LEISHMANIASIS
Leishmaniasis is a
protozoal disease caused by Leishmania tropica parasite, which is
transmitted by the Phlebotomus sand fly .The reservoir hosts are the dog
in the Mediterranean area , man in the Middle East and the wild rodents in
Asia and Africa .
Leishmaniasis has
three different morphological features ; cutaneous leishmaniasis ,
muco-cutaneous and the visceral (Kala-azar ).
CUTANEOUS
LEISHMANIASIS
Cutaneous
leishmaniasis has many local synonym such as Tropical sore, Oriental sore,
Aleppo sore or Baghdad sore. The disease is caused by Leishmania tropica
protozoa, which is endemic in Asia minor, Southwest Asia, the
Mediterranean and gulf regions.
Modes
of Infestations
The Phlebotomus
sand fly is the vector,
transmitting the disease from the reservoirs to human being.
Direct
infection from
infected sores to a traumatized skin may rarely cause the disease .
Children are more
susceptible, where solid immunity is acquired after the first infestation.
This is why some natives sometimes inoculate their children with the
protozoa on the shoulder or thighs to have the disease there in order to
protect the face from scarring if they are infested in the future with
leishmania.
Clinical
Features
The disease has a very chronic
course. The incubation period may take from weeks to two months
from the beginning of the sand fly bite .
Leishmaniasis
usually affects children more than other age groups where the face ,
extremities and the neck are the most common sites involved.
Fig.115. Cutaneous leishmaniasis
(Ulcerative & Destructive type) |
Fig. 116. Cutaneous leishmaniasis |
Fig. 117. Cutaneous leishmaniasis
(Ulcerative type)
|
Cutaneous
leishmaniasis has different clinical manifestations :
Oriental
sore
The primary lesion
is a papule mainly on the exposed areas such as the face and extremities .
The papule enlarges after few weeks to form a round plaque, which later on
ulcerates exuding a sticky secretion and forming a brownish , thick
adherent crust .
Secondary
bacterial infection of the ulcers is common causing more tissue
destruction and disfiguring of the skin.
One of the characteristic
of tropical ulcer lesion is its long chronic course and the satellites,
which develop nearby the primary lesion . These satellites may fuse
together forming punched out rounded or oval ulcers that may heal
after a few months causing disfiguring scars.
Abortive
type :
Some lesions are dry where the papule changes into a nodule that may
enlarge in size without ulceration .
The
monorecidive type : is a
relapsing type where infection occurs again after healing of the primary
lesion .
The
disseminated form -
Multiple lesions may involve the extremities. |
Fig.118. Cutaneous leishmaniasis
(Abortive type)
Fig. 118b. Cutaneous
leishmaniasis (Abortive type) |
Fig.120. Cutaneous leishmaniasis
(Disseminated type) |
Fig. 119. Cutaneous leishmaniasis
(Monorecedive
type) |
Different
Clinical Manifestations
Cutaneous
leishmaniasis due to L. infantum :
Infants infested
with this parasite, may have visceral leishmaniasis, while adults usually
get only the cutaneous lesions.
Cutaneous
leishmaniasis due to L. major:
(This type is endemic in wet and rural zoonotic areas)
The cutaneous
lesions are red, furuncle-like nodule appears at the site of inoculation
where after 2 weeks a central crust forms which may be followed by
ulceration . The ulcer has a raised red margin , enlarges over the next
2-3 months where the lesion reaches a diameter of 3-6 cm. Multiple
satellite nodules may develop near the primary lesion .
Spontaneous healing even without
treatment usually takes place within six months leaving a scar.
Cutaneous
leishmaniasis due to L. tropica
The incubation
period is more than 2 months . The lesion appears as a small, brownish
nodule that enlarges gradually to a plaque 1-2 cm in diameter in about 6
months forming shallow ulceration with adherent crust. Secondary satellite
lesions are minimal with this type .
Cutaneous
leishmaniasis due to L. Ethiopia
Lesions are most
commonly involve central of the face and theses are usually single. Satellite papules acuminate
may form a large spreading nodule without crusts .
Mucocutaneous
lesions around the mouth and nose may occur .
Diagnosis
of Leishmaniasi
-
An ulcer or
nodules having a chronic course of few months duration with satellites
in an endemic area is considered important cardinal signs.
-
Smear from the
base of the ulcer stained with Wright‘s stain detects round or ovoid
parasite in the cytoplasm with polymorph and mononuclear leukocytes
and epithelial cells .
-
Leishman test:
Intradermal injection of leishmanial antigen causes a delayed
tuberculin type of reaction.
Differential
Diagnosis
Oriental sore may
simulate different skin diseases such as tuberculosis cutis, tropical
ulcer, tuberculus ulcer and others.
MUCOCUTANEOUS
LEISHMANIASIS
Mucocutaneous
leishmaniasis is caused by Leishmania Brazilians parasite, which has the
affinity to involve the skin and mucous membranes. The disease is endemic
in Latin America, Peru and Brazil .
Etiology
The Phlebotomus
fly transmitting the disease lives in the forests and causes the infection
by biting their hosts .
The parasite is
present in two forms; the
flagellate, which is found
in the digestive tract of the vector and the non
flagellate form
which, is found in the tissues of human and animals infested by the
parasite .
Clinical
Picture
The incubation
period is from 2-4 weeks.
Skin
manifestations
The primary lesion
is a nodule that may abort after few weeks or enlarge into a nodule which
becomes vegetative and eventually forms a well-defined, irregular,
infiltrating ulcer .
Mucous
membranes manifestations
The characteristic
of the mucocutaneous lesion is its tendency to metastasis to the mucous
membrane of buccal and nasopharynex probably via lymphatics or blood
stream.
General
manifestations
The mucous
membrane lesions may involve the adjacent cartilage while bones are spared
.
Disfiguring of the
nose, soft palate, larynx, and pharynx .
Ulceration of
tongue, ocular and genital mucosa.
Regional
lymphadenopathy.
Differential
Diagnosis
-
Tropical
ulcer
-
Sporotrichosis
-
Tuberculosis
-
Yaws and
Syphilis .
Treatment
of Leishmaniasis
Most sores will
heal spontaneously within one year .
Treatment of
cutaneous and muco cutaneous leishmaniasis is the same while the latter
needs more intensive treatment due to the more severe and destructive
complications.
** Pentavalent
antimony: used for sores
that may cause scarring and disfiguring on the face, lower leg or over a
joint; mucosa or cartilage, or sores that might be due to parasites of the
L. braziliensis.
Unfortunately some
cases of leishmaniasis, may be seen treated by topical steroid
preparation. This changes the clinical picture, deteriorates the lesion ,
which becomes later more chronic and decreases its response to the
specific medications.
For adults, we
give 6 cc of Pentostam I.M. daily for 10 days. This usually gives very
good results, causing rapid healing of the ulcers. The dose is adjusted
according to the age.
** El-Zawahry
reported good results with dihydroemetine (Ciba) 2 tablets daily
for adult age for one month
** Neostibosan
(Bayer): is also an effective medication . The daily dose is 5mg./kg. body
weight . A dose of 200-300 mg. can be given for older children and adults
daily for 16 days is proved to be also effective .
Other medications
such as Chloroquine , Fouadin and antibiotics such as Tetracycline
have been found to be effective.
** Pentamidine
isethionate can be used
for Leishmania tropica in a dose of 4 mg/kg body weight once weekly for as
long as necessary .
Patients with
diffuse cutaneous leishmaniasis require treatment for a longer time.
Leishmaniasis
recidivans may respond to local infiltration, or systemic antimonies.
** Local infiltration
with 1-2 ml sodium
stibogluconate for solitary lesions.
** CO2 snow for small
sores may be frozen and curetted under local anesthesia.
Severe scarring
lesions may require plastic surgery .
** We used Co2
laser to resurface and ablate cutaneous leishmaniasis lesions. In our
medical center we recorded encouraging results especially in lesions
complicated by scarring .
Fig. 121. Cutaneous leishmaniasis (Scar) |
Fig. 122. leishmaniasis Scar treated by Co2 Laser |
**
Zithromx and Muperacin
This child
has cutaneous leishmaniasis since eight months. Different types of
standard treatment even carbon dioxide and surgical debridement were tried
in different centers.His father was advised for the last to be treated by
Co2 Laser. I was not sure that is the best in such an area were scarring
was clear due to different treatments.
I prescribed for
him muperacin cream (Bactroban cream and Zithromax suspension for one
week) Dramatic relief of the lesion was noticed. The same line of
treatment (Muperacin cream &Zithromax) was applied to other patients
and the results were rappid healing of the lesion.
Therefore
, this safe , un expensive new line of treatment for cutaneous
leishmaniasis can be tried.
Fig.122 b. Cutaneous leishmaniasis (before
treatment) Fig.122cOne week after treatment with Zithromax &Muperacin cream
(The deep scar is mainly due to the previous cautary)
Fig.117a. Oriental sore
Fig.117b. Oriental sore
(After treatment)*
*(One week after treatment with Muperacin cream (Bactroban)
and Zithromycin uspension
(Zithromax) .
VISCERAL
LEISHMANIASI
This is known also
"Kala-azar" and "dum-dum fever."
The disease is
widely distributed in Asia, South Europe, around the Mediterranean,
Africa, and in rural and poor communities .
Clinical
Picture
Irregular fever of
long duration .
- Fever is characteristic
and sometimes diagnostic to Kala-azar. The temperature rises in the
afternoon, declines towards the evening and rises once more around
midnight.
-
Hepatosplenomegaly
-
Emaciation
.
-
Anemia
and Leukopenia .
-
Visceral
manifestations; hepatosplenomegaly
-
Skin
manifestation - A peculiar grayish color of the skin, particularly on
the hands, nails, forehead, and central line of the abdomen; hence the
name "black disease" is derived .
POST
KALA-AZAR DERMAL LEISHMANIASIS
Clinical
Features
Cutaneous apple
jelly nodules surround the healing scars mainly on the face may appear few
years after healing of the primary lesions.
Hypopigmented
patches particularly on the face, neck, and extensor surface of the
forearms and inner side of the thighs resembling lepromatous leprosy .
Nodular and
granulomatous lesion may appear on the skin and rarely Papillomatous on
the eyelids, lips and ala nasi.
REFERENCES
-
Bryceson A.
Therapy in man. In: Peters W. Killick-Kendrick R, eds. The
-
Leishmaniases
in Biology and Medicine Vol 2. London: Academic Press, 1987: 848-907.
-
Ho M, Koech
DK, Iha DW et al. Immunosuppression in Kenyan visceral leishmaniasis.
Clin Exp Immunol 1983; 51: 207-14.
-
Kumar PV,
Sadeghi E, Torabi S. Kala azar with disseminated dermal leishmaniasis.
Am J Trop Med Hyg 1989; 40: 150-3.
-
Rashid JR,
Chunge CN, Oster CN et al. Post kala-azar dermal leishmaniasis
occurring after long cure of visceral leishmaniasis in Kenya. E Afr
Med J 1986; 63: 365-71.
-
WHO. The
leishmaniases. Report of WHO Expert Committee. Technical Report Series
701. Geneva: World Health Organization, 1984.
-
Ballou WR,
McClain JB, Gordon DM et al. Safety and efficacy of high dose sodium
stibogluconate therapy of American cutaneous leishmaniasis. Lancet
1987; ii: 12-16.
-
Bryceson A.
Therapy in man. In: Peters W. Killick-Kendrick R, eds. The
Leishmaniases in Biology and Medicine Vol 2. London: Academic Press,
1987: 848-907.
-
El-On J,
Weinrauch L, Livshin R et al. Topical treatment of recurrent cutaneous
leishmaniasis with ointment containing paromomycin and
methylbenzathonium chloride. Br Med J 1985; 291: 704-5.
-
Kumar PV,
Sadeghi E, Torabi S. Kala azar with disseminated dermal leishmaniasis.
Am J Trop Med Hyg 1989; 40: 150-3.
-
Montalban CK,
Martinez-Fernandez R, Calleja JL et al. Visceral leishmaniasis
(kala-azar) as an opportunistic infection in patients infected with
the human immunodeficiency virus in Spain. Rev Infect Dis 1989; 11:
655-60.
HUMAN
TRYPANOSOMIASIS
CHAGAS DISEASE
SOUTH
AMERICAN TRYPANOSOMIASIS
This is a systemic
disease caused by Trypanosome cruzi.
Modes of
Infection
Direct
infection:
Infection from
infected animals .
From animal
reservoirs such as cats, dogs and wild rodents.
Indirect
infection :
From man to man by
the "kissing bugs" either, by the bug bite where trypanosomes
are seeded into the skin, or infection from contamination with the bug
feces .
Human infection
occurs chiefly through the skin and rarely through the mucous membrane .
Clinical
Features
Infection is more
severe in infants and young children .
The
primary stage: may be
acute accompanied by constitutional symptoms such as fever, malaise and
fatigue .
Skin
manifestations: severe
reaction at the site of entrance of the parasite that may be in the form
of erythema multiforme and edema .
Late stage
: This is due to
hematogenous spread of the parasite to the viscera, the heart, brain and
liver which may lead to serious complications and may be fatal .
SLEEPING
SICKNESS
(African Trypanosomiasis)
The transmitting
vector is the tsetse fly which inocthe trypanosoma( (T.
Rhodesian and T. gambiense) present in its salivary glands into the skin
of the victim.
Clinical
Picture
Acute
stage :
This stage is
characterized by:
Skin
manifestations :
Chancre:
nodule appears at the site of the bite, which is hot, red, tender and
accompanied by lymphangitis and regional lymphadenopathy.
Pruritus
and painful edema involves
the hands, feet and eyes. The joints become swollen.
Late
stage:
Develops after a
chronic course where there may be cerebral impairment that develops
gradually leading to the clinical picture that is the "sleeping
sickness".
There is no skin
manifestation in this stage .
Diagnosis
Detection of the
parasites in the fluid aspirated from lymph nodes .
Parasites are rare in blood .
TOXOPLASMOSIS
Toxoplasmosis is a
zonosis caused by the parasites, protozoon Toxoplasma gonadii.
The disease is
congenital, transmitted either from the infected mother to the fetus
through the placenta or acquired from animal reservoirs such as cats , dogs
and birds.
Congenital
Toxoplasmosis
Infection of a
pregnant woman may lead to abortion or delivery of a full term fetus with
triad manifestations which are:
-
Hydrocephalus
-
Chorioadenitis
-
Cerebral
calcifications.
-
Skin
manifestations - skin rash appears which is macular and hemorrhagic
eruption .
-
Systemic
manifestations - Hepatosplenomegaly and jaundice.
-
The
mortality rate is about 10 per cent. Those who survive may show
complications such as hydrocephalus, mental retardation and impaired
vision .
In subsequent
pregnancies the fetus is not affected.
Acquired
Toxoplasmosis :
The disease is
contracted by contact with cats, rabbits, chicken, cattle and pigeons.
Skin
manifestations:
Scarlitiniform eruption, urticarial, pinkish papules or subcutaneous
nodules and rarely vesicles appear on the skin sparing the face, palms and
soles.
Systemic
manifestations: multiple
organ involvement causing encephalitis, hepatitis and other systemic
manifestations.
Diagnosis
-
Typical
clinical picture.
-
Wright‘s
stain or Giemsa stain to blood or lymph node.
-
Sabin-Feldman
test which is positive within two weeks. This test is positive in
early infection and antibodies decline after 1-2 years.
-
Direct
agglutination of formalinized parasites tests are useful for
screening purposes. These tests detect IgM and IgG antibodies .
-
Indirect
fluorescence is a simple and safe test that can be used to distinguish IgM from IgG
antibodies.
-
Spinal fluid
inoculated to a mouse . This is not a routine test and rarely used in
the clinical practice.
Treatment
Combination of Sulfonamides
(adult dose 3g. daily) and pyrimethamine (Daraprim), given in a
dose of 1mg/kg. daily for one month.
It should be noted
that Daraprim is a folic acid antagonist, so concomitant folic acid
therapy is recommended.
Rovamycin
can give good results .
Spiramycin
(adult dose 2g. Daily ) is
also effective .
These medications
reduce the incidence of fetal defects. When the proper medication is given
to infected pregnant women. This drug can control the constitutional symptoms
such as
fever and improves the ocular lesions when combined with corticosteroids.
REFERENCES
-
McCabe RE,
Remington JS. Toxoplasma gondii. In: Mandell GL, Douglas RG.
-
Bennett JE,
eds. Principles and Practice of Infectious Disease 2nd edn. New
York: John Wiley, 1983: 1540-9.
-
Beverley
JKA. Congenital toxoplasma infections. Proc Roy Soc Med 1960;
53:111-13.
-
Topi GC, D‘Alessandro
L, Catricata C et al. Dermatomyositis-like syndrome due to
toxoplasma. Br J Dermatol 1979; 101: 589-91.
ZOONOSIS
Zoonosis include
the diseases that are caused by parasites. These parasites may be living
on the skin surface (epizoonosis) or may pierce the epidermis
(endozoonosis).
The parasites may
cause different skin manifestations :
Scabies- Sarcopetes scabeii
parasites cause itchy skin lesions due to their burrow into the skin.
Bird mites infest birds such
as chicken, canaries and other birds that may cause severe pruritic skin
reaction. Some strains cause viral encephalitis when the mites attack
human beings.
Mouse mites cause
skin reaction
at the site of biting human beings and these also transmits rickettsia
pox.
Grain itch mite causes severe
dermatitis due to the pediculoides mite. The disorder is called also
"straw itch " . This occurs in families during the harvest time
due to contact with the infested straw with the parasite.
The eruption
usually presents with severe itchy bright red papules surmounted by
vesicles or pustules with urticarial hemorrhagic lesions. This reaction is
sometimes misdiagnosed as varicella especially in children. |
Fig. 123. Straw itch mites
|
Pulicosis is an acute epizoonosis
due
to fleabite .
Pediculosis is a chronic epizoonosis , caused by lice .
Cimicosis is a chronic skin reaction,
caused by bed bugs
Epizoonosis is a skin manifestations,
due to insects such as wasps , bees and ants.
Culicosis
is due to mosquito bite
causing pruritic macular and nodular lesion. The reaction may be severe in
sensitized persons. In children the reaction may be severe causing papular
urticaria, bullous reaction or reaction simulating lichen urticatus .
Trombidiosis
(hay or harvest itch ) is
an acute epizoonosis that is caused by soil mite whose larvae may be attached
to skin eliciting skin reaction in the form of erythematous
papulovesicular lesions or exanthemas with excoriations and secondary
bacterial infection such as furunculosis and impetigo.
Creeping
eruption
is a skin disease that is caused by migrating nematodes during a
stage of their development such as ancylostoma, hook worms, ascaris. The
larvae migrate beneath the skin, forming burrows that cause pruritus and
erythematous wheals .
SKIN
MANIFISTATIONS DUE TO MITES
HUMAN
SCABIES
Human scabies is
caused by the female parasite "Sarcopetes scabeii" which is
capable of completing her life cycle in man. The female burrows into the
skin after impregnation forming the characteristic lesion for scabies,
which is known "the tunnel or burrow" where larvae are
produced after eggs hatching. After copulation, larvae burrow into the
skin and start again a new life cycle.
Fig. 124. Sarcopetes scabeii
(Adult female) |
Modes of
Infestation
-
Direct contact
with infested individual .
- Contact with infested clothes ,
towels and bed linens .
-
Direct
infestation :from infested animals such as cats, dogs, cattle, sheep or
camels.
Clinical Picture
The disease has a
chronic course. The incubation period may take weeks or even months
without any apparent manifestations.
The clinical
picture varies according to age, sites involved and the type of host
transmitting infestation .
Scabies is
characterized clinically by severe itching especially at night and when
the skin becomes warm.
Excoriation marks
are due to severe scratching which may be accompanied by secondary
bacterial infections in the form of impetigo or carbuncles.
In the early
stage, the burrows, where the Sarcopetes scabeii are impregnated into the
skin can be seen easily as a grayish tortuous line where the mites are
embedded at one site of the line.
The sites infested
by scabies have characteristic distribution. The commonest sites involved
are the interdigital spaces of the fingers, the palms, the flexor surface
of the wrests around the umbilicus, the region of the belt line, nipple,
buttocks, genitalia and characteristically the glans penis in males.
The face and neck
are not involved except in infants .
ANIMAL SCABIES
Scabies
transmitted from animals such as dogs and cats may have severe clinical
picture such as macular , papular, pustular, impetigo or wheal like
reaction . Itching is severe and may be distressing causing sleep
disturbance.
Fig. 126. Scabies
(Umbulical & Glans penis lesions are characteristic) |
Fig. 125. Scabies
(Burrows of the antecubital area) |
PARASITOPHOBIA
Some neurotic
patients who had scabies may continue to have a belief that the skin is
still infested in spite of all the curative treatments he received. He
considers any mild pruritus even insect bite is an attack of scabies. He
moves from one clinic to the other and sometimes carrying with him in a
container some skin debris to convince the doctor that he is still having
the disease .
In spite of
that it is not
easy to convince such patients. Alll the possible efforts should be
considered in order to reassure him and to try all the possible clinical and psychic
methods to get relief of such problem.
NORWEGIAN SCABIES
This is a rare
type of scabies in which the clinical picture is more severe than the
ordinary scabies. This type of scabies is found in poor communities, low
sanitary conditions and in malnourished individuals .
Clinical Features
Crusted purulent
lesions appear on the face and genitalia .
Hyperkeratotic
lesions appear on the palms and soles with subungual and nail dystrophy.
Psoriasiform scaly
lesions appear on the trunk and extremities .
SCABIES IN BABIES
The clinical
features of scabies in infants differ in certain respects from the lesions
that occur in older children and adults.
Clinical Features
Extensive
distribution of burrows .
Vesicular and Vesiculopustular
lesions on the hands and feet are not uncommon, and bullous lesions have
been described.
Extensive
eczematization is frequently present .
Fig.
125b Scabies in babies
Fig. b. Scabies in babies
(Papulovesicular and bullous
lesions)
Fig.126 b. Scabies in babies
(Papulovesicular and bullous
lesions)
There may be
multiple crusted nodules on the trunk and limbs.
Diagnosis of
Scabies
-
Severe itching which
is more at night .
-
Typical sites
of distribution of the skin rash.
-
Detection of
the mites in the burrow is diagnostic . This can be seen by the naked eye
or by the help of a magnifying lens, which appears, as a grayish tortuous
line.
The mite can be
detected either by superficial pricking and raising the end of the burrow
with 25 gauge needle, where the mite may be seen sticking to the edge of
the needle. This can be detected also by very superficial shaving of the
burrow and examining the materials shaved under the low power microscope.
Treatment
General measures
The whole body,
except the head and neck should be treated.
All members of the
family and close contacts should be treated, whether they are symptomatic
or not.
Treatment of
scabies is easy if the patient follows the instructions and to use the
medications in the proper way besides measures to prevent
re-infestation .
When scabies is
suspected in any patient it is wise to begin treatment of this case as
scabies until the diagnosis is confirmed. A pruritic skin disease whether
scabies or not may benefit from the medications used for scabies where
these can help at least to stop itching which is sometimes a big problem
for patients and may interfere with sleeping.
In children the
mother is instructed to apply medications (Eurax or Kwell Lotion) to any
part of the body involved especially the intertriginous and between the
interdigital spaces of the fingers. The lotion or cream is left on the
skin and washed next day using newly washed clothes preferred ironed on
both sides .
Boiling and
ironing the clothes from both sides is usually enough to eradicate the
mites. Some clothes may be damaged by boiling, dry cleaning and the usual
method for laundery for the bed linen may be also sufficient to kill the
mite.
Disinfestations of
clothing and bedding, other than by ordinary laundering, is not always
necessary.
Specific treatment
Benzyl benzoate is
available in concentrations of 25 per cent. This should be diluted with 2
or 3 parts water for use to infants and young children. Prolonged or
repeated applications of Benzyl benzoate or Lindane should be avoided.
Treatment of
scabies is usually effective by rubbing the skin from neck to toe by Kwell
lotion or Eurax after taking a hot bath and rubbing the skin
with a sponge .
Crotamiton lotion and
cream may be used to treat burrows on the head and neck.
The adverse
effects of these medications may be contact dermatitis and toxic epidermal
necrolysis attributed to Monosulfiram have been reported.
Antihistamines are
necessary to stop itching.
Antibiotics orally
may be needed to control secondary bacterial infections. Erythrocin,
Cephalosporin or Fluxacillin orally are effective in controlling
carbuncles or pustular lesions that complicate some cases of scabies.
SKIN MANIFESTATIONS
OF OTHER MITES
-
Grain itch
-
Chiggers mite
-
Rat mite itch
-
Grocer‘s itch
- House dust mites
The eruption
provoked by these mites is commonly composed of minute, intensely pruritic
papules or papulovesicles on the exposed parts of the body, principally on
the head, neck, and forearms but occasionally more widespread. The
appearance of the eruption on the face may suggest an acute contact
dermatitis.
Dermatophagoides
pteronyssinus (the
house-dust mite) is widely distributed in the human environment especially
in house
dust and beds. It occurs worldwide and has been reported from all
inhabited continents. The largest numbers of mites are found in houses
that are damp and inadequately heated. Numbers vary seasonally, increasing
in early summer to reach a maximum by early autumn.
The main food of
D. pteronyssinus is human skin scales. Xerophylic moulds, especially
Aspergillus Penicilloides, are essential for the growth and survival of D.
pteronyssinus. The moulds digest lipid in the scales that is toxic to the
mites.
Fig. 128. Rat mite
|
Fig. 127. Harvest mite |
The role of the
house-dust mite in the pathogenesis of atopic eczema remains
controversial.
The houses of
patients with moderate to severe atopic eczema had more house-dust mites
than normal individuals. However, convincing direct evidence that
house-dust mite exposure exacerbates atopic eczema is lacking.
Measures to reduce
house-dust mite numbers include regular vacuum cleaning of bedroom
carpets, mattresses, and the use of plastic mattress covers. The
antifungal drug "Natamycin " can be considered in the treatment.
These types of
mites attack infants and children in their beds, which may elicit or
exacerbate dermatitis and allergic bronchial asthma in some patients. Skin
tests can detect these mites. Skin desensitization may be of help for some
patients.
PYEMOTES MITES
(Grain Itch Mite)
Skin lesion is due
to contact with infested straw . The dermatitis has been known as
"barley itch," "grain itch," "straw itch,"
"cotton-seed dermatitis."
The lesions are
urticarial papules surmounted by vesicles and occasionally bullous. They
are often very numerous, and their distribution depends upon the mode of
exposure.
TROMBIDOSIS
Different members
of these mites are distributed worldwide. The most important of these
mites are
the red bug, which live in grasses, shrubs and even in houses. They are
present in crowded places as refugee , military camps and prisons.
The parasites
attack human skin sucking their blood and fall down when the body is
engorged .
Infants and young
children may have more severe skin reactions due to their delicate skin
mainly on the legs , belt site , face and other areas of the body .
Clinical Features
Skin
manifestations
Itchy papules
appear at the site of the parasite bite . These may enlarge to form a
nodule .
Systemic
manifestations
Some species of red bugs may be a
vector for systemic diseases such as Tsutsu gamushi fever.
HARVEST MITES
(Trombidiosis,
Scrub itch)
Dermatitis is due
to the parasitic larvae, or free-living nymphs. The larvae may cause
troublesome dermatitis . Some of these mites are important vectors of Rickettsial
disease.
The eggs are laid
in soil. The six-legged larvae that emerge climb onto low vegetation to
wait for suitable vertebrate hosts. On the host, the larvae move to areas
where the skin is thin, such as the ears, axillae, groins and genitalia.
They pierce the skin with their claws and inject saliva, which has
cytolytic properties into the epidermis and feed on fluids and cell
debris. Once engorged, they fall to the ground. The larval mites are most
numerous from May to October, with a peak in September. The most favored
natural host is the rabbit.
Eutrombicula are
the most common chiggers attacking man .
Clinical Picture
Infestation to
children occurs while playing on grassy areas or whilst walking bare
footed through grass or low vegetation. The response to the bites of
harvest mites appears to be determined by the irritant effect of the mites‘
saliva and an acquired hypersensitivity to salivary antigens.
Erythematous
macules appear at the sites of the bites. Later on these gradually develop into
extremely itchy papules or papulovesicles. In heavy infestations the
lesion may cover extensive skin sites .
The distribution
and the type of lesion is determined by the preference of mites for thin
skin as that of the crural areas of young children besides the type of
clothing of the host. Lesions commonly occur around the feet and ankles,
the groins and genitalia, the axillae, the wrists , antecubital fossa, and
areas constricted by clothing, such as the waistline.
CHEYLETIELLA MITES
Species of
Cheyletiella mites are non-burrowing. Obligatory parasites of certain
mammals, predominantly in dogs, cats and rabbits. The entire life cycle is
completed on the host. Skin lesions manifest when there is contact with
infested animals.
Clinical Features
The typical
clinical picture is large numbers of intensely itchy papules surmounted by
a vesicle. Infection occurs on the areas coming in contact with the
infested animals during fondling of these animals. These lesions become
necrotic and the eruption may become extensive covering the chest and
abdomen manifesting with severe itching.
Secondary
bacterial infection may complicate the skin lesions due to severe
scratching .
DERMANYSSID MITES
( Bird, rodent and
reptile Mites )
Dermanyssid mites
are hematophagous parasites of birds and mammals. Dermanyssus gallinae
(the poultry mite), is a common parasite of domestic and wild birds.
Infestation is by
playing or dealing with domestic birds such as pigeons, chicken or their
cages. Mites enter houses from bird‘s nests via windows or air
conditions causing dermatitis .
Liponyssoides
sanguineus, the house mouse mite, is an Ectoparasite of small rodents. It
is of medical importance because it is the vector of Rickettsia akari that
transmits Rickettsia disease.
FAMILY
MACRONYSSIDAE
Members of the
Macronyssidae are hematophagous Ectoparasite of birds, mammals and
reptiles.
Clinical Picture
The clinical
manifestations vary according to the route , severity of infestation and
the degree of the host‘s response.
Skin manifestations are
pruritic papular or urticarial lesions . A profuse eruption of small, intensely itchy wheals or
papules appear which are sometimes grouped, and often asymmetrical. The lesions may have
a central punctum, and vesicles occasionally occur in the center of the
papules, especially in children.
Secondary
infection may occur due to
severe itching.
Persons attacked
by mites in bedding have more extensive bites. Occasionally lesions are
grouped adjacent to areas of tight clothing around the waistline.
In heavy
infestations the causative mites may be detected at the site of the
parasite bite .
SKIN MANIFISTATIONS
DUE TO FLIES
Flies are an
important vector of certain infectious diseases . Skin manifestations are
either due to the adult fly bite or due to the larvae within the skin
causing skin myiasis .
Clinical Picture
-
Fly bite
The severity of
manifestations vary depending on to the type of the insect family :
Family Tabanidae:
This is a fly animals such as horses and deers that causes a severe
painful bite.
Family Helediae:
Known also as "no see ums" because of their extraordinarily
small size. These have the characteristic of savage biting and cause itchy
and irritable lesions that may last for a few days.
Fig. 129. Black fly |
Fig. 130. Deer fly |
Fig. 131. Larva of bottle fly |
Family Simuliidae (black
flies) - are endemic in temperate and suburban areas. These are dangerous
and curious flies .
Clinical
Manifestations
Black flies -
cause painful bite, preferring the eyes, nostrils and ears. They cause
severe local and systemic manifestations.
Systemic
manifestations - fever and gastrointestinal problems .
Local reaction: an
erythematous and edematous lesions appear, swelling of the face and may
cause ulceration and distortion.
Family
Psychodidae: Species of
the genus Phlebotomus are the vectors of cutaneous leishmaniasis and
kala-azar, Carrion‘s disease, Verruga peruana and others. Phlebotomus
attack their victims at night and prefer the ankles, wrist, knees and
elbows.
Family Chloropidae.
This group is usually endemic in rural and urban areas with decreased
sanitary care. They feed on human blood and eye secretions causing
epidemic conjunctivitis , sores and open wounds.
-
Cutaneous
myiasis
This skin disorder
is due to infestation of the skin by fly larvae . The most common fly
causing dermal myiasis is the screw worm fly.
The larvae of
several varieties of flies produce different cutaneous manifestations
creating a tortuous telltale inflammatory ridge or line to mark the path
of their migrations . The eggs , living larvae or both are deposited on
the skin , genitourinary and gastrointestinal tract , eyes , ears and even
nose.
Clinical
Manifestations
-
Primary Myiasis:
The larvae can
burrow normal intact skin.
The pathogenesis and mode of
transmission of the disease depends on the type of the fly
|
Fig. 132. Cutaneous myiasis |
-
Some species of
flies puncture the skin and extrude the ova beneath the surface, where
others deposit their eggs on open wounds or ulcers .
-
Other species
such as Walfahrtia vigil gravid fly lays its eggs on the skin , then
hatched larvae migrate to the folds of skin as the intertriginous areas
causing inflammatory reactions as papules , furuncles and then pustules.
-
The female
human bottle fly , D. Hominin uses an intermediate host to lay its eggs on
the body of a mosquito , stable fly or ticks . When the mosquito bites the
skin , the hatched larvae on the mosquito body enter the skin through the
site of the bite causing skin myiasis .
-
The Tumbu fly
in tropical Africa lays its eggs on the ground, which after hatching, the
larvae attack and penetrate the skin of the scrotum or extremities
causing, inflamed tumor from which larvae emerge after one week from the
lesion .
-
Secondary
myiasis
This type depends
on the behavior of certain larvae.
-
Migratory -
where the larvae wander in the tissues causing inflammation at the site
the parasites migrate known as "creeping eruption".
-
Non-migratory -
larvae localize on the skin and becomes resident to the primary site.
Cutaneous myiasis
due to larvae of flies of the genera Gasterophilus and Hypoderma may cause
a creeping eruption similar to that caused by the hookworms.
Treatment of
Myiasis
Surgical
extraction
of the larvae
with a sharp needle and douching of the wound with 15 per cent chloroform
in vegetable oil .
Anaesthetizing the
larva using cotton pad moistened with Chloroform can treat nasal myiasis
and then blocking the nostril for 2-3 minutes. Remove the larvae with
forceps.
Preventive measures
by eradication of screw worm fly.
REFERENCES
-
Poindexter
HA. Cutaneous myiasis. Arch Dermatol 1979; 115: 235.
-
Reames MK,
Christensen C, Luce EA. The use of maggots in wound debridement. Ann
Plast Surg 1988; 21: 388-91.
-
Spigel CT.
Opportunistic cutaneous myiasis. Arch Dermatol 1988; 124: 1014-15.
-
Wildy GS,
Clover SC. Myiasis due to tumbu fly larva. Lancet 1982; i: 1130-1.
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