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  • Author or Editor: Ton Willemse x
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Abstract

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 observed.

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)

Full access
in American Journal of Veterinary Research

Abstract

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 healthy cats.

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)

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in American Journal of Veterinary Research

Abstract

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 pedigrees.

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)

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in American Journal of Veterinary Research

Abstract

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 2001;219:1411–1414)

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in Journal of the American Veterinary Medical Association

Abstract

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.

Full access
in American Journal of Veterinary Research