Parasites and the skin: parasitic infections may be confined to the skin or may have skin involvement as part of their pathology.
This article seeks to familiarise readers with the management of those conditions that are encountered in daily practice and to remind you of those rare and wonderful infestations that you might never see. I will focus on and deal with parasitic infestations and the skin. Skin pathology often provides important clues to systemic infections. This article will discuss common clinical presentations and tabulate the rarer diseases.Parasitic infestations are common in the tropics due to a combination of heat, humidity and ultimately poor socioeconomic and health care conditions.
Parasitic infections can be solely confined to the skin, as seen with human scabies, cutaneous larva migrans, the chigger flea, cutaneous myiasis and cutaneous leishmaniasis. Parasites not confined to the skin include onchocerciasis, loiasis, the guinea worm, schistosomiasis, cutaneous amoebiasis and the cutaneous involvement in trypanosomiasis.
Common scenarios
Scabies
The common scenario of a child brought to a busy rural outpatient department or public hospital is shown in Figs 1 and 2. The history is that of severe pruritis persisting for a few weeks, worse at night and there are family members or friends with the same affliction as shown in Fig. 1. The diagnosis is scabies until proven otherwise, and treatment consists of topical scabicides.
[FIGURE 1 OMITTED]
[FIGURE 2 OMITTED]
Human scabies is caused by the host-specific mite Sarcoptes scabie var. hominis. A hypersensitivity reaction to the mite is responsible for the intense pruritis experienced by infested individuals. This burrowing mite lives its entire life cycle within the epidermis of the skin. Secondary infection with group A Streptococcus pyogenes or Staphylococcus aureus may occur. Transmission occurs by direct contact and sometimes spreads through fomites. Drug resistance to topical scabicides is occurring.
The diagnosis is confirmed by direct microscopy of skin scraping from a burrow, mounted on a glass slide. The findings are demonstrated in Fig. 3. Dermoscopy, epiluminescence microscopy and skin biopsy are other diagnostic aids. Treatment is shown in Table I.
[FIGURE 3 OMITTED]
Table I. Treament of scabies
Drug Dose Comment
Gamma-bezenehexachloride: Apply and leave on for Contraindicated
Lindane 1% lotion 8 hours; repeat 1 week during pregnancy and
later in children <2 years
of age
Resistance is
emerging
Aplastic anaemia
recently reported in
children treated with
Gambex shampoo
Precipated sulphur 5 - Apply for 3 Safe in children and
10%: Tetmosol soap 5% consecutive days, then in pregnancy
wash off Preparations include
Tetmosol soap 5%
Useful for
prophylaxis
Ineffective in
established
infestation Sulphur
ointments in soft
white paraffin
effective in children
Crotamiton: Eurax Apply on 2 consecutive Eurax not as
days, repeat in 5 effective as the
days others
Benzyl benzoate 10% Apply for 24 hrs then Dilute in water for
lotion: Ascabiol emulsion wash off May need to children Safe in
25% repeat pregnancy Rare
side-effects Skin
irritation
Ivermectin 200 Stat dose Can repeat Highly effective,
[micro]g/kg after a week especially in
Norwegian crusted
scabies
Can be obtained on a
named-patient basis
from MSD with
permission from the
MCC
Pyrethroids: Spregal Spray entire body Esdepallethrin is a
aerosol except the face; leave pyrethroid pesticide,
on overnight and which is scabicidal
repeat one week later
Repeated sprays may be Piperonyl butoxide
needed in HIV+ acts by blocking the
patients defense system that
the parasite uses to
counteract the latter
All persons affected Contraindicated in
in same household to children <2 years and
treat at the same during pregnancy
time
Do in well-ventilated
room and avoid any
flames
Disinfect clothes and
bed linen
Treatment of scabies
Effective management of scabies requires the following:
* Treat all contacts.
* Apply scabicides from the neck down over the entire body, especially unaffected intertriginous areas of the skin.
* Avoid using antiseptic such as dettol and savlon.
* Avoid overuse of tetmosol soap, which may worsen existing pruritis.
* Disinfect towels, clothing and bedding.
* Use systemic antibiotics and/or systemic antihistamines in severe cases.
* Short courses of topical or systemic steroids may be effective in treating post-scabetic pruritis, which is common. Avoid the continuous use of topical antiseptics.
* Use sulphur-based ointments in neonates, infants and in pregnancy.
Norwegian scabies
The second clinical scenario of Norwegian scabies is commonly seen in HIV-positive patients. Fig. 4 shows the eczematous, psoriasiform rash reminiscent of psoriasis.
[FIGURE 4 OMITTED]
Diagnosis will be assisted by considering the following:
* One or more skin biopsies may be required to confirm the diagnosis.
* This illness is highly contagious and often health care workers become afflicted after contact.
* Norwegian scabies is commonly seen in old age homes and psychiatric facilities.
* The most effective treatment for Norwegian scabies is oral ivermectin, which requires permission for use from the Medicines Control Council.
* Several applications and prolonged use of stronger concentrations of sulphur ointments, Ascabiol or Spregal spray need to be used in these patients to obtain cure.
* Keratolytics and occasionally anti-proliferative agents are needed to clear the hyperkeratosis that is teeming with mites before using the above agents.
Myiasis
Scenario 3 demonstrates a typical case of myiasis. A backpacker ventured into rural Zimbabwe for a few months and subsequently returned to Johannesburg with numerous boils on his back (Fig. 5). These irritating lesions persisted for approximately 3 weeks and did not respond to topical antiseptics and systemic antibiotics.
[FIGURE 5 OMITTED]
Myiasis is caused by the larvae of flies, which lay their eggs on skin or clothing. The eggs hatch and the larvae penetrate the skin. Worldwide the most common flies that cause human infestation are Dermatobia hominis (human botfly) and Cordylobia anthropophaga (tumbu fly).
The route of transmission differs with different flies. The botfly lays her eggs on mosquitoes, which in turn deposit them on warm-blooded mammals. The tumbu fly deposits its eggs on moist clothing, soiled blankets and in sand. In endemic areas people usually iron their clothes after hanging them out to kill the fly eggs.
There are essentially two types of myiasis:
* Furuncular myiasis (Fig. 6), which is what the patient described in our scenario has, usually caused by the botfly.
[FIGURE 6 OMITTED]
* Wound myiasis (Fig. 7), where larvae are deposited in suppurating wounds or on decomposing flesh. Cochliomyia hominovorax is the causative fly in the Americas and Chrysomia in Africa.
[FIGURE 7 OMITTED]
The main aim of treatment is literally to suffocate the larvae. Occlusive ointments such as vaseline are effective as they interfere with the larva's respiration and force it to extrude itself. Alternatively, surgical nicking of the furuncle followed by extraction of the larvae can be curative (Fig. 6).
Topical and systemic antibiotics may be needed to cure any secondary infection. The approach in wound myiasis would be surgical debridement and the principles of surgical management.
Cutaneous larva migrans
In the fourth scenario a young child is brought for a rash on his foot, as shown in Fig. 8. The family had just returned from a coastal holiday. This is typical of cutaneous larva migrans or 'creeping eruption'. The latter term is being used because of the slow crawling movement of the worm, which is visible. This condition is due to the incomplete development of hookworm larvae, whose natural hosts are cats and dogs, in man. The larvae are found in damp soil contaminated by dog and cat faeces. Invasion of human skin usually takes place on beaches, where shoes are seldom worn.
[FIGURE 8 OMITTED]
Treatment of larva migrans
Spontaneous cure can take place over months. Do not try to catch, freeze or surgically clip the worm. The treatment of choice is a single dose or 3-day course of albendazole.
Alternatively, a 500 mg tablet of thiabendazole is ground up in 25 g of vaseline and applied once a day for 2 days.
Chigger fleas or tungiasis
In scenario 5 a child from a rural, economically poor area of KZN is brought to you. Fig. 9 demonstrates the clinical picture. The primary lesions are black dots, papules, nodules and burrowing excoriations. There is some resemblance to a minor abscess with a central punctum. The child complains of mild discomfort. The differential diagnosis includes infected warts or scabies but the primary lesions of these are fairly typical ofchigger fleas, therefore always consider tungiasis or chiggers in this setting.
[FIGURE 9 OMITTED]
This is common in the tropics (endemic in Central and South America, the Caribbean, tropical Africa, India and Pakistan), and is caused by the wingless flea Tunga penetrans. The condition is called tungiasis.
The flea's eggs are found in clusters in soil, from which infestation of the bare-footed patient occurs. The impregnated female burrows itself into the skin of the foot, the toe webs, around the nails and on the heels. The flea's abdomen expands rapidly, forming a large white sphere like a mistletoe berry. Rare complications include gangrene, tetanus and auto-amputation.
Treatment of tungiasis
* Maintaining a high index of suspicion for this condition.
* Removal of the flea with a sterile needle.
* Surgical curettage and electrodessication.
* Topical thiabendazole or ivermectin.
* Systemic thiabendazole or ivermectin.
* Systemic antibiotic cover.
* Tetanus prophylaxis.
Leishmaniasis
In this scenario, a 26-year-old medical doctor visited Israel over a period of a month and returned with a small sore on his upper lip. This increased in size with time. He took an empiric dose of a broad-spectrum antibiotic in addition to a topical antibiotic for 2 weeks, with no response. He had no associated constitutional symptoms. Fig. 10 shows the ulcerating plaque, which is clinically non-diagnostic.
[FIGURE 10 OMITTED]
The differential diagnoses include:
* furunculosis resistant to antibiotics
* an actinic cheilitis (this would occur on the lower lip)
* granulomatous conditions which may be fungal such as sporotrichosis, or mycobacterial such as tuberculosis
* atypical mycobacteria
* syphilis or other sexually transmitted infections
However, his visits to the Middle East would make one consider leishmaniasis.
Diagnosis requires the mandatory performance of an adequately sized deep skin biopsy.
The presence of amastigotes in neutrophils is in keeping with leishmaniasis. This doctor had the oriental sore of cutaneous leishmaniasis.
Leishmaniasis is a genus of flagellate protozoa found in Africa, the Mediterranean basin, the Caribbean and Latin America. It is transmitted by the bite of the phlebotomus sandfly.
Dogs and rodents are the intermediate hosts.
There are three forms of leishmaniasis:
* cutaneous leishmaniasis, which is restricted to the skin and is seen more often in the old world, as seen in our patient
* mucocutaneous leishmaniasis, which affects the skin and mucous surfaces and occurs exclusively in the so-called new world (Fig. 11)
[FIGURE 11 OMITTED]
* visceral leishmaniasis, which affects the organs of the mononuclear phagocytic system, such as the lymph nodes and spleen.
There are various species and subspecies of Leishmania. The commonest old-world form is L. major or L. tropica.
The clinical picture begins with a small papule at the inoculation site, which enlarges into a nodule or plaque. This may become verrucous or ulcerate. The lesions are often solitary but may be multiple, with the formation of satellites in a lymphatic or sporotrichoid spread. These lesions can resolve spontaneously in people living in endemic areas or may become chronic and disseminate. The latter occurs more often in immunosuppressed patients with poor cell-mediated immunity.
Diffuse cutaneous leishmaniasis develops in the setting of infections with L. aethiopica and L. amazonensis. After a prolonged time period of years and decades some patients develop mucocutaneous disease. Additional forms of cutaneous leishmaniasis are L. recidivans, which follows a sporotrichoid pattern with dry erythematous plaques. L. recidivans is characterised by recurrences at the site of an original ulcer, generally within 2 years and often at the edge of a scar.
Diagnosis of leishmaniasis
The diagnosis is confirmed by tissue or skin histology which demonstrates the presence of amastigotes in dermal macrophages. This is sometimes found in dermal scrapings or fine-needle aspirate (FNA) of affected tissue--so-called Leishman-Donovan bodies in large histiocytes. However, in older lesions parasites may not be found. Here the delayed skin reaction test (Montenegro test or Leishman reaction), which uses leishmania antigens to induce a cell-mediated (CMI) response can be an important diagnostic tool.
This test is positive in 50% of patients with cutaneous and mucocutaneous leishmaniasis. It is negative in diffuse leishmaniasis. Another drawback is that the test does not distinguish between past and current infection. Other adjunctive tests are tissue culture, ELISA and PCR.
Treatment of cutaneous leishmaniasis
Treatment depends on the type and severity of infection. Old-world disease is often self-limiting. Severe cases of L. tropica and L. major can be treated with pentavalent antimonials. New-world disease, e.g. L. brazilienzes, can progress to mucocutaneous disease. Treatment of choice is pentavalent antimonials, e.g. sodium stiboglutamate or meglumine antimonials.
Adjunctive treatments for cutaneous and mucocutaneous lesions include heat and cryotherapy, and drugs such as itraconazole, amphotericin B, ketaconazole and allopurinol. Prevention measures include insect repellants, insecticides and destruction of animal reservoirs.
Parasites not confined to the skin include onchocerciasis, loiasis, the guinea worm, schistosomiasis, cutaneous amoebiasis and the cutaneous involvement in trypanosomiasis. These are listed in Table II and depicted in Figs 12 - 14.
[FIGURE 12 OMITTED]
[FIGURE 13 OMITTED]
[FIGURE 14 OMITTED]
Table II. Summary of parasitic diseases not confined to the skin
Disease Pathogen Vector Geographic
distribution
Onchocerciasis Onchocerca Blackflies Equatorial
(Fig. 12) volvulus Simulium Africa,
Along Central and
free-flowing South
rivers Larvae America,
develop well Yemen
in aerated
water
Loiasis (Fig. Loa loa Chrysops West and
13) flies Central
Africa
Dracunculosis Guinea worm Ingest larva Africa, Latin
(Fig. 14) Dracunculous in America,
medinensis contaminated India
water
containing
cyclops
Cutaneous S. haematobium Humans are Haematobium
schistosomiasis S. mansoni infected by North Africa
S. japonicum contact with Middle east
fresh water Sub-Sahara
The parasite Mansoni
penetrates Sub-Saharan
intact skin Africa Middle
Water snails East Brazil
are Caribbean
intermediate Japonicum
hosts China
Philippines
Indonesia
Trypanosomiasis American T. American: Tropical
cruzi Reduviid bug America
(Chagas' Occasionally Tropical
disease) contaminated Africa
African T. blood Tsetse
rhodesiense fly
(acute) T. (Glossina)
gambiense
(chronic)
Filarial Wuchereria Mosquitoes Africa, West
elephantiasis bancrofti, Genus: Aedes Indies
Brugia
malayi
Disease Diagnostic Disease and
tests complications
Onchocerciasis Skin snips for Chronic pruritis
(Fig. 12) unsheathed and excoriations
microfilaria Eye involvement
DEC with gradual
(Mazotti test impairment of
vision and
blindness (river
blindness)
Loiasis (Fig. Microscopy of Calabar swellings
13) day blood for (migrating
microfilaria swelling) Transient
subcutaneous
nodules often on
the arm Irritation
of eye as an adult
worm traverses the
sclera
Dracunculosis Clinical: see Ingested larva
(Fig. 14) adult worm reach the skin,
stringing out of where adult worm
skin ulcer literally breaks
through
Cutaneous Identification Papules, nodules
schistosomiasis of viable eggs Cercarial
Microscopy of dermatitis
terminal urine (swimmer's itch)
in S. Main pathology is
haematobium granuloma formation
Stool in S. around eggs
mansoni and S. Katayama fever:
japonicum Eggs development of
from all on adult worms and the
rectal biopsy early stages of egg
Serology: does deposition, days to
not distinguish weeks after
acute from past infection May cause
infection severe systemic
reaction including
fevers, rigors,
myalgia, urticaria,
lymphadenopathy and
hepatosplenomegaly
High eosinophilia
Chronic established
disease:
granulomatous
disease affecting
all organs
Trypanosomiasis American: In Clinical includes a
acute stage necrotic chancre at
stage micro exam the site of
for inoculation,
trypomastigotes pruritis in the
in blood specs later stage, and
Thereafter: PCR 'trypanides', more
African: or less discoid or
Detection of annular
trypanosomes in erythematous
blood film, eruptions African
chancre, lymph Trypanides Cervical
node aspirate, lymphadenopathy In
buffy coat, bone American Tryp
marrow or CSF Affects ANS, GIT
PCR and CVS systems
Myocarditis is
critical in these
patients When
conjunctiva is the
portal of entry
oedema of the
palpebral and
periocular tissue
is seen--Romana's
sign Chagoma:
painful nodule at
site of
inoculation
Filarial Microfilaria in Thickened
elephantiasis peripheral blood oedematous skin
at night
Disease Treatment
Onchocerciasis Ivermectin
(Fig. 12) effective against
microfilaria
Adjunctive
doxycycline
sterilises female
worm Add systemic
steroids in cases
of eye involvement
Suramin for adult
worms
Loiasis (Fig. Oral DEC 1 - 6 tabs
13) dly for 2 weeks
Repeated courses
are necessary
Ivermectin
Dracunculosis Excision and
(Fig. 14) extraction
Metronidazole
(anti-inflammatory
more than
antihelmintic)
Wound care
Cutaneous Praziquantel 40
schistosomiasis mg/kg/day stat
Sometimes repeated
Systemic steroids
in Katayama fever
Avoidance of water
in endemic areas
Snail control
Trypanosomiasis Nifurtimox (with
gamma interferon
Suramin,
pentamidine
Eflornithine WHO
control measures
Filarial Ivermectin
elephantiasis Adjunctive
albendazole,
doxycycline
Surgical
correction
DEC = diethylcarbamazine; ANS = autonomic nervous system; GIT =
gastrointestinal; CVS = cardiovascular system; CSF = cerebrospinal
fluid; PCR = polymerase chain reaction.
RELATED ARTICLE: In a nutshell
* Skin pathology often provides important clues to systemic infections.
* Parasitic infestations are common in the tropics due to a combination of heat, humidity and ultimately poor socioeconomic and health care conditions.
* Parasitic infections can be solely confined to the skin, as seen with human scabies, cutaneous larva migrans, the chigger flea, cutaneous myiasis and cutaneous leishmaniasis.
* Parasites not confined to the skin include onchocerciasis, loiasis, the guinea worm, schistosmiasis, cutaneous involvement in trypanosomiasis.
DEEPAK MODI, MB BCh, DTM &H (RCP Lond), MSc (Lond), FFDerm (SA)
Professor and Academic Head, Division of Dermatology, University of the Witwatersrand, Johannesburg
E-mail: howzat@iafrica.com
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| Author: | Modi, Deepak |
|---|---|
| Publication: | CME: Your SA Journal of CPD |
| Article Type: | Disease/Disorder overview |
| Geographic Code: | 6SOUT |
| Date: | Jan 1, 2010 |
| Words: | 2808 |
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