ETIOLOGY

Five species of flies of are known to parasitize domestic equids; Gasterophilus nasalis, G. intestinalis, G. haemorrhoidalis, G. pecorum, and G. inermis. Their larvae are the ‘stomach bots’ of horses, donkeys, and mules. Three species, G. intestinalis, G. nasalis, and G. haemorrhoidalis, are the most important and have a world wide distribution. The later larval stages inhabit the stomach and duodenum. These creamy pink larvae are thick, segmented, and about 5–15 mm long. The adult flies are golden brown, hairy, and about the size of a bee with two wings and vestigial mouth parts.

LIFE CYCLE AND EPIDEMIOLOGY

Flies do not feed and only live a few days.¹ They are active during the summer months and there may be overlap among the species in their periods of activity. In areas with mild winters the flies may be active throughout the year. In colder regions fly activity ceases with the first frost and there is usually only a single generation per year. In these regions the second and third instars remain in the stomach over the winter.

Eggs are attached to hairs while the fly hovers close to the horse. Fecundity is roughly correlated to the size of the fly. G. haemorrhoidalis matures about 50–200 eggs, G. nasalis 300–500 eggs, and G. intestinalis up to 1000.¹ Eggs of the various species are laid in specific locations and are attached in a specific manner, allowing identification of eggs to species. The eggs are laid on the horse’s coat except for G. pecorum which lays up to 2000 eggs in batches of 100–200 on pasture plants. The eggs of G. pecorum and G. haemorrhoidalis are dark brown; the eggs of the others are yellow and are readily visible glued to the hairs, usually one to a hair. The eggs of G. intestinalis, the most common fly, are laid on the front legs, particularly the lower parts; those of G. nasalis in the intermandibular area; the others species’ eggs are laid on the cheeks and lips.

The eggs are ready to hatch in about 2–10 days and the first instars enter the mouth either by host biting or licking or by subcutaneous migration from the cheeks into the oral cavity. The eggs of G. intestinalis and G. pecorum require a stimulus, provided by licking (moisture) or rubbing (friction), before they will hatch. The larvae penetrate oral mucosa, migrate to inner surfaces and emerge in the inter-dental spaces. The larvae of G. intestinalis penetrate the anterior end of the tongue and burrow in the buccal mucosa for about 3–4 weeks before invading pockets between the teeth or between the gum and molars.² G. nasalis may also accumulate in pockets alongside the molars and cause mouth irritation. G. haemorrhoidalis can penetrate the skin of the cheek and after wandering in the tissues of the mouth may attach in the pharynx. The second instar of G. intestinalis may also attach for a few days to the pharynx and the sides of the epiglottis before passing to the stomach. The first instars of G. pecorum burrow into the mucous membranes of the hard palate, cheek and tongue where they develop into second instars. They then move to the pharynx where they develop into the third instar.³ Occasional larvae migrate to abnormal sites including the brain, the cranial sinuses, the heart, and lungs.

Third instars of G. intestinalis are found attached to the mucosa, usually in bunches, at the junction of the glandular and non-glandular portion of the stomach, where they become attached to the mucosa. G. nasalis larvae are found in the pyloric region of the stomach and the duodenum. G. pecorum larvae may be found in the pharynx and upper part of the esophagus and in the fundus of the stomach. G. haemorrhoidalis larvae are found in the tongue, the pharynx, and the gastric fundus.

In the host, two molts are made and the larvae pass out in the droppings 10–12 months after infestation, usually in the spring and early summer. Some larvae may attach temporarily to the rectal mucosa on their way through. The larvae migrate into the ground, pupate, and adult flies emerge after 3–5 weeks to recommence the late summer attacks on horses.

PATHOGENESIS

The adult fly causes considerable annoyance when ovipositing. The droning noise and the sudden attacks to lay eggs causes head tossing and running in the host. G. nasalis is particularly troublesome as it darts at the lips and throat.

There is some doubt as to the importance of the lesions associated with the larvae. At the sites where they adhere there is an area of thickening and inflammation and in rare cases gastric perforation occurs. It is probable that there is some chronic gastritis and interference with digestion in most infestations. G. intestinalis, the most common species, attaches to the squamous epithelium and this has a relatively slight impact on digestion in the horse. However, the ulceration, edema, and abscessation associated with this species cannot be overlooked and one must expect some effect from such lesions although it is difficult, in practice, to separate these findings from those associated with a concurrent worm burden. Occasional perforation of the gut has been documented.⁴ The larvae do not remove sufficient blood to cause anemia, feeding mostly on tissue exudate. In rare cases pleurisy may occur following perforation of the esophagus close to the cardia.⁵ In very heavy infestations with G. pecorum the presence of large numbers of larvae (100–500) on the soft palate and base of the tongue can cause stomatitis and some deaths. Migration of first instars in the tongue and interdental gingiva and the aggregation of larvae in periodontal pockets may produce irritation or pain and may prevent foals eating.

CLINICAL FINDINGS

A non-specific syndrome of unthriftiness, poor coat, occasional mild colic, and lack of appetite, plus bad temper and unwillingness to work is usually ascribed to bot infestations. Adult flies frighten horses by their hovering, darting flight, especially around the head of the horse, and may be a cause of shying and balking.

CLINICAL PATHOLOGY

The eggs on the hairs can be seen by direct inspection but the presence of larvae in the stomach and intestines can only be detected after treatment with a suitable boticide.

NECROPSY FINDINGS

A few larvae are present in the stomach of most horses at necropsy but clinical illness is usually associated with very large numbers. The areas of larval attachment are pitted and the gastric wall thickened. There may be an adhesive peritonitis with attachment and abscessation of the spleen over such areas.

TREATMENT

Many of the organophosphates are effective. Trichlorfon 40 mg/kg is effective and is usually given with a benzimidazole to control strongyles as a common broad-spectrum mixture in the horse. It can also be used as a paste. Ivermectin 0.2 mg/kg has high efficacy against the oral and gastric Gasterophilus larvae⁷ as well as all gastrointestinal nematodes, including migrating and hypobiotic large strongyles, microfilaria of Onchocerca cervicalis and larval stages of Habronema spp. and Draschia megastoma in the skin. Ivermectin has gained high acceptance in horse practice. Moxidectin 2% oral gel has been shown to have excellent efficacy.^6,8

CONTROL

Treatment should preferably be administered after fly activity has ceased and the larvae have reached the stomach but before gastric damage has occurred. In most districts two doses should be given in winter, or in late winter and early spring. In foals showing pain on mastication, treatment with ivermectin paste or dichlorvos should be given as needed throughout the fly season.

The use of repellents or agents to kill the larvae in manure has not been successful, nor has bathing the affected hairs to encourage mass hatching and death of the larvae. The use of fringes, veils and tassels on the head harness helps protect horses against fly worry but is of little use in preventing bot infestation.

ETIOLOGY

A single species, known as the sheep nose bot, affects sheep and goats in most regions, but is particluarly significant in the Mediteranean basin, central America southern Africa, and eastern Europe. The larvae inhabit the nasal passages and sinuses, eventually being expelled through the nares. Goats are less dramatically affected than sheep. The slightly dorso-ventrally flattened, segmented larvae are light cream in color, but as they reach maturity dark bands appear on each segment.

LIFE CYCLE AND EPIDEMIOLOGY

The adult fly is stout, mottled gray in color, and about 1 cm long. Its mouthparts are rudimentary and it does not feed. In North America, flies emerge in the late spring, mate, and the females begin larviposition activities approximately 2–3 weeks later.¹ Adult flies attempting to deposit larvae on the nares annoy the sheep and cause them to bunch or seek shelter. Stamping of the feet and shaking of the head are common. Sheep may bunch together and press their heads into the fleece of others. Fly activity occurs primarily during the warmer parts of the day, but still may result in the loss of a good deal of grazing time. Behavioral changes in goats are less dramatic,² presumably because of their browsing habit.²

Larval development takes place within the dorsal turbinates and frontal sinuses. The period of development can vary from 3 weeks to several months after which they migrate to the nostrils. Larvae feed on the mucosal secretions and cells eroded from the mucosal epithelium. The larvae are thick, yellow-white in color and when mature there is a dark dorsal band on each segment. The ventral surface has rows of small spines on each segment. Mature larvae exit the host, usually during a bout of sneezing, and actively burrow beneath the upper layers of soil and ground litter. Pupation occurs at these locations and development of the adults requires 4–5 weeks, but may take longer at low temperatures.³ In temperate areas there may be one or two generations per year but several generations may be completed in hot areas. O. ovis are adapted to the various climates prevailing wherever sheep and goats are kept. When winters are cold, the larvae can overwinter by remaining dormant in the first instar (hypobiosis), but in warmer climates development may continue throughout the winter. In those regions where summer temperatures are extreme the larvae will also undergo hyopobiosis.

O. ovis are an important zoonosis as the females may larviposit in the eye, nose or on the lips of humans. In some countries ophthalmomyiasis or infection of the upper respiratory tract is a common occurrence.

PATHOGENESIS

The stress of the larviposition attacks can be significant with reduced grazing time and over-heating resulting from bunching. Herdsmen find the animals are more nervous and difficult during the fly activity periods.

Larvae induce a gradually increasing rhinitis and sinusitis as the infestation persists. Marked changes in the structure of the epithelial tissues are noted with a marked cellular degeneration and a loss of the ciliary layer. The changes are a result of both mechanical activity of the larval spines and mouthhooks as well as the effect of proteolytic enzymes excreted or secreted.⁴ Varying degrees of mucous discharge are observed in the later stages of the infestation. This can lead to the nostrils being occluded by adherent straw and dust.

CLINICAL FINDINGS

Early in the infestation there is a distinct rhinitis accompanied by a muco- to muco-purulent discharge. Later as larvae mature, a sinusitis is evident. Presence of mature larvae in nasal cavities may induce excessive sneezing which assists larval exit.

Activity of the larvae in the nasal cavities and the changes they induce lead to an increased incidence of secondary pathology. The number and severity of lung abscess are more significant in nose bot infested sheep.⁵ The presence of bots also is correlated with increased carcinomas⁶ and may lead to reactivation of latent ‘orf’ symptoms.

TREATMENT

Closantel 7.5 mg/kg⁸ and ivermectin 0.2 mg/kg⁹ as well as other macrocyclic lactones^10,11 are effective and the use of these compounds for fluke or worm control also controls nasal bots.

CONTROL

Treatment should preferably be applied after the cessation of fly activity, although it may be necessary to apply treatments during prolonged fly activity in order to give relief.

ETIOLOGY

There are two species which specifically parasitize cattle: Hypoderma bovis and H. lineatum. A third species, H. sinense, affects cattle and yaks in central Asia.¹ The adult flies are robust and hairy, about the size of a bee (12–18 mm long), are yellow-orange in color and have two wings. They are not easily seen because of the rapidity of their flight. Repeated infestation results in an acquired immunity that results in older animals being less severely affected than younger animals.

Horses are occasionally infected with Hypoderma species of cattle. The larvae are found in subcutaneous cysts on the back, but have not been reported to complete development. This location causes problems if they are in the saddle region.

Losses to the cattle industry associated with warble fly have not been estimated recently, but in 1965 the loss was estimated to be US$192 million per annum in the United States, and in 1976 approximately CAN$100 million in Canada. In 1982 the cost of warble fly was estimated as £35 million for Great Britain, but the parasite has now been eradicated from the UK and Ireland. Advent of the macrocyclic lactone endectocides have greatly reduced the prevalence of the cattle species in North America, but they persist in localized areas.²

Hypoderma tarandi, H. acteon, and H. diana infect reindeer/caribou and deer respectively. H. diana is found throughout Europe in several deer species but may also occur in sheep. H. actaeon, also found throughout Europe, is known only from the red deer. These species do not undergo deep tissue migrations that characterize the lifecycle of the cattle species.

Przhevalskiana silenus is similar to the above and parasitizes goats in the Mediterranean basin, parts of eastern Europe as well as in Pakistan and India. This species also does not have a deep tissue migration and larvae tend to develop subcutaneously very near the site of initial skin penetration. The losses resulting from this parasite are significant and result from reductions in carcass quality and reduced animal health.

The larvae of Dermatobia hominis, a small (12 mm long) related fly, parasitize a wide variety of hosts and cause major economic losses to cattle production in South America. They also affect man and are a major zoonosis for travelers in the region. Mature larvae are about 2.5 cm long and develop in a subcutaneous cyst that can be quite painful. Female Dermatobia oviposit on zoophilous, ‘porter’ flies such as mosquitoes and stable flies which they catch ‘on the wing’. The eggs are transported to mammalian hosts where they hatch in response to increased temperature as the fly lands. Larvae penetrate the skin, but do not migrate. Treatment and control measures are the same as for H. bovis.

LIFE CYCLE AND EPIDEMIOLOGY

Warble flies are common parasites of cattle in the northern hemisphere, including North America, Europe, and Asia. Precise distribution of these parasites have been changing recently with the widespread use of macrocyclic lactone endectocides and the adoption of eradication programs in many European countries. Infestations south of the equator are rare and are the result of imported cattle, although endemic cases have occurred in Chile.

Adult flies are active in the spring to late summer, H. lineatum usually appearing 3–4 weeks before H. bovis. H. lineatum attaches up 600 eggs, in strings of 5–25, to hairs on the legs or lower parts of the body while H. bovis attaches eggs, one at a time, to hairs on the rump and upper parts of the hindleg. The oviposition flight of H. bovis, darting in to lay each egg, will terrorize cattle. Eggs hatch in 4–6 days. The larvae penetrate the skin using protease enzymes and migrate through connective tissues to reach the esophagus (H. lineatum) or the epidural fat in the spine (H. bovis) where they stay, feeding and growing, for 2–4 months. They subsequently continue their migration to reach the subdermal tissue of the back in the early spring. Here they make a breathing hole and become encased in a granulomatous cyst. They complete development in 1–2 months, passing through second and third instars and emerge through the hole, fall to the ground and pupate. Adult flies emerge some 3–5 weeks later. The fully developed larvae are thick and long (25–30 mm), light cream in color, but darkening to almost black as mature third instars. A single animal may have up to 300 larvae each developing with granulomatous cysts, with breathing holes, under the skin of the back.

The timing of the life cycle, i.e. the period when grubs are present in the animals and the time at which the flies are present in large numbers, varies with the climate and is of importance in a control program. H. lineatum generally is 1–2 months ahead of H. bovis and where the two flies are present both ‘grub’ and ‘fly’ seasons may be very long. In the southern United States the ‘fly season’ is February and March; in Canada it is June to August. The period when grubs are present in the back is December in the south and February to May in Canada. In Europe the larvae begin to move to the back in January to July.

PATHOGENESIS

Migrating first instars cause little damage as they use their proteolytic enzymes to migrate through connective tissue. The enzymes, however, have an anti-inflammatory effect, partially through cleavage of complement components.³ Larvae maturing under the skin of the back form holes in the skin and the reaction of the host encloses each grub within a granulomatous cyst. On rare occasions an anaphylactic reaction may occur in a sensitized animal as the result of death of migrating larvae; chance migration into the brain may also occur. Intracranial myiasis due to H. bovis has also been recorded in the horse. Treatment of animals when the first instars are in the esophagus may cause a massive inflammatory edema which may prevent feeding and swallowing of saliva; eructation may stop and bloating may occur. Treatment of H. bovis while it is in the spinal canal may also cause edema and mild to severe paraplegia.

CLINICAL FINDINGS

If the fly population is heavy, cattle at pasture may be worried by their attacks which disrupt grazing and breeding behavior. Avoidance behavior, called gadding, may result in injury as cattle run into fences and other natural obstructions. Heavy infestations with larvae are commonly associated with poor growth, condition and production but such heavy infestations are often complicated by other forms of mismanagement including malnutrition and parasitic gastroenteritis. Immunosuppression results from the effect of larval secretions. Infected cattle milk poorly and a considerable increase in milk production and milk fat occurs after treatment.

The presence of the subcutaneous larvae causes obvious swelling with pain on touch. The swellings are usually soft and fluctuating. There may be as many as 200–300 such lesions on the back of one animal.

With involvement of the spinal cord there is a sudden onset of posterior paralysis without fever and without other systemic signs. The suddenness of onset and the failure of the disease to progress usually suggest traumatic injury. A similar disease can occur in horses and is reputed to be more common in horses than in cattle.

CLINICAL PATHOLOGY

An ELISA which detects antibodies to the secreted enzymes of H. lineatum and H. bovis has been developed. It has been used in the eradication program in Great Britain⁴ and in France.⁵ In addition, an antigen capture ELISA, used to detect the presence of circulating quantities of the predominant larval enzyme has been developed.⁶ This will be useful in differentiating active from cleared infestations and will be useful in detailed surveillance programs.

NECROPSY FINDINGS

The first instars, migrating within connective tissue, are usually surrounded by a zone of yellow-green discoloration. Later larval stages lie in a subcutaneous, granulomatous cyst which may contain a pale fluid. Rarely the cyst will contain a large amount of purulent discharge.

TREATMENT

CONTROL

While rotenone has been used successfully to kill the larvae in the subcutaneous tissues in the back, this technique does not prevent damage to the hide and has been largely superseded by the use of organophosphate insecticides and the macrocyclic lactone endectocides. In general, systemic treatments are given in the autumn (between September 15 and November 30) and in the spring after March 1.

Warble fly has been eradicated in Norway, Sweden, Denmark, Malta, Ireland, and Great Britain. Eradication programs have commenced in France. A joint Canadian–US study using sterile male Hypoderma species eradicated these species from the test area, but the difficulty of mass producing flies, in the absence of an in vitro rearing system, makes this technique impractical for large scale warble fly control.⁷

Vaccination of cattle using crude larval extracts has reduced both the number of warbles in the back and the number of larvae that could pupate.⁸ Results of vaccination studies with recombinant antigens have been variable,⁹ but show promise although there has been no commercial development.

ETIOLOGY

Despite there being a large number of species capable of causing the disease, grouped geographically below, there are two species that are the primary agents of blow fly strike: Lucilia cuprina and L. sericata.

LIFE CYCLE AND EPIDEMIOLOGY

The primary agents of fly strike are obligate parasites. Lucilia cuprina is overwhelmingly important in the initiation of strike in sheep from Australia, and South Africa. L. cuprina was introduced to New Zealand in 1988 and fly strike is now a major disease in that country. In northern Europe the primary agent of fly strike is Lucilia sericata although there are some other minor species that have been reared from struck sheep.¹

In sheep, the incidence varies widely depending largely on the climate, warm humid weather being most conducive to a high incidence. In summer rainfall areas fly strike may be seen most of the year, being limited only by dry winter conditions; while in winter rainfall areas it is usually too cold in the winter and too dry in the summer for outbreaks to occur. Under these conditions abnormally heavy summer or autumn rains may be necessary before an outbreak will occur.

PATHOGENESIS

The first instars feed on the exudate produced by the bacterial infection on the skin, but the larvae also produce excretory/secretory enzymes which may cause some skin degradation after egg hatch and provide soluble molecules on which the first instars can feed.^7,8 Later instars can cause severe skin damage to provide themselves with food. Larvae may also migrate from the original area of strike, along the surface of skin to establish additional focal lesions.

Many primary strikes remain small and are unnoticed by the farmer.⁶ Such covert strikes may outnumber overt strikes and are important as a source of future generations of flies. Once the initial strike is made, the site becomes suitable for the secondary flies that now invade and extend the lesion. The effects of strike include toxemia due to absorption of toxic products of tissue decomposition, loss of skin and subsequent fluid loss, and secondary bacterial invasion.

CLINICAL FINDINGS

Individual sheep may be ‘struck’ at any time provided they are in a susceptible condition. Massive outbreaks tend to be confined to periods of humid, warm weather and are therefore in temperate areas usually limited in length to relatively short periods of 2–3 weeks, but in sub-tropical areas characterized by summer rainfall severe strikes may occur over many months.

The clinical effects of ‘blowfly’ strike vary with the site affected but all struck sheep have a basic pattern of behavior caused by the irritation of the larvae. The sheep are restless, moving about from place to place with their heads held close to the ground and they become anorexic. They tend to bite or kick at the ‘struck’ area and continually wriggle their tails.

If the area is large there is an obvious odor and the wool can be seen to be slightly lifted above normal surrounding wool. The affected wool is moist and usually brown in color although in wet seasons when fleece rot is prevalent other colors may be evident. In very early cases the maggots may still be in pockets in the wool and not yet in contact with the skin. When they have reached the skin it is inflamed and then ulcerated and the maggots begin burrowing into the subcutaneous tissue.

Three days after the primary oviposition feed intake is reduced, rectal temperature rises to about 42°C (108°F) and pulse and respiratory rates increase. Some sheep may die. The wool may be too hot to handle as a result of the inflammation caused by the mass of maggots that can be seen when the wool over the strike is opened. When primary strikes are invaded by secondary flies, particularly Ch. rufifacies, the affected area is extended and the maggots may burrow deeply into the tissues. Affected sheep may lose their fleece over the affected area and may suffer a break in the remaining fleece. Tracts of discolored wool may lead to other affected areas of skin. As the struck area extends a scab forms over the center, the wool falls out and the maggots are active only at the periphery.

CLINICAL PATHOLOGY AND NECROPSY FINDINGS

A clinical examination is all that is necessary to make the diagnosis but identification of the flies responsible may be important if epidemiology is being considered. Identification of larvae should be carried out by a specialist. Molecular techniques for accurate identification are available from specialists.⁹ Preservation of the larval stages is critical to these techniques and larvae should be rapidly frozen or preserved in 70% ethanol. Fly trapping may not correlate with larval findings as not all flies are equally attracted by commonly used baits.

TREATMENT

A local dressing containing a larvicide and an antiseptic is applied. The prevention of reinfestations is also an important aim and as repellents have been largely unsatisfactory, it has become apparent that the larvicide in a suitable dressing must be one with maximum retention in the treated area. Modern dressings usually contain organophosphate insecticides but most products do not kill all the organophosphate resistant larvae and some perform poorly even against susceptible larvae. Variations in effectiveness with the same compound sold by different companies is probably related to formulation.¹⁰ Ivermectin at 0.03 mg/kg applied by hand jetting is highly effective in killing all larval stages.¹¹ Powder and liquid dressings containing diazinon, tetrachlorfenvinphos, propetamphos, and ivermectin are most generally favored.

Cyromazine, an insect growth regulator, is now widely used. It is particularly active against second and third instars, but is slow-acting and so live larvae may be seen in the fleece for some days after treatment.

CONTROL

Practical control of crutch strike in extensive farming areas depends on the use of the Mules operation to extend the bare areas around the perineum and tail, good worm control to prevent contamination of the perineal region, correct tail length and a midseason crutching. Control of strike in other situations is based on insecticidal treatment and treatment of wounds as they occur. Under conditions of extensive sheep raising, such as occur in Australia and South Africa and where climatic conditions are conducive to the development of the disease, the control of blow fly strike is a major undertaking and an extensive bibliography on the subject is available. Only a summary can be presented here.

The subject can be divided into three phases: reduction in fly numbers; prediction of fly waves followed by prophylactic crutching and application of larvicides; and reduction in susceptibility of sheep.

ETIOLOGY

Larvae of the flies Cochliomyia hominivorax and Chrysomyia bezziana cause myiasis or ‘screwworm disease’ of animals. The flies are typical blow flies, C. hominivorax (New World Screwworm) being blue-green with an orange head; Ch. bezziana (Old World Screwworm) is of similar coloring. C. hominivorax occurs in the Americas, Ch. bezziana in the Persian Gulf, Africa, and Asia. The occurrence of Ch. bezziana in Papua New Guinea provides a constant threat to livestock on the Australian mainland. A similar fly is Callitroga (Cochliomyia) macellaria which is not a true ‘screw-fly’ in that the larvae feed only on carrion or necrotic tissues.

EPIDEMIOLOGY

The screwworm maggots are obligatory parasites with no host-specificity. Thus, all domestic and wild, mammals, marsupials, and birds are potential hosts. Females are attracted to fresh wounds where they will oviposit. The navel of a newborn animal is a favored site, but fresh accidental or surgical wounds, such as those produced by castration, docking, and dehorning, are readily infested. Wounds which have already been infested are markedly attractive to the flies because of their odor. In bad seasons the flies will lay eggs on minor wounds such as areas of excoriation, tick bites, running eyes, peeling brands, and on the perineum soiled by vaginal and uterine discharges in animals which have recently given birth. Injury is not necessarily a prerequisite for screwworm strike in sheep, which can be struck in the intact infraorbital fossa and vulva. Wool loss and tenderness may occur and the remaining fleece may be stained.

The development of the fly is favored by hot, humid weather. The optimum temperature range for C. bezziana is 20–30°C (68–86°F). Below this the flies become sluggish and at 10°C (50°F) and below the flies will not move. Temperatures above 30°C (86°F) can be tolerated provided shade is available. C. hominovorax is active all year in areas where temperatures exceed 16°C and disperses rapidly from these areas as the temperature increases in the neighboring colder areas. The disease can be spread either by migration of flies or their carriage in livestock ships or commercial aircraft,¹ by shipment of infested cattle or other livestock, and by movement of affected wildlife. The mean distance that C. bezziana can travel and deposit eggs is 11 km. The maximum distance is 100 km, but long distances are probably wind assisted. In the new environment the flies may die out if the climate is unsuitable or persist to set up a new enzootic area. Persistence of the fly in an area may depend upon persistence in wildlife or in neglected domestic animals, although the latter do not usually survive unattended for more than about 2 weeks.

In many enzootic areas it is common for the fly to persist in neighboring warmer areas during winter, returning to its normal summer habitat as the temperature rises. This pattern is exemplified by the introduction of screwworms into the southeastern United States in 1933 where they had not previously occurred. The flies died out in most areas in winter but persisted in southern Florida. In succeeding summers migrations of flies northwards caused outbreaks. The disease has since been eradicated from the area.

The disease is of importance in tropical and subtropical areas of Africa, Asia, North and South America, especially Central America, the Caribbean islands, Mexico, and American states bordering on Mexico. The prevalence of the fly in enzootic areas places severe restriction on the times when prophylactic surgical operations can be carried out.

The potential worldwide geographical distribution and abundance of Ch. bezziana has been assessed using a computer program. The differences in the observed global distribution and the potential predicted distribution indicate the areas at risk of colonization.²

LIFE CYCLE

The screwworm flies have a typical fly lifecycle with eggs, three larval instars, and a pupal stage. Females lay 150–500 white eggs in shingle-like clusters at the edges of fresh wounds. Larvae hatch in about 12 hours and penetrate the tissues surrounding the wound. The larvae preferentially feed on fresh, living tissue which is digested by regurgitation of a wide variety of salivary enzymes. Oviposition by other screwworm flies is encouraged by the presence of larvae already in the wound. The larvae feed as a group and at their time of maturation will have created a deep lesion 10–12 cm in diameter. Larval development is complete in 5–7 days, after which they leave the wound and fall to the ground. These mature third instars burrow into the upper soil layers and pupate. On the ground, pupal development is highly temperature dependent requiring from 3–60 days. Emerging flies commence egg-laying in about 1 week, having completed the life cycle, under optimum environmental conditions, in less than 3 weeks. There may be 15 or more generations per year.

The temperature sensitivity of the pupal stage, which is unable to survive freezing for more than short periods, limits the distribution of this parasite. As with all flies pupal development is highly temperature regulated. The screwworm pupal development is inhibited at soil temperatures below 15°C (60°F). Temperatures below this point for more than 2 months cause death of the pupa. Thus the occurrence of the disease is limited to warm climates. Pupae are also affected by the moisture content of the soil. The emergence of adults is reduced when the moisture content is more than 50%, while temporary floods can drown pupae.

PATHOGENESIS

Following invasion of the wound a cavernous lesion is formed, characterized by progressive liquefaction, necrosis and hemorrhage. Anemia and decreased total serum protein results from hemorrhage into the wound. Secondary bacterial infection, toxemia, and fluid loss contribute to the death of the animal. Surviving calves frequently develop infectious polyarthritis.

CLINICAL FINDINGS

The young larvae invade the nearby healthy tissues vigorously and do not feed on necrotic superficial tissue. A profuse brownish exudate, composed of larval excreta, and host fluids, pours from the wound and an objectionable odor is apparent. This is highly attractive to other flies and multiple infestations of a single wound may occur within a few days. The resulting tissue damage may be so extensive that the animal is virtually eaten alive. Affected animals show irritation in the early phase of the infestation and by day 3 show pyrexia. Animals do not feed but wander about restlessly, seeking shade and shelter.

CLINICAL PATHOLOGY

It is imperative to differentiate screwworm infestation from infestation with other fly larvae. The appearance and smell of the wound are significant but careful examination of the larvae is necessary to confirm the diagnosis. Mature larvae are 1–2 cm long and pink in color; they are pointed anteriorly and blunt posteriorly; two dark lines are visible reaching from the blunt posterior to the middle of the body and they have rows of dark fine spines on the anterior part of each segment. Specimens forwarded to a laboratory for identification should be preserved in 70% alcohol.

NECROPSY FINDINGS

Superficial examination of infested wounds is usually sufficient to indicate the cause of death.

TREATMENT

Affected wounds should be treated with a dressing containing an efficient larvicide and preferably an antiseptic. The larvicide should be capable of persisting in the wound for some time to prevent reinfestation. A number of proprietary preparations and some of the newer insecticides have been compared.³ Lindane 3% and coumaphos 3% were the most effective but fenchlorphos 2.5%, diazinon 1.5%, chlorfenvinphos 0.05% and fenthion-methyl 0.2% were also very efficient. Stirofos (15%) and dichlorvos (20%) give season-long protection in the ears of cattle against C. hominivorax and Amblyomma maculatum.⁴ An ointment or gel base is preferred so that as much of the active ingredient as possible is left in the site. It should be liberally and vigorously applied with a paint brush to insure that larvae in the depths of the wound are destroyed. To avoid reinfestation in extensive lesions or in bad seasons the treatment should be repeated twice weekly.

When large numbers of animals are affected and individual treatment is impractical, spraying with a 0.25% solution of coumaphos, chlorfenvinphos, or fenchlorphos, using a power sprayer, is recommended. The spray is directed forcibly into wounds and, except for young calves, applied generally over the body to provide protection for about 2 weeks. Young calves may show signs of toxicity if sprayed too liberally and application should be restricted to the belly. These sprays can be used to protect animals which are not infested but are exposed to considerable risk or are to be shipped to free areas. In the latter situation dusts are also available if spraying is undesirable in cold weather. A pyrophyllite dust containing 5% coumaphos and 2% mineral oil is effective as a protectant if applied at the rate of 60–180 g per animal. Residual protection lasts for 3–7 days.

Thirteen acaricides, commonly used for Boophilus microplus control, have been tested against Ch. bezziana larvae. While they are not sufficiently active to use as a primary treatment, their continued use for tick control would reduce screwworm populations.

Ivermectin 200 mg/kg given subcutaneously kills all Ch. bezziana larvae up to 2 days old and many older larvae. It provides residual protection for 16–20 days. Bull calves treated with ivermectin at the time of castration were completely protected against strike.⁵ A preliminary study showed that closantel at 15 mg/kg body weight was effective with a residual protection of 8–15 days.⁶ Doramectin 200 mg/kg subcutaneously caused complete expulsion of C. hominovorax larvae within 8 days.⁷ Prophylactic use of ivermectin and doramectin significantly reduced occurrence of screwworm strike in cattle.⁸ Fipronil had a prophylactic effect, reducing occurrence of screwworm infestations in cattle and providing efficacious treatment in those that did become infested.⁹

CONTROL

The eradication of screwworm by genetic means, chemical control, trapping techniques and lures, and dispersal of flies has been reviewed.¹⁰ In an enzootic area the incidence of the disease can be kept at a low level by the general institution of measures designed to break the life cycle of the fly. Surgical procedures should be postponed where possible until cold weather. In the warm months all wounds including shearing cuts must be immediately dressed with one of the preparations described under treatment. All range animals should be inspected twice weekly and affected animals treated promptly. Infestation of fresh navels is common and newborn animals should be treated prophylactically. If possible the breeding program should be arranged so that parturition occurs in the cool months. The routine use of ivermectin for internal parasite control provides protection for about 2 weeks.⁵

In the United States, the Caribbean, and central America an eradication program has been successfully carried out against C. hominivorax using the sterile insect technique (SIT). Huge numbers of pupae are mass reared on semi-artificial media and exposed to the sterilizing effects of cobalt 60. The resulting sterile male flies are released over large areas, primarily by aerially drops, where they compete with wild males for available females which mate only once. C. hominivorax has now been eliminated from the United States, the Caribbean, and all of Central America, up to the Darien Gap in Panama.¹¹ C. hominivorax appeared in Libya in 1988, apparently with a load of sheep transported from South America, but has been eradicated using sterile male flies from the USA.¹²

Attractants may also be used to reduce the fly population. A chemical bait has been developed, and when combined with an insecticide forms a screwworm adult suppression system (SWASS) which reduces the fly population and the incidence of strikes. An examination of the efficacy of various methods of baiting showed that polythene sachets containing sworm-lure 2, a pungent mixture of 11 chemicals, attracted flies (not C. bezziana) for at least 2 weeks and was as efficient as jar baits.¹³ This result needs confirming in a screwworm endemic country.

LIFE CYCLE AND EPIDEMIOLOGY

Larvae of this species are obligatory parasites developing only in the living flesh of warm-blooded vertebrates. They are not host specific. Adults are typical for this group of flies, being dark gray in color with three distinct black stripes on the thorax where the wings are attached.

Female flesh flies, which are active during the warm parts of the day, deposit first instar larvae on the host, usually in small groups of 15–20. Each female may produce up to 170 larvae. Completion of the three larval stages takes from 5 to 7 days after which the mature third instars leave the lesion and fall to the ground where they pupate. Development of the fly within the pupa is regulated by temperature and may require between 7 and 21 days.

Larvae are usually deposited near small wounds (bites of blood-feeding arthropods are sufficient to attract the larvae), but the favored sites appear to be the genitalia.³ Irritation of the vulva associated with the use of vaginal sponges for estrus synchronization may be a predisposing factor in sheep.

Flies are active between April and October with several generations being produced. Little information is available on overwintering. Wildlife are suspected as being reservoir hosts, but little information is available on which are the most important.

PATHOGENESIS

Larvae have well developed mouthhooks which are used to abrade the skin surface and with the aid of a wide variety of salivary enzymes they quickly produce a dramatic lesion. Lesions increase in size as the larvae grow and require additional fresh tissue. Each animal may have one or more focal lesions, each packed with larvae. In severe cases several lesions may coalesce into one larger site.

Animals are often struck multiple times during a season, suggesting the absence of protective immunity. This adds to the impact of this disease as animals must be constantly monitored.

CLINICAL PATHOLOGY AND NECROPSY FINDINGS

A clinical examination is all that is necessary to make the diagnosis. Larvae can be distinguished from those of the screwworm or the strike flies by the presence of a large posterior cavity surrounded by a number of prominent tubercles. However, specific identification should be done by a specialist. Larvae should be preserved in 70% ethanol.

Affected animals are clearly stressed, showing restlessness and anorexia.³ Lesions formed at the vulva or prepuce are the most significant causing great discomfort and dysfunction. Lightly infested animals shown no impairment of productivity.³ Infested animals develop strong antibody responses to salivary secretions, particularly of the third instars.⁴

TREATMENT

There are currently no products specifically registered for management of this disease. Evaluations of several drugs and treatment approaches have been made. Of particular interest is the equivocal results of trials with macrocyclic lactones. In sheep, ivermectin and moxidectin had no effect on existing infestations and no prophylactic effect⁵ or only short protection against early instars.⁶ In contrast, doramectin provided complete prophylactic protection for 21 days and significant reductions for 40 days.⁷ The pyrethroid, cypermethrin, was less effective.⁷

The insect growth regulator dicyclanil has also been evaluated and shown to reduce prevalence of infestation in sheep.³ The reduction not only occurred in treated animals, but was seen in untreated herdmates possibly as a result of the overall reduction in fly numbers.

LIFE CYCLE

Keds live their entire life cycle on the host. Adults of both sexes are blood feeders and although the degrees of infestation usually encountered cause only irritation with resulting scratching, biting, and damage to the fleece, very heavy infestations may cause severe anemia. Spread is generally the result of direct contact between hosts. A recent review² suggests this exchange is primarily between dams and their offspring and that it is predominantly the newly emerged adults that migrate to new hosts. Larvae develop within the female one at a time and are deposited on the host as mature third instars which pupate within a few hours. The female ked lives for 4–5 months and may lay up to 10–15 larvae, so build-up of infection is slow. The larvae are attached to the wool fiber some distance above the skin and many larvae and pupae are removed at shearing. The young ked usually emerges in 20–22 days but this period may be prolonged for up to 35 days in winter. The complete life cycle takes 5–6 weeks under optimal conditions. Heavy infestations usually occur in winter months and they decline in the summer. The parasite is mainly seen in colder, wetter areas and infestations may be lost when sheep are moved to hot dry districts. Resistance is acquired in time and resistant sheep grow better and produce more wool.

A seasonal pattern of infestation occurs. Keds are sensitive to hot, dry weather and numbers decrease markedly over the summer. Populations increase slowly over the autumn and winter. While keds that have been dislodged from the host can live for up to 2 weeks if in mild moist conditions, most die in 3–4 days and probably do not play a part in reinfesting sheep.

CONTROL

At shearing a large proportion of adults and pupae will be removed. This can provide effective control on adult sheep particularly where a combination of hot conditions and a short fleece will kill most of the remaining keds. However, some may remain alive in protected places such as the ventral neck and breech regions and on younger stock. If treatment is carried out within the next 2–4 weeks eradication will be achieved as long as all sheep are included and the insecticide used has a residual protection longer than the time taken for the last pupae to hatch.

Keds are particularly susceptible to organophosphates and most of those used to eliminate lice will also remove keds. They can also be used in higher dose rates in pour-on applications. Diazinon used as a pour-on removed all keds and prevented re-establishment for 9 weeks.³ The synthetic pyrethroids are also active against keds; deltamethrin, cyhalothrin and cypermethrin are used. Cyfluthrin 2 mg/kg pour-on in sheep also eradicates ked and protects for 50 days. Amitraz will kill adult keds but has little residual action and is therefore usually combined with another compound to provide sufficient residual action to eliminate infections. Ivermectin given at the standard anthelmintic dose will also eliminate keds. Closantel which is mainly used against Haemonchus or Fasciola is effective against keds.

ETIOLOGY

The important species are:

LIFE CYCLE AND EPIDEMIOLOGY

CLINICAL FINDINGS AND DIAGNOSIS

TREATMENT AND CONTROL

Self-grooming and grooming by headmates effectively regulates louse populations on most hosts, but the effectiveness is limited when hair coat or fleece become too long for the tongue surface to effectively remove the lice and eggs. Similarly, shearing is an important factor in reducing body lice populations on sheep. Between 30 and 50% of the population is removed with the fleece and those remaining are subjected to a more variable microclimate. Populations are at their lowest 30–60 days after shearing. Reversing temperature gradients as sheep move in and out of shade, and very wet conditions, will also reduce lice numbers.

Body lice of sheep are relatively easy to eradicate if a clean muster is achieved, if the sheep are thoroughly treated and reinfestation is avoided. However, in practice, failure to eradicate commonly occurs due to the inability to thoroughly wet the fleece because of poor maintenance of dips or poor formulation of products, or because the lice are resistant to the chemical used. The most difficult problem when attempting to eradicate lice from flocks over a large area is the diagnosis of lice in lightly infested flocks. Dipping clean sheep is wasteful but if lightly infested flocks are not dipped the infestation will build up and may cause serious economic loss in the next year. Techniques have been devised to test for lice by digesting the wool and examining the residue for lice, but the delays inherent in such a system often mean that by the time the farmer obtains the results, the optimum time to treat sheep has passed. On-farm tests have been examined but none are yet sufficiently accurate.¹¹

Affected sheep can be effectively treated in a plunge or shower dip with organophosphate insecticides (diazinon, coumaphos, chlorfenvinphos, carbophenothion, propetamphos), synthetic pyrethroids, or carbamates. The synthetic pyrethroids, cypermethrin and cyhalothrin, have been shown to be effective in sheep and give good residual protection. Products formulated as emulsifiable concentrates wet the fleece better and give better results than wettable powders.¹² Cypermethrin, alphamethrin, and deltamethrin are marketed as pour-ons for sheep and goats. They must be used immediately after shearing. A small proportion of sheep show irritation after application and some may show fleece damage. Further, most of the chemical that is applied remains in the tip of the fleece and grows out with the wool and so is not in contact with the lice.¹³

The spread of synthetic pyrethroid following backline treatment of sheep is slower than in cattle and horses and takes some days to reach maximum concentrations along the midside. However, the ease of application, low capital outlay required, and the need for only one muster has led to rapid acceptance of backline treatments. It is important that the pour-on is applied along the spine from the poll to the tail. Failures to eradicate occur if the sheep are not cleanly shorn, and in large-bodied sheep with extensive neck folds which are difficult to shear cleanly. The presence of unshorn lambs, cotted or Dermatophilus-affected fleeces, wrinkly sheep or inexpert shearers make backline pour-on application an inappropriate method. Heavy rain following application may also cause failure. Some lice remain alive for up to 6 weeks after backline treatment and so sheep are infective for this time. Jetting races have been used to treat sheep because of their ease of use and the speed with which sheep can be treated. However none of the machines marketed in Australia is able to eradicate lice even from sheep with short wool.¹⁴

The manufacturer’s recommendations should be accurately followed, particularly when using shower dips. The most common cause of failure when using shower dips is poor maintenance of the pump so that insufficient volume of dip wash is applied from the overhead sprays. Blocked jets, incorrect speed of rotation of the top spray and leaving sheep in the shower for insufficient time are also common faults.

Infested long-woolled sheep can be jetted to reduce the population until the sheep can be shorn and dipped. Treatment of sheep in long wool leads to residue problems in the wool presented for sale. Every effort should be made to treat sheep properly in the first 2 weeks after shearing to insure eradication of lice and to present wool without insecticidal residues. Cyhalothrin has been shown to eradicate body lice from long-woolled sheep when applied by jetting at 20 ppm, but in field use eradication is rarely achieved. Phoxim 125 mg/L has also been reported to eliminate lice in long-woolled sheep, while 250 mg/L gave at least 4 months of protection against reinfestation. An ivermectin 0.03% jetting fluid was reported to have high efficacy in treating lice in sheep with 3–9 months wool, but failed to eradicate. High concentrations of cyhalothrin (1500 ppm) and diazinon (36000 ppm) in 100 mL applied to sheep has also proved effective but requires a practical method of application. No treatment is known that can eradicate lice from long-woolled sheep under field conditions. Following treatment of foot lice, sheep should be moved to a paddock that has been free of sheep for a month.

Treatment of goats has not been studied extensively and the treatments used on sheep and cattle are thought to be effective in goats. Lactating goats should not be treated.

Organophosphates (e.g. fenthion, famphur, chlorpyrifos, temephos, methidathion, fenchlorphos, phosmet) and pyrethroids (e.g. deltamethrin and flumethrin) have been used in pour-on application on cattle.^12,13 While pour-on applications are easy to use, none will kill all lice; they are expensive compared with sprays if large numbers are to be treated, and in many countries they should not be used on lactating cows. Similarly, organophsphates (diazinon, coumaphos, ethion) and pyrethroids (cypermethrin) or combinations (bromophos-ethyl combined with chlorfenvinphos) are used as sprays or dips for cattle. Macrocyclic lactone based products (ivermectin, moxidectin, doramectin and eprinomectin) are available as pour-on or injectable formulations for cattle and have shown excellent efficacy against both sucking and chewing lice. Persistence of activity is one of the exceptional benefits of these products.^14,15

Fenthion 2% has been widely used on horses in Australia with good results although coat color changes and, rarely, hair loss does occur. A single subcutaneous injection of 0.2 mg/kg ivermectin will remove sucking lice but is not completely effective against chewing lice. Moxidectin, a compound with ivermectin-like activity, performs similarly.¹² Treatment of horses with a shampoo containing 1% selenium sulfide three times at 10 day intervals eradicated lice; most horses showed a marked improvement after treatment.¹³

Sheep lice have been shown to quickly develop insecticide resistance and strains of D. ovis which are resistant to the chlorinated hydrocarbon insecticides are common in the United Kingdom, while strains of lice resistant to the synthetic pyrethroids have followed inappropriate backline use of these compounds.¹⁴ Resistance management strategies that involve rotational use of the various insecticide/parasiticide active ingredient categories should be adopted wherever practical. For example, if pyrethroid-resistant lice are present an organophosphate or macrocyclic based product should be used. Subsequent treatments should involve another change of compound class.

Treatments should be timed to coincide with the beginning of population growth (i.e. autumn or early winter). Extremely early treatments often result in spring outbreaks that result from very small residual populations on a few animals. When products with short residual activity are used (e.g. organophosphates) two treatments separated by 10–14 days are required. The second treatment will kill any newly hatched nymphs. Products with persistent activity in excess of 21 days (e.g. macrocyclic lactones) do not require a second application.

Effective management of lice in a herd requires that new animals be isolated for a period of time sufficient for all lice to be eliminated by treatment. The introduction of one or two lousy sheep to a flock, such as occurs when stray infested sheep enter a clean mob, leads to a slow build-up of infestation.

TREATMENT AND CONTROL OF TICK INFESTATIONS

Four methods are now available to control ticks:

Crude vaccines made from extracts of semi-engorged adult female B. microplus give effective immunity. Antibody destroys cells lining the tick’s gut and allows blood to escape into the hemocele, some ticks die and the fertility of those remaining is reduced by up to 70%. The fertility of males is also reduced.⁷ A recombinant vaccine based on a membrane bound glycoprotein Bm86 has been isolated and shown to be as effective as the native antigen, and to be effective against acaricidal resistant ticks.⁸ Its major effect is a progressive control in tick numbers in successive generations through a decrease in their reproductive capacity.⁹ Because the vaccine acts against an antigen in the tick’s gut to which cattle are never exposed, they must be given booster injections at regular intervals.

This was the first recombinant parasite vaccine sold commercially and is marketed in Australia as Tickgard. A similar product, using the same antigen produced in a eukaryotic expression system, was produced in Cuba and has been trialed in other countries.¹⁰ A second antigen has now been added to the vaccine (Tickgard 2). This significantly enhances efficacy and does not impair the response to Bm86. Addition of a saponin adjuvant has greatly increased the efficacy of the vaccine.²

Although vaccines offer long term control, they need to be used with pasture management, dips and tick resistant cattle as part of an integrated pest management control system. Certain Stylosanthes spp., tropical legumes, can kill or immobilize larval ticks and the use of these plants may simultaneously improve pasture quality and reduce the pasture contamination of larval ticks if high legume to grass ratios are achieved. Brachiaria brizantha has also been shown to be lethal to Boophilus larvae.¹¹

Integrated management of ticks requires the use of several complementary approaches to reduce populations below acceptable thresholds. One component of these strategies is the development of acaricidal pathogens that may augment other approaches such as vaccination and selective acaricide application. Fungal pathogens are under evaluation for use in this type of program, in particular Metarhizium anisopliae and Beauvaria bassiana.^12,13

CONTROL AND ERADICATION

In most countries all that is attempted is reduction of the tick population by periodic dipping or spraying. Complete eradication is extremely difficult because of the persistence of ticks, especially multihost ticks, on wild fauna, and the ability of adult ticks to live for very long periods away from a host. On the other hand, continuous treatment to restrain the tick population is highly conducive to the development of resistance, a problem which has become apparent in many tick areas. Boophilus annulatus was eradicated from the southeastern United States by a program of continuous dipping at short intervals of all livestock in the area. B. microplus was also eradicated from Florida by a similar procedure but 20000 deer, the important alternate host in the area, had to be slaughtered. Concern has been expressed that deer and other wildlife species may threaten efforts to prevent B. microplus and B. annulatus becoming re-established in southern USA after they are introduced from Mexico.²⁷ Attempts to eradicate other single-host ticks in other countries have not been generally successful.

Although both dipping and spraying are recommended for the control of ticks, complete wetting of the animals, which can only be effected by dipping, is essential if eradication is to be undertaken. This adds another impediment to eradication plans because of the cost of constructing proper dips and yards. When one considers that dipping may have to be carried out every 14 days for 15 months, that every animal in the eradication area must be dipped, and that a strict quarantine of the area must be maintained, it is obvious that eradication cannot be undertaken lightly. The use of pour-on applications, which allow a longer period between treatments, and of ivermectin, will necessitate a review of control and eradication techniques.

Measures other than the application of insecticides used in the control of tick infestation include burning of pasture, removal of native fauna, plowing of fields, and rotational grazing. So little is known of the bionomics of specific ticks in specific areas that these measures have been largely unsuccessful and it is impossible to provide details for their proper implementation.¹

In those areas where the epidemiology is known it has been shown that in regions with a cold winter the females stop laying eggs, and that the development of eggs is prolonged. This results in few larvae being available in the spring, and if repeated treatments are given at this time, pasture contamination will remain low for some months. In hot tropical areas where the required temperatures for tick breeding are always present, the dry period may cause mortality by desiccation.

Pasture spelling and rotational grazing have been shown to be capable of greatly reducing the tick population on farms in some areas. If cattle are placed on spelled pastures early in winter when the ticks are producing few or no progeny and then alternated at 4-monthly intervals, the tick population can be controlled with a markedly lower number of treatments. The practicability of the procedure depends upon a full-scale financial assessment of the increased weight gains relative to the costs of management. Duration of the spelling period varies between 2 and 3 months in summer to 3–4 months in the winter, but these intervals need to be determined for each district. In practice, pasture spelling is rarely used.

It is possible to reduce the impact of ticks and tick-borne diseases by the introduction of Brahman and Brahman-cross cattle which are more resistant than British breeds. The resistance has been shown to be largely acquired, and is mainly expressed against the larvae in the first 24 hours after attachment.²⁸ In Australia the possibility that B. microplus might escape from its control area because of increased resistance to acaricides has been realized. For this reason a great deal of attention is being paid to the possibility of selecting cattle for tick resistance. In most tick-infested areas, cattle should have up to 50% Bovis indicus breeding, as this allows a reduction in the frequency of treatments. Penalties such as reduced liveweight gains, late maturity and poor temperament become evident when cattle have more than 50% B. indicus. With successive infestations cattle differ in their response to Boophilus microplus. Thus there is increased irritation and more licking²⁸ and a decrease in the number of ticks carried. Resistance to ticks has been shown to be heritable²⁹ and can be increased by breeding from cows and bulls selected for resistance. Selection for tick resistance does not affect milk production.³⁰

Other special cases include Otobius megnini, the nymphs of which drop off to molt and lay eggs in protected spots, necessitating the spraying of buildings, fence posts, feed troughs, and tree trunks in feedlots where heavy infestations are most common. Ornithodorus spp. ticks are difficult to control because the nymphs and adults attach to feed for brief periods only. Where ticks which cause paralysis are common it may be necessary to apply an insecticide as a dust and dip at short intervals.

LIFE CYCLE AND EPIDEMIOLOGY

The entire lifecyle of this mite, eggs, larvae, two nymphal stages, and adults, takes place entirely on the host. In sheep the cycle takes 4–5 weeks. All stages occur in the superficial layers of the skin. The adults are extremely small and can be seen only with the aid of a microscope. Only the adults are mobile on the skin surface and they effect spread of the disease by direct contact. In sheep this often occurs between recently shorn animals when contact is close and prolonged such as when shorn sheep are packed in yards after shearing, or from ewe to lamb while suckling. Mite feeding activity, in addition to excreta causes skin irritation leading to rubbing and biting of the affected parts (principally the sides, flanks, and thighs) and raggedness, sometimes shedding, of the fleece. Wool over these areas becomes thready and tufted and contains dry scales.²

PATHOGENESIS

The skin shows no gross abnormality other than an increase in scurf. Histologically there is hyperkeratosis, desquamation, and increased numbers of mast cells.³ The irritation appears to be a hypersensitivity and results in biting and chewing of the fleece on the flanks and rump behind a line approximately from the elbow to the hips. In the individual sheep and in flocks the disease spreads slowly so that it may be several years before clinical cases are observed and an appreciable number are visibly affected. The incidence of clinical cases in a neglected flock may be as high as 15%. Sheep on poor nutrition have significantly higher mite populations, more scurf and greater fleece derangement.³ Affected sheep may become tolerant after 1–2 years and show no signs, even though they remain infested.

Amongst sheep, Merinos are most commonly affected. The highest incidence is observed in this breed, particularly in areas where the winter is cold and wet. There is a marked seasonal fluctuation in the numbers of mites; the numbers are very low in summer, commence to rise in the autumn, and peak numbers are found in the spring. Spring or summer shearing exacerbates the decline in numbers. Clinically, the disease resembles louse infestation, but may be distinguished on the smaller proportion of the flock affected (10–15%), the less severe irritation and tendency of the sheep to bite those areas it can reach. Hence lesions are confined to parts of the flank and the hindquarters and the wool tufts have a chewed appearance.

CLINICAL FINDINGS

Diagnosis depends on finding the mites in a skin scraping. The selection of sheep with excess scurf and fleece derangement increases the chance of finding mites and in the absence of lice, ked, and grass seed infestation, about 75% of such sheep prove positive for P. ovis. The wool should be clipped as close as possible, the skin smeared lightly with oil and scraped over an area of about 25 cm². The mites have a seasonal incidence and may be very difficult to find in summer and autumn. For best results the scraping should be made on the ribs or shoulder in winter or spring. Scrapings are usually teased out in oil and examined microscopically without digestion. A number of scrapings may be needed from each sheep before mites can be demonstrated. Because of the difficulty of finding mites in summer and autumn, sheep dipped at that time cannot be said to be free of infestation until they prove negative on skin scraping in the following spring, when mite numbers should be at the highest levels.

TREATMENT AND CONTROL

There is no compound available that will eradicate itchmite after a single treatment. Arsenic, lime sulfur, or finely divided sulfur have been used and markedly reduce the number of mites. Because the mites are slow to build up, dipping every second year will mask the signs of infestation. However, arsenic is no longer used in most countries. Finely divided rotenone by itself or mixed with the synergist piperonyl butoxide reduces the mite population. It is usually combined with an organophosphate to include lice and ked control in the one product. Phoxim, an organophosphorus compound, has good activity but two dippings 1 month apart are necessary to eradicate infestations. Amitraz causes a marked reduction in mites that will be maintained for some months.

A single subcutaneous injection of 0.2 mg/kg ivermectin freed sheep of mites up to 56 days post-treatment.⁴ However these sheep would have to be examined over a longer period to insure eradication. Other macrocyclic lactone products, in various formulations, have been shown to have good efficacy.

ETIOLOGY

Mites infesting the different host species are considered to be specific and are designated as Demodex bovis for cattle, D. ovis for sheep, D. caprae for goats, D. equi for horses, and D. phylloides for pigs.

Demodicosis may occur in farm animals of any age, especially those in poor condition but most cases in cattle occur in adult dairy cattle in late winter and early spring. This differs from the well-known condition in the dog which occurs in young, immunodeficient animals.

LIFE CYCLE AND EPIDEMIOLOGY

The entire life cycle is spent on the host. Adult mites invade the hair follicles and sebaceous glands which become distended with mites and inflammatory material. The life cycle consists of the egg, larval, and two nymphal stages. The disease spreads slowly and transfer of mites is thought to take place by contact, probably early in life. Calves can acquire mites from an infected dam in half a day.¹ However in horses grooming instruments and rugs may transmit infection.

PATHOGENESIS

Invasion of hair follicles and sebaceous glands leads to chronic inflammation, loss of the hair fiber and in many instances the development of secondary staphylococcal pustules or small abscesses. It is these foci of infection which cause the small pinholes in the hide which interfere with its industrial processing as well as reducing the value dramatically. In most farm animals the lesions are difficult to see externally and only the advanced ones will be diagnosed.

CLINICAL FINDINGS

The important sign is the appearance of small (3 mm diameter) nodules and pustules which may develop into larger abscesses, especially in pigs and goats. The small lesions can be seen quite readily in short-coated animals and on palpation feel like particles of bird-shot in the hide. In severe cases there may be a general hair loss and thickening of the skin in the area, but usually there is no pruritus and hair loss is insufficient to attract attention. The contents of the pustules are usually white in color and cheesy in consistency. In large abscesses the pus is more fluid. In cattle and goats the lesions occur most commonly on the brisket, lower neck, forearm, and shoulder, but also occur on the dorsal half of the body, particularly behind the withers. Larger lesions are easily visible but very small lesions may only be detected by rolling a fold of skin through the fingers. In horses the face and around the eyes are predilection areas. Demodicosis in pigs usually commences on the face and spreads down the ventral surface of the neck and chest to the belly. There is little irritation and the disease is observed mainly when the skin is scraped at slaughter. The disease may be especially severe in goats, spreading extensively before it is suspected and in some instances causing deaths. Severe cases in goats commonly involve several skin diseases such as mycotic dermatitis, ringworm, besnoitiosis and myiasis. Demodicosis is rare in sheep. In this species pustules and scabs appear on the coronets, nose, tips of the ears, and around the eyes, but clinical signs are not usually seen and mites may be found in scrapings from areas of the body not showing lesions.

CLINICAL PATHOLOGY

The characteristically elongated mites are usually easy to find in large numbers in the waxy material which can be expressed from the pustular lesions. They are much more difficult to isolate from squamous lesions. Lesions in hides can be detected as dark spots when a fresh hide is viewed against a strong light source. However, lesions may not be readily seen until the hair has been removed and the skin has been soaking for some time.

TREATMENT AND CONTROL

Repeated dipping or spraying with the acaricides recommended for other manges is usually carried out but is more to prevent spread than cure existing lesions. Ivermectin which does not eradicate the infection in dogs, possibly because of the difficulty in getting the acaricide to the mite, has been reported to cure 98% of beef bulls when used at 0.3 mg/kg.² Ivermectin in a premix, fed for 7 consecutive days has been reported to clear the infestation in pigs.³

ETIOLOGY

The causative mite, Sarcoptes scabiei, is usually considered to have a number of varieties each generally specific to a particular host species. Morphological, immunological and molecular research confirms the close relationship among the varieties,¹ but do not explain the biological differences, particularly with respect to host specificity. Because host specificity is not strict and transference from one host species to another can occur there is some concern when attempting to control the disease.

Animals in poor condition appear to be most susceptible, but conditions, especially overcrowding, in which sarcoptic mange occurs often go hand in hand with poor feeding and general poor husbandry. The disease is most active in cold, wet weather and spreads slowly during the summer months.

LIFE CYCLE AND EPIDEMIOLOGY

Female mites form shallow burrows in the lower stratum corneum of the skin in which they deposit eggs. Development for both sexes includes a larval stage, two nymphal stages prior to molting to the adult. All life cycle stages, except the eggs, can be found moving on the skin surface and are thus easily transferred to other hosts. The normal exfoliation of the skin eventually exposes the tunnels exposing eggs as well. The life cycle from egg to egg takes 10–13 days.

Although direct contact between hosts is the most effective method of transmission inert materials such as bedding, blankets, grooming tools, and clothing may act as carriers. Adult mites do not usually survive for more than a few days away from the host but in optimum laboratory conditions they may remain alive for up to 3 weeks. In pigs adult sows are often the source of infestation for young pigs even though they show no signs of the disease. Large numbers of mites can often be found in the ears of normal sows and the mites are transmitted soon after farrowing. Significant scratching does not occur until a hypersensitivity develops some 8–10 weeks later and may continue until slaughter.² A small proportion of young pigs do not develop a hypersensitivity and these become chronically affected.²

Amongst domestic species pigs are most commonly affected, but it is an important disease in cattle and camels and occurs in sheep. It has been a notifiable disease in most countries, because of its severity, but a decline in prevalence accompanying the advent of new therapeutics has resulted in the removal of this requirement in some countries. People handling infested animals may become infected but lesions will disappear if further contact is prevented.

Infested animals develop protective immunity³ and are able to clear challenge infestations rapidly. A proportion of infested hosts do however remain chronically infested and mite populations may show a post-partum recrudescence thereby facilitating transfer to the susceptible offspring.

PATHOGENESIS

Young animals, in particular piglets, become infected in the first few weeks of life and develop a hypersensitivity within 8–10 weeks. This allergic phase lasts for 8–9 months⁴ and during this time affected animals are constantly itchy. The disease, if untreated, progress to a localized crust formation characteristic of a chronic hyperkeratotic state.

Many infestations in pigs have little or no effect on weight gain although there is some controversy⁵ and treatments improve productivity (see below). There are suggestions in other hosts of reduced feed efficiency. In some pigs the loss of condition, production and vitality may be severe, and the appearance of affected animals is esthetically displeasing. Erythema, papules and intense pruritis may be seen. Few mites may be necessary to cause a reaction in a previously sensitized animal. A chronic condition is uncommon but is seen in pigs with an immunodeficiency.

In cattle and camels, severe hypersensitivity lesions occur and often lead to death. Sheep initially show an intense pruritus and rub the affected part against fences or bite at the skin. Later papules and vesicles occur and the skin becomes thickened, covered with pale scabs and the hair is lost.⁶

CLINICAL FINDINGS

Early lesions are characterized by the presence of small red papules and general erythema of the skin. The affected area is intensely itchy and frequently excoriated by scratching and biting. Loss of hair, thick brown scabs overlying a raw surface, and thickening and wrinkling of surrounding skin soon follow. In pigs the lesions commence on the trunk, in sheep and goats on the face, in cattle on the inner surface of the thighs, the underside of the neck and brisket and around the root of the tail, and in horses and camels on the head and neck. Except in sheep where the lesions do not spread to the woolled skin, lesions become widespread if neglected and such animals may show systemic effects including emaciation, anorexia, and weakness, and in neglected cases death may occur.

The course of sarcoptic mange is rather more acute than in the other forms of mange and may involve the entire body surface of cattle in a period as short as 6 weeks.

CLINICAL PATHOLOGY

Necropsy examinations are not usually undertaken. Deep scrappings which draw blood are required for accurate diagnosis and must be taken from the edges of any evident lesions (scrappings taken from the central portions of lesions are very often negative). Examination of scrapings either directly or after digestion in 10% potassium hydroxide will reveal mites and/or eggs. When practical multiple scrapings from affected animals should be taken. Examination of the ear wax of pigs often shows mites when none can be seen in scrapings.

Change in behavior, a result of the intense pruritis, have been used in swine as an initial diagnostic tool. An increase in the rubbing index is indicative of infestation, but other clinical confirmation is required.⁷

An ELISA for detection of antibodies to Sarcoptes scabiei has been developed.⁸ The test has high specificity and moderate sensitivity, being more sensitive in young animals undergoing their first infestation. It has been shown to work well in herd level eradication programs and functions afterward as an effective surveillance tool.⁹

TREATMENT AND CONTROL

Macrocyclic lactone endectocides (including ivermectin, eprinomectin, moxidectin, and doramectin) are the preferred products for treatment of sarcoptic mange. Use of these products in pour-on or injectable formulations are highly efficacious when used at the label recommended dose. Because of the residual activity of these compounds¹⁰ retreatment is not usually necessary although moxidectin given subcutaneously at 0.2 mg/kg to infested sheep resulted in a rapid clinical improvement but did not eliminate the mites. Two doses 10 days apart resulted in negative skin scrapings by 14 days post-treatment.¹¹ A single injection to cattle eliminated the mites by day 14.¹² The resolution of the lesions may take considerable time, but should not be misconstrued as product failure.

Prefarrowing treatment with ivermectin to prevent transmission to the newborn piglets improves weight gains and early feed conversion.

If other treatments are used they must be thoroughly applied so that all parts of the skin, especially under the tail, in the ears and between the legs are wetted by the acaricide. Although buildings, bedding, and other inert materials do not support the mite for more than a few days they should also be treated unless they can be left in a dry state for 3 weeks.

Treatments should be repeated three times at 7-day intervals. For sows this should commence 3 weeks before farrowing. Special attention should be paid to the ears. Trichlorfon, maldison (0.5%), diazinon (0.02%), coumaphos (0.05–0.1%), fenchlorphos, chlorfenvinphos, amitraz (0.1%), and phoxim (0.025%) have been used. All animals should be treated. Phosmet 20% applied as a pour-on at weaning eliminated Sarcoptes and allowed 12% increase in live weight gain.¹³

ETIOLOGY

The various species of Psoroptes have now been reduced to two or three species.² Based on molecular evidence³ P. ovis, P cuniculi, and P. cervinus are identical despite differences in morphology and biology. It is clear that P. ovis from cattle and sheep are identical⁴ although cross-transmission is not always successful.⁵ P. equi occurs on horses, donkeys, and mules in Great Britain and P. natalensis on cattle and the water buffalo. The ear mites are all P. cuniculi and recent work has suggested this is a variant of P. ovis adapted to the aural environment. P. cervinus assumes a dual role, being an ear mite of the American bighorn and a body mite of the wapiti.

LIFE CYCLE AND EPIDEMIOLOGY

Psoroptic mange is a major disease in sheep which was once virtually eliminated in most progressive countries where wool production is an important industry. With the cessation of organophosphate dips in the UK there has been a resurgence of the problem. The disease in cattle was widespread in the United States but has now largely been brought under control. It can spread rapidly and cause serious losses in cattle if neglected as shown by the serious losses that can occur in feedlots. The ear manges cause irritation and, in horses, a touchiness around the head.

Psoroptic mites abrade the surface and feed on lipid exudate, bacteria, and skin debris.⁶ Erythrocytes are not normally a constituent of the diet and may be accidentally ingested when host scratching results in skin breakage.⁶ They cause the formation of scabs, under which they live. The eggs are laid on the skin at the edge of a scab and hatch in 1–3 days, although this is prolonged if eggs are not in contact with the skin. There are the usual larval and nymphal stages and the whole life cycle is complete in 10–11 days.⁷ All stages are capable of survival away from the host for up to 10 days and under optimum conditions adult females may survive for 3 weeks.

Optimum conditions for development include high humidity and cool temperatures. Thus the disease is most active in autumn and winter months. This is a result of not only increased activity of the mites but also the more rapid development in housed animals and the tendency for the disease to be most severe in animals in poor condition. When conditions are adverse, as in summer, mites survive in sheep in protected parts in the perineum, in the inguinal and interdigital regions, the infraorbital fossae, inside the ear and the scrotum. Spread occurs from sheep to sheep but transmission from infected premises and by passive spread of pieces of wool also occurs.

While P. ovis has been shown to survive for up to 17 days away from the host,⁸ no natural transmission has taken place where premises have been rested for more than 10 days.⁵ Premises left free of sheep for at least 2 weeks can be assumed to be safe.⁵ If cattle are housed in stanchions that prevent grooming infestation will be more severe.⁷ Although individual mites survive for only 4–6 weeks the disease is continuous and a very rapid increase in mite numbers may occur.⁷

The life cycle of the other species is thought to be similar. Spread of ear mite in horses can occur by grooming or by the use of infected harness.

PATHOGENESIS

The mite migrates to all parts of the skin and prefers areas covered with hair or wool. Salivary secretions and mite excreta contain proteinases that result in a severe allergic pruritis. The exudation of serum accumulates to form a crust. In cattle the mites are most active at the edge of the crust and the lesion spreads peripherally. Infested calves have lower weight gains, lower feed conversion and lower energy retention than non-infested calves.⁷ In sheep the mites are more generally distributed and bacterial invasions of the skin are more common.⁴

CLINICAL FINDINGS

CLINICAL PATHOLOGY

The mites can be easily demonstrated in scrapings taken from the edges of the lesions. Examination is facilitated by prior digestion of the scraping in warm, 10% potassium hydroxide solution.

An ELISA has been developed for diagnosis of Psoroptes infestation in sheep.¹⁰ It has been applied to monitoring of infestations as part of efficient control programs.¹¹

TREATMENT AND CONTROL

Macrocyclic lactone endectocides are used most frequently for control of psoroptic scabies. Cattle treated with ivermectin must be separated from non-infested cattle for between 9 and 14 days, otherwise spread and re-infection¹² may occur. In sheep two treatments of ivermectin 0.2 mg/kg subcutaneously are necessary to eliminate infestations.¹³

Moxidectin applied as a 0.5% pour-on at 0.5 mg/kg to cattle is effective against P. ovis as well as lice and Chorioptes bovis¹⁴ and was equally effective against P. ovis as 0.2 mg/kg by subcutaneous injection.¹⁵ In sheep, although a single subcutaneous dose of 0.2 mg/kg moxidectin gave a rapid clinical improvement, two doses 7 days apart were necessary to eliminate mites.¹⁶ In large scale field use, sheep receiving a single injection in the autumn remained free of the infestation throughout the winter, while two injections 10 days apart were effective in treating outbreaks.¹⁷

Doramectin injectable at 200 μg/kg was highly effective in eliminating mites in scrapings of infested cattle.¹⁸ The same treatment was found to protect cattle from infestation for up to 3 weeks.¹⁸

If sheep are to be dipped, it is important to wet the skin thoroughly and pay special attention to severe cases where mites are likely to be present in inaccessible sites on the body. Thus a plunge dip is almost essential and the sheep must be kept immersed in the dipping fluid for at least one minute. Prior shearing may be advisable but may lead to further spread of the infestation. Care must be taken to insure that the concentration of the acaricide in the dip is maintained, especially when large numbers of sheep are being treated. Badly affected animals should be set aside and inaccessible sites including ears, horn bases, and perineum treated manually with the dipping fluid. Dipped sheep should not be returned to their pastures, nor to the barn unless the latter has been thoroughly cleaned and sprayed with the dipping fluid.

Diazinon (0.01%), propetamphos (0.0125%), and flumethrin (0.055%) will all eliminate P. ovis from sheep with a single dipping and will give at least 4 weeks of protection.¹⁹ Coumaphos (0.1%), phoxim (0.05%), and amitraz (0.05%) require two treatments at 7–10 day intervals to eliminate infestations. The synthetic pyrethroids are variable in their efficacy. Flumethrin, used as a non-stripping dipping compound, eradicated P. ovis from sheep when used at 55 ppm and gave at least 7 weeks of protection.²⁰ Fenvalerate (0.05%) used twice will also clear infested cattle, but another synthetic pyrethroid, cypermethrin, when used at 150 ppm did not eliminate infestations after three treatments.²¹

In horses, affected ears should be cleaned of all wax and ear preparations containing benzene hexachloride should be used at weekly intervals. Local treatment of diazinon or propetamphos could also be used. Benzyl benzoate is a safe and effective treatment when given every 5 days for three treatments. Ivermectin is highly effective against P. equi.²²

Eradication of sheep scab on an area basis is usually undertaken by quarantine and compulsory treatment of all susceptible animals in the area at the same time. Now that there are effective treatments that do not require dipping, eradication of scab from areas should be more easily accomplished. The necessity to dip all animals in the area during a short period presents difficulties and the cost of construction of dips and lack of desire to dip in cold climates are other obstructing factors. The use of pour-ons or injections is an attractive alternative to autumn dipping, and has the added advantage of providing helminth control in late season lambs and in ewes. Further, even pregnant animals can be yarded and treated by subcutaneous injection or pour-on as long as care is taken in the yards. Where it is desired to keep the disease at a low level short of eradication, the disease is made notifiable, movement of stock is restricted and infested farms are quarantined.

ETIOLOGY

Chorioptic mites were formerly named according to the host species but those on cattle, horses, goats, and sheep are now considered to be one species, Chorioptes bovis. Another species, C. texanus, has been reported on goats, cattle, and Canadian reindeer. In cattle, the mites are much more active in the latter part of the winter and tend to disappear in cattle at pasture. This diminution in activity is not noted in cattle kept housed in the summer.

LIFE CYCLE AND EPIDEMIOLOGY

Chorioptes bovis feed on the skin surface, abrading the upper layers with their mouthparts and contaminating the area with salivary secretions and excreta. Developmental stages are similar to that of Psoroptes and a complete cycle, from egg to adult, requires approximately 3 weeks. The number of parasites is influenced by temperature and humidity; the mite populations beginning to increase on sheep in early autumn, numbers reach a peak in late autumn or early winter and decline in spring. In cattle the cycle is longer, peak numbers occurring in late winter and early spring and declining in summer. Transmission is probably effected by direct contact in most instances although in animals housed in barns, grooming tools may be an additional method of spreading the disease. Infestation of bedding is not a common method of transmission.

In horses, the parasites occur almost entirely in the long hair on the lower parts of the legs and are rarely found on other parts of the body. In cattle the disease is most evident in the winter, lesions occurring most commonly on the perineum, and back of the udder, extending in severe cases to the backs of the legs and over the rump. In the summer months the mites persist in the area above the hooves, particularly the pasterns of the hind leg. In sheep, lesions are confined to the wool-less areas, chiefly the lower parts of the hindlegs and scrotum. Rams are more heavily infected than ewes and probably infect ewes while copulating. Lactating ewes probably act as the source of infection for lambs.

PATHOGENESIS

The mites cause an allergic, exudative dermatitis; the yellowish serous exudate coagulates and breaks as the hair grows so that small scabby lesions are seen on the hair. In horses the mites cause severe irritation and itchiness. The initial lesion in cattle is a small nodule which exudes serum causing matting of the hair. In severe cases these coalesce to form heavy scabs and cause thickening and wrinkling of the skin. Mites can be isolated from many animals which show no clinical evidence of the disease. While most cases do not cause any symptoms, a rapidly spreading syndrome characterized by coronitis, intense irritation and a marked fall in milk production has been reported. C. bovis is a common parasite of sheep in the United States, New Zealand, and Australia, and causes an allergic exudative dermatitis on the scrotum of rams. This may cause a rise in temperature of the scrotal contents and a severe testicular degeneration if the lesion has an area greater than 10 cm².¹

CLINICAL FINDINGS

The first sign in horses is usually violent stamping of the feet and rubbing of the back of the hind pasterns on wire, rails, or stumps. This is most evident during periods of rest and at night. Examination of the area is difficult because of the long hair present and the horses may resent manipulation. In cases of long duration the skin is seen to be swollen, scabby, cracked, and usually greasy; small amounts of serous exudate may be attached to most hair in the affected area.

Cattle show little evidence of cutaneous irritation but the small crusty scabs (3 mm diameter) on the escutcheon, udder, and thighs are unsightly. Although the mites appear to cause little trouble in the summer, occasional animals are seen which have thick, crusty scabs on the skin, just above the coronets and around the muzzle.

The main lesion in sheep is seen on the scrotum of rams where an allergic dermatitis results in the production of a yellowish serous exudate over areas from a few millimeters to several centimeters.¹

CLINICAL PATHOLOGY

Scrapings from the affected areas usually contain large numbers of mites.

TREATMENT AND CONTROL

The macrocyclic lactone endectocides have shown efficacy against Chorioptes spp., but eradication of the parasites from a herd is difficult. Moxidectin 0.5 mg/kg applied as a pour-on eliminated C. bovis as well as sucking lice and Psoroptes ovis.³ When given as a single injection of 0.2 mg/kg there was a marked decline in the number of mites but few cattle were cleared of infection.⁴ Doramectin has high efficacy at the label rate in cattle, but a single treatment did not clear mites from all of the trial animals.⁵ Treatment with eprinomectin at recommended rates was completely effective, but mites persisted for at least 14 days.²

Two doses of 2 mg/kg flumethrin applied to the whole body 1 week apart eliminates mites from cattle, while treatment of 2 mg/kg was successful if applied to the caudal region.⁶ Fenvalerate 0.05% also killed all mites while amitraz 0.05% removed 98%.⁷ Phoxim 0.05% and 0.1% used twice at 10-day intervals has also eradicated the infection from cattle.⁸ Other compounds if used repeatedly will reduce mite numbers but recrudescences may occur. Ivermectin 0.2 mg/kg given subcutaneously on two occasions reduced but did not eliminate the infestation on cattle. A single treatment of infested horses with ivermectin paste did not remove all mites but when combined with hair removal, washing encrusted areas with oil of salicylic acid and the later removal of crusts with a stiff brush, eradication was achieved.⁹