Flea allergy dermatitis

From Dog
Ctenocephalides canis, the cause of flea allergy dermatitis[1]

Flea allergy dermatitis (FAD) or flea bite hypersensitivity is the most common [[skin diseases|skin disease of domestic dogs worldwide, caused by an allergy to Ctenocephalides canis.

The disease is characterized by variable degrees of dermatitis, intertrigo and in severe cases, pyoderma.

When feeding, fleas inject saliva that contains a variety of histamine-like compounds, enzymes, polypeptides, and amino acids that span a wide range of sizes (40-60 kD) and induce Type I, Type IV, and basophil hypersensitivity[2]. Dogs which suffer from flea allergy have a greater propensity of eosinophils and this condition is thought to result in immune-dysregulation[3].

Clinical signs in affected dogs vary from intermittent pruritus to generalized dermatitis, otitis externa, pododermatitis and atopy. As the condition progresses and becomes chronic, affected skin areas become alopecic, lichenified, and hyperpigmented and the dog develops secondary bacterial and yeast infections. Interestingly, clinical signs are less and shorter in duration for continuously exposed dogs compared to episodic exposed dogs[4].

In extremely hypersensitive dogs, extensive areas of alopecia, erythema, and self-trauma are evident. Traumatic moist dermatitis (hot spots) can also occur. As the disease becomes chronic, the dog may develop generalized alopecia, severe seborrhea, hyperkeratosis, and hyperpigmentation.

Intradermal skin testing may be used to support a presumptive diagnosis of flea allergy dermatitis[5] but their use has been controversial[6].

A differential diagnosis would include food allergy, atopy[7], folliculitis, Dirofilaria repens[8], Demodex spp, Sarcoptes spp, Malassezia spp), pyoderma, cutaneous lymphoma and lupus erythematosus. Skin scrapings, skin cultures and skin biopsies are recommended in most cases.

Treatment is aimed primarily at flea control both on the dog and its environment[9] as well as reducing doses of prednisolone to minimize pruritus-associated self-injury. Systemic antibiotics are required in cases where bacterial cultures return a positive growth.

Hyposensitization consists of administering allergens to a hypersensitive animal on a regular basis in an attempt to obtain a state of clinical nonreactivity to flea bites[10]. The effectiveness of currently available whole flea extracts is controversial.

References

  1. AH Montgomery
  2. Merck Veterinary Manual
  3. Wuersch K et al (2006) Immune dysregulation in flea allergy dermatitis - a model for the immunopathogenesis of allergic dermatitis. Vet Immunol Immunopathol 110(3-4):311-323
  4. Wilkerson MJ et al (2004) The immunopathogenesis of flea allergy dermatitis in dogs, an experimental study. Vet Immunol Immunopathol 99(3-4):179-192
  5. Laffort-Dassot C et al (2004) Diagnosis of flea allergy dermatitis: comparison of intradermal testing with flea allergens and a FcepsilonRI alpha-based IgE assay in response to flea control. Vet Dermatol 15(5):321-30
  6. Olivry, T et al (2007) Food for thought: pondering the relationship between canine atopic dermatitis and cutaneous adverse food reactions. Vet Dermatol 18:390–391
  7. Bruet V et al (2012) Characterization of pruritus in canine atopic dermatitis, flea bite hypersensitivity and flea infestation and its role in diagnosis. Vet Dermatol 23(6):487-493
  8. Rocconi F et al (2012) Allergic dermatitis by Dirofilaria repens in a dog: clinical picture and treatment. Parasitol Res 111(1):493-496
  9. Stanneck D et al (2012) The synergistic action of imidacloprid and flumethrin and their release kinetics from collars applied for ectoparasite control in dogs and cats. Parasit Vectors 5:73
  10. Marro A et al (2011) Successful immunotherapy of canine flea allergy with injected Actinomycetales preparations. Immunotherapy 3(8):971-978