Parasitic Skin Diseases Part 1
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Transcript Parasitic Skin Diseases Part 1
Small Animal Dermatology
2007/03/23
Parasitic Skin Diseases
Part 1
Cheng-Hung Lai, DVM, PhD.
Assistant Professor
Department of Veterinary Medicine
National Chung Hsing University
Animal skin is exposed to attack by many
kinds of animal parasites.
Each species has a particular effect on the
skin; the effect can be mild, as in the case of
an isolated fly or mosquito bite, or severe, as
in the case of generalized demodicosis or
canine scabies.
When ectoparasites are vectors or
intermediate hosts of bacterial, rickettsia, or
parasitic diseases, they become more
important than when they produce only their
own effect.
The most serious dermatological concern
occurs when the dermatosis produced by
parasites living in or on the skin produces
irritation and sensitization.
The reaction of the skin to these insults
varies from trivial to lethal but usually
includes inflammation, edema, and an attempt
to localize the foreign body, toxin, or
excretory products of the parasite.
These secretions are often allergenic and
cause itching and burning sensations.
Helminth parasites
Arthropod parasites
Arachnids------parasitic ticks
parasitic mites
Insects---- ----lice
flea
Helminth
Hookworm Dermatitis
Hookworm dermatitis is a skin reaction at
sites of percutaneous larval penetration in
dogs previously sensitized to hookworm.
The disease is caused by Ancylostoma in the
tropics and in worm temperate areas, and by
Uncinaria in temperate and subarctic areas.
The highest incidence reported in dogs
housed or exercised in contaminated
environments.
Helminth
Helminth
Lesions are characterized by mildly to
intensely pruritic, papular eruptions that
appear interdigitally and on other skin areas
that frequently contact the ground.
Affected skin becomes uniformly
erythematous, alopecic, and thickened.
The feet often become swollen, hot, and
painful.
Helminth
Diagnosis
1. Fecal flotation
2. Dermatohistopathology
3. Response to treatment
Treatment
1. fenbendazole, mebendazole, or pyrantel pamoate
twice 3-4 weeks apart
2. environmental sanitation
Helminth
Pelodera Dermatitis
Pelodera (Rhabditis) strongyloides is a small
saprophytic nematode that lives in decaying
organic matter.
On rare occasions, it can invade the mammalian
skin, causing a pruritic, erythematous, alopecic
and crusting dermatitis on skin sites that come
into contact with the ground.
Helminth
Clinical features
A pruritic, alopecic, erythematous and
crusting dermatitis affecting body sites in
contact with the ground was a typical clinical
feature
Secondary pyoderma may be present
Helminth
Diagnosis of the disease is based on case
history (a dog living outdoors on damp straw
bedding) with characteristic skin lesions and
on the demonstration of typical larvae in skin
scrapings or biopsy.
Pelodera (rhabditic) dermatitis cases have
been reported mainly from Central European
countries and the United States.
Helminth
(Saari and Nikander, 2006)
Helminth
Skin scrapings and histopathology as
diagnostic tools
Skin scraping is an easy, fast, inexpensive and
reliable method for the diagnosis of Pelodera
dermatitis. The length of larvae in skin
scrapings varied from 600 to 750 μm, and the
width from 30 to 40 μm
Helminth
Hyperkeratosis
paired lateral alae (a)
(Saari and Nikander, 2006)
Helminth
The oesophagus of the larvae was of the
rhabditiform type, consisting of an elongated
corpus, followed by a distinct swelling midway
down the oesophagus and narrow isthmus,
ending aborally with a clearly defined
valvulated bulb. The cuticle was distinctly
transversally striated. The oral opening was
surrounded by lips, but their number and
arrangement could not be determined with LM.
Helminth
buccal capsule
narrow isthmus
(Saari and Nikander, 2006)
Helminth
(Saari and Nikander, 2006)
Helminth
Dracunculiasis
Dracunculiasis is a skin disease that is caused
by Dracunculus, a nematode that parasitizes
subcutaneous tissues. Infection occurs when
the mammalian host ingests an infected
microscopic crustacean (intermediate host)
while drinking contaminated water. Over the
next 8 to 12 months, the larvae develop into
adults within the mammalian host's
subcutaneous tissue.
Helminth
In North America, Dracunculus insignis
primarily parasitizes raccoons, mink, and
other wild mammals, with infection in dogs
and cats occurring uncommonly.
In Africa and Asia, D. medinensis (the guinea
worm) infects many mammals, including dogs,
horses, cattle, and humans.
Lesions are often painful or pruritic, chronic,
single or multiple subcutaneous nodules on the
legs, head, or abdomen that eventually
fistulate (and through which female worms
are stimulated to discharge their larvae when
the skin contacts water).
Helminth
Diagnosis
1. Cytology (fistulous exudate): eosinophils,
neutrophils, macrophages, and 500μm-long
nematode larvae that have tapered tails
2. Dermatohistopathology: subcutaneous
pseudocyst that contains adult and larval
nematodes surrounded by eosinophilic
pyogranulomatous inflammation
Helminth
Persian physicians removing Guinea worm from legs
of patients (by Velschius, 1624-1677)
A plate by Fedchenko showing the Guinea worm rolled up
on a stick, larvae in the body cavity of cyclops
Helminth
Helminth
Pyogranulomatous inflammation
surrounding an adult Dracunculus
insignis with larvae
Treatment and Prognosis
1. Nodules should be surgically excised.
2. Water supplies should be decontaminated.
3. The prognosis is good. However,
dracunuliasis is contagious to other animals
and humans via animal-crustacean-animal
transmission.
Arachnids
Canine scabies
Highly contagious parasitic dermatosis caused
by the multiplication in the epidermis of an
acarine mite of the species Sarcoptes scabiei
var canis (200 to 400 μm).
Intensely pruritic.
Quite common.
Arachnids
• Parasitic life cycle (egg-larva-nymph-adult)
short, 2 to 3 weeks.
• The fertilised females on the skin surface
move rapidly towards the warmer areas of
the skin and burrow into the epidermis
to lay eggs.
• Life expectancy of adult mites: 4 to 5
weeks.
• In the environment (off the host), the
different parasitic stages survive for only
short periods (2 to 6 days at 25°C).
Nevertheless, at lower temperatures and
high humidity, nymphs and females can
survive for up to 3 weeks and may lead to
reinfection.
Arachnids
■
Clinical signs
◙ There is severe and constant pruritus often
leading to a rapid appearance of extensive
excoriations.
◙ Primary lesions: erythematous papules,
crusted papules. Typical primary lesions (to
be scraped!) are crusted papules which
represent the exact points where the
fertilised females entered the epidermis.
They appear either just prior to, or
simultaneously with the development of
increasing pruritus.
◙ Secondary lesions: crusts, excoriations,
hyperpigmentation, lichenification.
Arachnids
◙ Associated dermatological findings: scaling
and seborrhoeic problems, alopecia, pyotraumatic dermatitis, otitis externa affecting the
margins of the ear flaps.
◙ Lesion distribution: the favourite habitats of
the mites and thus the sites of the lesions
are the margins of the ear pinnae and the
bony prominences, especially elbows and hocks,
and then the ventral portions of the chest
and abdomen. When the disease spreads, the
entire body may be involved, but the dorsal
midline is always spared.
Arachnids
■
Diagnosis
◙ History
◙ Clinical elements
◙ Pinnal-pedal reflex
◙ Scrapings
◙ Skin biopsies
◙ Response to scabicidal treatment
Pinnal-pedal reflex
■
Treatment
◙ Topical treatment
• Selamectin (6 mg/kg) and moxidectin (2.5
mg/kg) are effective when applied as spoton preparations at monthly intervals.
Treatment for 2-3 months is advisable.
◙ Systemic treatment
• Ivermectin (250 to 400 μg/kg, 2 or 3
times at 10 or 15 day intervals) by
subcutaneous injection.
• Milbemycin oxime (2 mg/kg, 3 times at 1
week intervals) orally.
◙ Additional therapy.
• Keratolytic, antiseborrhoeic, antipruritic and
emollient topical shampoos and lotions.
• Possible systemic corticosteroid treatment
for the first week in cases with very intense
pruritus (prednisolone, 0.5 to 1 mg/kg/day
orally, 2 or 3 days): only when a definitive
diagnosis has been made by scrapings.
Feline Scabies
Feline scabies is a disease that is caused by
Notoedres cati, a sarcoptic mite that burrows
superficially in the skin.
Feline scabies is noted as intensely pruritic,
dry, crusted lesions that usually first appear
on the medial edges of ear pinnae, then
spread rapidly over the ears, head, face, and
neck. Lesions may subsequently spread to the
feet and perineum.
Infested skin becomes thickened, lichenified,
alopecic, crusted, or excoriated.
Diagnosis
1. Microscopy (superficial skin scrapings):
detection of notoedric mites, nymphs, larvae,
or ova
2. Dermatohistopathology: superficial
perivascular or interstitial dermatitis with
varying numbers of eosinophils and
pronounced focal parakeratosis.
Treatment
1. Traditional therapy is to bathe the animal with a
mild antiseborrheic shampoo to loosen crusts,
followed by a total body application of 2 to 3 lime
sulfur solution every 7 days
2. Ivermectin 0.2-0.3 mg/kg PO or SC twice, 2 weeks
apart
3. Doramectin 0.2-0.3 mg/kg SC once
4. 0.015% amitraz solution applied to entire body q 7
days for 21 days
Canine localized demodicosis
Canine localized demodicosis is associated
with overpapulation of the mites Demodex
canis, which are normal inhabitants of the
hair follicle, and sometimes of the sebaceous
glands.
Predisposing factor
endoparasitism, poor nutrition, immunosurpressive drug therapy, transient stress
(e.g., estrus, pregnancy, surgery, boarding)
Highest incidence in puppies 3 to 6 months old
Clinical features
◙ Canine localized demodicosis may appear as
one to five patchy areas of alopecia with
variable erythema, hyperpigmentation, and
scaling localized to one region of the body.
◙ Lesions are most common on the face, but
they can be anywhere on the body.
◙ Lesions are not usually pruritic unless they
are secondarily infected.
Diagnosis
◙ Deep skin scraping
◙ Dermatohistopathology
Treatment
1. Any predisposing factors and secondary pyoderma
should be identified and treated.
2. Lesions should be treated topically with 2.5% to
3% benzoyl peroxide shampoo, lotion, or cream
every 24 hrs.
3. 0.03% to 0.05% amitraz solution applied to lesions
every 24 hours is often effective.
4. Topical therapy is continued until follow-up skin
scrapings are negative and lesions have resolved.