Objective—To evaluate skin test reactivity to environmental
allergens in healthy cats and in cats with
atopic dermatitis (AD).
Animals—10 healthy cats and 10 cats with AD.
Procedure—10 allergens in serial dilutions were
injected ID on the lateral aspect of the thorax of
sedated cats. Histamine (0.01% solution) and buffer
solutions were used as positive and negative controls,
respectively. Immediately after the last injection,
10% fluorescein solution was administered IV. Skin
test results were evaluated with ultraviolet light after
15 to 30 minutes and at 4 and 6 hours by 2 independent
observers. In the control group, skin tests were
repeated after 6 weeks. Skin test reactivity and the
nature of the immunoglobulin involved were investigated
by use of the Prausnitz-Küstner test with
untreated and heat-treated cat sera.
Results—Intertest and interobserver agreement
were high when measurement of the diameter of the
fluorescent wheal was used to evaluate skin test
responses, compared with assessment of its intensity.
In both groups of cats, immediate skin test reactivity
was observed as an IgE-mediated reaction, as
an IgG-mediated reaction, and as a result of nonspecific
mast cell degranulation. There was no correlation
between allergen concentration and the type of reaction
Conclusions and Clinical Relevance—Skin test
reactivity in cats should be evaluated after IV administration
of 10% fluorescein solution by means of a
Prausnitz-Küstner test to differentiate among IgEmediated,
IgG-mediated, and nonspecific reactions.
(Am J Vet Res 2003;64:773–778)
Objective—To investigate the role of Felis domesticus
allergen I (Feld I) in the pathogenesis of
eosinophilic granuloma complex (EGC) in cats.
Animals—7 healthy cats and 6 cats with EGC.
Procedure—Epidermis was removed from 4 areas.
Rubber stoppers filled with Feld I, saline (0.9% NaCl)
solution, and PBS solution were glued to the skin lesions
and removed 48 hours later. Fluid within each stopper
was collected. Biopsy specimens were obtained at each
site, snap frozen, and stored at –70 C. Total and differential
numbers of cells in fluid were counted. Biopsy specimens
were stained by use of monoclonal antibodies
against feline CD4, CD8 and CD3. Data were analyzed
by use of multivariate repeated-measures analysis.
Results—Healthy cats had a significant increase in
number of CD3+ cells, compared with number of
CD4+ and CD8+ cells, and Feld I caused a significant
increase in number of CD3+ cells, compared with
PBS or saline solutions. Cats with EGC had a significant
increase in number of CD3+ cells, compared
with number of CD4+ and CD8+ cells, and Feld I
caused a significant increase in number of CD3+ and
CD4+ cells, compared with PBS or saline solutions.
Cats with EGC had an increased CD4+ response, a
significantly decreased CD8+ response, and a significantly
increased CD4-to-CD8 ratio compared with
Conclusions and Clinical Relevance—The increased
CD4+ response, significantly decreased CD8+
response, and significantly increased CD4-to-CD8
ratio are comparable to results in atopic people and
allergic cats. Therefore, Feld I could be an autoallergen
responsible for chronic inflammatory reactions in
cats with EGC. (Am J Vet Res 2002;63:338–341)
Objective—To investigate the possibility that variants
in the acidic or basic keratin genes or in desmoglein 1
may cause the clinical manifestation of familial footpad
hyperkeratosis in Irish Terriers.
Animals—11 dogs belonging to 2 related affected
pedigrees of Irish Terriers.
Procedure—Genomic DNA was extracted from blood
samples obtained from each dog. The DNA markers
linked to the genes keratin 2, keratin 9, and
desmoglein 1 were amplified by use of a polymerase
chain reaction technique, and length of the products
was determined by use of an automatic DNA analyzer.
Results—All tested markers yielded information.
None of the markers (genotype) cosegregated with
the clinical status of the dogs (phenotype) in the 2
Conclusions and Clinical Relevance—Mutations in
the genes encoding keratin 2 and 9 as well as
desmoglein 1 are highly unlikely to be the primary
cause of familial footpad hyperkeratosis in Irish
Terriers. (Am J Vet Res 2003;64:715–720)
Objective—To evaluate 3 commercially available
selected-protein-source diets as maintenance diets in
dogs with pruritus caused by adverse food reactions.
Design—Randomized crossover trial.
Animals—40 dogs > 6 months of age with pruritus
caused by adverse reactions to foods.
Procedure—Diagnosis was confirmed by use of diet
elimination and provocation studies. Subsequently,
dogs were fed 3 commercial diets for 3 weeks each
in a randomized, blinded, crossover trial. Dogs were
evaluated for pruritus, vomiting, diarrhea, and flatulence.
Results—Pruritus recurred in 52.5% of dogs fed a
chicken-rice diet, 47.5% of dogs fed a catfish-rice diet,
and 85% of dogs fed a venison-rice diet. Overall, 95%
of the dogs could be managed successfully with at
least 1 of the 3 diets.
Conclusions and Clinical Relevance—Results indicated
that commercially available limited-allergen
diets with selected protein sources may be appropriate
for long-term management of pruritus caused by
adverse food reactions. Testing of various protein
sources is usually required. (J Am Vet Med Assoc
Objective—To determine whether skin-related clinical signs in cutaneous food hypersensitivity (CFH) coincide with immune reactivity in the intestine in dogs.
Animals—11 dogs with CFH without intestinal clinical signs and 8 healthy control dogs.
Procedures—After a provocation and elimination diet, the duodenal gene expression levels of Th1-, Th2- and Treg-related cytokines and transcription factors were investigated by means of quantitative PCR assay. The presence of CD3+, CD8+, CD4+, CD1c+, γδ T-cell receptor+, and major histocompatibility complex II+ cells in duodenal epithelium and lamina propria were determined.
Results—The expression of Th1-, Th2-, and Treg-related genes in dogs with CFH and healthy control dogs was similar. Although clinical signs disappeared, there was no effect of the elimination diet on cytokines, transcription factors, or cellular phenotypes.
Conclusions and Clinical Relevance—No change in T-cell phenotypes or a distinct Th1, Th2, or Treg profile was detected in the duodenum of dogs with only cutaneous clinical signs of food hypersensitivity. This suggested that the intestinal mucosa is not the primary site of T-cell activation that eventually leads to cutaneous food hypersensitivity.