Fipronil

Fipronil is an insecticide and acaricide in the phenylprazole class. It acts as an antagonist at the insect γ-aminobutyric acid (GABA) receptor. Fipronil is marketed in a spray (Frontline, Merial) or spot application product (Frontline Top Spot, Merial) for flea, tick, scabies, and chewing lice control in dogs and cats. Its efficacy in nonfollicular mite and lice infestations has been demonstrated in horses.

Formamidines

These acaricidal agents act by inhibition of monoamine oxidase. They are also prostaglandin synthesis inhibitors and α-adrenergic agonists. Amitraz is available as rinse, collar, and spot application products for control of ticks and Demodex mites in the dog. Amitraz is contraindicated in horses. Horses sprayed with a 0.025% solution developed somnolence, depression, ataxia, weakness, and colonic impaction.⁵

Pyrethrins

Pyrethrin is a volatile oil extract of the chrysanthemum flower. It contains six active pyrethrins that are contact poisons and have a fast knockdown action and flushing action on insects, but no residual activity. It is rapidly inactivated by moisture, air, and light. Pyrethrins, because of their low toxicity, rapid inactivation, and lack of tissue residue and buildup, are relatively environmentally safe, although they are still toxic to fish and bees. For clients concerned with chemicals, the use of pyrethrins may be more acceptable, because they are organic natural insecticides.

Pyrethrin demonstrates a rapid kill but low toxicity, and the low concentration of 0.06-0.4% is effective if it is synergized with 0.1-2% piperonyl butoxide, which forms a stable complex with cytochrome P450, thus limiting the metabolism of pyrethrins in insects. Spray, foam, spot-on, and wipe-on formulations are available.

Pyrethroids

These synthesized chemicals are modeled after pyrethrin and include d-trans-allethrin, bioallethrin, resmethrin, tetramethrin, deltamethrin, fenvalerate, and permethrin. A fourth-generation of potent and long-lasting pyrethroids is available for ear tag use. The LD₅₀ varies with the agent selected. In action and toxicity, the pyrethroids are relatively comparable, although not identical, to pyrethrin. They produce a quick kill that is improved by the addition of a synergist and pyrethrin. Some of the early pyrethroids degrade on exposure to ultraviolet light, so there is little or no residual activity. The new pyrethroids are relatively photostable compared with pyrethrin.

The most popular pyrethroid agent in equine products is permethrin. Part of permethrin’s desirability is its low toxicity, relative stability on exposure to ultraviolet light, and potential for use as a repellent. As with pyrethrins, the synthetic pyrethroids are often combined with other active agents, particularly repellents.

Repellents

Although these chemicals are capable of keeping insects away, they need frequent applications (often every few hours depending on temperature, humidity, the density of insects, the movement of the animal, and the drying effect of the wind). Compounds with repellent action include pyrethrin, permethrin, citronella, diethyltoluamide (DEET), ethohexadiol, dimethyl phthalate, butoxypropylene glycol, MGK-264, and ingredients in Skin-So-Soft (Avon) bath oil (some believe that the fragrance is the effective ingredient).

Sulfur

With the emphasis on newer, more effective drugs, it is sometimes forgotten that sulfur and its derivatives are excellent and safe parasiticides. The commercial lime sulfur solution (Sulfurated Lime Sulfur Concentrate, DermaPet) is safe for horses of all ages; is an inexpensive effective treatment of infestations of nonfollicular mites; and is fungicidal, bactericidal, keratolytic, and antipruritic. A 28% lotion (Happy Jack Mange Medicine, Happy Jack) and 10% sulfur ointment are other forms of sulfur medications. These high concentration products can be irritating.

Sulfur is a natural parasiticide that is relatively nontoxic and environmentally safe. Its major drawback is the foul odor. It also stains jewelry and temporarily discolors hair, especially white hair. It is drying, but only rarely irritating when used at therapeutic concentrations. A 2-5% lime sulfur solution is effective against Sarcoptes, Psoroptes, Chorioptes, chiggers, bird and straw mites, and lice.

Systemic endectocides

These parasiticides were developed from macrocyclic lactones produced by the fermentation of various actinomycetes. This class of drugs includes avermectins (ivermectin, doramectin, abamectin, selamectin, eprinomectin) and milbemycins (milbemycin, moxidectin). At present, the product used most in equine dermatology is ivermectin. Preliminary studies suggest that all of these products may have equal efficacy when administered at the appropriate dosage. All partly act by potentiating the release and effects of GABA. GABA is a peripheral neurotransmitter in susceptible nematodes, arachnids, and insects. Avermectins and milbemycins are also agonists of glutamate-gated chloride channels. In mammals, GABA is limited to the central nervous system. Because these drugs do not cross the blood-brain barrier in most adult animals, they are relatively safe and have a wide margin between efficacy and mammalian toxicity. If the horse has some preexisting defect in the blood-brain barrier, neurotoxicity can be seen at recommended doses.⁶ Their use in foals less than 4-months-old is contraindicated. In general, these drugs are effective for nematodes, microfilaria, lice, and mites.

Ivermectin

Ivermectin is a derivative of avermectin B from fermentation products of a Streptomyces avermitilis. This drug is licensed for the treatment of various intestinal parasites, including pinworms, bots, summer sores caused by Habronema and Draschia spp., and Onchocerca spp. It is also highly effective in the treatment of sucking lice, chiggers, Sarcoptes, Psoroptes, Demodex, and other serum-feeding mites. A partial response is seen when chewing lice or Chorioptes mites are treated. Ivermectin does not affect trematodes and cestodes, because GABA is not involved in neurotransmission in those species. Parasite paralysis is the main action of ivermectin, but it also suppresses reproduction. Ticks are not killed, but their egg production and molting are suppressed.

Ivermectin is rapidly absorbed orally (PO) and has a plasma resident time of up to 20 days.^3,5 Intramuscular administration results in longer lasting plasma levels: 8.9 ± 0.7 days versus 4.2 ± 0.4 days.⁴ Ninety percent of the dosage is eliminated in the feces within 4 days. The dosage used to treat all nonfollicular mites is 0.2 mg/kg at 14-day intervals.

Moxidectin

Moxidectin (Quest, Fort Dodge) is derived from fermentation products of Streptomyces cyaneogriseus subsp. noncyanogenus. It is marketed for the treatment of various intestinal parasites, including pinworms and bots. It is administered at 0.4 mg/kg PO. Its plasma resident time is approximately 18 days.⁵ Since it is equally as effective in treating onchocerciasis as is ivermectin, the two products probably can be used interchangeably.

Doramectin

Doramectin (Dectomax, Pfizer) is derived from fermentation of selected strains of S. avermitilis. In the United States, it is marketed for the treatment and control of various nematodes, mites, and lice in cattle and swine. In horses, when given at 0.2 mg/kg PO, plasma levels are measurable for 30 days.³

Cause and pathogenesis

Psoroptes spp. mites are large (0.4-0.8 mm long) (Fig. 6-1) and nonburrowing and feed on tissue fluids.⁵ Their life cycle on the host is completed in approximately 10 days. Median life expectancy of an adult female is about 16 days. Off-host survival time is significantly influenced by local temperature and humidity. Environmental conditions in the corners of stalls, organic debris, and bedding, etc. can be very different from those in the rest of the barn with a prolonged off-host survival time. High temperatures and low humidity disfavor survival. In the typical barn, a 14- to 21-day off-host survival can be expected.^1,5,8 However, P. ovis and P. cuniculi maintained under various environmental conditions survived for up to 48 and 84 days, respectively.⁵ The researchers suggested stable quarantine periods of 7 and 12 weeks, respectively.

Figure 6-1 Psoroptes mite (×100).

(Courtesy J. Georgi.)

As mentioned earlier, the number of distinct species with Psoroptes mites is probably much smaller than previously described. Presently, P. equi, Psoroptes natalensis, P. ovis, and P. cuniculi are reported to parasitize the horse. Since Psoroptes mites show little-to-no host specificity and appear to be genetically homogeneous, it is probably best not to assign a specific clinical presentation to any individual species (e.g., otoacariasis due to P. cuniculi).

Psoroptic mites from horses have not been reported to cause disease in humans. Since Otodectes cynotis, the ear mite of companion animals, behaves like a Psoroptes mite and can cause disease in humans, it is likely that humans could be infested by Psoroptes mites from a horse if the horse had a high parasite burden and the contact time was long.

Clinical features

Transmission of Psoroptes mites is by direct or indirect contact. In herds, up to 10% of contact animals may be infected.⁷ The incubation period varies from 2 to 8 weeks. If the horse has been infested previously and became hypersensitive during the initial exposure, the incubation period will be shorter.

Clinical signs are quite variable.⁵ Infested horses may be asymptomatic or may show signs of ear disease, truncal dermatitis, mane and tail disease, or combinations of these. Signs of ear disease include head shaking, ear scratching, or head shyness, and the horse may have a lop-eared appearance (Fig. 6-2). The dermatitis tends to be focused around the ears, mane (Fig. 6-3), and tail (Fig. 6-4). Pruritus is variable but can be intense. In mildly pruritic horses, the presentation will be of mane and tail seborrhea (see Chapter 11). In more pruritic horses, one sees nonfollicular papules, crusts, excoriation, and alopecia. In severe cases the entire topline may be involved.

Figure 6-2 Psoroptic mange. Lop-eared head carriage due to parasitic otitis externa.

(Courtesy W. McMullen.)

Figure 6-3 Psoroptic mange. Excoriations of the mane.

Figure 6-4 Psoroptic mange. Tail head rubbing in the horse with mane pruritus.

Diagnosis

The differential diagnosis includes sarcoptic mange, chorioptic mange, lice, insect-bite hypersensitivity, fly-bite dermatitis, atopic dermatitis, and food allergy. Definitive diagnosis is based on history, physical examination, skin scrapings, and otoscopic examination. Body mites, depending on the degree of infestation, may or may not be demonstrated in skin scrapings. Ear mites can be very difficult to demonstrate even with a thorough otoscopic examination (usually requires chemical restraint) and microscopic examination of material gathered from deep within the ear canal. Skin biopsy reveals varying degrees of superficial perivascular-to-interstitial dermatitis with numerous eosinophils.⁵ Eosinophilic microabscesses and focal areas of epidermal edema, leukocytic exocytosis, and necrosis (epidermal “nibbles”) may be found. Mites are rarely seen.

Clinical management

There are various reports on the treatment of Psoroptes otoacariasis with numerous topical parasiticides.⁵ After a thorough ear cleaning, the product is applied twice weekly for 3 weeks. If the horse is extremely head shy, owner compliance will be a problem and relapses can be expected. Since mites can survive outside the ear canal, simultaneous treatment of the body is recommended to prevent a relapse. Pyrethrin, pyrethroid, or lime sulfur sprays or dips can be effective when applied every 7-14 days for 3-4 weeks. Amitraz is contraindicated in horses.

Ivermectin (0.2 mg/kg PO) or moxidectin (0.4 mg/kg PO) are very effective in the treatment of psoroptic otoacariasis and/or dermatitis.^5,9 A single dosage rapidly decreases mite and egg counts with parasitologic cure within 30 days of treatment. To ensure a cure, a second dose 14 days after the initial treatment is recommended. The cattle product, eprinomectin, can be applied as a pour-on at a dosage of 0.5 mg/kg once weekly for 4 treatments.⁸ Since ivermectin and other parasiticides do not kill eggs, the treated horse should be considered infectious for the first few weeks of treatment.

Cause and pathogenesis

Sarcoptes spp. mites (0.25-0.6 mm in diameter) (Fig. 6-5) tunnel through the epidermis and feed on tissue fluids and possibly epidermal cells. The life cycle on the host is completed in 2-3 weeks. The mites are quite susceptible to drying and survive only a few days off the host. Transmission is by direct and indirect contact. The incubation period varies from a few hours to several weeks, depending on the method and severity of exposure and on prior sensitization of the host.

Figure 6-5 Sarcoptes mite (×100).

(Courtesy J. Georgi.)

Sarcoptes scabiei mites are found on a number of different hosts. It is currently believed that all the various mites are genotypically identical.⁵ Through adaptations for survival on a particular host, the mites may be phenotypically different, but these phenotypic differences do not confer strict species specificity. Cross-infestation among animals and between animals and humans are common.

The primary clinical sign in sarcoptic mange of any species is pruritus, and much of this is associated with a hypersensitivity reaction to mite product(s).

Clinical features

Once common, equine sarcoptic mange is now rare throughout the world.⁵ In the United States, equine sarcoptic mange has been eradicated. There are no apparent age, breed, or sex predilections. The chief clinical sign is pruritus, which usually begins on the head, ears, and neck (Fig. 6-6), and spreads caudally. Nonfollicular papules, crusts, excoriations, alopecia, and lichenification are usually seen. If the mite is acquired from a fox during a hunt, the horse can develop a distal limb dermatitis mimicking many other conditions.¹

Figure 6-6 Sarcoptic mange. Facial pruritus with involvement of the edges of the pinnae.

(Courtesy I. Yeruham.)

Diagnosis

The differential diagnosis includes psoroptic mange, lice, fly-bite dermatoses, and allergic skin diseases. Definitive diagnosis is based on history, physical examination, skin scrapings, skin biopsy, and response to therapy. Mites are often very difficult to find in scrapings. If the pinnae are involved, scrapings along cranial edge should be most rewarding.

Skin biopsy reveals varying degrees of superficial perivascular-to-interstitial dermatitis with numerous eosinophils.⁵ Eosinophilic microabscesses and focal areas of epidermal edema, leukocytic exocytosis, and necrosis (epidermal nibbles) may be seen. Mites may be seen within parakeratotic scale-crusts and in subcorneal “tunnels,” but this is uncommon. Occasionally, deep perivascular dermatitis with lymphoid nodules may be seen.

Because of the frequently negative results of skin scrapings and skin biopsy, response to therapy is often employed in determining a presumptive diagnosis. A positive response to treatment, especially when ivermectin is used, strongly supports the diagnosis of a nonfollicular mite infestation but does not differentiate scabies from the other mite infestations. Because sarcoptic mange would be disastrous if it entered the horse population, state or federal veterinarians should be notified when the disease is confirmed or strongly suspected. Since quarantines might be imposed while the point source of infestation is determined, some barn owners will try to talk the veterinarian out of placing the call. If the clinical presentation is strongly suspicious of sarcoptic mange, the regulatory agencies should be called.

Clinical management

Sarcoptic mange is a severe disease. Intense, constant pruritus results in annoyance, irritability, anemia, secondary infections and myiasis, increased susceptibility to other diseases, and even death. All animals that have been exposed to infected animals should be treated. Since mites can be transferred by grooming tools and other fomites, serious consideration should be given to the treatment of all horses in the barn.

Sarcoptic mange may be treated with spray or dip applications of 0.5% malathion, 0.03% lindane, 0.06% coumaphos, 0.5% methoxychlor, or 2% lime sulfur.⁵ At least two treatments at 14-day intervals should be administered. Ivermectin or moxidectin are effective.^1,5,9

Cause and pathogenesis

Chorioptic mites (0.3-0.5 mm long) (Fig. 6-7) are surface-inhabiting parasites that feed on epidermal debris.⁵ The life cycle takes about 3 weeks and is completed on the host. Adult mites can survive off-host for nearly 70 days, depending on the presence of epidermal debris as a food source and the local environmental conditions. Transmission is by direct and indirect contact.

Figure 6-7 Chorioptes mite (×100).

Four species of mites, Chorioptes bovis (cattle), C. caprae (goats), C. equi (horses), and C. ovis (sheep) are listed in texts as individual species. However, once genotypic testing is performed, it is likely that C. caprae, C. equi, and C. ovis will be phenotypic variants of C. bovis. Currently, interspecies transmission with chorioptic mange has not been reported and the mite has not been reported to cause human disease.

Mite populations are usually much larger during cold weather.⁵ Thus, clinical signs are usually seen, or are more severe, in winter. This seasonality of mite populations and clinical signs is thought to be influenced by temperature, humidity, and wetting of the host. Hot and dry conditions decrease mite survival times. The signs of disease often spontaneously regress during summer when mite numbers become very small. During this clinically inapparent stage of infestation, mites may only be demonstrated around the coronet.

Clinical features

Chorioptic mange occurs in horses in most parts of the world.* In general, there are no apparent age, breed, or sex predilections.

Chorioptes spp. infestations are most commonly seen in draft horses and other horses with feathered fetlocks, especially during winter. Clinical signs are seen on the distal hand limbs (Fig. 6-8) with the fetlocks, pasterns (Fig. 6-9), and tail being particularly affected. Pruritus may be intense or absent. Horses with widespread lesions have been seen (Fig. 6-10).

Figure 6-8 Chorioptic mange. Alopecia and crusting of the distal limb secondary to self-trauma.

Figure 6-9 Chorioptic mange. Crusted, ulcerated lesions on the pastern of a draft horse. The feathers have been clipped.

Figure 6-10 Chorioptic mange. Severe infestation with involvement of the hind limbs and ventrum.

Diagnosis

The differential diagnosis includes tail rubbing (insect-bite hypersensitivity, food allergy, atopic dermatitis, lice, oxyuriasis, or stable vice) and pastern dermatitis (see Chapter 15). Definitive diagnosis is based on history, physical examination, and examination of skin samplings collected by scraping, brushing, or combing. In feathered horses, combings and brushings are more likely to be positive.¹¹ During cool weather, Chorioptes spp. mites are usually easy to demonstrate. These mites are usually active and fast-moving. To prevent them from walking off the slide, the authors recommend using an insecticide-containing solution for the skin-scraping solution. Skin biopsy reveals variable degrees of superficial perivascular-to-interstitial dermatitis with numerous eosinophils.⁵ Eosinophilic epidermal microabscesses and focal epidermal necrosis, leukocytic exocytosis, and edema (epidermal nibbles) may be seen (Fig. 6-11). Mites are not usually seen.

Figure 6-11 Chorioptic mange. Superficial perivascular-to-interstitial dermatitis with focal epidermal damage beneath a mite segment (arrow) in the surface keratin.

Clinical management

All animals that have encountered infected animals should be treated simultaneously. Horses stabled near the infected animal are at risk and probably should be treated.

Because of the mites’ feeding habits, treatment with conventional systemic endectocide regimens may or may not be effective.* Treatment with higher dosages of ivermectin (0.3 mg/kg) at higher frequencies (weekly for four treatments) can improve the response rate, but therapeutic failures will occur.

Topical treatments are labor-intensive but effective. To allow better access of agent to the mites, feathers should be clipped from draft horses. The most labor-intensive treatment involves bathing the horse with a 2% selenium sulfide shampoo.⁵ The shampoo is prediluted with water (1:2), and the horse is bathed three times at 5-day intervals. After a 10-min contact time, the lather is rinsed off and the horse is allowed to dry.

Over the years, various topical insecticides, applied at 7- to 14-day intervals, have proven to be effective. Effective agents include 0.25% crotoxyphos, 0.5% malathion, 0.5% methoxychlor, 0.06% coumaphos, and 2% lime sulfur.⁵ A 0.25% fipronil spray has been reported to be curative in one treatment.⁵ Horses are sprayed from the elbows and stifles down with 125 mL of product applied to each leg. To ensure cure, a second treatment in 3-4 weeks is recommended.^5,12 This application constitutes an extra-label use of an EPA-registered pesticide. A 5% lime sulfur solution applied at 7-day intervals can be effective even when other treatments fail.^5,10

Regardless of the treatment selected, the barn should be cleaned thoroughly. Grooming tools, tack, and other fomites should also be disinfected.

Cause and pathogenesis

Demodectic mites are normal residents of the skin in all large animals.⁵ The mites live in hair follicles and sebaceous glands, are host-specific, and complete their entire life cycle on the host. The life cycle of most demodicids has not been carefully studied, but is assumed to be completed in 20-35 days.

Under most environmental conditions, demodicids can survive only several minutes to a few days off the host. Studies in cattle and dogs have shown that: (1) demodectic mites are acquired during the first 2-3 days of life by direct contact with the dam, (2) animals delivered by cesarean section and raised away from other animals did not harbor demodectic mites, and (3) confining normal adult animals with severely infested and diseased animals for several months did not produce disease in the normal animals.⁵

In addition, attempts to transmit clinical demodicosis to horses by direct contact and by applying mites to the skin were unsuccessful.⁵ Thus, demodectic mange is not thought to be a contagious disease.

Because demodectic mites are normal residents of the skin, it is likely that animals manifesting clinical disease resulting from this parasite are, in some manner, immunocompromised. Demodicosis in dogs is known to occur due to immunosuppression (drugs or diseases) and genetic predilection (selective immunodeficiency?).⁵ In large animals, many authors have suggested that clinical demodicosis probably occurs only in animals that are immunocompromised (debilitation, concurrent disease, poor nutrition, or stress). In horses, demodicosis has been reported in association with chronic treatment with systemic glucocorticoids or pituitary pars intermedia dysfunction.^1,5

Clinical features

Equine demodectic mange is recognized worldwide but is very rare in occurrence and has no apparent age, breed, or sex predilections.⁵ The authors have rarely seen equine demodicosis and only in association with long-term glucocorticoid administration. Horses possess two species of demodicid mites: Demodex caballi (264-453 μm in length; eyelids and muzzle) and D. equi (179-236 μm in length; body) (Fig. 6-12). Clinical signs consist of usually asymptomatic hypotrichosis, alopecia, scaling, and occasionally crusting, especially over the face (Fig. 6-13), neck, shoulders (Fig. 6-14), and forelimbs. Papules and pustules may be seen.

Figure 6-12 Demodex equi mite (×400).

Figure 6-13 Demodectic mange. Patchy alopecia and scaling on the face.

Figure 6-14 Demodectic mange. Follicular hair loss on the lower chest wall.

Diagnosis

The differential diagnosis includes other follicular dermatoses: staphylococcal folliculitis, dermatophytosis, dermatophilosis, and sterile eosinophilic folliculitis. Definitive diagnosis is based on history, physical examination, skin scrapings, and skin biopsy. Alopecic, erythematous, and scaling areas of skin should be squeezed firmly and scraped deeply until blood is drawn.

The skin biopsy reveals hair follicles distended to varying degrees with demodectic mites and keratin.⁵ In many cases, there is minimal inflammatory response (Fig. 6-15). Alternatively, varying degrees of perifolliculitis, folliculitis, furunculosis, and foreign body granuloma formation may be seen.

Figure 6-15 Demodectic mange. Mites (arrows) visible in the follicular keratin in a horse receiving glucocorticoids.

Clinical management

Because demodectic mange (1) is usually asymptomatic, (2) may spontaneously regress, and (3) has been refractory to most therapeutic agents and regimens, treatment is not usually attempted.⁵ There is one report in which a horse received ivermectin for 15 days and was cured.⁵

Cause and pathogenesis

Trombiculid adults and nymphs are free-living and feed on invertebrate hosts or plants.⁵ Eggs are laid in the soil and hatch to larvae in approximately 1 week. The larvae normally feed on tissue fluids of small rodents, but are not host-specific and will attack horses and humans. Skin lesions produced by feeding larvae consist of papules and wheals. Because some animals manifest extreme pruritus, and other animals none, it is theorized that the pruritic animals may have developed a hypersensitivity reaction to larval salivary antigen(s).

Trombiculid larvae measure 0.2-0.4 mm in length and vary in color from red-to-orange-to-yellow. In North and South America, Trombicula (Eutrombicula) alfreddugesi (Fig. 6-16) and T. splendens are important trombiculids that inhabit forested and swampy areas. T. (Neotrombicula) autumnalis—the harvest mite, or heel bug, of Europe and Australia—inhabits chalky soils, grasslands, and cornfields. T. sarcina is the blacksoil itch, or leg itch, mite of Australia.

Figure 6-16 Trombicula (Eutrombicula) alfreddugesi (×100). Six-legged larva collect in a skin scraping.

Trombiculid larvae are usually active in summer and fall. After feeding (7-10 days), the larvae drop off the host to molt. The entire life-cycle typically takes 50-70 days.

Clinical features

Trombiculiasis generally occurs in the late summer and fall, when larvae are active.⁵ The infestation is seen primarily in pastured animals, horses in infested paddocks, or horses taken on trail rides through infested fields and woods. The larva may persist in hay or straw bailed in late summer and infest stalled horses that encounter it.¹³ There are no apparent age, breed, or sex predilections.

Skin lesions consist of papules and wheals at the site of larval attachment. Typical sites include the muzzle, nares, false nostril, face, ears, neck, and distal limbs (Fig. 6-17

Stay updated, free articles. Join our Telegram channel

Join