アレルギー性皮膚炎 : 犬の食物アレルギー (CARF)
要約
- ペットの食餌に含まれる原因アレルゲン(もっとも頻繁に摂取する成分)の摂取に関連する非季節性のそう痒性アレルギー性皮膚炎
- ヒトが食物アレルゲンを摂食して死に至る場合があるのとは異なり、通常は生命を脅かす疾患ではない。
- 犬では正確な病因についてすべてわかっているわけではないが、多様な免疫学的反応(I型、III型、IV型、またはそのいずれか1つ)が関わっている可能性も考えられる。
- 最もよくみられるものは、食物中の糖タンパク質に対する異常な免疫反応である。糖タンパク質は通常、熱安定性、水溶性であり、大きさは10~70 kDaである。
- 犬ではアトピー性皮膚炎(AD)と併せて診断されることが多い(ADを除外しない)。
- 犬では、ノミアレルギー性皮膚炎およびアトピー性皮膚炎に次いで3番目に多いアレルギー性皮膚炎である(10~15%)。
どのような疾患か?
- No age or sex predilection, but many cases begin at less than 1 year of age, and more common than AD in dogs younger than 6 months
- Any breed can be affected but reported predisposed breeds include: American cocker spaniel, English springer spaniel, Labrador retriever, collie, miniature schnauzer, Chinese shar pei, poodle, West Highland white terrier, boxer, dachshund, Dalmatian, Lhasa apso, German shepherd dog, Rhodesian ridgeback, pug, and golden retriever
- Distribution of clinical signs are similar to AD – face, ears, axillae, inguinal area, abdomen; pattern with pruritus of mainly ears and perineal area (“ears and rears”) is often attributed to CARF (24%)
- Concurrent gastrointestinal signs – 10-30%; flatulence and increased frequency of defecation occur more commonly than vomiting or diarrhea
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Recurrent secondary staphylococcal (pruritic or non-pruritic) dermatitis and yeast (Malassezia) infections can occur
- Rarely, vasculitis, urticaria and erythema multiforme
What Else Looks Like This?
- Atopic dermatitis (non-seasonal)
- Sarcoptic mange
- Staphylococcal / Malassezia infections
- Cheyletiellosis
- Dermatophytosis
- Flea allergy dermatitis
HOW DO I DIAGNOSE IT?
- The only accurate method of diagnosis is a food trial that lasts up to 12 weeks during which time the pet’s clinical signs resolve (followed by recurrence of signs upon provocation—see below)
- This diet can be home-cooked or carefully selected prescription prepared food
- There is insufficient evidence that blood or skin testing for food allergies is diagnostic
- Ingredients must be novel proteins for the pet or hydrolyzed proteins (proteins broken down to peptides smaller than 10kDa)
- All treats, chewable medications (including parasite preventatives and NSAIDs) must be replaced with non-flavored versions or topical therapy where appropriate
- If pruritus resolves with the trial, a food challenge (provocation for up to two weeks) should be done to confirm the offending protein. This can be done with the initial diet, with ingredients from that diet, or specific treats. Once the offending protein is identified, avoiding its ingestion is the goal of long-term management.
How Do I Manage It?
- Once it is determined that the dermatitis is due to a reaction to something the pet has been fed, avoiding its ingestion is the goal of long-term management.
- Pruritus associated with CARFs generally has partial to no response to treatment with corticosteroids and/or cyclosporine (some animals show a partial response and then relapse when dose is tapered)
Comments:
- Cross-reactions may occur among foods within a food group (e.g., beef and venison) and also between food allergens and other allergens (e.g., milk and beef; crustaceans and cockroaches; birch pollen may cross-react with a variety of fruits and vegetables) Beef has been reported as the most common reactant in dogs, followed by soy, chicken, milk, corn, wheat and eggs
- Hydrolyzed diets may work best for dogs with immediate (Type I) hypersensitivity reactions and may not work for dogs with delayed CAFR
- More than one elimination diet trial may be required to diagnose a CAFR
- If a home-cooked diet is used long-term consultation with a nutritionist is necessary to ensure the diet is nutritionally adequate for the patient
References:
- Bowlin, CL. Novel Proteins and Food Allergies. NAVC Clinician’s Brief. March 2010. pp 37-40.
- Bruet V, Bourdeau PJ, Roussel A, et al. Characterization of pruritus in canine atopic dermatitis, flea bit hypersensitivity and flea infestation and its role in diagnosis. Vet Dermatol. 2012; 23. 487-492.
- Bruner, S. Dietary Hypersensitivty, in Small Animal Dermatology Secrets, KL Campbell, 2004, pp 196-201.
- Gaschen, FP, Merchant SR. Adverse Food Reactions in Dogs and Cats. Vet Clin Small Animal. 41, 2011, pp 361-379.
- Handbook of Small Animal Practice, 5th ed. Morgan, RV, ed. 2008 pp 825-826.
- Jackson, H. Dermatologic manifestations and nutritional management of adverse food reactions. Vet Med. Jan 2007. pp 51-64.
- Kennis RA. Food allergies: update of pathogenesis, diagnosis and management. Vet Clin North Am Small Anim Pract. 2006; 35:175-184.
- Loeffler A, et al. A retrospective analysis of a case series using home prepared and chicken hydrolysate diets in the diagnosis of adverse food reactions in 181 pruritic dogs. Vet Dermatol. 2006, 17. pp 272-279.
- Martin A, et al. Identification of allergens responsible for canine cutaneous adverse food reactions to lamb, beef, and cow’s milk. Vet Dermatol. 2004, 15. pp 349-356.
- Miller, WH et al. Muller and Kirk’s Small Animal Dermatology, 7th ed. pp 397-404.
- Nett, C. Food allergy: new insights in the diagnosis and management. WCVD, 7/2012. pp 81-86.
- Olivry T, Bizikova, P. A systematic review of the evidence of reduced allergenicity and clinical benefit of food hydroylsates in dogs with cutaneous adverse food reactions. Vet Dermatol. 2010, 21. pp 32-41.
- Raditic DM, Remiilard, RL, Tater KC. ELISA testing for common food antigens in four dry dog food used in dietary elimination trials. J Animal Physiol Anim Nutrition. 2011. 95. pp 90-97.
- Ricci. R, et al. A comparison of the clinical manifestation feeding whole and hydrolyzed chicken to dogs with hypersensitivity to the native protein. Vet Dermatol. 2010, 21. pp 358-366.
- Williamson, NL. Chronic Skin Problems in a cocker spaniel. NAVC Clinician’s Brief. July 2008, pp 45-47.
- Zimmer A, et al. Food allergen-specific serum IgG and IgE before and after elimination diets in allergic dogs. Vet Immunol Immunopathol. Dec 15, 2011, 144(3-4), pp 442-447.
abscess
A discrete swelling containing purulent material, typically in the subcutis
alopecia
Absence of hair from areas where it is normally present; may be due to folliculitis, abnormal follicle cycling, or self-trauma
alopecia (“moth-eaten”)
well-circumscribed, circular, patchy to coalescing alopecia, often associated with folliculitis
angioedema
Regional subcutaneous edema
annular
Ring-like arrangement of lesions
atrophy
Thinning of the skin or other tissues
bulla
Fluid-filled elevation of epidermis, >1cm
hemorrhagic bullae
Blood-filled elevation of epidermis, >1cm
comedo
dilated hair follicle filled with keratin, sebum
crust
Dried exudate and keratinous debris on skin surface
cyst
Nodule that is epithelial-lined and contains fluid or solid material.
depigmentation
Extensive loss of pigment
ecchymoses
Patches due to hemorrhage >1cm
epidermal collarettes
Circular scale or crust with erythema, associated with folliculitis or ruptured pustules or vesicles
erosion
Defect in epidermis that does not penetrate basement membrane. Histopathology may be needed to differentiate from ulcer.
erythema
Red appearance of skin due to inflammation, capillary congestion
eschar
Thick crust often related to necrosis, trauma, or thermal/chemical burn
excoriation
Erosions and/or ulcerations due to self-trauma
fissure
Excessive stratum corneum, confirmed via histopathology. This term is often used to describe the nasal planum and footpads.
fistula
Ulcer on skin surface that originates from and is contiguous with tracts extending into deeper, typically subcutaneous tissues
follicular casts
Accumulation of scale adherent to hair shaft
hyperkeratosis
Excessive stratum corneum, confirmed via histopathology. This term is often used to describe the nasal planum and footpads.
hyperpigmentation
Increased melanin in skin, often secondary to inflammation
hypopigmentation
Partial pigment loss
hypotrichosis
Lack of hair due to genetic factors or defects in embryogenesis.
leukoderma
Lack of cutaneous pigment
leukotrichia
Loss of hair pigment
lichenification
Thickening of the epidermis, often due to chronic inflammation resulting in exaggerated texture
macule
Flat lesion associated with color change <1cm
melanosis
Increased melanin in skin, may be secondary to inflammation.
miliary
Multifocal, papular, crusting dermatitis; a descriptive term, not a diagnosis
morbiliform
A erythematous, macular, papular rash; the erythematous macules are typically 2-10 mm in diameter with coalescence to form larger lesions in some areas
nodule
A solid elevation >1cm
onychodystrophy
Abnormal nail morphology due to nail bed infection, inflammation, or trauma; may include: Onychogryphosis, Onychomadesis, Onychorrhexis, Onychoschizia
onychogryphosis
Abnormal claw curvature; secondary to nail bed inflammation or trauma
onychomadesis
Claw sloughing due to nail bed inflammation or trauma
onychorrhexis
Claw fragmentation due to nail bed inflammation or trauma
onychoschizia
Claw splitting due to nail bed inflammation or trauma
papule
Solid elevation in skin ≤1cm
papules
Solid elevation in skin ≤1cm
paronychia
Inflammation of the nail fold
patch
Flat lesion associated with color change >1cm
petechiae
Small erythematous or violaceous lesions due to dermal bleeding
phlebectasia
Venous dilation; most commonly associated with hypercortisolism
plaques
Flat-topped elevation >1cm formed of coalescing papules or dermal infiltration
pustule
Raised epidermal infiltration of pus
reticulated
Net-like arrangement of lesions
scale
Accumulation of loose fragments of stratum corneum
scar
Fibrous tissue replacing damaged cutaneous and/or subcutaneous tissues
serpiginous
Undulating, serpentine (snake-like) arrangement of lesions
telangiectasia
Permanent enlargement of vessels resulting in a red or violet lesion (rare)
ulcer
A defect in epidermis that penetrates the basement membrane. Histopathology may be needed to differentiate from an erosion.
urticaria
Wheals (steep-walled, circumscribed elevation in the skin due to edema ) due to hypersensitivity reaction
vesicle
Fluid-filled elevation of epidermis, <1cm
wheal
Steep-walled, circumscribed elevation in the skin due to edema