CONSULTANT ON CALL hDERMATOLOGYh PEER REVIEWED

Canine Atopic
Dermatitis
Maite Verde, DVM, PhD
University of Zaragoza

1 d Dog with atopic

dermatitis and
generalized lesions.

PROFILE

h Canine atopic dermatitis (CAD) is a geneti- T

 his definition assumes that IgE is not CAD is a complex,
cally predisposed inflammatory, pruritic necessary for clinical manifestations of multifactorial
skin disease. the disease and that other mechanisms disease;
h Characteristic signs, associated with immu- (eg, skin barrier dysfunction) can lead to genetic and
noglobulin (IgE), are most commonly directed dermatitis clinically indistinguishable environmental
against environmental allergens1; however, from classic atopic dermatitis.
factors play a
CAD can be associated with other systemic
fundamental role.
signs (eg, GI, respiratory). Pathophysiology
A  llergens not associated with environ- hC
 AD is a complex, multifactorial disease;

ment (primarily food) may trigger derma- genetic and environmental factors play a
titis flare-ups with signs indistinguishable fundamental role.
from CAD. hC AD is triggered mainly by aeroallergens;

F  ood can induce atopic dermatitis. diverse factors (eg, bacterial or yeast over-
h Atopic-like dermatitis (ALD) is an inflamma- growth, physiologic or weather factors) can
tory, pruritic skin disease with clinical fea- affect its presentation.3
tures identical to those in CAD, in which an hT he 2 major mechanisms of the disease are:

IgE response to environmental or other A bnormalities of the epidermal structure

AD = atopic dermatitis
allergens cannot be documented.2 and function.
ALD = atopic-like
A  LD, similar to intrinsic atopy in humans, C utaneous inflammation due to inappro- dermatitis
describes patients with clinical features of priate immune response to antigens CAD = canine atopic
CAD and no detectable IgE increase.2 encountered on the skin. dermatitis

18 cliniciansbrief.com March 2016

h A defective cutaneous barrier is consid-
ered crucial for development of atopic
dermatitis.3
I n patients with atopic dermatitis (AD), the
epidermal elements that should form a
compact wall are unstructured; this
leaves weak points, which allergens can
penetrate.
D  efects or dysfunction in structural skin
integrity (eg, corneodesmosomes, inter-
cellular lipids, terminally differentiated
keratinocytes), are associated with CAD
development.4
h Cutaneous barrier dysfunction can be
caused by5:
I ntercellular lipid lamellae structural
defects in the stratum corneum and at the
junction with the stratum granulosum.
D  efects of skin lipid composition with
reduced ceramides and reduced expres-
sion of and mutations of filaggrin (ie,
structural protein isolated from the stra-
tum corneum that binds to keratin fila-
ments and causes aggregation into
macrofibrils contributing to cellular com-
paction and a highly insoluble keratin
matrix).
T  he matrix acts as a protein scaffold for the
attachment of cornified-envelope proteins
and lipids that form the stratum corneum.6
A  berrant lamellar organization and
increased transepidermal water loss.
h An overactive T-helper type 2 (Th2) immune
response against environmental allergens
that penetrate the epidermis can lead to
increased production of allergen-specific
IgE (not in ALD cases) and to an inflamma-
tory dermal reaction that worsens cutane-
ous barrier function, appearance of lesions,
and pruritus.
h Bacteria and yeast (eg, Staphyloccocus
pseudintermedius, Malassezia pachyderma-
tis), which easily colonize the skin surface,3
adhere and multiply faster in individuals
with AD.
O  vergrowth is common and can produce
recurrent pyoderma and Malassezia spp
dermatitis.
Bacteria and Malassezia spp may also act
as antigens producing bacterial and
Malassezia spp hypersensitivity, which
worsens the inflammatory process.
h The enteric barrier and immunologic toler-
ance mechanisms in the GI tract may pres-
ent functional defects.
S ome patients could develop hypersensi-
tivity to allergens, particularly protein, in
the diet.
h Factors that can trigger flares or worsen
In patients
the disease include flea bites, food, inhal- with atopic
ant, and contact allergens.7
S ome detergents, some textile fibers,
dermatitis
extreme temperatures and humidity, and (AD), the
cutaneous microbial colonization can
have the same effect. epidermal
elements
Signalment
h Age of onset can range from 6 months to that should
6 years,8 depending on factors such as
breed and geographical location.
form a
H  ighly susceptible dogs in warm climates, compact
with pollen present year-round, have
increased risk for early onset of signs.8
wall are
F  rench bulldogs and shar-peis appear to unstructured;
develop CAD earlier in life than other
breeds.9
this leaves
D  ogs with food-induced CAD are more weak points,
likely to be presented with clinical signs at
<1 year of age in 50% of cases; for CAD
which
related to environmental allergens, it is allergens can
38%.3
I n general, clinical signs appear before
penetrate.
3 years of age in 68% of cases.10,11
h Breed predisposition and breed-specific
clinical phenotypes have been reported.9,12
Clinical Signs
h C AD is a clinical syndrome, not a uniform
disease.
C
 linical manifestations can evolve
throughout the life of affected dogs.
h Some dogs are presented with year-round
March 2016 cliniciansbrief.com 19
CONSULTANT ON CALL hDERMATOLOGYh PEER REVIEWED
2A
d An acute case of erythema and pruritus
located in axillae, interdigital, and inguinal
regions.
clinical signs from the onset of CAD.
I n about 30% of cases, signs are seasonal
and associated with environmental
allergens.8
 In these cases, signs may become pres-
ent year-round as the disease pro-
gresses.
D  ogs with food-induced atopic dermatitis
or CAD caused by dust mites are pre-
sented with year-round clinical signs.8
h Pruritus without lesions (ie, sine materia) at
onset is the main sign of the disease.
T  his can be accompanied by erythema
and papules as initial lesions in affected
areas.
E  arly in the disease process, pruritic
intensity can be mild (eg, 4-5 on a scale
CAD = canine atopic of 1-10) but increases progressively as the
dermatitis process becomes chronic and/or is com-
20 cliniciansbrief.com March 2016
2B
d A chronic case of hyperpigmentation and
alopecia in the same areas.
plicated with secondary infections
(eg, bacterial or yeast overgrowth) or
other aggravating factors (eg, food, fleas,
contact irritants).
h Lesions are not specific, but their distribu-
tion pattern can be highly suggestive of
CAD (Figure 1).
L esions observed in the acute phase
include erythema and papulopustular
rash that evolve to squamous lesions,
lichenification, and alopecia as the dis-
ease progresses.
A  reas most commonly affected are ven-
tral hairless zones (axillae, inguinal
region, and interdigital areas; Figure 2,
page 18), similar to the lesions seen in
allergic contact dermatitis.
Other affected areas include the muzzle,
periocular region, pinnae (Figure 3, next
 page), and flexural surface of the elbow
(Figure 4).
h Other signs may include conjunctivitis, oti-

tis (Figure 5, next page), hyperhidrosis,

chronic changes from pruritic behavior (eg,
salivary staining, lichenification, hyperpig-
mentation; Figures 6 and 7, pages 22 and
23), acute moist dermatitis, acral pruritic
nodules, and acral lick granulomas.
I n up to 43% of cases, external otitis can

be the first sign.8

h Some dogs with CAD are predisposed:

T  o develop reactions to allergens (eg, 3

food, flea, contact allergens).
T  o develop secondary bacterial infections
d C AD in a Labrador retriever. Skin
(66%) and yeast infections (33%) with some
hyperpigmentation is present in muzzle,
breed propensity (eg, West Highland white periocular, and facial areas; erythema and
terrier, German shepherd dog).7 lichenification in the pinna are seen.
Concurrent environmental and food aller-
gens have been observed in 13% to 30% of
cases10; in these patients, GI manifestations
(eg, increased frequency of defecation, soft
and light-colored feces, flatulence, scoot-
ing) can accompany the cutaneous signs.
Other noncutaneous signs (eg, rhinitis,
reverse sneezing, alteration of the estrus
cycle) can be observed.

DIAGNOSIS

h Based on presentation frequency of differ-

ent signs, a set of diagnosis criteria has

been proposed (see Favrots Clinical Crit-
era Sets, page 25).12 4
W  hen 5 of these criteria are present, this

provides 85.4% sensitivity and 79.1% d Erythema and lichenification located in

specificity for CAD diagnosis.
h Diagnosis must be based on clinical his-
tory, signs, and exclusion of other pruritic
causes of dermatitis with similar clinical
presentations.
ventral thorax and flexural surface of the
elbow.
A  differential diagnosis should be made

T  here is no definitive test for CAD
diagnosis.
h For a patient with a clinical history and
signs suggestive of CAD, these steps can be
followed to reach a definitive diagnosis:
based on information from clinical history
and physical and dermatological exam-
ination (Table 1, page 24).
I t should be verified that the patient meets
at least 5 of Favrots diagnostic criteria.

March 2016 cliniciansbrief.com 21

CONSULTANT ON CALL hDERMATOLOGYh PEER REVIEWED
5A
5B
d Otitis externa in2 dogs with CAD. Clinical
aspects in an acute otitis (A) and in a
chronic case (B).
B
 asic dermatological diagnostic tests and/
or therapeutic trials should be conducted
to rule out Sarcoptes scabiei, Demodex spp
mite infestation, pyoderma, and yeast
overgrowth as causes of pruritus.
Sarcoptic mange should be ruled out.
Superficial scrapings on the periphery of
alopecic lesions and squamous scabs;
lesions on edge of the pinnae, hocks,
and elbows; and evident pinnal-pedal
response can help in diagnosing Sarcoptes.
In case of doubt, 4 doses of selamectin
or moxidectin spot on should be
applied every 2 weeks for 2 months;
other options (eg, PO/SC ivermectin,
lime sulfur dips) may be considered.
 Demodex spp mites can be found in
22 cliniciansbrief.com March 2016
6A
6B
d Different aspects of salivary staining in
CAD.
deep skin scrapings of dogs with signs
similar to those seen with CAD.
These mites are readily found on deep
skin scrapings of alopecic lesions; blood
should be visible on cytologic samples.
 Demodex spp mites may be noted in
dogs previously treated with systemic
corticosteroid medications; in this situ-
ation, demodicosis may resolve strictly
with discontinuation of steroid therapy.
h Bacteria overgrowth, surface folliculitis,
and pyoderma are common in CAD.
T
 opical therapy (ie, antiseptic shampoos
2 times a week at onset and later once a
week) may be indicated and can resolve
pyoderma in some patients (Table 2,
page 26).
 I n other cases, treatment with systemic
antibiotics may be warranted, although
they should be used judiciously to help
prevent the development of bacterial
resistance.
h Yeast overgrowth, common in CAD, can sig-

nificantly contribute to pruritus.

M  alassezia spp can trigger hypersensitiv-

ity reactions; if yeast is found on surface

cytology, topical therapy (eg, chlorhexi-
dine and miconazole baths) or systemic
therapy with antifungals (eg, itraconazole
ketoconazole, fluconazole, terbinafine)
7A 7B
should be initiated.
h Control of internal and external parasites

(eg, fleas) should be verified.

A  dulticidal flea preventative should be

administered consistently to all poten-

tially allergic patients in geographical
regions endemic for fleas.
h A strict elimination diet can detect whether

diet components are responsible for >75%

of pruritus and clinical signs.13
I n many CAD cases, patients are presented
with clinical signs caused by a combination

7D
of food and environmental allergens.
In these cases, in the authors experience, 7C
only a mild improvement (<25%) may be
d Chronic generalized CAD in a German shepherd dog, with lichenification
observed during the elimination diet.
and hyperpigmentation.
h If no substantial improvement of signs and/

or pruritus has been seen following the steps

listed above, and if the patient has at least 5
of Favrots clinical criteria, the patient can be
TREATMENT
diagnosed CAD to aeroallergens, with 85.4%
sensitivity and 79.1% specificity. h Treatment must be adapted to each

O  nce diagnosed, the patient can be patient; there is no set formula for CAD
treated based on signs (Table 2, page 26), treatment.
or an intradermal or serological ELISA T he right therapeutic approach for each

allergen test can be performed to identify
environmental allergens involved in
development of clinical signs.
If positive results are obtained in the
intradermal or serologic test, and these
are in line with the epidemiological char-
patient will be based on concomitant fac-
tors (eg, geographical area, severity of
clinical signs, duration of signs, acute or
chronic presentation, patient age, owner
resources).
h Pruritus threshold and summary effects are

acteristics and the patient history, immu- critical in managing CAD.

notherapy may be recommended. h All pruritus-inducing factors should be

March 2016 cliniciansbrief.com 23

CONSULTANT ON CALL hDERMATOLOGYh PEER REVIEWED

TABLE 1

CANINE ATOPIC DERMATITIS DIFFERENTIAL DIAGNOSIS: CAUSES TO BE RULED OUT

Nonseasonal Causes Seasonal Causes Less Frequent Causes

Scabies (Sarcoptes scabiei) Flea-allergy dermatitis Internal parasitism with hypersensitivity

Demodicosis Contact allergy to seasonal plants Cheyletiellosis

Otocariasis (Otodectes cynotis) Insect bite hypersensitivity Pediculosis

Dermatophytosis Trombiculiasis

Food hypersensitivity Primary seborrhea

Contact allergy to perennial allergens (eg, carpet Mycosis fungoides (cutaneous

fibers) lymphoma)

Contact allergy to plants (eg, Chrysanthemum Drug reactions

cinerariifolium, Achillea millefolium, Curcuma longa,
Anthemis nobilis, Taraxacum officinale, Tanacetum
vulgare, Chamomilla recutita)

Flea-allergy dermatitis

Insect bite hypersensitivity

analyzed in determining which are most Minimizing Allergen Exposure

important to control or eliminate. h Allergen exposure can be minimized by:

G  iving baths to reduce epicutaneous

Client Communication
h Clients should be informed that:
C AD is a chronic, incurable disease.
P ruritus may not resolve completely; how-
ever, with therapy it should markedly
improve to a reasonably tolerable level.
T he veterinary team will try to use as few
drugs as possible to minimize or control
signs.
T he patient can relapse, and the condition
can worsen with age.
It is important to be strict with diet and
flea control.
Measures to lower the concentration of
CAD = canine atopic aeroallergens may help prevent
dermatitis relapses.
exposure.
P  reventing atopic dogs from walking on
grass, particularly recently cut grass.
E  liminating carpets and rugs from the
house.
F requently vacuuming curtains and
fabric-covered furniture.
F requently laundering the dog bed with
hot water to reduce mites.
K  eeping the home free of tobacco smoke.
C  ontrolling the relative humidity and tem-
perature using air conditioning.
Skin Barrier Repair
h The following methods can repair the skin
barrier:

24 cliniciansbrief.com March 2016

 F requent baths (2 times a week initially,
then less frequently) with products con- FAVROTS CLINICAL
taining antiseptics, antifungals, emollients, CRITERIA SETS12
and moisturizers can help control bacterial
and/or Malassezia spp overgrowth, folliculi- All sets of criteria should be used only after
tis, and superficial pyodermas. ruling out other causes of pruritus (eg,
B  aths also have a hydrating effect and can
ectoparasites, infections, food).
wash allergens off of the skin surface. Set 1 Criteria
S  ystemic antibiotics for at least 4 weeks
h Age at onset <3 years
(in superficial pyodermas) or 8 weeks (in
deep pyodermas) if pyoderma cannot be h Mostly indoor

controlled with topical treatment.

h Corticosteroid-responsive pruritus
S  ystemic antifungals in case of Malassezia

spp overgrowth and the associated signs h Chronic or recurrent yeast infections

are significant and not controlled with

h Affected front feet
topical treatment.
h Affected ear pinnae

Antiparasitic Control h Non-affected ear margins

h Use GI parasite and flea control year-round.

h Adjust the preventive program to fit the h Non-affected dorsolumbar area

areas climate, the patients living environ-
ment (eg, indoor, outdoor, additional pets),
and bathing frequency.
Diet
h In CAD cases in which a dietary component
Dogs exhibiting 5 of these criteria have
85.4% sensitivity and 79.1% specificity for
diagnosis of CAD12
Dogs exhibiting 6 of these criteria have
58.2% sensitivity and 88.5% specificity for
diagnosis of CAD12

is suggested, patients should be fed a Set 2 Criteria

hypoallergenic diet with specific or hydro-
h Age at onset <3 years
lyzed proteins.
h In cases that are not food-induced, diet h Mostly indoor
should be supplemented with essential
h Pruritus sine materia (ie, without lesions) at
fatty acids.
onset

Pruritus Therapy h Affected front feet

h These drugs may control pruritus and inflam-

h Affected ear pinnae
matory lesions that could not be resolved
with therapies described previously14: h Non-affected ear margins

H
 1 antihistamines with essential fatty acids.
h Non-affected dorsolumbar area
O
 clacitinib at 0.5 mg/kg twice a day for
Dogs exhibiting 5 of these criteria have
1 to 2 weeks, then lower the dose and 77.2% sensitivity and 83.0% specificity for
frequency to control acute crises and for diagnosis of CAD12
mid- and long-term therapy. Dogs exhibiting 6 of these criteria have
C
 orticosteroids (prednisolone and 42.0% sensitivity and 93.7% specificity for
methylprednisolone) at 0.5 mg/kg twice a diagnosis of CAD12
day for 1 week, then lower to once a day and
once every other day to treat acute crises.

March 2016 cliniciansbrief.com 25

CONSULTANT ON CALL hDERMATOLOGYh PEER REVIEWED

M odified cyclosporine A at 5 mg/kg once a

TABLE 2
day for a month, then lower the fre-
quency, for long-term treatment. CANINE ATOPIC DERMATITIS THERAPY
Modified cyclosporine A can be com-
bined with oclacitinib and corticoste-
roids for the first 2 weeks of treatment.
T opical therapy with corticosteroids and Systemic (PO) Administration
tacrolimus in focal-localized cases.
TYPE-1 ANTIHISTAMINES
Immunotherapy Cetirizine 0.5-1 mg/kg once or twice a day
h Allergen-specific immunotherapy (ASIT) or

hyposensitization is considered the only Chlorpheniramine 0.4 mg/kg twice a day

treatment that could alter the course of the
Clemastine 0.05-0.1 mg/kg twice a day
disease.
A  SIT may be a good option for long-term Cyproheptadine 1-2 mg/kg twice a day
control of CAD, but it is not effective for
every patient. Diphenhydramine 2.2 mg/kg twice a day
A  SIT allows for modulation of the immune
Hydroxyzine 2.2 mg/kg twice a day
system through administration (SC or sub-
lingual) of allergen concentrates to which ANTIMICROBIALS
the patient has shown to be sensitive
Cephalexine 22-35 mg/kg twice a day
(based on the results of allergen testing),
with increasing doses and frequencies. Cefadroxil 22-30 mg/kg twice a day
h Immunotherapy is the best option, particu-

larly with young patients with nonseasonal Cefovecin 8 mg/kg SC once every 2 weeks, 2 times
CAD and in patients that are expected to Cefpodoxime 5-10 mg/kg once a day
stay in the same area in the future.
h In the authors experience, once good Amoxicillinclavulanic acid 20 mg/kg twice a day
results are achieved, hyposensitization
Clindamycin 5.5 mg/kg twice a day
therapy should be maintained for life.
N  ot every CAD patient will benefit from ANTIFUNGAL
immunotherapy, which has been shown
Fluconazole 5 mg/kg once a day
effective in approximately 50% to 75% of
cases.15 Ketoconazole 5-10 mg/kg once a day
H  owever, when a formulation has been

unsuccessful (eg, a patient has not bene- Itraconazole 5 mg/kg once a day
fited from injectable immunotherapy),
Terbinafine 30-40 mg/kg once a day for 2 days, after 5
another (eg, sublingual administration) days out (for 1 month)
may have beneficial results. CORTICOSTEROIDS
h Monoclonal antibody therapy for the

immediate future.16 Prednisolone/prednisone 0.5 mg/kg twice a day and tapering to

P  roposed to inhibit IgE production via its
once a day to once every 2 days
promoting cytokines (IL-4/ IL-13), their
cytokine receptors, or IgE itself.
Methylprednisolone 0.4 mg/kg twice a day and tapering to
T  he itch sensation itself could be altered, once a day to once every other day
at least theoretically, by antibodies tar-
Table continues on next page.

26 cliniciansbrief.com March 2016

 geting itch-promoting cytokines such as IL-31.
T  he newly available monoclonal antibody prod-

uct against IL-31 can be administered SC once-

monthly.
 Safety and efficacy studies are still ongoing
with the conditional license. n
Systemic (PO) Administration

CALCINEURIN INHIBITORS
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IgE = immunoglobulin

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