Download Approach to the Pruritic Dog

PRURITIC DERMATOSES OF THE DOG –
DIAGNOSIS AND TREATMENT
Candace A. Sousa, DVM
Diplomate (Emeritus) American Board of Veterinary Practitioners,
Canine and Feline Practice
Diplomate American College of Veterinary Dermatology
Canine Pruritus
“Infectious Diseases”
1.
2.
3.
Sarcoptes scabiei
Malassezia colonization
Staphylococcal pyoderma
Demodex
Allergic Diseases
1.
2.
3.
Flea allergy dermatitis
Food allergy dermatitis
Atopic dermatitis
4.
Other allergic dermatoses
Hypothyroidism
Conformation (obesity)
4.
Other (dermatophytosis,
Cheyletiella, lice, etc)
(drugs, contact, etc)
Pruritus is one of the most common presenting complaints of pet owners in a
dermatology practice. Clinical signs may be manifested by licking, chewing, and/or rubbing,
resulting in visible alopecia, dermatitis and/or odor. Sometimes the only complaint is the owner’s
irritation.
“Infectious” Causes of Pruritus
Sarcoptes scabiei
Sarcoptes scabiei mites are a cause of one of the most pruritic diseases seen in dogs.
The mites are also known to cause disease in foxes, humans and rarely in cats. The mites
burrow through the cornified layer of the epidermis where they lay eggs. The pruritus is most
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likely caused by an allergic (IgE-mediated) reaction to the intestinal proteins secreted in the mite
fecal material. Puppies, very old dogs, dogs that are treated with immunosuppressive amounts
of corticosteroids, or dogs that have not yet developed an immunologic reaction to the mites
may be asymptomatic carriers of the disease.
Affected dogs exhibit generalized pruritus with the edges of the pinnae, elbows, hocks,
and ventral abdomen having the most severe lesions. Alopecia, erythematous papules, thick,
yellowish crusts, and excoriations are noted on the physical examination. In many dogs a
positive pinnal-pedal reflex can be elicited by rubbing the edge of the dog’s pinnae and noting
an attempt to scratch the ear region.
Collection and identification of the mites can be difficult. The crusted lesions on the ear
margins, elbows, or hocks are most likely to yield a positive scraping. There are commercial
laboratories that will perform an ELISA test for sarcoptid antigens. The test will be positive 2 to
4 weeks after infection. A presumptive diagnosis of scabies can be made by a positive
response to treatment with a miticidal product. All in-contact dogs also need to be treated.
One topical application of selamectin (Revolution) is effective in killing more than 93% of
the S. scabiei after 1 administration and 100% effective after a second application 30 days later.
Currently available topical insecticide therapies include 2% lime sulfur rinses, to be applied
weekly for 4 weeks, amitraz rinses, to be used every 7 to 14 days for 1 month, or an
organophosphate rinse, such as phosmet, applied weekly for 4 weeks. AdvantageMulti and
Frontline spray are also effective in the treatment of Sarcoptes.
Ivermectin, 200 to 400 µg/kg given either orally or by injection every 7 to 14 days for 4 to
6 weeks (potentially very toxic in collies, Shetland sheepdogs, and other breeds of dogs that
may be P-glycoprotein deficient; submit sample to WSU for PCR for ABCB Δ1 mutation) or
milbemycin, 2 mg/kg given orally every 7 days for 3 or 4 treatments, have both been shown to
be effective in treating scabies. No matter which treatment method is selected the majority of
dogs will experience about a 50% reduction of pruritus 7 days after the first treatment, an 80%
reduction in pruritus 14 days after the initiation of treatment, and clinical cure within 1 month.
Isoxazolines are a new class of parasiticides recently approved for the treatment and
prevention of fleas and ticks in dogs. These are oral products. Fluralaner (Bravecto), afoxolaner
(NexGard) and sarolaner (Simparica) have all been shown to be effective in the treatment of
scabies.
Malassezia Dermatitis
Malassezia spp. are lipophilic, non-mycelial, saprophytic yeast that can be found on the
skin, in the ears, anal sac, rectum, and vagina of normal dogs and cats. In the dog, disease is
caused by colonization or infection with Malassezia pachydermatis (Pityrosporum canis, P
pachydermatis, Malassezia canis). In the normal animal, commensal bacteria and yeast and the
animal's immune system keep the Malassezia from overgrowing and causing disease. If the
skin barrier is "disrupted", the immune system compromised, or there is a change in the
microclimate (i.e. skin folds), the yeast can increase in numbers and cause disease. Underlying
conditions such as cornification defects, allergic diseases, or endocrine imbalances are
commonly identified. The yeast are not considered to be a contagious disease. Breeds of dogs
that are predisposed to develop yeast colonization include the West Highland white terrier,
German shepherd, Shih Tzu, basset hound, spaniels, silky terrier, Maltese, Shetland sheepdog,
and dachshund.
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Clinical signs of Malassezia dermatitis can include pruritus, erythema, greasiness,
waxiness, scaling, hyperpigmentation, lichenification, and/or odor. Lesions can be focal,
multifocal or generalized. Common sites of involvement include the lip folds, ear canals, ventral
neck, abdomen, interdigital and ventral paws, perianal area, and skin folds. The affected areas
may be sharply demarcated. Occasionally dogs are reported to have fits of muzzle or facial selftrauma.
The diagnosis is best made using cytology. Direct impression smears are one method of
choice. The glass slide is pressed or rubbed firmly several times onto the skin surface to collect
loose surface material. Double-sided clear acetate tape can first be applied to the slide and
then used to collect squamous epithelial cells and bacteria and yeast. Some practitioners use
single-sided clear tape to collect material for an impression smear. A cotton swab is useful for
collecting material from the ear canals and interdigital spaces. A skin scraping can be used to
collect material from a dry surface. The slide is then stained with new methylene blue or Dif
Quik® (heat fixing is not necessary). Malassezia are oval to peanut-shaped budding organisms
that stain blue varying from faint to dark. It is best to record the numbers of yeast by examining
10 to 20 oil immersion fields (rather than noting 1+ to 4+).
Since Malassezia is a commensal organism that is well adapted to the host, treatment
will most likely never eliminate them all. The aim of treatment is to confirm the clinical
significance of the yeast in the disease process observed, reduce the population to normal or
below normal amounts to eliminate clinical signs, and to maintain the population at a level
unlikely to produce clinical signs. It is very important to try to identify and correct the underlying
and predisposing cause of the infection to help prevent reoccurrence.
Systemic therapy involves the use of ketoconazole (Nizoral) 10 mg/kg PO SID for 30
days. Occasionally this is associated with gastrointestinal upset and in rare cases the dog will
develop a toxic hepatopathy. The drug should be given with food to facilitate absorption.
Itraconazole (Sporanox) 5 -10 mg/kg q 24 hours and fluconazole (Diflucan) are also effective in
treating Malassezia. Terbenifine (Lamasil) has recently been shown to also be effective in the
treatment of Malassezia. All of these therapies can be quite costly. Griseofulvin is not effective
against Malassezia.
Topical therapy is an important part of the treatment protocol. If the lesions are localized
they may be controlled with lotions or creams. Miconazole (Conofite) or thiabendazole
(Tresaderm) are good products. Shampoos should be left on a minimum of 10 minutes before
rinsing to allow them to work. Initially they can be used often, as the owner is able and as often
as the dog needs it. The frequency can then be tapered. Miconazole, ketoconazole, selenium,
and chlorhexidine are all active ingredients that have efficacy against Malassezia. Using a final
leave-on rinse will help in preventing re-colonization of the skin. Enilconazole, miconazole, or
white vinegar - 1:2 to 1:3 dilutions, are all useful products.
Staphylococcal Pyoderma
In dogs, bacterial pyoderma is the second most commonly diagnosed skin disorder,
behind flea allergy dermatitis; however, with the advent of newer, highly effective flea-control
products, this order may well have switched. Staphylococcus spp can be identified in about
94% of canine patients with bacterial pyoderma, with S. pseudintermedius identified in
approximately 84% of these pyodermas. S. schleiferi subsp. coagulans and S. aureus are a
less common cause of bacterial pyoderma, isolated from approximately 8% and 1% of patients,
respectively.
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Bacterial pyoderma in dogs develops is always secondary to something as a dog will
never be cured of staphylococcus. When we can’t identify the underlying cause, we call it
primary, which is another way of saying idiopathic. Successful management involves
identification of the causative underlying factor(s), recognition of the type, correct antibiotic
treatment and appropriate supportive care.
The diagnosis of bacterial pyoderma involves evaluation of signalment, history and
physical findings. Consideration of breed, age and the role physical characteristics is important.
In most cases this is a clinical diagnosis. Cytologic examination of skin surface or lesion
exudates is a key and routine adjunctive diagnostic step. In some situations, additional
diagnostic steps such as culture and sensitivity, biopsy and/or laboratory testing may be
needed.
Characteristic clinical lesions are erythema, alopecia, pustules, papules, crusts, and
epidermal collarettes (raised borders of detaching stratum corneum present at the margins of
circular areas of inflammation). With a deep pyoderma, there are often nodules, erosions,
ulcers, and draining tracts. If cytologic examination of material from the surface of the skin, a
pustule, or a draining tract shows large cocci, usually in pairs, it is highly suggestive of
pyoderma caused by S. pseudintermedius. The concurrent presence of rods is indicative of a
mixed infection. When bacteria are seen within the cytoplasm of a neutrophil it confirms that
they are not just contaminants. Skin biopsy is another valuable tool for the diagnosis of
bacterial pyoderma. A response to treatment with oral antibiotics alone strongly supports the
diagnosis of a pyoderma.
Treatment of bacterial pyoderma in dogs must address both the bacteria and the
underlying causative factors. The choice of an appropriate antibiotic can be made empirically or
based on results of a culture and sensitivity test. A culture and sensitivity test is usually
recommended for those cases of bacterial pyoderma that have made no clinical improvement
after 2 weeks of treatment with an antibiotic that is typically effective against staphylococcal
infections, used at the correct dose and frequency. The depth of the infection can interfere with
and/ or delay successful therapy. A culture and sensitivity can be of value at the initiation of
treatment of deep pyoderma, for infections suspected to be caused by Gram-negative
organisms or if the animal has been treated previously with several different antibiotics.
Beta-lactam antibiotics (amoxicillin-clavulanate [Clavamox], cephalexin, cefpodoxime
[Simplicef] and cefovecin [Convenia]) are all good empirical first choice antibiotics. The duration
of treatment has not been well studied. There is only 1 blinded study that supports treatment for
2 weeks, with 94% “cure.” Treatment “beyond a clinical cure” may be one of the major factors in
the selection of methicillin-resistant bacteria.
Topical antibacterial therapy is an integral part of the treatment of a bacterial pyoderma
and is also useful in preventing reoccurrences of the condition. The owner can be instructed to
shampoo the dog as often as the dog needs it and as often as they are able (generally 2-3
times per week initially then once weekly once the infection is under control). Shampoos
containing benzoyl peroxide, chlorhexidine, triclosan, or ethyl lactate have antimicrobial activity
and are good choices for this adjunctive therapy. Owners are advised to let the shampoo
contact the dog for a minimum of 10 minutes before rinsing. Use of a final leave-on rinse after
bathing will assure that the active ingredient remains in contact with the skin and hair coat.
Antibiotic creams or ointments are useful for spot treatment. Generic 2% mupirocin is a
bactericidal antibiotic with excellent activity against Gram-positive cocci. Topical products that
contain corticosteroids should be avoided when treating staphylococcal pyoderma.
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Allergic Causes of Pruritus
Flea Allergy Dermatitis
Ctenocephalides felis is the most prevalent species of flea found on dogs and cats. Flea
bite hypersensitivity (flea allergy dermatitis; FAD) is the most common hypersensitivity disorder
of these animals. Up to 40% of the dogs in a flea-endemic area can produce IgE to the
allergenic components in flea saliva. Affected animals generally manifest their pruritus on the
caudal half of the body including the tailhead, caudal thighs, and ventral abdomen. Lesions are
usually secondary to the pruritus and consist of partial alopecia, papules, erythema,
lichenification, hyperpigmentation, and excoriations. In cats, crusted papules can also be noted
around the neck.
The diagnosis of flea allergy dermatitis is made using several pieces of information. In
the history, the owner should be questioned about the presence of fleas or “flea dirt”. On
physical examination, the presence fleas or flea feces on the dog or cat is noted as well as the
lesions and distribution of the dermatitis. An intradermal test using flea antigen (Greer
Laboratories) at a 1:1000 w/v dilution along with a negative and positive control will yield a
positive immediate reaction in the majority of flea allergic dogs. The intradermal test in cats is
not easy to perform or interpret.
One of the current methods of flea control involves the use of a collar. Most are helpful
when they contain an insect growth inhibitor (IGI) such as methoprene or nylar. These have no
effect on the adult flea that is biting the animal and producing clinical disease. Sprays that are
sold by veterinarians usually contain pyrethrins, synthetic pyrethrins or permethrin in an alcohol
or water-based vehicle. Some are combined with an IGI. The systemic IGI lufenuron will
interrupt the life cycle of the flea but does not have any effect on adult fleas and therefore is of
minimal use in the flea allergic animal.
Monthly topical flea killers such as imidacloprid (Advantage, K9 Advantix, Advantage
Multi), spot-on products, fipronil + / precor (Frontline, Frontline Plus), used as either a spray or
spot-on, and selamectin (Revolution), a spot-on product, all kill about 98% of adult fleas within
24 hours of application. Revolution is an FDA-labeled product that has also been shown to
decrease egg production by 99% and to decrease egg hatchability by 99%. Fleas will usually
take a blood meal prior to dying but recent research shows that the amount of blood consumed
from Revolution-treated cats is significantly less than from cats treated with either Advantage or
Frontline.
The isoxazolines are the newest class of flea products approved for use in dogs.
Fluralaner (Bravecto), administered orally every 12 weeks, and afoxolaner (Nexgard) and
sarolaner (Simparica) administered orally monthly, are all effective in killing fleas as well as ticks
and other parasites.
The clinical signs of pruritus in the allergic animal will improve about 80% within 1 week
of elimination of the fleas and 99% within 14 days. To provide animals with immediate relief,
oclacitinib (Apoquel) or anti-inflammatory doses of oral prednisone can be prescribed to be
used for the first 7 days. Antihistamines provide minimal relief from the pruritus caused by FAD.
In many dogs, antibiotics are also useful to control secondary pyoderma.
Food Allergy (Cutaneous Adverse Food Reaction)
Cutaneous adverse food reactions (CAFR) were previously called “food allergy.” Adverse
reactions to food (food sensitivities) are suspected when an association is noted between the
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ingestion of a certain foodstuff and the appearance of a particular clinical sign or group of signs.
The true incidence of immunologically mediated disease in the dog is currently unknown. A type
I hypersensitivity reaction has been reported in up to 70% of the cases in man and is suspected
in 80 to 85%of the cases in domestic animals. Both types III and IV hypersensitivity reactions
are also suspected to be important in the pathogenesis.
Food allergy is a non-seasonal, pruritic skin disorder associated with a reaction to a
variety of antigenic materials in the diet. It accounts for a diagnosis in about 10% of the allergic
dogs and cats and as much as 1% of all canine and feline dermatoses. Some investigators
believe that the signs of pruritus may be poorly responsive to corticosteroids. Approximately 1015% of the food allergic animals with dermatologic signs will have GI disease concurrently.
Twenty to 30% of dogs will have another concurrent allergic dermatitis.
A recent study identified food hypersensitivity in 7.6% of all dogs presented to a referral
dermatology practice over a one-year’s period. This represented 32.7% of all dogs presenting
with allergic skin disease. Sensitization usually takes a minimum of 3 months to develop. Many
studies report the majority of the animals have been exposed to the offending substance for 2
years before signs appear. Therefore, it is not usually a "new" foodstuff that is implicated. The
reaction is usually specific to a certain protein substance in the diet. Since most commercial pet
foods have similar ingredients, merely changing brands of food has little effect on the disease.
Forty percent of dogs in one study reacted to one allergen on dietary provocation, 40% to
two allergens, 10% to three allergens and 10% to five allergens. Cross reactivity between
allergens from the same animal species (e.g. beef and cow’s milk) is possible. In a study
published in 2004, Bovine IgG was the major allergen in cow’s milk and appeared to be a
source of cross-reactivity with beef and probably with lamb because of high homology with
ovine immunoglobulins. In addition, there were several other proteins found in bovine and ovine
meat to which sera from food allergy dogs showed reactivity.
Dogs of any age can be affected. In one study, Labrador Retrievers, Cocker Spaniels,
Golden Retrievers and German Shepherd Dogs were over-represented. Another source noted
that the Shar-Pei and Poodle might be at greater risk.
The onset of signs is usually sudden and signs may be very severe from the outset.
Typically the problem is perennial, but can be episodic if the offending food is only fed
intermittently or obtained intermittently.
The clinical signs seen in animals with food allergy are nonspecific and can mimic any
other allergic dermatosis. The owner’s major complaint is pruritus, usually non-seasonal. CAFR
in dogs often assumes the clinical presentation commonly attributed to atopic dermatitis
triggered by environmental allergens; thus, dogs are presented with pruritus primarily of the
ventral abdomen, axillae, groin, muzzle, periocular, perianal and palmar or plantar and dorsal
interdigital skin. Not all body regions are necessarily affected in individual dogs. “Ears and
rears” may be a pattern attributed to CAFR while some dogs may have only perianal pruritus.
Otitis externa with erythema of the pinnae and vertical canal only (no horizontal canal
involvement) may be the only cutaneous manifestation of the CAFR. In one study, the ear
region was involved in 80% of the cases, feet 61%, inguinal region 53%, and axillary, anterior
foreleg and periorbital region 31- 37%. In the study above, the ear was the only area affected in
24% of the cases. Secondary yeast/bacterial otitis externa is a common occurrence. A
manifestation comparable to the appearance of canine scabies (generalized papular pruritic
disease) has also been associated with CAFR and may be more common in Labrador
Retrievers.
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A primary papular eruption may also be present. Secondary infections with Staphylococci
or Malassezia often occur. Other presentations of CAFR are recognized such as a recurrent
superficial pyoderma and pruritic papular eruptions over the trunk and head. Recurrent otitis
externa is a common complaint and may be present in 56% to 80% of cases. Dogs may present
with only otitis externa. There is debate over the frequency of concurrent gastrointestinal signs
in patients with dermatologic signs of CAFR. It has been reported that canine CAFR may
respond poorly to antipruritic doses of glucocorticoids, but most clinicians now agree this
distinction is not a useful diagnostic feature. Two studies report that the majority of dogs with
CAFR present before three years of age. However, this disorder can occur at any age and
should be considered in the older dog with no previous history of pruritus.
Signs can appear within an hour of eating the offending allergen, but may be delayed
with a peak in clinical signs noted to be up to 14 days in one study. Signs may become
continuous with repeated exposure. Secondary changes resulting from chronic pruritus
(lichenification, Malassezia or staphylococcal colonization) may continue the clinical signs of
pruritus even after the offending substance is avoided. Thus it is important to treat these
secondary changes prior to evaluation of the patient with an elimination diet.
Prior to embarking on a diagnostic work up for the possibility of the presence of other
pruritic skin diseases should be ruled out. Ectoparasitic infestations in particular should be ruled
out. If skin scrapings are negative, then a therapeutic trial with a parasiticide may be warranted.
A diagnosis of CAFR is made using the history and physical examination and evaluating
the animal’s response to a hypoallergenic elimination diet trial after ruling out the infectious
causes of pruritus. Results of an IDT are not useful in diagnosing food allergy. RAST and
ELISA tests are currently available to aid in the diagnosis of food allergy but their diagnostic
accuracy or validity is unproven. The diagnosis is best made by feeding a "hypoallergenic"
home-cooked diet for a minimum of 4 weeks. One study demonstrated that some dogs showed
no improvement until completing 10 weeks of a diet trial.
The diet should be composed of two ingredients to which the animal has not been
commonly exposed. If possible, the diet should be free of additives including preservatives,
colorings, and flavorings. In dogs, rice, potatoes, sweet potatoes, yams, turnips, oats, barley or
polenta might be a suitable carbohydrate choice. Lamb, poultry, pork, beef, venison, rabbit or
fish are possible novel protein sources. There may be cross-reactivity of allergens between
similar proteins (i.e. chicken and turkey; beef and venison; etc) but this has not been proven.
Simply switching to another brand or form of commercial dog or cat food is often not a valid test.
Strict control over the feeding of the diet includes no treats, no flavored medications, etc, other
than the designated diet for the trial period.
I recommend a home prepared diet for 4 to 8 weeks. Six cups of carbohydrate plus 1
pound of “meat” yields 4 pounds of food. A 20 pound dog can be fed 1 pound per day.
Commercial novel protein diets contain whole proteins which are not commonly found in
dog foods. Although a truly “novel” protein is becoming more difficult to find as commonly fed
diets increasingly contain more varied and exotic ingredients. The diet should be selected on
the basis of the protein content which should be one which has not routinely been fed to the pet
in the past, may not be cross-reactive and ideally not fed ever.
Hydrolyzed diets theoretically negate the need to find a “novel” protein. The parent
protein in these diets is usually a readily available source such as chicken or soy in which the
peptide bonds have been broken to create small peptide fragments. These peptides are too
small to bridge adjacent allergen specific IgE molecules on the surface of mast cells thus
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degranulation does not occur. The rationale behind the use of these diets assumes that canine
CAFR is mediated by IgE, which as previously discussed has not been determined. Various
studies have examined the performance of hydrolyzed diets in a clinical setting and found them
to be well tolerated. There is less critical evaluation however on the performance of these diets
in dogs known to be hypersensitive to the parent protein. A small number of studies suggest
that 20-50% of individuals will react adversely to the hydrolyzed diet if they are sensitive to the
parent protein. Furthermore, these diets tend to be costlier and less palatable.
If the animal’s signs and disease improve on the test diet a challenge with the original
diet should be performed to confirm the diagnosis. Signs of pruritus usually return within a week
of feeding the offending diet.
After the diagnosis has been made, the owner can try feeding the animal one of several
different commercial diets to see if they can be maintained sign-free on any of them. If the
animal’s condition relapses with a challenge, the owner can go back to feeding the
hypoallergenic diet before the next challenge. Many owners will elect to continue on the “food
trial” commercial diet. If they do not wish to pinpoint the individual allergen, they should be
encouraged to keep a list of the food substances that have previously been fed to their pet.
With this information, if they desire to change diets or if the diet being fed becomes unavailable,
they may be able to choose another commercially available diet that avoids proteins from the
“potentially offending protein” list.
Oclacitinib (Apoquel) can be used to control the pruritus and dermatitis during the diet
trial. It has been shown effective in treating dogs with any allergic dermatitis, and at some time
during the trial, when the Apoquel is discontinued, it can be determined if the new diet is
controlling the signs.
Canine Atopic Dermatitis (CAD)
Currently accepted pathogenesis of CAD
In the acute phase of the disease, possible epidermal barrier defects are thought to
facilitate contact of environmental (and possibly microbial) allergens with epidermal immune
cells. These Langerhans cells have allergen-specific IgE on their surface which aids in their
capture of specific allergens. These cells migrate to the dermis and regional lymph nodes.
Microbial products and immune cell-derived inflammatory mediators activate keratinocytes,
which, in turn, release more chemokines and cytokines. IgE-coated dermal mast cells release
histamine, proteases, chemokines and cytokines following contact with allergens. There is an
early influx of granulocytes (neutrophils and eosinophils), allergen-specific T-lymphocytes and
dermal dendritic cells. Eosinophils degranulate and release proteins that induce dermal and
epidermal damage. Th2 lymphocytes that have been activated by the antigen-presenting
Langerhans cell release cytokines promoting further IgE synthesis and eosinophil survival.
Microbes, self-trauma and neuromediators might also contribute to persistent inflammation in
chronic skin lesions. There is a continuous cycle of chemokine release that leads to the influx
and activation of leucocytes and the release of additional pro-inflammatory mediators. The
failure to down-regulate pro-inflammatory mechanisms is followed by self-perpetuating
cutaneous inflammation. Despite the advances in our knowledge of the pathogenesis of canine
AD, the mediators that elicit the sensation of pruritus have not been elucidated. Importantly,
histamine injected intradermally does not appear to cause pruritus in dogs.
Current views as to the immunopathogenesis of CAD assume a central role for allergenspecific IgE. In a small number of cases (approximately 10%) of what clinically appears to be
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otherwise classical CAD, allergen-specific IgE is undetectable – either by intradermal testing
(IDT) or by serology. The term “atopic-like dermatitis” is proposed for such cases. The
pathogenesis of this subset is not fully understood.
Clinical signs
In dogs with CAD, pruritus is the overwhelming owner complaint. Primary skin lesions
(e.g. papules, wheals) are not commonly seen. Pruritus and the resultant lesions usually involve
the face, particularly the periocular and perioral areas, inner surface of the pinnae, and ear
canals; the feet, especially the caudal carpi and tarsi; the axillae; and the ventrum, or some
combination thereof. There are generalized cutaneous signs in about 40% of the cases. Otitis
externa is present in about 50% of the cases. Bacterial pyoderma (i.e. folliculitis, furunculosis,
acute moist dermatitis) caused by Staphylococcus intermedius accompanies approximately
33% of the cases. Atopy is one of the many possible underlying causes of recurrent pyoderma.
Many dogs with AD will experience secondary colonization of their skin with Malassezia
pachydermatis. Secondary seborrheic skin disease is present in about 12% of the atopic dogs.
Hyperhidrosis has been reported in about 10% of the cases. Dogs often have concurrent
allergic conjunctivitis (50%) but rarely allergic rhinitis, asthma, or gastrointestinal signs.
The diagnosis of CAD is made by the history, physical examination, and by ruling out
other causes of pruritic dermatoses. Questions to be addressed in the history include the
signalment; age of onset of the pruritus; seasonality, especially in the beginning; distribution of
the pruritus; and known responsiveness of the disease to corticosteroid therapy.
Therapy
An evidence-based systematic review of the therapies recommended for the treatment of
CAD showed good evidence for recommending the use of oclacitinib, oral glucocorticoids and
cyclosporine. The report found fair evidence for using topical triamcinolone spray, topical
tacrolimus lotion, oral pentoxifylline or oral misoprostol. Insufficient evidence is available for or
against recommending the prescription of oral first- and second-generation type-1 histamine
receptor antagonists, tricyclic antidepressants, cyproheptadine, aspirin, Chinese herbal therapy,
ascorbic acid, immune-modulating antibiotics, topical pramoxine or capsaicin. Finally, there is
fair evidence against recommending the use of oral arofylline, leukotriene synthesis inhibitors
and cysteinyl leukotriene receptor antagonists. In this review fatty acid supplementation and
allergen-specific immunotherapy were not evaluated. Oclacitinib has been shown to be safe
and effective for the long term management of the clinical signs of CAD.
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