Flea allergy dermatitis (FAD) or flea bite hypersensitivity is the most common dermatologic disease of domestic dogs in the USA. Cats also develop FAD, which is one of the major causes of feline miliary dermatitis. FAD is most prevalent in the summer, although in warm climates flea infestations may persist throughout the year. In north temperate regions, the close association of pets and their fleas with human dwellings creates conditions that permit a year-round problem. Temperature extremes and low humidity tend to inhibit flea development.
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. Flea-naive dogs exposed intermittently to flea bites develop either immediate (15 min) or delayed (24–48 hr) reactions, or both, and detectable levels of both circulating IgE and IgG antiflea antibodies. Dogs exposed continuously to flea bites have low levels of these circulating antibodies and either do not develop skin reactions or develop them later and to a considerably reduced degree. This could indicate that immunologic tolerance may develop naturally in dogs continually exposed to flea bites. Although the pathophysiology of FAD in cats is poorly understood, similar mechanisms may exist.
Clinical signs associated with FAD are variable and depend on frequency of flea exposure, duration of disease, presence of secondary or other concurrent skin disease, degree of hypersensitivity, and effects of previous or current treatment. Nonallergic animals may have few clinical signs other than occasional scratching due to annoyance of flea bites. Those that are allergic will typically have a dermatitis characterized by pruritus.
In dogs, the pruritus associated with FAD can be intense and may manifest over the entire body. Classic clinical signs are papulocrustous lesions distributed on the lower back, tailhead, and posterior and inner thighs. Dogs may be particularly sensitive in the flanks, caudal and medial thighs, ventral abdomen, lower back, neck, and ears. Affected dogs are likely to be restless and uncomfortable, spending much time scratching, licking, rubbing, chewing, and even nibbling at the skin. Hair may be stained brown from the licking and is often broken off. Common secondary lesions include areas of alopecia, erythema, hyperpigmented skin, scaling, papules, and broken papules covered with reddish brown crusts. The rump and tailhead areas are typically the first, most evident, areas affected. As FAD progresses and becomes chronic, the areas become alopecic, lichenified, and hyperpigmented, and the dog develops secondary bacterial and yeast infections.
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, generalized alopecia, severe seborrhea, hyperkeratosis, and hyperpigmentation may develop.
In cats, clinical signs vary from minimal to severe, depending on the degree of sensitivity. The primary dermatitis is a papule, which often becomes crusted. This miliary dermatitis is typically found on the back, neck, and face. The miliary lesions are not actual flea bites but a manifestation of a systemic allergic reaction that leads to generalized pruritus and an eczematous rash. Pruritus may be severe, evidenced by repeated licking, scratching, and chewing. Cats with FAD can have alopecia, facial dermatitis, exfoliative dermatitis, and “racing stripe” or dorsal dermatitis.
A number of factors must be considered in the diagnosis of FAD, including history, clinical signs, presence of fleas or flea excrement, results of intradermal testing, and exclusion of other causes of dermatologic disease.
Most cases are seen in the late summer, corresponding to the peak of flea populations. In these cases, history can be highly suggestive. Age of onset is also important, because FAD does not ordinarily occur before 1 yr of age. Usually, diagnosis is made by visual observation of fleas on the infested pet. Demonstration to the owner of the presence of fleas or flea excrement is helpful. Slowly parting the hair against the normal lay often reveals flea excrement or the rapidly moving fleas. Flea excrement is reddish black, cylindrical, and pellet- or comma-shaped. Placed in water or on a damp paper towel and crushed, the excrement dissolves, producing a reddish brown color.
Extremely hypersensitive animals are likely to be virtually free of fleas because of excessive self-grooming. In these cases, it is usually difficult to find evidence of fleas, thus making it harder to convince owners of the problem. Use of a fine-toothed flea comb (32 teeth/in.) facilitates finding of fleas and their excrement. Examination of the pet's bedding for eggs, larvae, and excrement is also useful.
Intradermal skin testing may be used to support a presumptive diagnosis of FAD. Positive immediate reactions are characterized by a wheal 3–5 mm larger in diameter than the negative control. Alternatively, a positive wheal measurement can be defined as a response that is at least equal to the halfway point between the size of positive and negative control reactions. Observations for an immediate reaction (15–20 min) and, if negative, a 24-hr delayed reaction are recommended. The delayed reaction may not be seen as a discrete wheal but rather as a diffuse erythematous reaction. A positive reaction does not conclusively indicate that the clinical condition is FAD—it indicates only that the animal is allergic to the flea antigen, either from present or past exposure. The reliability of intradermal skin testing in cats to diagnose FAD is variable.
Serologic testing of IgE directed against flea-specific salivary antigens can be used to aid in the diagnosis of FAD.
FAD must be differentiated from other causes of dermatologic disease. The presence of fleas or a positive reaction to an intradermal test does not exclude the presence of another dermatologic disease responsible for the clinical signs. In dogs, differential diagnoses include atopic dermatitis, food allergy dermatitis, sarcoptic or demodectic mange, other ectoparasites, and bacterial folliculitis. In cats, other conditions that can result in miliary dermatitis include external parasites (cheyletiellosis, trombiculosis, notoedric mange, and pediculosis), dermatophytosis, drug hypersensitivity, food allergy, atopic dermatitis, bacterial folliculitis, and idiopathic miliary dermatitis.
Treatment and Control
Also see Ectoparasiticides Used in Small Animals.
Flea control measures have changed dramatically over the years. The development of insecticides and insect growth regulators (IGRs) with convenient dosage formulations and prolonged residual activity has dramatically improved owner compliance and helped eliminate recurrent infestations. The goals of flea control are elimination of fleas on pet(s), elimination of existing environmental infestation, and prevention of subsequent reinfestation. The first step is still the elimination of existing pet flea infestations. Elimination of those fleas currently established on the dog or cat is necessary to eliminate pet discomfort. One common consideration is termed rate or speed of flea kill on a pet. However, it is important to differentiate between speed of elimination of established infestations and speed of elimination of newly acquired fleas after a product has been applied. When treating a dog or cat with a topically applied formulation, it could take several hours (12–36 hr) until the compound has spread sufficiently or reached sufficient systemic concentrations to eliminate all existing fleas. If a more rapid rate of kill is needed, a flea spray or oral product such as nitenpyram, afoxolaner, fluralaner, or spinosad may be desirable.
Several available insecticides provide excellent elimination of established flea infestations on both dogs and cats, including afoxolaner (dogs only), dinotefuran, fipronil, fluralaner (dogs only), imidacloprid, indoxacarb, metaflumizone, nitenpyram, selamectin, spinosad, and pyrethroids.
The second step is to eliminate the existing infestation in the pet's environment. This can be accomplished in several ways: 1) topical application of residual insecticides that kill newly acquired fleas (within 24 hr) before they can initiate reproduction, 2) administration of topical, injectable, or oral IGRs to stop flea reproduction, 3) repeated application of insecticides and/or IGRs to the premises, or 4) combinations of the above.
Administration of topical or systemic residual insecticides and administration of topical, injectable, or oral IGRs have become the preferred methods to eliminate flea infestations. Several of these insecticides and IGRs have very effectively controlled fleas on pets living in infested premises. Field studies have shown that afoxolaner, fipronil with or without the addition of (S)-methoprene, imidacloprid, indoxacarb, fluralaner, lufenuron (with an adulticide), selamectin, and spinosad can effectively control flea infestations, without the need for premise treatment. Flea infestations can be eliminated via regular monthly use of topical and systemic approaches, because most fleas are killed before and/or directly inhibited from reproducing. However, even if the systemic or topical insecticide used is 100% effective, control of an existing infestation will typically take 2–3 mo because of the existing flea life stages in the environment.
If residual flea products are applied at the appropriate dose and treatment intervals, there may be adequate residual activity between applications to kill many newly acquired fleas before egg production is initiated. However, flea survival and reproduction may occur before the next application for a variety of reasons: 1) residual activity <100% within the labeled time frame, 2) rate of flea kill slows during the third or fourth week, 3) delayed or infrequent product reapplication, 4) simple under-dosing, and 5) mechanical removal of water-soluble insecticides during bathing or swimming. These problems may result in delays in control or outright treatment failures.
Some of the currently available residual flea products may not be 100% effective against all cat flea strains between labeled reapplication periods because of genetic variability of different flea populations. Many of the factors that allow flea infestations to persist could possibly lead to genetic selection of resistant flea populations. Surviving fleas may be capable of producing viable eggs. Continued reproduction must be halted to prevent persistent flea infestations and selection for resistant fleas. Reproduction can be prevented by administration of topical or systemic IGRs, which provide prolonged residual ovicidal activity, interrupting future flea development even after residual activity of an insecticide is diminished. Application of methoprene or pyriproxyfen to the hair coat of dogs and cats rapidly kills developing flea eggs in addition to residual ovicidal activity. The combination of fipronil/(S)-methoprene or other adulticidal/ovicidal products has demonstrated activity against adult fleas and provides prolonged residual ovicidal activity, thus reducing the potential for genetic selection. Not only have topically applied IGRs been shown to be ovicidal, but orally administered or injectable (cats only) lufenuron also provides ovicidal activity. Although not an IGR, selamectin also demonstrates ovicidal activity in cats.
Many pet owners mistakenly think that flea products either kill all newly acquired fleas within seconds to minutes or completely repel them. But repellency may sometimes be nonexistent, and residual products do not kill most fleas within minutes. Often fleas may live for 6–24 hr and consume blood before being killed. Therefore, close scrutiny of treated pets in an infested environment occasionally results in a few flea sightings on pets for up to 8 wk and occasionally longer until the infestation is eliminated.
An additional complication for pet owners is infestation of the yard by wildlife, feral cats and dogs, or other infested pets. Often pet owners will treat their pets, but do not realize the environment their pet frequents may be constantly infested with fleas by wildlife or feral animals (especially cats). Even when pets only go outdoors for brief periods, they are susceptible to becoming infested. Additionally, people can act as carriers, bringing fleas into the household and infesting unprotected pets.
In cases of severe, massive flea infestations or severe pet or human flea allergy, treatment of the premises may be necessary. Pet owners should begin by conducting a mechanical control program. Helpful procedures include washing pet blankets, throw rugs, and pet carriers; in addition, pet sleeping and resting areas should be vacuumed thoroughly to help remove flea eggs and larvae. Seat cushions and pillows on sofas and chairs should be removed and vacuumed, and special attention given to crevices in sofas and chairs and to areas beneath sofas or beds where flea eggs and feces may drop from the pet and accumulate. Intermittent-light flea traps can also be beneficial. The overall goal of mechanical intervention is to reduce preexisting biomass of immature and adult life stages in the premises. In addition, treatment of the premises with adulticides and IGRs may still be necessary in some infestations. Control may be achieved by using insecticides with residual activity (or by repeated application of short-acting insecticides) in combination with an IGR to prevent development of flea eggs and larvae. Methoprene and pyriproxyfen are the currently available IGRs for premise application. Insecticides and IGRs can be applied by broadcast treatment (hand pump sprayers or pressurized aerosols) or with total release aerosols or “foggers.” During application, the surface of all rugs and carpets must be treated adequately. Efforts should be directed to areas where flea eggs and larvae accumulate, such as carpets, cracks, grooves in hardwood floors, behind baseboards, under the edge of rugs, beneath furniture (beds, tables, and sofas), and within closets. In severe infestations, a second treatment may be necessary 7–10 days later because of continued emergence of adult fleas from cocoons hidden deep within carpets.
Elimination of fleas in the yard can be an important aspect of flea control. Outdoor treatments (eg, imidacloprid, cyfluthrin, fenvalerate) should concentrate on primary areas of flea development, including protected microhabitats such as dog houses, within garages, under porches, and in animal lounging areas beneath shrubs or other shaded areas. Spraying flea control products over the large expanse of a shade-free lawn generally is not beneficial in control efforts and is poor environmental practice.
Despite the efforts of pet owners, the total elimination of fleas may not be feasible in some situations or may not occur rapidly enough to control clinical signs of FAD. Supportive medical therapy must be instituted to control pruritus and secondary skin disease in hypersensitive animals. Systemic glucocorticoids are often needed to control inflammation and associated pruritus. Short-acting prednisone or prednisolone can be administered initially at a dosage of 0.5–1 mg/kg/day, tapering the dosage and using alternate-day therapy until the lowest dose possible that still controls the pruritus is given. As soon as flea control is accomplished, the glucocorticoid can be discontinued. Anti-inflammatory therapy should never be used as a substitute for flea control.
Secondary bacterial skin infection can be associated with FAD. Systemic antibiotics are commonly used to control the pyoderma and thus reduce the associated inflammation and pruritus. Selection of an appropriate antibiotic should be based on bacterial cultures and results of antibiotic sensitivity tests.
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. The effectiveness of currently available whole flea extracts is controversial.
Last full review/revision December 2014 by Michael W. Dryden, DVM, PhD, DACVM