, N. and Clemence, P. The effects of the
bites of Argas brumpti (Acarina: Argasidae) on humans. C. Afr. J. Med. 1980; 26:
212-213.

44. Graves, S. Rickettsial diseases: An Australian perspective. Annals of the ACTM.

2005; 5: 17-21.

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Correspondence:

Professor John Goldsmid, BSc (Hons), MSc, PhD, FRCPath, CBiol., FIBiol,
FAIBiol, FASM, Hon FACTM, Hon FRCPA.
Emeritus Professor of Medical Microbiology
Discipline of Pathology
University of Tasmania,
Hobart, Tasmania, Australia
[email protected]

Dr Wayne Melrose, DrPH, MPH&TM, BApplSci, ThDip, FACTM,

FAIMS, MNZIMLS.
Acting Director,
W.H.O. Collaborative Centre for Control of Lymphatic Filariasis,
Senior Lecturer,
Anton Breinl Centre for Public Health and Tropical Medicine,
James Cook University,
Townsville, Queensland, Australia
[email protected]

***

© Copyright 2005.

All rights reserved, The Australasian College of Tropical Medicine

Primer of Tropical Medicine

Enquiries to: [email protected]

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