Fleas and Flea Allergy Dermatitis: Introduction

Transmission, Epidemiology, and Pathogenesis

There are >2,200 species of fleas recognized worldwide. In North America, only a few species commonly infest dogs and cats: Ctenocephalides felis (the cat flea), C canis (the dog flea), Pulex simulans (a flea of small mammals), and Echidnophaga gallinacea (the poultry sticktight flea). However, by far the most prevalent flea on dogs and cats is C felis . Cat fleas cause severe irritation in animals and humans and are responsible for flea allergy dermatitis. They also serve as the vector of typhus-like rickettsiae and Bartonella sp , and are the intermediate host for filarid and cestode parasites. Cat fleas have been found to infest >50 different mammalian and avian hosts throughout the world. In North America, the most commonly infested hosts are domestic and wild canids, domestic and wild felids, raccoons, opossums, ferrets, and domestic rabbits.

Ctenocephalides felis, female

Ctenocephalides felis, male

Ctenocephalides spp, larvae

Transmission, Epidemiology, and Pathogenesis:

Cat fleas deposit their eggs in the pelage of their host. The eggs are pearly white, oval with rounded ends, and 0.5 mm long. They readily fall from the pelage and drop onto bedding, carpet, or soil, where hatching occurs in ~1-6 days. Newly hatched flea larvae are 1-5 mm long, slender, white, segmented, and sparsely covered with short hairs. Larvae are free-living, feeding on organic debris found in their environment and on adult flea feces, which are essential for successful development. Flea larvae avoid direct light and actively move deep in carpet fibers or under organic debris (grass, branches, leaves, or soil).

Larvae are susceptible to desiccation, with exposures to relative humidity <50% being lethal. The areas within a home with the necessary humidity are limited, and suitable outdoor sites are even rarer. Flea development occurs outdoors only where the ground is shaded and moist (1-20% soil moisture content) and where the flea-infested pet spends a significant amount of time so that adult flea feces will be deposited into the larval environment. In the indoor environment, flea larvae probably survive only in the protected microenvironment deep within carpet fibers, in cracks between hardwood floors in humid climates, and on unfinished concrete floors in damp basements. The larval stage usually lasts 5-11 days but may be prolonged for 2-3 wk, depending on availability of food and climatic conditions.

After completing its development, the mature larva produces a silk-like cocoon in which it pupates. The cocoon is ovoid, ~0.5 cm long, whitish, and loosely spun. Flea cocoons can be found in soil, on vegetation, in carpets, under furniture, and on animal bedding.

Once the pupa has fully developed (1-2 wk), the adult flea emerges from the cocoon when properly stimulated by physical pressure, carbon dioxide, substrate movement, or heat. The preemerged adult (which is a fully formed adult flea) residing in the cocoon is the stage that can extend the longevity of the flea. If the preemerged adult does not receive the proper stimulus to emerge, it can remain quiescent in the cocoon for several weeks until a suitable host arrives. Emergence can be delayed up to 350 days if preemerged adults are protected from desiccation. Newly emerging fleas move to the top of the carpet pile or vegetation, where they are more likely to encounter a passing host. A newly emerged cat flea can survive 24-72 hr before requiring a blood meal. It is the newly emerged unfed fleas that infest pets and bite people. Cat fleas that have found a preferred host (eg, dog, cat, opossum, etc) generally do not leave their host unless forced off by grooming or insecticides.

Depending on temperature and humidity, the entire life cycle of the cat flea can be completed in as little as 12-14 days or can be prolonged for up to 350 days. However, under most household conditions, cat fleas complete their life cycle in 3-6 wk.

Adults begin feeding almost immediately once they find a host. Female cat fleas can consume 13.6 µL of blood daily. After rapid transit through the flea, the excreted blood dries within minutes into reddish black fecal pellets or long tubular coils (flea dirt). Fleas mate after feeding, and egg production begins within 24-48 hr of females taking their first blood meal. Female cat fleas can produce up to 40-50 eggs/day during peak egg production, averaging 27 eggs/day through 50 days, and may continue to produce eggs for >100 days.

Cat fleas are susceptible to cold. No stage of the life cycle (egg, larva, pupa, or adult) can survive exposure to <3°C (37.4°F) for several days. Therefore, cat fleas survive winters in north temperate climates as adults on untreated dogs and cats or on small wild mammals (eg, raccoons or opossums) in the urban environment. As these animals pass through yards in the spring or set up nesting sites in crawl spaces or attics, the eggs laid by surviving female fleas drop off and subsequently develop to adults. Cat fleas may also survive the winter as preemerged adults in microenvironments protected from the cold.

Fleas can cause iron deficiency anemia in heavily infested hosts, particularly in young animals. Fleas in the genus Ctenocephalides have been reported to produce anemia in poultry, dogs, cats, goats, cattle, and sheep.

Cat fleas are also involved in disease transmission. Murine typhus, caused by Rickettsia typhi and R felis , is a mild to severe febrile disease of humans characterized by headaches, chills, and skin rashes, with infrequent involvement of the kidneys and CNS. The disease occurs in humans and many small mammals along the southeastern, southwestern, and Gulf coasts. In the USA, the principal transmission cycle involves opossums and cat fleas. Cat fleas also serve as the intermediate host of the nonpathogenic subcutaneous filarid nematode of dogs, Dipetalonema reconditum . Dipylidium caninum , the common intestinal cestode of dogs and cats (and rarely children), develops as a cysticercoid in C felis , C canis , and P irritans . Flea larvae ingest the eggs of the tapeworm, which develop into cysticercoids in the body of the flea. When grooming themselves, dogs and cats may ingest infected fleas, and the cysticercoids are released.

Flea allergy dermatitis (FAD) or flea bite hypersensitivity is the most common dermatologic disease of domestic dogs in the USA. Cats are also afflicted with 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 continuously exposed to flea bites. Although the pathophysiology of FAD in cats is poorly understood, similar mechanisms may exist.

Clinical Findings:

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 that is 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, the dog may develop generalized alopecia, severe seborrhea, hyperkeratosis, and hyperpigmentation.

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.

Diagnosis:

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 ruling out other causes of dermatologic disease.

Most cases occur 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 due to excessive self-grooming. In these cases, it is usually difficult to find evidence of fleas, thus making it more difficult 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 occur 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 has been 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 rule out the presence of another dermatologic disease responsible for the clinical signs. In dogs, differential diagnoses include allergic inhalant dermatitis (atopy), 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, atopy, bacterial folliculitis, and idiopathic miliary dermatitis.

Treatment and Control:

See also ectoparasiticides of small animals, Ectoparasiticides Used in Small Animals: Overview.

Flea control measures have changed dramatically in recent years. Historically, flea control was achieved through repeated application of on-animal products and application of insecticides and insect growth regulators (IGR) on the premises. The difficulty with this approach was achieving consistent compliance with treatment protocols. The recent development of insecticides and IGR with convenient dosage formulations and prolonged residual activity has dramatically improved owner compliance and has 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 term commonly employed when discussing flea kill on a pet is rate or speed of flea kill. However, it is important to differentiate between speed of elimination of established infestations and speed of elimination of newly acquired fleas after the product has been applied. When treating a dog or cat with a topically applied formulation, it could take several hours (12-36 hrs) 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 nitenpyram may be desirable.

Several currently available insecticides provide excellent elimination of established flea infestations on both dogs and cats; these include fipronil, imidacloprid, nitenpyram, selamectin, and pyrethroids. Orally administered nitenpyram will eliminate fleas within 3-4 hr, while the topically applied residual spot-on formulations containing fipronil, imidacloprid, or selamectin take 12-42 hr.

The second goal is to eliminate 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 IGR to stop flea reproduction, 3) repeated application of insecticides and/or IGR to the premises, or 4) combinations of the above.

Topical application of residual insecticides and administration of topical, injectable, or oral IGR have become the preferred methods of eliminating flea infestations. Several of these new insecticides and IGR have been shown to be extremely effective in controlling fleas on pets living in infested premises. Field studies have shown that fipronil (with or without the addition of (S)-methoprene), imidacloprid, lufenuron (with pyrethroid spray or nitenpyram tablets), and selamectin may be effective in controlling flea infestations, without the need for premise treatment. Flea infestations can be eliminated via chronic use of topical and systemic approaches because most fleas are killed prior to and/or directly inhibited from reproducing.

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 prior to the next application for a variety of reasons such as: 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.

None of the currently available residual flea products is 100% effective against all cat flea strains between labeled reapplication periods due to 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 IGR, 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 IGR been shown to be ovicidal, but orally administered or injectable (cats only) lufenuron also provides ovicidal activity. While not an IGR, selamectin also demonstrates ovicidal activity in cats.

In cases of massive flea infestations or severe pet or human flea allergy, treatment of the premises with adulticides and IGR may still be necessary. 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 the development of flea eggs and larvae. Methoprene and pyriproxyfen are the 2 currently available IGR for premise application. Insecticides and IGR 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 due to 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, 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. Entomopathogenic nematodes that parasitize flea larvae and pupae also can be used in these areas to inhibit the buildup of the flea population. Spraying flea control products over the large expanse of a shade-free lawn generally is not beneficial.

Pet owners should also conduct mechanical control. 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 should be 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.

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 0.5-1.0 mg/kg, sid, 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.