Treatment of canine atopic dermatitis: 2015 updated guidelines from the International Committee on Allergic Diseases of Animals (ICADA)

Abstract

Background:
In 2010, the International Task Force on Canine Atopic Dermatitis (now International Committee on Allergic Diseases of Animals, ICADA) published the first consensus guidelines for the treatment of atopic dermatitis (AD) in dogs. This is the first 5-year minor update of this document.

Results:
The treatment of acute flares of AD should involve the search for, and then elimination of, the cause of the flares, bathing with mild shampoos, and controlling pruritus and skin lesions with interventions that include topical and/or oral glucocorticoids or oclacitinib. For chronic canine AD, the first steps in management are the identification and avoidance of flare factors, as well as ensuring that there is adequate skin and coat hygiene and care; this might include more frequent bathing and possibly increasing essential fatty acid intake. The medications currently most effective in reducing chronic pruritus and skin lesions are topical and oral glucocorticoids, oral ciclosporin, oral oclacitinib, and, where available, injectable recombinant interferons. Allergen-specific immunotherapy and proactive intermittent topical glucocorticoid applications are the only interventions likely to prevent or delay the recurrence of flares of AD.

Conclusions:
This first 5-year minor update of the international consensus guidelines for treatment of AD in dogs further establishes that the treatment of this disease is multifaceted, and that interventions should be combined for a proven (or likely) optimal benefit. Importantly, treatment plans are likely to vary between dogs and, for the same dog, between times when the disease is at different stages.

Full text

C O R R E S P O N D E N C E Open Access
Treatment of canine atopic dermatitis: 2015
updated guidelines from the International
Committee on Allergic Diseases of Animals
(ICADA)
Thierry Olivry
1*
, Douglas J. DeBoer
2
, Claude Favrot
3
, Hilary A. Jackson
4
, Ralf S. Mueller
5
, Tim Nuttall
6
, Pascal Prélaud
7
and for the International Committee on Allergic Diseases of Animals
Abstract
Background: In 2010, the International Task Force on Canine Atopic Dermatitis (now International Committee on
Allergic Diseases of Animals, ICADA) published the first consensus guidelines for the treatment of atopic dermatitis
(AD) in dogs. This is the first 5-year minor update of this document.
Results: The treatment of acute flares of AD should involve the search for, and then elimination of, the cause of
the flares, bathing with mild shampoos, and controlling pruritus and skin lesions with interventions that include
topical and/or oral glucocorticoids or oclacitinib. For chronic canine AD, the first steps in management are the
identification and avoidance of flare factors, as well as ensuring that there is adequate skin and coat hygiene and
care; this might include more frequent bathing and possibly increasing essential fatty acid intake. The medications
currently most effective in reducing chronic pruritus and skin lesions are topical and oral glucocorticoids, oral
ciclosporin, oral oclacitinib, and, where available, injectable recombinant interferons. Allergen-specific immunotherapy
and proactive intermittent topical glucocorticoid applications are the only interventions likely to prevent or delay the
recurrence of flares of AD.
Conclusions: This first 5-year minor update of the international consensus guidelines for treatment of AD in dogs
further establishes that the treatment of this disease is multifaceted, and that interventions should be combined for a
proven (or likely) optimal benefit. Importantly, treatment plans are likely to vary between dogs and, for the same dog,
between times when the disease is at different stages.
Keywords: Atopic dermatitis, Canine, Dogs, Evidence-based medicine, Guidelines, Treatment
Background
In 2010, the International Task Force on Canine Atopic
Dermatitis (ITFCAD), now International Committee on
Allergic Diseases of Animals (ICADA; www.icada.org)
generated the first guidelines for treatment of atopic
dermatitis (AD) in dogs [1]. These recommendations,
published in English and translated in 17 other languages,
were designed and made freely downloadable for a global
general practitioner audience. While new drugs have
become available in the last 5 years, others are no longer
so, and therapeutic regimens have continued to evolve.
For these reasons, the ICADA membership decided to up-
date these guidelines on a 5-year basis. While complete re-
writes are planned to occur every 10 years, minor updates
are to be written 5 years into each decade; this is the first
quinquennial minor rewrite to the 2010 canine AD treat-
ment guidelines [1].
As for the first version of these directives, readers
should remember several basic principles that underlie
this document:
* Correspondence: tolivry@ncsu.edu
1
Department of Clinical Sciences, College of Veterinary Medicine, North
Carolina State University, 1060 William Moore Drive, Raleigh 27606 NC, USA
Full list of author information is available at the end of the article
© 2015 Olivry et al.
Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a
link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain
Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this
article, unless otherwise stated.
Olivry et al. BMC Veterinary Research (2015) 11:210
DOI 10.1186/s12917-015-0514-6

1) Recommendations are generally made from evidence
derived from previously published randomized
controlled trials (RCTs) and systematic reviews [2–4].
Practitioners must keep in mind that statistically
significant changes in trial’s outcome measures do not
imply that the intervention will be effective in all
patients, or that the ownerswillbesatisfiedwiththe
recommended product. Moreover, clinical trials
generally test the efficacy of a single intervention, while,
in daily practice, the best clinical benefit normally
requires the combination of multiple treatments.
Consequently, results of clinical trials will usually
underestimate the synergistic potential of the tested
drug when it is included in a multi-intervention
treatment protocol.
2) In multiple sections of these guidelines, readers will
find that there is a lack of or insufficient evidence
supporting the efficacy of a specific intervention.
Such statement does not mean that the discussed
intervention will not be effective in their patient, but
rather that it has not been tested sufficiently to
assess if it offers any benefit.
3) As in the first version of these guidelines, when
recommendations are made for an intervention
supported by one or more trials done with a specific
product, we mention the generic drug name
followed by the brand and company indicated in the
paper reporting the study results. In all other cases,
recommendations only provide generic drug names.
Importantly, the recommendation for a specific
product does not imply the endorsement of the
product or its maker by the ICADA. A
recommendation only means that at least one
clinical trial exists that suggests the drug’s benefit,
or, in the absence of such trial, that there is
consensus among authors for recommending this
intervention.
4) Finally, and as done previously, this update is
divided into three different sections:
recommendations for i) the management of acute
flares of canine AD, ii) the treatment of chronic skin
lesions of AD, and, iii) the interventions to prevent
disease relapses. For typical case scenarios that could
benefit from these recommendations, the readers are
referred to the 2010 version of these guidelines [1].
In each section, treatment options are listed in a
particular order. By no means do we imply that all
interventions are recommended—or even
needed—for each patient in that very same order.
Recommendations must be evaluated by
veterinarians taking in consideration their unique
patient and pet owners. Practitioners should always
assess the benefit, side effects, practicability, cost
and availability of the proposed treatments, which
often will have to be combined for an optimal
outcome.
This paper is aimed at being a shorter update of the
longer original version of the guidelines [1]. Each section
will contain an abbreviated summary of the 2010 recom-
mendations, followed by a “2015 update”with support-
ing information for the proposed change or update.
Supporting data published in the 2010 guidelines will
normally not be repeated. In each section, we will clearly
state where there was no obvious need for updating the
2010 recommendations.
Importantly, the authors decided to change the strength
of recommendation (SOR) and category of evidence (COE)
grading schemes used in the 2010 guidelines to the simpli-
fied and less confusing SORT scoring system (Table 1) [5].
As before, an SOR of lower alphabetic order and a quality
of evidence (QOE) of lower Roman numeral should be con-
sidered of greater value than those with higher letters and
numbers. However, readers should not attempt to compare
the SORs and COEs/QOEs between the 2010 and 2015
versions of these guidelines, are these scores are not de-
signed to be transposable.
Furthermore, in this update, and to facilitate the com-
parison between this and future versions of the guide-
lines, each section will be numbered.
Finally, and as done previously, we provided, as an online
document, a one-page summary of the recommendations
developed herein (Additional file 1).
A. Treatment of acute flares of AD
This section is relevant to the treatment of dogs with
case scenarios 1a and 1b described in the 2010 version
of these guidelines [1]; these can be accessed freely on
the following site: http://onlinelibrary.wiley.com/doi/
10.1111/j.1365-3164.2010.00889.x/suppinfo.
A.1. Identification and avoidance of flare factors
Table 1 Strength of recommendation taxonomy (SORT)
Strength of recommendation (SOR)
A = based on consistent and good quality patient-oriented evidence
B = based on inconsistent or limited quality patient-oriented evidence
C = based on consensus, usual practice, opinion, disease-oriented
evidence or case series
Quality of the evidence (QOE):
1 = good quality, patient-oriented
2 = limited quality, patient-oriented
3 = other evidence (usual practice, opinion, disease oriented evidence)
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 2 of 15

A.1.a. Identification and removal of allergenic causes of
flares
Summary of the 2010 guidelines:
Recognized allergenic causes of acute flares of
canine AD are a recent increased exposure to
environment allergens (especially house dust mites
and pollens), the ingestion of food ingredients, and
flea or other insect bites. Flares will normally only
occur if the dog is hypersensitive to these different
allergens and if the allergen load is sufficiently high
to trigger flares. The identification and, if at all
possible, the elimination of contact with, or
ingestion of, such allergens are important to
prevent further worsening or recurrences of the
flares [1].
Updated 2015 recommendations:
There are no proposed changes to the 2010
recommendations (SOR C).
A.1.b. Evaluation of use of antimicrobial therapy
Summary of the 2010 guidelines:
Bacterial and yeast skin and ear infections are
common causes of flares in dogs with AD. The
treatment of such infections usually consists of
topical and/or systemic antimicrobials [1].
Updated 2015 recommendations:
There are no major changes to the 2010
recommendations (SOR C). To improve efficacy and
antimicrobial stewardship, veterinarians are advised
to follow antimicrobial treatment guidelines
established in their country of practice and/or in
international consensus recommendations (SOR C)
[6,7]. Importantly, veterinarians and pet owners
should watch for a drying or irritating effect of
topical antimicrobials—especially shampoos—that
might induce a flare of AD in their patient (SOR C).
A.2. Improvement of skin and coat hygiene and care
A.2.a. Bathing with a non-irritating shampoo
Summary of the 2010 guidelines:
Bathing with an emollient shampoo containing
lipids, complex sugars and antiseptics (Allermyl,
Virbac) has been shown to have a modest and
short-lived antipruritic effect. Other topical
emollients have not been proven to reduce pruritus.
The intensity and frequency of bathing may be the
most important factors to relieve itch [1].
Updated 2015 recommendations:
Emollient formulations containing either lipids,
complex sugars and antiseptics (Allermyl, Virbac)
or phytosphingosine, raspberry oil and lipids
(Douxo Calm, Ceva) have been shown to provide a
modest effect on skin lesions and pruritus in
allergic dogs (SOR B); this benefit is likely highest
in dogs with mild AD (SOR C). The intensity and
frequency of bathing may be the most important
factor in relieving pruritus (SOR B). Other topical
emollients have not been proven to consistently
reduce signs of AD in dogs (SOR C).
Basis for the updated recommendations:
A recent three-week small RCT revealed the nearly
equivalent reduction of skin lesions and pruritus in
allergic dogs using either Allermyl shampoo or a
Douxo Calm shampoo and foam combination
(QOE 2) [8]. These results mirror those from a
previous small trial employing Allermyl, Douxo
Calm shampoo or a Douxo Calm shampoo and
spray regimen (QOE 2) [9].
A.3. Reduction of pruritus and skin lesions with
pharmacological agents
A.3.a. Short-term treatment with topical glucocorticoids
Summary of the 2010 guidelines:
Topical glucocorticoid sprays are effective for the
treatment of acute flares of canine AD. Such
intervention is especially suitable for localized skin
lesions and for short durations. Treatment duration
and frequency should be tailored to the patients’
clinical signs [1].
Updated 2015 recommendations:
Topical glucocorticoid sprays (Cortavance, Virbac
[SOR A]; Genesis, Virbac US [SOR B]) are effective
for treatment of flares of canine AD. In the absence
of availability of these formulations, other topical
glucocorticoid formulations are theoretically likely
to be beneficial, but the efficacy and safety of these
medications will vary with the strength of
glucocorticoid and vehicle used (SOR C). Topical
glucocorticoids are especially beneficial for
localized skin lesions and for short durations; care
must be taken to avoid the steroid-induced skin
atrophy that will nearly always develop after
long-term daily application of the product at the
same skin sites (SOR C). Treatment duration and
frequency of use should be tailored to each patient;
applications should normally continue until
complete and stable remission of signs (SOR C).
Basis for the updated recommendations:
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 3 of 15

In addition to the previously available clinical
trial data, a small study confirmed that a one to
two-week daily application of an hydrocortisone
aceponate spray (Cortavance, Virbac) significantly
improved lesions and pruritus in atopic dogs
(QOE 2) [10].
A.3.b. Short course of oral glucocorticoids or oclacitinib
Summary of the 2010 guidelines:
Oral prednisolone, prednisone or
methylprednisolone at 0.5 mg/kg once to twice
daily improve clinical signs of dogs with severe or
extensive AD. Side effects of oral glucocorticoids
are generally proportional to drug potency, dosage
and duration of administration. The treatment of
acute flares of canine AD with long-acting injectable
glucocorticoids is not recommended. Because most
dogs with AD have signs that respond to oral
glucocorticoids, failure of rapid clinical benefit
with this intervention should prompt clinicians to
reconsider alternative diagnoses or the presence
of secondary complications (for example, skin
infections, ectoparasitism or other nonatopic
food reactions) [1].
Updated 2015 recommendations
Oral prednisolone, prednisone or methylprednisolone
given at 0.5 to 1.0 mg/kg per day, in one or divided
into two doses, is likely to improve clinical signs of
dogs with severe or extensive AD (SOR A). Adverse
effects of oral glucocorticoids are normally
proportional to drug potency, dosage and duration of
administration. The treatment of acute flares of
canine AD with long-acting injectable glucocorticoids
is not recommended (SOR C).
Oclacitinib (Apoquel, Zoetis) can be prescribed at
0.4–0.6 mg/kg orally twice daily for up to 14 days to
rapidly reduce skin lesions and pruritus in dogs with
AD (SOR A). Short-term treatment with oclacitinib
appears safe.
Because of theoretical concerns for a potential
dose-dependent drug-induced immunosuppression,
the concomitant use of oral glucocorticoids with
oclacitinib is likely contraindicated, especially in
case of infections, though such combined use has
not been evaluated (SOR C).
As most signs of canine AD are expected to
respond to oral glucocorticoids or oclacitinib,
clinicians should reconsider alternative diagnoses
and/or the presence of secondary complications
(for example, skin infections, ectoparasitism,
nonatopic food reactions etc…) if there is no rapid
clinical benefit after treating atopic dogs with these
drugs (SOR C).
Basis for such recommendations:
Additional studies, which used prednisone or
prednisolone as positive treatment controls for
comparison with oclacitinib (QOE 1) [11]or
ciclosporin (QOE 2) [12,13], have confirmed the
rapid efficacy of oral glucocorticoids for treatment of
canine AD. Oclacitinib has been shown to reduce
pruritus and clinical signs significantly better than
placebo (QOE 1) [14] and as well as—or, at the 14 day
time point, better than—prednisolone (QOE 1) [11].
Short-term adverse effects of oclacitinib appear minor.
A.3.c. Interventions likely to be of little or no benefit to
treat acute flares of canine AD
A.3.c.1. Antihistamines
Summary of the 2010 guidelines:
Type-1 antihistamines (i.e. H1 histamine receptor
antagonists) are not likely to be beneficial after a
flare of AD has occurred. There is no conclusive
evidence for the efficacy for type 1 antihistamines
for treatment of active AD in dogs [1].
Updated 2015 recommendations:
Oral type 1 antihistamines might provide a small
and limited benefit in some dogs with AD (SOR B).
Due to their mode of action and for an optimal
benefit, oral type 1 antihistamines should preferably
be given before a flare occurs to block the effects of
histamine (SOR C). Clinical benefit might also
occur due to the sedative effect of first generation
type 1 antihistamines (e.g. diphenhydramine,
chlorpheniramine…) (SOR C). Due to their limited
efficacy, type 1 antihistamines are likely to be more
beneficial in dogs with mild AD (SOR C). There is
no evidence supporting the use of topical type 1
antihistamine formulations to treat canine AD
(SOR C).
Basis for such recommendations:
Approximately 25 % of clients that gave oral
antihistamines to their atopic dogs reported these
to be at least very effective in a retrospective
survey (QOE 2) [15]. An RCT reported that two
oral antihistamines, a hydroxyzine and
chlorpheniramine combination (Histacalmine,
Virbac) and dimetindene (Fenistil, Novartis),
mildly improved pruritus and skin lesions in dogs
with AD (QOE 2) [16]. In contrast, the
administration of an oral type 1 antihistamine
(hydroxyzine) did not prevent the
development of skin lesions in an experimental
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 4 of 15

model of acute AD in house dust mite-sensitized
dogs (QOE 3) [17].
A.3.c.2. Essential fatty acids (EFAs)
Summary of 2010 guidelines:
Oral EFAs are not useful to treat acute flares of AD
due to the length of time needed for any possible
beneficial effect to occur [1].
Updated 2015 recommendations:
There are no proposed changes to the 2010
recommendations (SOR C).
Basis for such recommendations:
A systematic review identified no additional
evidence supporting the effectiveness of oral EFA
supplementation for treatment of acute flares since
the publication of the 2010 guidelines [4]. A small
RCT testing a topical lipid complex containing
EFAs (Allerderm Spot-on, Virbac) did not show an
effect in reducing skin or pruritus two weeks after
application. As a result, this formulation is unlikely
to offer any benefit in the management of acute
flares of canine AD (QOE 2) [18].
A.3.c.3. Calcineurin inhibitors
Summary of 2010 guidelines:
The slow onset of action of topical (e.g. tacrolimus)
and oral (e.g. ciclosporin) calcineurin inhibitors
makes them unsuitable for managing acute flares of
AD [1].
Updated 2015 recommendations:
There are no proposed changes to the 2010
recommendations (SOR C).
B. Treatment of chronic canine AD
This section is relevant to the treatment of dogs with case
scenarios 2a and 2b described in the 2010 version of these
guidelines [1]; these can be accessed freely on the follow-
ing site: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-
3164.2010.00889.x/suppinfo.
B.1. Identification and avoidance of flare factors
B.1.a. Performance of dietary restriction-provocation tri-
als in dogs with nonseasonal AD
Summary of the 2010 guidelines:
Dogs with adverse food reactions can present with
clinical signs of AD, and some dogs exhibit
concurrent allergy to environmental and food
allergens. Restriction-provocation dietary trials are
the standard method to diagnose food-induced
AD. Clinicians should consider repeating dietary
trials in dogs with a previously well-controlled AD
that is now relapsing [1].
Updated 2015 recommendations:
Overall, there are no major changes to the 2010
recommendations (SOR C).
In dogs, as in humans, food allergy can manifest
with clinical signs of AD or other syndromes (e.g.
urticaria or others) (SOR C) [19]. The current
gold standard for the diagnosis of food allergy
remains a restriction trial with novel and/or
hydrolysed diets followed by provocation with
original food items once signs have abated during
the restriction phase (SOR C). An 8-week
restriction-provocation dietary trial should permit
the diagnosis of food allergy in most dogs (SOR
A). In case of dubious response to the first food
change, additional dietary trials may be needed,
especially if: 1) the history suggests an inappropriate
diet selection (e.g. lack of “novelty”of ingredients or
over-the-counter ingredient diets, as opposed to
those designed for veterinarian prescription) for the
first trial, or 2) the dogs present with perianal
pruritus and/or associated gastro-intestinal signs,
or 3) previously well-controlled atopic dogs
experience a flare that cannot be controlled by
means that were helpful before (SOR C).
It is speculated that the presence of storage mites in
dry dog foods might cause some relapses of AD
because of their allergenic crossreactivity with house
dust mites to which atopic dogs are frequently
hypersensitive (SOR C). However, there is currently
no evidence suggesting that avoiding dry commercial
dog foods is beneficial in dogs hypersensitive to
storage and/or house dust mites (SOR C). Freezing
dry dog foods might reduce contamination with
storage mites, but the impact of such freezing on the
clinical signs of mite-hypersensitive dogs is unknown
(SOR C). Nevertheless, to decrease excessive storage
mite contamination, owners should be encouraged
to avoid storing dry dog foods in humid and warm
areas, and they should be advised to store foods in
clean and sealed containers (SOR C).
Basis for such recommendations:
A recent critically-appraised topic established that an
8-week elimination diet should lead to a remission of
signs in more than 90 % of dogs with cutaneous
adverse food reactions (QOE 1) [20].
Three studies have demonstrated that
“non-prescription”pet foods obtained from pet stores
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 5 of 15

or other retail channels (including foods supposedly
containing limited ingredients) frequently contain
traces of ingredients that are not listed on the label
[21–23]. Whether or not such contamination would
induce flares in dogs with food-induced AD is not
known.
Two thirds of dogs with concurrent AD and food
allergies exhibit perianal pruritus (QOE 2) [24].
House dust and storage mites and faeces are rarely
present in commercial dry dog foods (QOE 3) [25,26].
Storage of foods in paper bags (QOE 3) [25,26], and
especially in environmental conditions of moderate
temperatures and high humidity, increases Tyro phag us
storage mite numbers (QOE 3) [26]. Nevertheless, the
concentration of mite allergens on the floor adjacent to
stored dog food bags appears much higher than in the
food itself (QOE 3) [25].
B.1.b. Implementation of a flea control regimen
Summary of the 2010 guidelines:
Dogs with AD should be treated year-round with
an effective flea control regimen. Systemic and oral
adulticides are recommended in case of repeated
shampooing to prevent the wash off of topical flea
control products [1].
Updated 2015 recommendations:
There are no changes to the 2010 recommendations
(SOR C). Insecticides that demonstrate long effect
and fast residual speed of kill should be theoretically
more effective in dogs with AD that are
hypersensitive to flea bites (SOR C).
Basis for such recommendations:
Atrialestablishedthesuperiorityofspinosad
(Comfortis, Elanco) over a fipronil/(S) methoprene
combination (Frontline Plus, Merck) in the control of
flea-associated pruritus in field conditions; the higher
efficacy of spinosad could be due to its prolonged
activity and/or fast residual speed of kill (QOE 2) [27].
B.1.c. Performance of allergen-specific intradermal and/
or IgE serological tests to identify possible allergenic flare
factors
Summary of the 2010 guidelines:
Allergen-specific intradermal testing (IDT) and/or
IgE serologies are helpful to identify hypersensitivity
to environmental allergens in dogs with AD. Positive
immediate IDT reactions and IgE serology to
environmental allergens can also be observed in dogs
without signs of AD. As a result, these tests cannot
be used to differentiate dogs with AD from healthy
dogs or dogs with other pruritic dermatoses.
Serological and intradermal tests to determine
hypersensitivity to food allergens are not
recommended to assess the presence of food
hypersensitivity in dogs with food-induced
AD [1].
Updated 2015 recommendations:
There is increasing evidence that healthy dogs and/or
dogs with pruritic dermatoses other than AD might
have detectable serum allergen-specific IgE, and/or
positive IDT reactions to environmental allergens,
especially those that are not pollens. This reinforces
the concept that “allergy tests”must never be used to
diagnose AD; they should be requested only to define
IgE-mediated hypersensitivities in dogs already
diagnosed with AD by clinical criteria (SOR C). There
is currently no standardization in the performance of
serum allergen-specific IgE assays for environmental
allergens, and there is evidence that the results of IgE
serological tests can varysubstantiallybetween
laboratories (SOR C).
Because of inconsistent or limited data available,
additional studies are needed before
recommending the use of specific IgG and IgE
serology for, or intradermal or epicutaneous
(patch) or lymphocyte stimulation tests with, food
allergens to diagnose, or identify relevant food
allergens in dogs with food-induced AD (SOR C).
Basis for such recommendations:
A recent study that compared IgE serological assays at
four different laboratories showed a high variation in
tests results, except for mite allergens for which there
was generally a stronger agreement (QOE 3) [28]. A
recent evaluation of an IgG/IgE food allergen serology
test (Sensitest, Avacta Veterinary Laboratories)
reported that a negative serology result for a food
allergen predicted the lack of clinical reaction to this
food item in most dogs (negative predictive value of
~80 %); the reverse was not true for dogs with
positive serology to food allergens (low positive
predictive value) (QOE 2) [29]. Another study from
the United Kingdom demonstrated that food-specific
IgE/IgG serology offered by two unidentified
commercial laboratories did not permit the
differentiation of dogs with cutaneous adverse
food reactions from those with non-food induced
diseases (QOE 2) [30].
Patch testing with food items has been shown to
have a very high negative predictive value when
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 6 of 15

compared to the response to a restrictive diet trial
[29]. Consequently, this method might be useful to
identify food items to which dogs are not likely to
react clinically.
Finally, in a small study from Japan, most dogs with
signs of allergic skin disease that had a negative IgE
serology to environmental allergens and a positive
lymphocyte proliferation test to food allergens had
a favourable response to a dietary restriction trial
(QOE 3) [31].
B.1.d. Implementation of house dust mite control
measures
Summary of 2010 guidelines:
House dust mites are the most important source of
allergens for canine AD, worldwide. House dust
mite control measures should be relevant and
might be effective in dogs hypersensitive to such
allergens. The individual, or combinations of, house
dust mite control measures most effective to
prevent the flares of dogs with AD still have not
been determined [1].
Updated 2015 recommendations:
There are no major changes to the 2010
recommendations (SOR C).
Basis for such recommendations:
There is still only one uncontrolled study that
reported the benefit of house dust mite control
with a benzyl benzoate acaricidal spray (Acarosan
Spray, Bissell) for reduction of clinical signs of AD
in mite-hypersensitive atopic dogs (QOE 2) [32].
Recently, the isolation of dogs with AD in cages in
which house dust mites were controlled was shown
to lead to a rapid reduction in pruritus in most
dogs with IgE hypersensitivity to environmental
allergens (QOE 2) [33].
B.1.e. Evaluation of use of antimicrobial therapy
Summary of the 2010 guidelines:
Antimicrobial therapy is needed in an atopic dog
when a skin and/or ear infection with bacteria and/or
yeast is diagnosed based on compatible clinical signs
with or without supportive cytology or bacterial
culture. The treatment of such infections usually
consists of topical and/or systemic antimicrobials [1].
Updated 2015 recommendations:
There are no major changes to the 2010
recommendations (SOR C). Veterinarians are advised
to follow antimicrobial treatment guidelines
established in their country of practice and/or in
international consensus recommendations (SOR C)
[6,7]. Veterinarians and dog owners should watch
for a drying or irritating effect of topical
antimicrobials—especially shampoos—that might
induce a flare of AD in their patient (SOR C).
Terbinafine or itraconazole can be prescribed once
daily or for two consecutive days each week for
3 weeks to treat flares provoked or exacerbated by
Malassezia skin infections (SOR B).
Basis for such recommendation:
Treating dogs with Malassezia otitis or dermatitis
with 5 mg/kg itraconazole once daily or for two
consecutive days each week for 3 weeks, provides
comparable clinical and cytological results (QOE 2)
[34]. Terbinafine given to dogs with Malassezia
dermatitis at 30 mg/kg once daily for 3 weeks
resulted in a similar improvement in cytological and
skin lesion scores as in dogs given the drug at the
same dose twice weekly for 3 weeks; the
improvement in pruritus was higher with the daily
treatment (QOE 2) [35].
B.1.f. Investigation of the relevance of other flare factors
Summary of 2010 guidelines:
There is insufficient evidence to make general
recommendations regarding the importance of the
environment, humidity, detergents and stress as
flare factors in dogs with AD. Nevertheless, owners
should be educated to observe, and then avoid or
alter, the specific situations in which they see their
dog’s condition worsen [1].
Updated 2015 recommendations:
There are no changes to the 2010
recommendations (SOR C).
B.2. Improvement of skin and coat hygiene and care
B.2.a. Bathing with a non-irritating shampoo
Summary of 2010 guidelines:
Bathing at least once weekly with a mild non-irritating
shampoo and lukewarm water is likely to be beneficial.
The intensity and frequency of bathing may be
the most important factor in relieving pruritus.
The type of shampoo should be tailored to each
case: emollient shampoos are likely to be the most
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 7 of 15

soothing, but anti-seborrhoeic and antiseptic
products may be more appropriate in dogs with
skin greasiness, scaling and/or in case of
infection. Nevertheless, shampooing may be
drying and irritating. If necessary, clinicians
should consider changing products or protocols
and/or adding post-bathing topical moisturizers.
Practitioners should also be prepared to change
the topicals used if the state of the dog’sskin
and coat changes. The impact of frequent
bathing on the reduction of efficacy of
topical flea control products should also
be considered [1].
Updated 2015 recommendations:
There are no changes to the 2010
recommendations (SOR C).
B.2.b. Supplementation with oral EFAs
Summary of 2010 guidelines:
The oral intake of EFAs, especially those rich in
omega-6 EFAs either as supplement or in
enriched diets can influence superficial skin lipids
and improve the gloss and quality of the coat.
Oral EFAs might also provide some small benefit
in reducing clinical signs of AD in dogs, but the
limited degree of improvement expected makes it
unlikely that EFA supplementation would be
suitable for monotherapy of canine AD. The
benefit of EFAs, if any, might not be seen before
two months of supplementation. At this time,
there is no evidence of superiority for any
particular EFA combination, dosage, ratio or
formulation (including enriched diets) to improve
skin and coat quality in dogs with AD. In general,
EFA-enriched diets provide higher amounts of
EFAs than oral administration of EFA
supplements [1].
Updated 2015 recommendations:
There are no changes to the 2010
recommendations (SOR C).
Basis for such recommendations:
A systematic review did not uncover further
clinical trial evidence on the benefit of oral
EFAs for canine AD since 2010 (QOE 1) [4].
Supplementing the diet of dogs with AD with an
EFA liquid supplement (Megaderm/EFA-Z,
Virbac) for two months resulted in marked
changes in the biochemistry and ultrastructure
of stratum corneum intercellular lipids,
with both parameters becoming
closer to normal characteristics compared to
before supplementation (QOE 3) [36].
B.2.c. Application of topical EFA-containing
formulations
Summary of the 2010 guidelines:
There is insufficient trial-based evidence supporting
the use of lipid-containing topical formulations to
improve coat quality and/or to relieve signs of AD
in dogs [1].
Updated 2015 recommendations:
Topical lipid formulations can help normalize
existing stratum corneum lipid barrier defects in
dogs with AD (SOR C). Because of inconsistency in
outcomes of clinical trials, there is still insufficient
evidence for the benefit of lipid-containing topical
formulations to recommend these as monotherapy
for canine AD (SOR B). The benefit, cost and ease
of use of topical EFA-containing formulations as
adjuvant therapy for canine AD must be weighed
against those of feeding oral EFA supplements or
enriched diets (SOR C). The benefit of topical EFA-
containing formulations is likely minimal in dogs
already fed EFA-rich diets or EFA supplements
(SOR C).
Basis for such recommendations:
The application of a topical lipid complex
containing ceramides, cholesterol and EFAs in a
proportion aimed at reproducing that of
intercellular stratum corneum lipids (Allerderm
Spot On, Virbac) every three days for six
applications to atopic dogs normalized pre-
existing stratum corneum lipid profile anomalies
(QOE 3) [37]. This formulation had previously
been shown to increase the formation of normal-
appearing intercellular stratum corneum lipid la-
mellae in some dogs with AD (QOE 3) [38].
However, an RCT in dogs with mild-to-moderate
AD only reported a small and inconsistent clin-
ical benefit of this topical lipid complex (QOE 2)
[18]. A small RCT established the modest efficacy
of an omega-6 EFA and essential oil-containing
topical formulation (Dermoscent Essential
6 spot-on, Laboratoire de Dermo-Cosmétique
Animale) for reducing clinical signs of AD
(QOE 2) [39].
As orally administered EFAs can normalize
stratum corneum lipid in the same way as
a topical lipid mixture (QOE 3) [36–38], the
addition of topical EFA-containing formulations
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 8 of 15

to dogs already fed high levels of EFAs is likely
to provide little added benefit.
B.2.d. Administration of other dietary supplements
Summary of 2010 guidelines:
Some nutritional supplements can improve skin
barrier function in vitro, for example increasing
ceramide production and decreasing
transepidermal water loss, but there is no
evidence for the clinical benefit of such
supplements in dogs with AD [1].
Updated 2015 recommendations:
There are no changes to the 2010
recommendations (SOR C).
B.3. Reduction of pruritus and skin lesions with
pharmacological agents
B.3.a. Treatment with topical glucocorticoids or
tacrolimus
Summary of the 2010 guidelines:
Topical glucocorticoids and tacrolimus effectively
reduce clinical signs of canine AD, but there is a
risk of skin atrophy with the prolonged used of
the former [1].
Updated 2015 guidelines:
There is further evidence supporting the efficacy
of topical glucocorticoids for treatment of canine
AD. However, the risk of induced skin atrophy
means that they should be applied intermittently
after an induction phase of daily application
(SOR A). Treatment duration and frequency of
use should be tailored to each patient; the
application of topical glucocorticoids should
normally continue until a complete and stable
remission of signs is achieved (SOR C). Due to its
high cost, tacrolimus does not offer much added
value compared to topical glucocorticoids,
except for atopic dogs in which skin atrophy is
visible (SOR C).
Basis for such recommendation:
In a 12-week RCT, a hydrocortisone aceponate spray
(Cortavance, Virbac) showed a similar efficacy and
tolerance compared to oral ciclosporin (Atopica,
Elanco Animal Health) (QOE 1) [40].
B.3.b. Treatment with oral pharmacological
immunomodulators
Summary of the 2010 guidelines:
Oral glucocorticoids and ciclosporin are beneficial for
the treatment of canine AD, but the former lead to
faster improvement than the latter. Oral short-acting
glucocorticoids should be used to induce remission of
signs, and their dose should then be tapered; injectable
long-lasting glucocorticoids are not recommended.
The long-term concurrent administration of oral
ciclosporin and glucocorticoids (especially at higher
dosages of either or both drugs) is likely to result in a
higher risk of immunosuppression [1].
Updated 2015 recommendations:
Oral glucocorticoids (prednisone, prednisolone or
methylprednisolone), ciclosporin and oclacitinib are
effective for treatment of chronic canine AD (SOR
A), concurrently with or after control of known flare
factors (SOR C). Glucocorticoids and oclacitinib lead
to faster improvement than ciclosporin, but
ciclosporin can be combined with oral prednisolone
for the first 3 weeks to speed its onset of clinical
improvement (SOR A). The prolonged concomitant
administration of oral glucocorticoids, ciclosporin or
oclacitinib in any combination is not recommended
because of the theoretical higher risk of
immunosuppression predisposing to potentially
severe opportunistic infections of the skin or other
organs. There is no consensus on the need for
laboratory monitoring (e.g. haematology, serum
biochemistry and urinalysis) during prolonged
ciclosporin or oclacitinib administration. However, such
tests should be performed if signs of systemic illness
develop (SOR C). Due to the increased risk of urinary
tract infections, dogs treated with oral glucocorticoids
in the long term should be monitored periodically with
urinalyses and urine cultures (SOR C).
Oral glucocorticoids (prednisolone, prednisone or
methylprednisolone) should be used at 0.5 mg/kg
once to twice daily to induce remission of clinical
signs of AD. After such remission occurs, the dose of
oral glucocorticoids should be tapered to the lowest
dosage and frequency that maintains an absence of
signs to minimize the risk of side effects in the long
term (SOR C). Long acting injectable glucocorticoids
should be avoided wherever possible as the lack of
ability to taper their dose increases the risk of adverse
events (SOR C).
Oral ciclosporin should be administered at 5 mg/kg
once daily until satisfactory control of clinical signs,
which will usually take 4 to 6 weeks (SOR A).
Thereafter, the dose required to maintain remission
should be tapered by either decreasing the frequency
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 9 of 15

of treatment (e.g. from every day to every other day
and then twice weekly) or by decreasing the daily
dose (SOR A). Generic ciclosporin formulations
shown to be bioequivalent to the first approved
ciclosporin (modified) microemulsion (Atopica,
Elanco Animal Health) are acceptable substitutes for
it (SOR C).
Oral oclacitinib (Apoquel, Zoetis) should be given at
0.4 to 0.6 mg/kg twice daily for 14 days and then
once daily thereafter (SOR A). In case a complete
remission of signs is obtained, further tapering should
be attempted with the dose adjusted to maintain the
remission of signs (SOR C). This drug is not
approved for dogs less than 12 months of age. The
long-term administration of oclacitinib administered
once daily appears to be relatively safe whereas the
long-term safety of other dosing regimens is not
known.
The concomitant use of allergen-specific immunotherapy,
emollient shampoos, EFAs supplements or enriched diets
might allow for a further reduction in the dose and/or
frequency of oral glucocorticoids, ciclosporin (and
perhaps even oclacitinib) required to maintain remission
of clinical signs of AD. Outside of the oral
glucocorticoid-sparing effect of an EFA supplement
(Viacutan Plus, Boehringer Ingelheim) and an
antihistamine (trimeprazine)-prednisolone combination
(Temaril-P, Zoetis), which were both discussed in the
2010 version of these guidelines [1], the efficacy and
safety of other combined approaches has not yet been
published (SOR C).
Basis for such recommendations:
Three systematic reviews, as well as newly-published
randomized controlled trials, have confirmed the
efficacy of oral glucocorticoids [2–4,11,12],
ciclosporin [3,4,13,41,42] and oclacitinib [11,42,43]
for treatment of AD in dogs (QOE 1). Further details
on the treatment of chronic canine AD with oral
glucocorticoids and ciclosporin can be found in the
2010 guidelines [1].
In a RCT, ciclosporin orally given at 5 mg/kg daily for
4 weeks, concurrently with prednisolone at 1 mg/kg
daily for 7 days followed by alternate day dosing for
14 days, led to a quicker improvement of skin lesions
and pruritus scores than when ciclosporin was given
alone (QOE 2) [44]. A generic formulation of
ciclosporin (Equoral, Teva) was shown to be as
effective as prednisone in reducing skin lesions and
pruritus in dogs with AD in a small RCT (QOE 2) [13].
A novel liquid oral formulation of ciclosporin
(Cyclavance, Virbac) was recently reported to be better
accepted than ciclosporin capsules (Atopica, Elanco
Animal Health) (QOE 2) [45].
In RCTs, oclacitinib improved pruritus and clinical
signs significantly better than placebo (QOE 1) [43],
and as well or (at the 14 day time point) better than
prednisolone (QOE 1) [11]. The long term
administration of oclacinitib is associated with the
development of de novo urinary tract infections,
vomiting, otitis, pyoderma and diarrhoea in
approximately 5 to 10 % of dogs; serious adverse drug
events appear rare (QOE 1) [46]. Changes in
laboratory (haematology, chemistry panels and
urinalysis) parameters seem minimal after the
prolonged administration of oclacitinib to atopic dogs
(QOE 1) [46].
B.3.c. Treatment with biotherapeutic
immunomodulators
B.3.c.1 Treatment with recombinant interferons
Summary of the 2010 guidelines:
Recombinant canine interferon-gamma, given
subcutaneously at 5,000–10,000 units/kg three
times weekly for 4 weeks, then once weekly, is
effective for treatment of canine AD. Recombinant
feline interferon-omega seems to be beneficial, but
further trials are warranted before recommending
its use [1].
Updated 2015 recommendations:
Recombinant canine interferon-gamma (Interdog, Toray
Industries), given subcutaneously at 5,000–10,000
units/kg three times weekly for 4 weeks, then once
weekly, is effective for treatment of canine AD (SOR
A). Recombinant feline interferon-omega (Virbagen
omega, Virbac), administered subcutaneously or
orally, has been shown to provide some inconsistent
reduction of skin lesions and pruritus in dogs with
AD (SOR B).
Basis for such recommendations:
Two RCTs provided evidence for the efficacy of
recombinant canine gamma-interferon (Interdog,
Toray Industries) to treat dogs with AD in Japan
(QOE 1) [47,48]; suggested effective dosages are
5,000 to 10,000 units/kg subcutaneously three times
weekly for 4 weeks then once weekly. Side effects
appear to be minimal [47,48].
Results of two studies, including one RCT,
established that subcutaneous injections of
recombinant feline interferon-omega (Virbagen
Omega, Virbac), at 1 to 5 million units three times
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 10 of 15

weekly for 4 weeks and then monthly thereafter, offer
some clinical benefit in dogs with AD (QOE 1) [49].
Another RCT showed some inconsistent and mild
improvement in skin lesions and pruritus after either
subcutaneous injections or oral administration of
feline interferon-omega (QOE 2) [50].
B.3.d. Interventions likely to be of little or no benefit to
treat chronic canine AD:
Summary of the 2010 guidelines:
There is a lack of evidence for efficacy of type 1
antihistamines as monotherapy for the
management of chronic canine AD. Hydroxyzine
and its metabolite cetirizine have demonstrable
anti-histaminic action in the dog and should be
the preferable antihistamine in this species. Anti-
histamines should be used as preventatives, given on a
continuous daily basis, and a combination with other
antihistamines or other drugs may improve their
beneficial effects although further studies are required
to validate this. Other drugs appear to provide little
(misoprostol, tepoxalin) or nobenefit(e.g.leukotriene
inhibitors, capsaicin, dextromethorphan etc.) [1].
Updated 2015 recommendations:
Type 1 histamine receptor inverse agonists
(type 1 antihistamines) have modest efficacy
against pruritus, either alone or in combination
with each other, but their effect appears to be
variable between individuals. For optimal efficacy,
this class of drugs are best used as preventatives
before a flare occurs—not during or after it—and
they should preferably be given on a continuous
daily basis. In dogs, antihistamines with proven
bioavailability and/or demonstrated reliable
efficacy in this species should be the preferred
choices (SOR C).
Masitinib (Masivet/Kinavet, AB Science) appears
to offer some benefit in dogs with chronic AD,
but this effect must be weighed against the risk of
severe renal adverse drug events that requires the
performance of periodic urinalyses to detect
developing proteinuria (SOR A). Masitinib might
be a useful alternative for atopic dogs with signs
not responding to other approved drugs
(SOR C).
Further studies are needed to confirm the efficacy
and safety of high-dose oral pentoxifylline, oral
low-dose once weekly methotrexate and the ad-
junctive effect of vitamin E to antihistamines before
these drugs can be recommended for routine treat-
ment of AD in dogs (SOR C). Finally, oral fluoxet-
ine and low level laser therapy appear to have little
efficacy for treatment of canine AD (SOR B).
Basis for such recommendations:
An RCT evaluating the efficacy of the
antihistamines dimetindene (Fenistil, Novartis) and
the combination of chlorpheniramine and
hydroxyzine (Histacalmine, Virbac) confirmed the
small but variable efficacy of H1 antihistamines to
control pruritus in dogs with AD. The combination
of the two antihistamines did not show any added
benefit over the single drug, but this observation
cannot be extrapolated to other combinations of
drugs from this class (QOE 2) [16]. One small trial
suggested a possible benefit from the H1
antihistamine fexofenadine with a reported efficacy
similar to that of methylprednisolone (QOE 2) [51].
In another study, dogs were treated with
fexofenadine and oral vitamin E or placebo for
8 weeks. An improvement in skin lesions was seen
in dogs from both groups with a greater
improvement in dogs receiving vitamin E; there
was considerable individual response within groups,
however (QOE 2) [52].
A large RCT confirmed that masitinib at 12.5 mg/
kg once daily was moderately effective in reducing
clinical signs in atopic dogs. The development of
a protein-losing nephropathy in some dogs,
which, if unrecognized could be potentially fatal,
is a limitation of masitinib treatment
(QOE 1) [53].
An open RCT study evaluating pentoxifylline at the
high dose of 20 mg/kg three times daily, either
alone or in combination with oral EFA
supplementation, reported a significantly greater
improvement in skin lesions and pruritus of these
interventions over placebo; the effect seemed
highest for dogs treated with the combination of
pentoxifylline and EFAs (QOE 2) [54].
A small proof-of-concept trial reported the clinical
benefit and relative safety of low-dose once weekly
oral methotrexate for treatment of canine AD [55].
An RCT showed no benefit of low level laser
therapy in dogs with localized pedal AD (QOE 2)
[56]. Similarly, the selective serotonin reuptake
inhibitor (SSRI) fluoxetine, given at 1 mg/kg orally
once daily, showed no clinical efficacy in a small
RCT of dogs with AD (QOE 2) [57].
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 11 of 15

C. Implement strategies to prevent recurrence of signs
This section is relevant to the treatment of dogs with
case scenarios 2a and 2b described in the 2010 version
of these guidelines [1].
C.1. Avoidance of flare factors
Summary of the 2010 guidelines:
The identification and avoidance of known flare
factors (e.g. environmental and/or food allergens, flea
bites, infections etc.) is the best strategy to prevent
the recurrence of signs in patients with AD [1].
Updated 2015 recommendations:
There are no proposed changes to the 2010
recommendations (SOR C).
C.2. Implementation of proactive topical
pharmacotherapy
Summary of the 2010 guidelines:
In humans with AD, there is evidence for the high
benefit, cost effectiveness and low risk of proactive
intermittent applications of topical glucocorticoids
and tacrolimus to previously affected skin areas to
delay or prevent the appearance of such flares. There
is currently no evidence for the effectiveness of a
similar approach in dogs with AD, but the possible
benefit, low risk and low cost suggest that such
strategy is worth considering in suitable cases [1].
Updated 2015 guidelines:
The application of a topical hydrocortisone
aceponate spray (Cortavance, Virbac) to areas of
previous skin lesions, two consecutive days each
week, can delay the recurrence of lesions at these
sites without causing visible skin atrophy (SOR B).
A similar beneficial effect of proactive topical
glucocorticoid therapy is likely to be seen when
intermittently using other moderately potent
topical glucocorticoids at previously affected skin
sites (SOR C). When using potent topical
glucocorticoid formulations, even intermittently,
care must be taken to avoid glucocorticoid-induced
skin atrophy (SOR C).
Basis for such recommendation:
A small RCT tested the efficacy a hydrocortisone
aceponate spray (Cortavance, Virbac) applied to
previously affected areas on two consecutive days
after lesions had been controlled with the same
spray. The time to recurrence of flares at these
sites was nearly four times longer (median:
115 days) in dogs intermittently-treated with
topical glucocorticoids compared to those
sprayed with placebo (QOE 2) [58].
C3. Implementation of allergen-specific immunotherapy
Summary of the 2010 guidelines:
Allergen-specific immunotherapy (ASIT) is an
effective and safe way to reduce the clinical signs of
AD in dogs. There is no proven superiority of a
particular ASIT protocol over other alternatives
(traditional, rush or low-dose). Injection frequencies
and amounts injected must be tailored to each patient
depending upon the clinical improvement
observed and the presence of adverse events.
Because of the delay in the onset its beneficial
effects, anti-inflammatory drugs should be given
temporarily, as needed to maintain good quality
of life, until such time as the ASIT is judged to be
effective (see sections above). Because the onset
of clinical benefit might not appear for months,
ASIT must be continued for at least one year to
properly evaluate its efficacy. Whether or not
ASIT must be continued for the reminder of the
life of atopic dogs has not been established [1].
Updated 2015 recommendations:
The value of ASIT as a canine AD-modifying
treatment continues to be supported by (mostly
uncontrolled) studies reporting at least a moderate
efficacy (SOR B). There is some evidence that ASIT
administered via the sublingual route (sublingual
immunotherapy; SLIT), or in sped-up (i.e. “rush”)
protocol, are safe and effective for treatment of atopic
dogs (SOR C). While most patients appear to require
many years of ASIT, attempts should be made to
decrease the frequency of administration, or even stop
this intervention, in dogs exhibiting a prolonged
complete remission of signs (SOR C).
There is currently no standardization in the
performance of allergen-specific intradermal tests
or IgE serologies that are used used to select
allergens to be included in ASIT. Mounting
evidence suggests that the results of serological
tests can vary substantially between laboratories
(SOR C). A consequence of such assay variability
is that recommendations for immunotherapy
prescriptions are expected to vary substantially
between testing laboratories (SOR C).
Basis for such recommendation:
A recent study comparing IgE serological assays
offered by four different laboratories showed a
substantial variation in both results and
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 12 of 15

subsequent ASIT recommendations (QOE 3) [28].
Similarly, intradermal testing for allergens is not
standardized and its performance varies
substantially even between specialists of the same
geographical region [59].
In spite of these important limitations in
allergen hypersensitivity tests, an online survey
showed that one third of owners of atopic dogs
who had used this intervention for 5 to 10 years
rated it as “very or extremely effective”(QOE 2)
[15]. Moreover, approximately 5 % of dogs
having received ASIT as part of their treatment
had an apparent complete resolution of signs
without further need of anti-allergic treatment
[15]. Similarly, a large retrospective survey of
owners of atopic dogs having undergone 1 year
or more of ASIT established that nearly two
third of dogs had been rated as having a
“satisfactory-to-excellent”response to this
intervention (QOE 2) [60].
A small, open pilot study of SLIT in house dust
mite-sensitive atopic dogs reported clinical im-
provement and changes in mite-specific IgG and
IgE in most dogs (QOE 2) [61]. Similarly, a larger,
retrospective study of SLIT in house dust mite and
pollen-hypersensitive dogs reported a good-to-
excellent response to SLIT in about 60 % of evalu-
able dogs, and in half of those who had failed previ-
ous subcutaneous ASIT (QOE 2) [62].
Finally, in a small open study of rush alum-adjuvanted
ASIT, atopic dogs demonstrated a significant
improvement in pruritus andmedicationscoresafter
one year of treatment (QOE 2) [63].
C4. Implementation of nonspecific immunotherapy
Summary of the 2010 guidelines:
This is a new section that was not included in the
2010 guidelines [1].
Updated 2015 recommendations:
There is currently insufficient evidence supporting
the use of oral probiotics as nonspecific
immunotherapy for prevention or treatment of
canine AD (SOR C).
Basis for such recommendation:
Even though the pre- and post-natal exposure to
the probiotic Lactobacillus rhamnosus strain GG
(Culturelle HS, Culturelle) has shown some
possible lasting effect in reducing clinical signs
following allergen challenges in dogs experimentally
sensitized to house dust mites (QOE 3) [64], this oral
probiotic has not yet been shown to be of benefit in
dogs to treat or prevent clinical signs in dogs with
spontaneous AD.
Conclusion
This first 5-year minor update of the international
consensus guidelines for treatment of AD further high-
lights, as was done with the first version of this docu-
ment [1], that the treatment of this disease is clearly
multifaceted and that interventions should be com-
bined for a proven (or likely) optimal benefit. Further-
more, treatment should be tailored to each patient
depending upon the stage of the disease, its severity
and the distribution of lesions. Veterinarians should
also remember to evaluate and then discuss with the
pet owners the benefit of each recommended interven-
tion, its side effects, its ease of administration, and its
cost as a single or combined modality. Ultimately, the
quality of life of both dogs and their owners, as well as
the preferences of the latter, should be considered be-
fore a treatment plan is designed.
Additional file
Additional file 1: Treatment of canine atopic dermatitis: summary
statement of 2015 ICADA guidelines. (DOCX 148 kb)
Abbreviations
AD: Atopic dermatitis; RCT: Randomized controlled trial.
Competing interests
In the last five years, the authors report having lectured or consulted for,
and/or received research funding from the following animal health
companies:
Thierry Olivry: Aratana Therapeutics (Kansas City, Kansas, USA), Boehringer
Ingelheim Vetmedica (St Joseph, Missouri, USA), Ceva (Libourne, France),
Elanco Animal Health (Greenfield, Indiana, USA), Gour Medical (Zur,
Switzerland), NexVet (Melbourne, Australia), Novartis Animal Health (Basel,
Switzerland), Royal Canin (Aimargues, France), Vétoquinol (Paris, France),
Virbac (Carros, France) and Zoetis (Florham Park, New Jersey, USA).
Douglas DeBoer: Delmont Laboratories (Swarthmore, Pennsylvania, USA),
Elanco Animal Health (Greenfield, Indiana, USA), Heska (Fort Collins, Colorado
USA), Virbac (Carros, France) and Zoetis (Florham Park, New Jersey, USA)
Claude Favrot: Novartis Animal Health (Basel, Switzerland) and Virbac (Carros,
France)
Hilary Jackson: Greer Laboratories (Lenoir, North Carolina, USA).
Ralf Mueller: Bayer Animal Health (Leverkusen, Germany), Dechra
Pharmaceuticals (Lostrop, United Kingdom), Elanco (Bad Homburg,
Germany), Laboratoire de Dermo-Cosmétique Animale (Castres, France),
Novartis Animal Health (Basel, Switzerland), Royal Canin (Aimargues, France),
Virbac (Carros, France), Selectavet (Weyarn, Germany) and Zoetis (Berlin,
Germany).
Tim Nuttall: Virbac (Carros, France), Novartis Animal Health (Basel,
Switzerland), Zoetis (Walton Oaks, UK), Royal Canin (Aimargues, France), Iams
(Proctor & Gamble Pet Care, London, UK), Idexx Laboratories (Wetherby, UK),
Avacta Animal Health (Wetherby, UK), Vétoquinol (Buckingham, UK), Ceva
(Amersham, UK) and Dechra Veterinary Products (Shrewsbury, UK)
Pascal Prélaud: Elanco Animal Health (Neuilly, France), Novartis Animal Health
France (Rueil Malmaison, France), Zoetis (Paris, France), Merck-Merial (Lyon,
France), Biovac (Angers, France),
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 13 of 15

None of the companies above had any influence on the recommendations
included in these guidelines, and authors did not receive any honorarium for
writing this paper.
Authors’contributions
Each author wrote one or more sections of the outline of this update.
All authors reviewed and approved the outline and final version of these
document, which was written primarily by TO. The outline and final version
of this paper were also reviewed and accepted by the members of the
International Committee of Allergic Diseases of Animals (ICADA;
www.icada.org).
Acknowledgements
The authors thank the other members of the ICADA for their review of, and
suggestions for, these updated guidelines. These members are, in alphabetical
order, Drs. Emmanuel Bensignor, Petra Bizikova, Melissa Eisenschenk, Craig Griffin,
Richard Halliwell, Bruce Hammerberg, Patrick Hensel, Peter Hill, Alexander
Koutinas, Rosanna Marsella, Kenichi Masuda, Jon Plant, Christine Prost, Cherie
Pucheu-Haston (Chair, USA), Domenico Santoro, Manolis Saridomichelakis and
Regina Wagner. The authors acknowledge the editorial team of BMC Veterinary
Research for waiving the publication charges for this article.
Author details
1
Department of Clinical Sciences, College of Veterinary Medicine, North
Carolina State University, 1060 William Moore Drive, Raleigh 27606 NC, USA.
2
Department of Medical Sciences, School of Veterinary Medicine, University
of Wisconsin, 2015 Linden Drive, Madison 53706 WI, USA.
3
Clinic for Small
Animal Internal Medicine, Dermatology Department, Vetsuisse Faculty,
University of Zürich, Winterthurerstrasse 260, 8057 Zürich, Switzerland.
4
Dermatology Referral Services LTD, 528 Paisley Road West, Glasgow,
Scotland G51 1RN, UK.
5
Medizinische Kleintierklinik, Centre for Clinical
Veterinary Medicine, Ludwig-Maximilian University, Veterinärstrasse 13, 80539
Munich, Germany.
6
Royal (Dick) School of Veterinary Studies, The University
of Edinburgh, Easter Bush Campus, Roslin, Scotland EH25 9RG, UK.
7
Clinique
Advetia, 5 rue Dubrunfaut, Paris 75012, France.
Received: 24 July 2015 Accepted: 30 July 2015
References
1. Olivry T, DeBoer DJ, Favrot C, Jackson HA, Mueller RS, Nuttall T, et al.
Treatment of canine atopic dermatitis: 2010 clinical practice guidelines from
the International Task Force on Canine Atopic Dermatitis. Vet Dermatol.
2010;21:233–48.
2. Olivry T, Mueller RS. Evidence-based veterinary dermatology: a systematic
review of the pharmacotherapy of canine atopic dermatitis. Vet Dermatol.
2003;14:121–46.
3. Olivry T, Foster AP, Mueller RS, McEwan NA, Chesney C, Williams HC.
Interventions for atopic dermatitis in dogs: a systematic review of
randomized controlled trials. Vet Dermatol. 2010;21:4–22.
4. Olivry T, Bizikova P. A systematic review of randomized controlled trials for
prevention or treatment of atopic dermatitis in dogs: 2008-2011 update.
Vet Dermatol. 2013;24:97–e26.
5. Ebell MH, Siwek J, Weiss BD, Woolf SH, Susman J, Ewigman B, et al. Strength
of recommendation taxonomy (SORT): a patient-centered approach to
grading evidence in the medical literature. J Am Board Fam Pract.
2004;17:59–67.
6. Beco L, Guaguere E, Lorente Mendez C, Noli C, Nuttall T, Vroom M.
Suggested guidelines for using systemic antimicrobials in bacterial skin
infections: part 2—antimicrobial choice, treatment regimens and
compliance. Vet Rec. 2013;172:156–60.
7. Hillier A, Lloyd DH, Weese JS, Blondeau JM, Boothe D, Breitschwerdt E, et al.
Guidelines for the diagnosis and antimicrobial therapy of canine superficial
bacterial folliculitis (Antimicrobial Guidelines Working Group of the
International Society for Companion Animal Infectious Diseases). Vet Dermatol.
2014;25:163–75. e42–3.
8. Bensignor E, Pin D, Bourdeau P. A multicentric randomised controlled single
blinded study to evaluate the value of a new protocol with a shampoo and
a foam to treat canine allergic dermatitis (in French). Prart Méd Chir Anim
Comp. 2013;48:49–55.
9. Bourdeau P, Bruet V, Gremillet C. Evaluation of phytosphingosine-containing
shampoo and microemulsion spray in the clinical control of allergic
dermatoses in dogs: preliminary results of a multicentre study (abstract).
Vet Dermatol. 2007;18:177–8.
10. Nam EH, Park SH, Jung JY, Han SH, Young HY, Chae JS, et al. Evaluation of
the effect of a 0.0584 % hydrocortisone aceponate spray on clinical signs
and skin barrier function in dogs with atopic dermatitis. J Vet Sci.
2012;13:187–91.
11. Gadeyne C, Little P, King VL, Edwards N, Davis K, Stegemann MR. Efficacy of
oclacitinib (Apoquel®) compared with prednisolone for the control of
pruritus and clinical signs associated with allergic dermatitis in client-owned
dogs in Australia. Vet Dermatol. 2014;25:512–8. e86.
12. Taszkun I. The evaluation of Canine Atopic Dermatitis Extent and Severity
Index (CADESI) test in dogs with atopic dermatitis (AD) treated with
cyclosporine or prednisone. Pol J Vet Sci. 2010;13:681–8.
13. Kovalik M, Taszkun I, Pomorski Z, Kozak M, Pomorska D, Szczepanik M, et al.
Evaluation of a human generic formulation of ciclosporin in the treatment
of canine atopic dermatitis with in vitro assessment of the functional
capacity of phagocytic cells. Vet Rec. 2011;168:537–42.
14. Cosgrove SB, Wren JA, Cleaver DM, Martin DD, Walsh KF, Harfst JA, et al.
Efficacy and safety of oclacitinib for the control of pruritus and associated
skin lesions in dogs with canine allergic dermatitis. Vet Dermatol.
2013;24:479–e114.
15. Dell DL, Griffin CE, Thompson LA, Griffies JD. Owner assessment of
therapeutic interventions for canine atopic dermatitis: a long-term
retrospective analysis. Vet Dermatol. 2012;23:228–e47.
16. Eichenseer M, Johansen C, Mueller RS. Efficacy of dimetinden and
hydroxyzine/chlorpheniramine in atopic dogs: a randomised, controlled,
double-blinded trial. Vet Rec. 2013;173:423–6.
17. Baeumer W, Stahl J, Sander K, Petersen LJ, Paps J, Stark H, et al. Lack of
preventing effect of systemically and topically administered histamine H(1)
or H(4) receptor antagonists in a dog model of acute atopic dermatitis.
Exp Dermatol. 2011;20:577–81.
18. Marsella R, Genovese D, Gilmer L, Ahrens K, Gatto H, Navarro C.
Investigations on the effects of a topical ceramides-containing emulsion
(Allerderm Spot on) on clinical signs and skin barrier function in dogs with
atopic dermatitis: a double-blinded randomized controlled study. Intern J
Appl Res Vet Med. 2013;11:110–6.
19. Olivry T, DeBoer DJ, Prélaud P, Bensignor E. Food for thought: pondering
the relationship between canine atopic dermatitis and cutaneous adverse
food reactions. Vet Dermatol. 2007;18:390.
20. Olivry T, Mueller RS, Prélaud P: Critically appraised topic on adverse food
reactions of companion animals (1): duration of elimination diets. BMC Vet
Res 2015;in press
21. Ricci R, Granato A, Vascellari M, Boscarato M, Palagiano C, Andrighetto I, et
al. Identification of undeclared sources of animal origin in canine dry foods
used in dietary elimination trials. J Anim Physiol Anim Nutr (Berl). 2013;97
Suppl 1:32–8.
22. Okuma TA, Hellberg RS. Identification of meat species in pet foods using a
real-time polymerase chain reaction (PCR) assay. Food Control.
2015;50:9–17.
23. Maine IR, Atterbury R, Chang KC. Investigation into the animal species
contents of popular wet pet foods. Acta Vet Scand. 2015;57:7.
24. Maina E, Galzerano M, Noli C. Perianal pruritus in dogs with skin disease.
Vet Dermatol. 2014;25:204–9. e51–2.
25. Gill C, McEwan N, McGarry J, Nuttall T. House dust and storage mite
contamination of dry dog food stored in open bags and sealed boxes in 10
domestic households. Vet Dermatol. 2011;22:162–72.
26. Hibberson CE, Vogelnest LJ. Storage mite contamination of commercial dry
dog food in south-eastern Australia. Aust Vet J. 2014;92:219–24.
27. Dryden MW, Ryan WG, Bell M, Rumschlag AJ, Young LM, Snyder DE.
Assessment of owner-administered monthly treatments with oral spinosad
or topical spot-on fipronil/(S)-methoprene in controlling fleas and
associated pruritus in dogs. Vet Parasitol. 2013;191:340–6.
28. Plant JD, Neradelik MB, Polissar NL, Fadok VA, Scott BA. Agreement between
allergen-specific IgE assays and ensuing immunotherapy recommendations
from four commercial laboratories in the USA. Vet Dermatol.
2014;25:15–e6.
29. Bethlehem S, Bexley J, Mueller RS. Patch testing and allergen-specific serum
IgE and IgG antibodies in the diagnosis of canine adverse food reactions.
Vet Immunol Immunopathol. 2012;145:582–9.
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 14 of 15

30. Hardy JI, Hendricks A, Loeffler A, Chang YM, Verheyen KL, Garden OA, et al.
Food-specific serum IgE and IgG reactivity in dogs with and without skin disease:
lack of correlation between laboratories. Vet Dermatol. 2014;25:447–e70.
31. Kawano K, Oumi K, Ashida Y, Horiuchi Y, Mizuno T. The prevalence of dogs
with lymphocyte proliferative responses to food allergens in canine allergic
dermatitis. Pol J Vet Sci. 2013;16:735–9.
32. Swinnen C, Vroom M. The clinical effect of environmental control of house
dust mites in 60 house dust mite-sensitive dogs. Vet Dermatol. 2004;15:31–6.
33. Fujimura M. The study of canine atopic dermatitis involving the isolation of
dogs. Pol J Vet Sci. 2011;14:273–7.
34. Pinchbeck LR, Hillier A, Kowalski JJ, Kwochka KW. Comparison of pulse
administration versus once daily administration of itraconazole for the
treatment of Malassezia pachydermatis dermatitis and otitis in dogs. J Am
Vet Med Assoc. 2002;220:1807–12.
35. Berger DJ, Lewis TP, Schick AE, Stone RT. Comparison of once-daily versus
twice-weekly terbinafine administration for the treatment of canine
Malassezia dermatitis—a pilot study. Vet Dermatol. 2012;23:418–e79.
36. Popa I, Pin D, Remoue N, Osta B, Callejon S, Videmont E, et al. Analysis of
epidermal lipids in normal and atopic dogs, before and after administration
of an oral omega-6/omega-3 fatty acid feed supplement. A pilot study.
Vet Res Commun. 2011;35:501–9.
37. Popa I, Remoue N, Osta B, Pin D, Gatto H, Haftek M, et al. The lipid
alterations in the stratum corneum of dogs with atopic dermatitis are
alleviated by topical application of a sphingolipid-containing emulsion.
Clin Exp Dermatol. 2012;37:665–71.
38. Piekutowska A, Pin D, Rème CA, Gatto H, Haftek M. Effects of a topically
applied preparation of epidermal lipids on the stratum corneum barrier of
atopic dogs. J Comp Pathol. 2008;138:197–203.
39. Blaskovic M, Rosenkrantz W, Neuber A, Sauter-Louis C, Mueller RS. The effect
of a spot-on formulation containing polyunsaturated fatty acids and
essential oils on dogs with atopic dermatitis. Vet J. 2014;199:39–43.
40. Nuttall TJ, McEwan NA, Bensignor E, Cornegliani L, Lowenstein C, Reme CA.
Comparable efficacy of a topical 0.0584 % hydrocortisone aceponate spray
and oral ciclosporin in treating canine atopic dermatitis. Vet Dermatol.
2012;23:4–10. e1–2.
41. Steffan J, Favrot C, Mueller R. A systematic review and meta-analysis of the
efficacy and safety of cyclosporin for the treatment of atopic dermatitis in
dogs. Vet Dermatol. 2006;17:3–16.
42. Little PR, King VL, Davis KR, Cosgrove SB, Stegemann MR. A blinded,
randomized clinical trial comparing the efficacy and safety of oclacitinib
and ciclosporin for the control of atopic dermatitis in client-owned dogs.
Vet Dermatol. 2015;26:23–30. e7–8.
43. Cosgrove SB, Wren JA, Cleaver DM, Walsh KF, Follis SI, King VI, et al.
A blinded, randomized, placebo-controlled trial of the efficacy and safety of
the Janus kinase inhibitor oclacitinib (Apoquel(R)) in client-owned dogs
with atopic dermatitis. Vet Dermatol. 2013;24:587–97. e141–2.
44. Dip R, Carmichael J, Letellier I, Strehlau G, Roberts E, Bensignor E, et al.
Concurrent short-term use of prednisolone with cyclosporine A accelerates
pruritus reduction and improvement in clinical scoring in dogs with atopic
dermatitis. BMC Vet Res. 2013;9:173.
45. Navarro C, Crastes N, Benizeau E, McGahie D. Voluntary acceptance and
consumption of two oral ciclosporin formulations in dogs: two randomised,
controlled studies. Ir Vet J. 2015;68:3,015–0031–8. eCollection 2015.
46. Cosgrove SB, Cleaver DM, King VL, Gilmer AR, Daniels AE, Wren JA, et al.
Long-term compassionate use of oclacitinib in dogs with atopic and
allergic skin disease: safety, efficacy and quality of life. Vet Dermatol.
2015;26:171–e35.
47. Iwasaki T, Hasegawa A. A randomized comparative clinical trial of
recombinant canine interferon-gamma (KT-100) in atopic dogs using
antihistamine as control. Vet Dermatol. 2006;17:195–200.
48. Yasukawa K, Saito S, Kubo T, Shibasaki Y, Yamaoka K, Hachimura H, et al.
Low-dose recombinant canine interferon-gamma for treatment of canine
atopic dermatitis: An open randomized comparative trial of two doses.
Vet Dermatol. 2010;21:41–8.
49. Carlotti DN, Boulet M, Ducret J, Machicote G, Jasmin P, Reme CA, et al. The
use of recombinant omega interferon therapy in canine atopic dermatitis:
a double-blind controlled study. Vet Dermatol. 2009;20:405–
11.
50. Litzlbauer P, Weber K, Mueller RS. Oral and subcutaneous therapy of canine
atopic dermatitis with recombinant feline interferon omega. Cytokine.
2014;66:54–9.
51. Plevnik A, Kobal S, Domanjko-Petric A, Kotnik T. The efficacy of
antihistamine fexofenadine versus methylprednisolone in the treatment of
atopic dermatitis in dogs. Slov Vet Res. 2009;46:5–11.
52. Plevnik Kapun A, Salobir J, Levart A, Tavcar Kalcher G, Nemec Svete A,
Kotnik T. Vitamin E supplementation in canine atopic dermatitis:
improvement of clinical signs and effects on oxidative stress markers. Vet
Rec. 2014;175:560.
53. Cadot P, Hensel P, Bensignor E, Hadjaje C, Marignac G, Beco L, et al.
Masitinib decreases signs of canine atopic dermatitis: a multicentre,
randomized, double-blind, placebo-controlled phase 3 trial. Vet Dermatol.
2011;22:554–64.
54. Singh SK, Dimri U, Saxena SK, Jadhav RK. Therapeutic management of
canine atopic dermatitis by combination of pentoxifylline and PUFAs. J Vet
Pharmacol Ther. 2010;33:495–8.
55. Pin D, Fourel I, Lussiez C, Guinet C, Berny P, Videmont E. Pharmacokinetic
and toxicity of methotrexate in the dog and its efficacy in canine atopic
dermatitis. Vet Dermatol. 2012;23 Suppl 1:45–6. abstract.
56. Stich AN, Rosenkrantz WS, Griffin CE. Clinical efficacy of low-level laser
therapy on localized canine atopic dermatitis severity score and localized
pruritic visual analog score in pedal pruritus due to canine atopic dermatitis.
Vet Dermatol. 2014;25:464–e74.
57. Fujimura M, Ishimaru H, Nakatsuji Y. Fluoxetine (SSRI) treatment of canine
atopic dermatitis: a randomized, double-blind, placebo-controlled, crossover
trial. Pol J Vet Sci. 2014;17:371–3.
58. Lourenço-Martins AM, São-Braz B, Schmidt V, Rème CA, Nuttall TJ. Long-term
maintenance therapy of canine atopic dermatitis with a 0.0584 % hydrocortisone
aceponate spray (Cortavance) used ontwoconsecutivedayseachweek.
Veterinary dermatology. 2012;23 Suppl 1:39 (abstract).
59. Hensel P. Differences in allergy skin testing among dermatologists within
the same geographical region in the USA. Vet Dermatol. 2012;23 Suppl 1:60
(abstract).
60. Carlotti DN, Gribeauval C, Costargent FA, Ganiayre J, Viaud SE. A
retrospective survey of the results of allergen-specific immunotherapy in
205 atopic dogs in Aquitaine, France (1989–2001). Prat Méd Chir Anim
Comp. 2013;48:41–7.
61. DeBoer D, Verbrugge M, Morris M. Clinical and serological response of dust
mite-sensitive dogs with atopic dermatitis to sublingual immunotherapy.
Allergo J. 2010;19:317. abstract.
62. DeBoer DJ, Morris M. Multicentre open trial demonstrates efficacy of
sublingual immunotherapy in canine atopic dermatitis. Vet Dermatol.
2012;23 Suppl 1:65. abstract.
63. Hobi S, Mueller RS. Efficacy and safety of rush immunotherapy with alum-
precipitated allergens in canine atopic dermatitis. Tierarztl Prax Ausg K
Kleintiere Heimtiere. 2014;42:167–73.
64. Marsella R, Santoro D, Ahrens K, Thomas AL. Investigation of the effect of
probiotic exposure on filaggrin expression in an experimental model of
canine atopic dermatitis. Vet Dermatol. 2013;24:260–e57.
Submit your next manuscript to BioMed Central
and take full advantage of:
• Convenient online submission
• Thorough peer review
• No space constraints or color figure charges
• Immediate publication on acceptance
• Inclusion in PubMed, CAS, Scopus and Google Scholar
• Research which is freely available for redistribution
Submit your manuscript at
www.biomedcentral.com/submit
Olivry et al. BMC Veterinary Research (2015) 11:210 Page 15 of 15