Veterinary · Para-clinical · also MSVE VPA-221
Flies, mosquitoes, midges, lice, fleas, ticks and mites: the damage they do themselves and the diseases they carry, and the ectoparasiticides used against them.
In the exams: ICAR AICE-JRF core group 06; ICAR AIEEA-PG 13 (Parasitology)
Veterinary entomology studies the insects that feed on or annoy animals: flies, mosquitoes, biting midges, lice and fleas. Veterinary acarology studies ticks and mites (the Acari). Together they cover the ectoparasites and the arthropod vectors that carry viruses, bacteria, protozoa and worms between animals. Babesiosis, theileriosis, bluetongue, lumpy skin disease, trypanosomosis and African swine fever all reach their hosts through arthropods.
Arthropods harm animals directly, through blood loss, irritation, disturbed grazing, hide and wool damage, hypersensitivity, toxicosis and myiasis (invasion of living tissue by fly larvae), and indirectly, by transmitting pathogens. A practitioner must identify the arthropod, know which stage of its life cycle can be attacked, name what it transmits and how, and choose an ectoparasiticide that works, is legal and does not select for resistance faster than necessary.
The manual follows the order of most curricula, including the Indian MSVE course VPA-221: structure and vector principles, flies, mosquitoes, Culicoides, myiasis, lice, fleas, ticks and mites, the vectors of babesiosis, theileriosis, bluetongue and lumpy skin disease, and ectoparasiticides and resistance. Examiners worldwide ask the same core things: features that separate genera, one-, two- and three-host tick cycles, which vector carries which pathogen by which route, and the mode of action and toxicity of each drug class. Species, licensing and withdrawal periods differ by country. Drugs are discussed by class; no product dose is given, so use the product label and your national formulary.
Arthropods have a jointed chitin exoskeleton that must be shed (moulted) for growth; several ectoparasiticides act by disrupting moulting. Insects have three body parts (head, thorax, abdomen), three pairs of legs and one pair of antennae. The Acari (ticks and mites) have two: the gnathosoma or capitulum, carrying the mouthparts, and the idiosoma, carrying the legs. Acarine nymphs and adults have four pairs of legs, larvae three pairs, and there are no antennae, so a six-legged acarine larva is not an insect.
The insect orders of veterinary importance are the Diptera (flies, mosquitoes, midges), Phthiraptera (lice), Siphonaptera (fleas) and, less often, Hemiptera (bed bugs, triatomine bugs). Ticks form the order Ixodida, with hard ticks (Ixodidae) and soft ticks (Argasidae). Mites include the Astigmata (Sarcoptes, Psoroptes, Chorioptes, Otodectes, Knemidocoptes), Prostigmata (Demodex, Cheyletiella, chiggers) and Mesostigmata (Dermanyssus, Ornithonyssus).
In complete metamorphosis (holometabolous: flies, fleas) the cycle is egg, larva, pupa, adult, and larvae live somewhere quite different from adults: dung, water, wounds or bedding. Control can target those habitats. In incomplete metamorphosis (hemimetabolous: lice) the cycle is egg, nymph, adult, and all stages share the host. Ticks and mites pass through egg, six-legged larva, eight-legged nymph(s) and adult; hard ticks have one nymphal stage, soft ticks several. Most ectoparasiticides do not kill louse eggs or flea pupae, so treatment must be repeated or persistent.
In mechanical transmission the pathogen is carried on the mouthparts or body without developing or multiplying, like a contaminated needle. It must happen quickly and is favoured by flies whose feeding is interrupted, such as tabanids and stable flies. Trypanosoma evansi (surra), equine infectious anaemia virus and Anaplasma marginale are classic examples.
In biological transmission the pathogen must develop, multiply or both in the vector. Propagative transmission is multiplication without change of form (bluetongue virus in Culicoides, Yersinia pestis in fleas). Cyclo-developmental transmission is development without multiplication (Dirofilaria immitis in mosquitoes: one microfilaria becomes at most one infective larva). Cyclo-propagative transmission is both (Plasmodium in mosquitoes, Babesia in ticks, trypanosomes in tsetse). The interval from the infective meal until the vector can transmit is the extrinsic incubation period; it shortens as temperature rises, which makes vector-borne disease seasonal.
Ticks feed once per stage, so a pathogen acquired by one stage must survive the moult to be passed on by the next: transstadial transmission, as with Theileria parva in Rhipicephalus appendiculatus. Transovarial transmission is passage from female through the egg to the next generation; pathogens of one-host ticks, such as Babesia bigemina and B. bovis in Rhipicephalus (Boophilus), depend on it. Some arthropods are intermediate hosts that must be swallowed: fleas and the dog chewing louse for Dipylidium caninum, and the brown dog tick for Hepatozoon canis. Vector competence is the intrinsic ability of a species to become infected and transmit; vectorial capacity adds field factors such as density, biting rate on the host, daily survival and extrinsic incubation.
Diptera have one pair of wings; the hind wings are reduced to club-shaped halteres. Nematocera (mosquitoes, midges, blackflies, sandflies) are small with long, many-segmented antennae. Brachycera (tabanids) are large with short antennae. Cyclorrhapha (house flies, stable flies, blowflies, bots, tsetse, keds) have short antennae bearing a bristle, the arista, and pupate inside a barrel-shaped puparium. Non-biting flies such as Musca have sponging mouthparts. In muscids and tsetse both sexes suck blood; in tabanids, mosquitoes, midges, blackflies and sandflies only females do.
Musca domestica breeds in manure and rotting matter, carries bacteria and parasite eggs mechanically, and is the intermediate host of the equine stomach worms Habronema muscae and Draschia megastoma, whose larvae in wounds cause cutaneous habronemosis (summer sores). The face fly, Musca autumnalis, feeds on eye and nose secretions of cattle, is associated with spread of Moraxella bovis (infectious keratoconjunctivitis) and is the intermediate host of Thelazia eyeworms and Parafilaria bovicola.
Stomoxys calcitrans, the stable fly, resembles a house fly but has a rigid, forward-pointing piercing proboscis. It breeds in decaying vegetable matter mixed with manure, such as waste around hay feeders. Its painful bites reduce weight gain, and it transmits T. evansi, EIA virus and lumpy skin disease virus mechanically and Habronema microstoma biologically. Haematobia irritans, the horn fly (with the buffalo fly H. irritans exigua in Asia and Australia), is small, stays on the host almost continuously, rests head-down on the back, and leaves only to lay eggs in fresh dung. Insecticide ear tags have selected strongly for resistance in this species.
Tabanids (Tabanus, Chrysops, Haematopota) are large, fast flies of warm, sunny weather near water; larvae develop in mud. Only females bite, with cutting mouthparts that leave bleeding wounds. Painful bites interrupt feeding, making them efficient mechanical vectors of T. evansi, EIA virus, A. marginale and Bacillus anthracis.
Blackflies (Simuliidae) are small humped flies whose larvae attach to stones in fast-flowing, well-oxygenated streams. Mass attacks can kill cattle through toxaemia and blood loss. They transmit Leucocytozoon to birds and some Onchocerca species of cattle.
Phlebotomine sandflies (Phlebotomus in the Old World, Lutzomyia in the New World) are small, hairy flies that hold their wings in an erect V at rest and bite at night; larvae develop in moist organic debris in soil and cracks, not in water. They are the biological vectors of Leishmania infantum, the cause of canine leishmaniosis in the Mediterranean, Middle East, South Asia and Latin America. The dog is the main reservoir of human visceral leishmaniosis caused by L. infantum, so pyrethroid collars and spot-ons with repellent effect protect dogs and people.
Tsetse (Glossina) occur only in sub-Saharan Africa. At rest the wings fold flat, one directly over the other like closed scissors; each wing has a hatchet-shaped discal cell, and the palps are as long as the proboscis. Both sexes feed on blood. Reproduction is by adenotrophic viviparity: the female nourishes one larva at a time in her uterus from milk glands and deposits a mature larva, which pupates in soil within hours. Because each female has few offspring, populations recover slowly, so traps, insecticide-treated targets and cattle, and the sterile insect technique can suppress them. Tsetse are cyclo-propagative vectors of Trypanosoma congolense, T. vivax and T. brucei (nagana). T. vivax can also be transmitted mechanically by other biting flies, which is how it persists in South America without tsetse.
Keds (Hippoboscidae) are flattened, leathery flies with strong claws. The sheep ked, Melophagus ovinus, is wingless and lives permanently in the fleece; the female deposits a mature larva that pupates on the wool. Keds cause pruritus, fleece staining and cockle, a hide defect, and carry the non-pathogenic Trypanosoma melophagium. The pigeon fly Pseudolynchia canariensis transmits Haemoproteus columbae.
Mosquitoes (Culicidae) are slender Nematocera with a long, forward-projecting proboscis and scales on the wing veins and wing margin. Males have bushy (plumose) antennae and feed on plant sugars; females take blood to mature each batch of eggs. In Anopheles the female palps are about as long as the proboscis; in culicine (Culex, Aedes) females they are short. Anopheles rests with the body at an angle to the surface, culicines parallel to it. Anopheles lays single eggs with lateral floats on water; Culex lays eggs stuck together in a floating raft; Aedes lays single eggs without floats on damp surfaces above the water line, and these survive drying for months and hatch when flooded, so Aedes populations surge after rain. Anopheles larvae lack a breathing siphon and lie parallel to the water surface; culicine larvae hang from the surface by a siphon, long with several hair tufts in Culex, short with one tuft in Aedes.
All larvae are aquatic, pass through four instars and become a comma-shaped pupa that is mobile but does not feed. The aquatic stages take one to two weeks in warm weather. Each cycle of blood meal, egg maturation and laying is a gonotrophic cycle and a chance to acquire or transmit a pathogen; only older females have survived the extrinsic incubation period. Host preference, biting time and indoor or outdoor biting decide which diseases a species carries and which control reaches it.
Mosquitoes are biological vectors of filarial worms. Dirofilaria immitis, canine heartworm, is transmitted by many Culex, Aedes and Anopheles species: microfilariae develop to infective third-stage larvae in the Malpighian tubules and move to the mouthparts. Development needs sustained warmth, so transmission is seasonal in temperate areas. Setaria digitata, normally harmless in the cattle peritoneal cavity, is mosquito-borne and causes cerebrospinal nematodosis (kumri in India) when larvae invade the nervous system of horses, sheep and goats.
Mosquitoes transmit arboviruses propagatively. Japanese encephalitis virus is carried by Culex tritaeniorhynchus and related Culex; wading birds are reservoirs, pigs are amplifying hosts that suffer reproductive failure, and horses and humans are dead-end hosts. West Nile virus circulates between Culex and birds, with horses and people as dead-end hosts. Rift Valley fever virus causes abortion storms and heavy lamb losses in Africa and Arabia; floodwater Aedes pass it transovarially and keep it in dry eggs between epidemics, and Culex amplify it after heavy rains. The equine encephalitis viruses of the Americas are also mosquito-borne. Mosquitoes transmit avian Plasmodium, carry fowlpox and myxoma viruses mechanically, and with Culicoides transmit bovine ephemeral fever virus.
Culicoides (family Ceratopogonidae) are tiny midges, mostly 1 to 3 mm, small enough to pass through ordinary insect screens, with spotted wings folded flat over the body at rest. Only females bite, mainly at dusk, night and dawn in warm, humid, still weather. Larvae are semi-aquatic, living in wet mud at pond and stream margins, waterlogged pasture, manure and, for some species, dung pats. Breeding sites are small and scattered, so larval control is rarely practical. Adults fly weakly but are carried by wind over tens of kilometres, sometimes across the sea. Temperature governs adult activity, survival and virus replication; in temperate climates activity stops for part of the winter, and authorities can declare a seasonally vector-free period from trap catches.
The main direct harm is allergic. Insect bite hypersensitivity of horses (sweet itch, Queensland itch) is a seasonal, intensely pruritic dermatitis caused by hypersensitivity, predominantly type I, to Culicoides salivary proteins. Lesions affect the mane, tail base, withers, face or ventral midline, depending on where local species feed. Management reduces exposure: stabling from late afternoon to after dawn, fine-mesh screens, fans, full-body rugs and repellents, with treatment of the dermatitis.
Culicoides are biological, propagative vectors of bluetongue virus, epizootic haemorrhagic disease virus, African horse sickness virus, Schmallenberg virus and Akabane virus (the last two cause congenital malformations in ruminants), and, with mosquitoes, bovine ephemeral fever virus. Culicoides imicola is the main Old World vector of bluetongue and African horse sickness across Africa, southern Europe, the Middle East and South Asia. In northern Europe the C. obsoletus and C. pulicaris groups, which breed in farm habitats, transmitted bluetongue serotype 8 from 2006. C. sonorensis is the main North American vector and C. brevitarsis the main Australian one. African horse sickness, endemic in sub-Saharan Africa, causes very high mortality in horses, and its spread outside Africa has followed the distribution of C. imicola. The same midge species can carry several viruses, so surveillance for one serves others.
Culicoides are also intermediate hosts of Onchocerca cervicalis of horses and Onchocerca gibsoni, which causes subcutaneous worm nodules in cattle in Asia and Australia, and they transmit Leucocytozoon caulleryi of chickens in Asia and Haemoproteus of birds.
Myiasis is infestation of living vertebrate tissue by fly larvae. In obligatory myiasis larvae develop only in living tissue (screwworms, bots, warbles). In facultative myiasis larvae normally live in carrion but can invade living animals: facultative primary flies, such as the sheep blowflies Lucilia cuprina and L. sericata, initiate strike on soiled or damp intact skin; facultative secondary flies, such as Calliphora, Phormia and Chrysomya other than C. bezziana, follow a primary strike or wound. Myiasis is also described by site: cutaneous, nasal, gastric or furuncular.
Screwworm larvae burrow deep into wounds and can kill. The New World screwworm, Cochliomyia hominivorax, was eradicated from the United States, Mexico and Central America to Panama by the sterile insect technique (SIT): irradiated males are released in huge numbers, and because females mate once, those mating sterile males lay infertile eggs. SIT also eliminated an introduction to Libya around 1990. Since 2023 the fly has spread north again through Central America into Mexico. The Old World screwworm, Chrysomya bezziana, occurs in Africa, the Indian subcontinent, South-East Asia and Papua New Guinea. Wohlfahrtia magnifica, a flesh fly, deposits larvae in wounds and orifices around the Mediterranean and in Asia.
Blowfly strike of sheep is caused mainly by L. cuprina in Australia and South Africa and L. sericata in the United Kingdom. Females are attracted to wool soiled by faeces and urine (breech strike) or kept wet long enough for fleece rot or dermatophilosis (body strike). Larvae cause severe inflammation and toxaemia and can kill within days. Prevention combines crutching and shearing, worm control to prevent scouring, breeding for plain breeches and fleece-rot resistance, carcass disposal and preventive chemicals before the fly season.
Oestrus ovis, the sheep nasal bot, deposits first-stage larvae around the nostrils of sheep and goats; larvae develop in the nasal passages and sinuses and are sneezed out to pupate. Flies disturb grazing; larvae cause mucopurulent discharge and sneezing. It also causes ocular myiasis in shepherds. Cephalopina titillator is the nasal bot of camels.
Hypoderma bovis and H. lineatum lay eggs on the leg hairs of cattle, H. bovis singly with attacks that cause panic (gadding), H. lineatum in rows. Larvae migrate for months: H. bovis overwinters in the epidural fat of the spinal canal, H. lineatum in the oesophageal submucosa. They then reach the back and form warbles that damage the hide. Killing many larvae in the spinal canal or oesophagus can cause paralysis or bloat, so systemic treatment is given after fly activity ends and before larvae reach these sites. National campaigns eradicated warbles from the United Kingdom, Ireland and other European countries. Przhevalskiana silenus is the goat warble.
Gasterophilus bots of horses lay eggs on hairs: G. intestinalis on the forelegs and shoulders, G. nasalis under the jaw, G. haemorrhoidalis on the lips. Larvae enter the mouth, then attach in the stomach or duodenum for months. Dermatobia hominis of Latin America lays eggs on mosquitoes and other flies, which deliver larvae to cattle, dogs and people (phoresy); each larva forms a furuncle.
Lice (Phthiraptera) are small, wingless, dorsoventrally flattened, highly host-specific insects that spend their whole life on one host species. Sucking lice (Anoplura) have a narrow head, narrower than the thorax, and piercing mouthparts; they feed on blood and can cause anaemia. Chewing lice (Amblycera and Ischnocera, formerly Mallophaga) have a broad head, wider than the thorax, with mandibles, and feed on skin debris and feather fragments. The difference matters for treatment: injected systemic drugs reach blood-feeding sucking lice well but chewing lice poorly, so chewing lice need topical products.
Cattle carry the chewing louse Bovicola (Damalinia) bovis and the sucking lice Linognathus vituli, Haematopinus eurysternus and Solenopotes capillatus; the tail louse H. quadripertusus matters in the tropics, and buffalo carry H. tuberculatus. In sheep the chewing louse Bovicola ovis is the most damaging, causing fleece derangement and cockle. Pigs have only the sucking louse Haematopinus suis, the largest louse of domestic animals, which transmits swinepox virus. Horses carry Bovicola equi and Haematopinus asini. Dogs carry Trichodectes canis (chewing), Linognathus setosus (sucking) and, in warm climates, Heterodoxus spiniger. Cats have only the chewing louse Felicola subrostratus. Poultry have only chewing lice; Menacanthus stramineus, the body louse, is the most pathogenic, with Menopon gallinae, Lipeurus caponis, Cuclotogaster heterographus and Goniocotes gallinae.
Eggs (nits) are cemented to hairs or feathers near the skin and hatch in about one to two weeks. Three nymphal instars follow, and the egg-to-egg cycle takes roughly three to four weeks. Lice survive only days off the host, so transmission is mainly by direct contact.
Livestock louse numbers rise in winter, when a long coat gives a stable microclimate, animals are housed together and nutrition is often poor, and fall in summer. Heavy infestation (pediculosis) causes pruritus, rubbing, hair and wool loss, hide and fleece damage and reduced growth; sucking lice can cause marked anaemia in calves. Heavy burdens usually point to poor husbandry or concurrent disease, as in adult cats with Felicola. Trichodectes canis is an intermediate host of Dipylidium caninum.
Diagnosis is by parting the coat over the neck, back and tail head. Because most treatments do not kill eggs, a product must persist beyond the egg stage or be repeated after about two weeks, and all in-contact animals are treated together. Sheep louse control is complicated by resistance to pyrethroids and insect growth regulators and by withdrawal periods before shearing.
Fleas (Siphonaptera) are wingless, laterally compressed, with long jumping hind legs; both sexes feed on blood. Combs (ctenidia) of stout spines are the key features: the genal comb on the lower margin of the head and the pronotal comb behind it. Ctenocephalides has both. C. felis, the commonest flea of both cats and dogs worldwide, has a long head with a sloping forehead, and the first genal spine is about as long as the second. C. canis has a rounded head and a first genal spine clearly shorter than the second. Pulex irritans, the human flea, which also infests pigs and dogs, and Xenopsylla cheopis, the oriental rat flea and vector of plague and murine typhus, have no combs. Echidnophaga gallinacea, the sticktight flea of poultry, lacks combs and has an angular head; females attach in clusters on the comb, wattles and around the eyes. Tunga penetrans females burrow into the skin of people and pigs. Spilopsyllus cuniculi, the rabbit flea, is the main vector of myxomatosis in Britain.
C. felis adults stay on the host, feed within minutes and lay eggs within a day or two. Eggs fall into bedding and carpets. Larvae avoid light, live deep in carpets and shaded soil, and feed on debris and adult flea faeces (dried blood). After three larval stages they spin a cocoon and pupate. The adult can wait in the cocoon for weeks to months, emerging in response to vibration, warmth, pressure and carbon dioxide. The cycle takes about three weeks in warm, humid conditions, longer when cool. Most of a flea population is therefore eggs, larvae and pupae in the home, and pupae resist most insecticides. New fleas keep appearing for weeks after treatment, so every dog and cat in the household is treated, adulticide cover is maintained, an insect growth regulator may be added and bedding is washed and floors vacuumed.
Heavy infestations cause iron-deficiency anaemia that can kill kittens and puppies. Flea allergy dermatitis (FAD), hypersensitivity to flea salivary antigens, is the most important disease. In dogs it produces pruritic papules over the lumbosacral area, tail base, caudal thighs and ventral abdomen; in cats, miliary dermatitis, self-induced alopecia or eosinophilic granuloma complex lesions. Few bites are needed to trigger itching, so control must be strict and continuous in all in-contact pets. Diagnosis rests on lesion distribution, finding fleas or flea faeces (which leave a red-brown stain on damp white paper) and response to control.
Fleas are the intermediate host of Dipylidium caninum: flea larvae eat tapeworm eggs, the cysticercoid develops as the flea matures, and pets are infected by swallowing fleas while grooming. Fleas transmit Bartonella henselae among cats, mainly through infected flea faeces in skin wounds; cats pass it to people as cat scratch disease. C. felis carries Rickettsia felis and is implicated in transmitting feline haemotropic mycoplasmas. In Xenopsylla cheopis, Yersinia pestis multiplies and blocks the foregut, so the hungry flea regurgitates bacteria into each bite, a classic propagative transmission.
Hard ticks (Ixodidae) have a dorsal shield, the scutum, covering the whole back of the male but only the front of the female, so she can engorge enormously. The capitulum projects forward and is visible from above; it carries palps, cutting chelicerae and the hypostome, a plate with backward-pointing teeth that anchors the tick, often aided by cement.
Genera are separated by palp length, the shape of the basis capituli, eyes, festoons (rectangular grooves on the rear margin), ornamentation and the anal groove. Ixodes has the anal groove curving in front of the anus (Prostriata) and has no eyes or festoons. Haemaphysalis has festoons but no eyes, and its second palpal segment projects sideways. Rhipicephalus has short palps, a hexagonal basis capituli, eyes and festoons; Boophilus, now a subgenus of Rhipicephalus, has very short palps, a hexagonal basis and no festoons. Dermacentor is usually ornate, with a rectangular basis capituli. Amblyomma and Hyalomma have long palps; Amblyomma is brightly ornate, Hyalomma large and inornate, often with pale-banded legs.
The hard tick passes through egg, larva, nymph and adult. Each stage takes one large blood meal lasting days, then moults. The engorged female drops off, lays one batch of several thousand eggs and dies. Most of the life is spent off the host, and ticks survive months unfed.
In one-host ticks all stages feed on one animal and only the engorged female drops: Rhipicephalus (Boophilus) microplus, R. (B.) annulatus, R. (B.) decoloratus and Dermacentor albipictus. The parasitic phase of R. microplus lasts about three weeks. In two-host ticks larva and nymph share the first host and the adult finds a second: Rhipicephalus evertsi and some Hyalomma. In three-host ticks every stage drops off and finds a new host: most species, including Ixodes ricinus, R. sanguineus, R. appendiculatus, Haemaphysalis and Amblyomma. Three-host ticks often feed on different host species at each stage, moving pathogens between wildlife, livestock and people. One-host ticks spend longer on the host, so host treatment controls them better, and their pathogens must pass transovarially. R. sanguineus, the brown dog tick, uses dogs for all stages and completes its cycle indoors in kennels. Haemaphysalis longicornis can reproduce parthenogenetically and established rapidly after its introduction to the eastern United States.
Heavy burdens cause blood loss, tick worry, lower growth and milk yield, damaged hides and teats, and wounds that attract blowflies; Amblyomma bites favour abscesses and dermatophilosis. Tick paralysis is an ascending flaccid paralysis from salivary neurotoxins of feeding females: Ixodes holocyclus in eastern Australia, which can progress even after tick removal, Dermacentor andersoni and D. variabilis in North America, where removal usually brings recovery, and I. rubicundus in South Africa. Sweating sickness is a toxicosis of calves caused by Hyalomma truncatum in southern and eastern Africa.
Soft ticks (Argasidae) lack a scutum, have a leathery wrinkled cuticle, and in nymphs and adults the capitulum lies underneath, invisible from above. There are several nymphal stages. Nymphs and adults feed quickly, often in under an hour at night, then hide in cracks, nests, burrows and animal houses; females lay several small batches of eggs. Control therefore targets housing and hiding places.
Argas persicus and relatives are the fowl ticks of warm climates. Larvae stay attached for several days; nymphs and adults feed at night. They cause anaemia, lower egg production and deaths, transmit Borrelia anserina (avian spirochaetosis) and Aegyptianella pullorum, and can cause paralysis in birds. Ornithodoros moubata lives in warthog burrows in eastern and southern Africa and maintains African swine fever virus in the sylvatic cycle, passing it transstadially and transovarially; O. erraticus did so in the Iberian Peninsula. O. coriaceus transmits the agent of epizootic bovine abortion in the western United States. Otobius megnini, the spinose ear tick, is parasitic only as larva and nymph, deep in the ear canals of cattle, horses and dogs; adults do not feed.
Besides Babesia and Theileria (next chapter but one), Anaplasma marginale of cattle is transmitted biologically by Rhipicephalus (Boophilus) and Dermacentor ticks and mechanically by biting flies and needles. Ehrlichia ruminantium (heartwater) is carried by Amblyomma in sub-Saharan Africa and the Caribbean; Ehrlichia canis by R. sanguineus; Anaplasma phagocytophilum (tick-borne fever of ruminants, granulocytic anaplasmosis of dogs, horses and people) and Borrelia burgdorferi sensu lato (Lyme borreliosis) by Ixodes; Rickettsia rickettsii by Dermacentor. Crimean-Congo haemorrhagic fever virus is carried by Hyalomma; livestock are infected without signs but infect farm and slaughter workers. Nairobi sheep disease virus is carried by R. appendiculatus, louping ill and tick-borne encephalitis viruses by Ixodes ricinus. Hepatozoon canis is acquired when a dog swallows an infected R. sanguineus, and Cytauxzoon felis of cats is carried by Amblyomma americanum. Because one tick can carry several agents, co-infections are common, and a dog with ehrlichiosis in an area with R. sanguineus should also be checked for Babesia vogeli, Hepatozoon canis and Anaplasma platys.
Mites are tiny Acari, mostly under 0.5 mm, that in many species complete the whole cycle (egg, larva, nymphs, adult) on the host in about two to three weeks, spreading by contact or fomites.
Sarcoptes scabiei is round with short legs and dorsal spines and scales; some legs end in suckers on long, unjointed stalks (pedicels). Host-adapted varieties infect dogs, pigs, cattle, sheep, goats, camels, horses and people. Females tunnel in the epidermis, and intense pruritus arises largely from hypersensitivity. In dogs lesions start on the ear margins, elbows, hocks and ventral abdomen, and rubbing the ear margin often provokes a hind-leg scratch (pinnal-pedal reflex). Scrapings are often negative, so a negative scraping does not rule out scabies; serology and response to treatment help. In-contact people develop transient itchy papules. In pigs sarcoptic mange causes crusted ears and hypersensitivity dermatitis with poor growth; whole-herd treatment can eradicate it. It is severe in camels and small ruminants.
Notoedres cati causes crusting, intensely itchy mange of the head and ears of cats; it resembles Sarcoptes but is smaller with a dorsal anus. Knemidocoptes mutans causes scaly leg of poultry, K. gallinae depluming itch, and K. pilae crusts on the beak and cere of budgerigars.
Psoroptes is oval with long legs and long, jointed pedicels ending in trumpet-shaped suckers; it lives on the skin surface feeding on exudate. Psoroptes ovis causes sheep scab: intense pruritus, wool loss, yellow crusts over moist lesions, weight loss and death. Mites survive off the host for up to a few weeks, so handling facilities and trucks spread infection. Sheep scab was eradicated from Australia and New Zealand in the nineteenth century and is under statutory control in some countries; an antibody ELISA detects early infestation. Psoroptes also causes body mange in cattle and ear canker in rabbits. Chorioptes bovis has short, unjointed pedicels with cup-shaped suckers and causes mild crusting dermatitis of the tail base, perineum and legs of cattle and of the feathered legs of heavy horses. Otodectes cynotis lives in the ear canals of cats, dogs and ferrets, producing a dark brown waxy discharge; all in-contact animals are treated.
Demodex mites are cigar-shaped with stubby legs and live in hair follicles as normal fauna. D. canis passes from bitch to pups during the first days of nursing and is not otherwise contagious. Disease arises when immune control fails. Localised juvenile demodicosis often resolves; generalised demodicosis, often with deep pyoderma, is serious. Juvenile-onset generalised disease has a hereditary component, so affected dogs should not be bred; adult-onset disease prompts a search for hyperadrenocorticism, hypothyroidism, neoplasia or immunosuppressive drugs. Diagnosis is by deep skin scraping to capillary ooze or trichogram, and treatment continues past repeated negative scrapings. D. gatoi of cats is short, pruritic and contagious; D. bovis causes hide nodules in cattle.
Cheyletiella are large surface mites with hooked palpal claws (C. yasguri on dogs, C. blakei on cats, C. parasitivorax on rabbits) that cause scaling along the back, "walking dandruff," and readily infest people. Diagnosis is by acetate tape, flea combing or superficial scraping. Trombiculid mites (chiggers, harvest mites) are parasitic only as orange larvae, which attach to the feet, legs and ears of animals and people in late summer and autumn.
Dermanyssus gallinae, the poultry red mite, feeds on birds at night and hides in cracks of the house by day; in warm conditions its cycle can be completed in about a week. It causes anaemia, restlessness, lower egg production, deaths in heavy infestations and dermatitis in workers, and is a major problem in laying hens. Ornithonyssus sylviarum, the northern fowl mite, spends its whole life on the bird, concentrated around the vent. Red mite control therefore treats the house between flocks as well as the birds.
Babesia are intra-erythrocytic protozoa causing fever, haemolytic anaemia, haemoglobinuria and jaundice. In tropical and subtropical cattle the key species are B. bigemina and B. bovis, transmitted by one-host Boophilus ticks: Rhipicephalus (Boophilus) microplus, R. (B.) annulatus, and R. (B.) decoloratus (B. bigemina). In 1893 Smith and Kilborne showed that Texas cattle fever was tick-borne, the first proof that an arthropod transmits a protozoan; the United States later eradicated the disease by eradicating Boophilus.
Because the vector never changes host, Babesia passes transovarially: the engorging female ingests parasites, they invade her eggs, and the next generation transmits. B. bovis is transmitted by larvae, B. bigemina mainly by nymphs and adults. B. bigemina is large, in pairs at an acute angle; B. bovis is small, paired at an obtuse angle and more virulent, causing cerebral babesiosis when infected red cells stick in brain capillaries. In Europe B. divergens is transmitted by Ixodes ricinus and is zoonotic in splenectomised people; B. major by Haemaphysalis punctata. In small ruminants B. ovis is carried by Rhipicephalus bursa.
In dogs, B. canis is transmitted by Dermacentor reticulatus in Europe, B. vogeli by R. sanguineus worldwide (usually mildest), and B. rossi by Haemaphysalis elliptica in southern Africa (most virulent). B. gibsoni is carried by Haemaphysalis ticks but also spreads by bites and blood among fighting dogs. Equine piroplasmosis is caused by B. caballi (transovarial) and Theileria equi (transstadial, also transplacental and iatrogenic) and is transmitted by Dermacentor, Hyalomma and Rhipicephalus; carriers make testing necessary for international horse movement.
Theileria multiply as schizonts in leucocytes and then as piroplasms in red cells. Unlike Babesia, they pass only transstadially: a larva or nymph is infected and the next stage transmits, after sporozoites develop in its salivary glands during feeding.
Theileria parva causes East Coast fever in eastern, central and southern Africa and is transmitted by the three-host brown ear tick, Rhipicephalus appendiculatus. Schizonts transform lymphocytes; signs are fever, generalised lymph node enlargement and terminal pulmonary oedema with frothy nasal discharge. Buffalo-derived T. parva causes the acute corridor disease. Immunisation is by infection-and-treatment: live sporozoites given with a long-acting tetracycline.
Theileria annulata causes tropical theileriosis from North Africa and southern Europe through the Middle East to India and China, transmitted mainly by Hyalomma anatolicum and, in some regions, H. scupense. Exotic and crossbred cattle are far more susceptible than indigenous zebu, which is why crossbreeding raised its importance in South Asia. Macroschizonts (Koch's blue bodies) are found in lymph node smears; live attenuated cell-culture schizont vaccines are used in several countries. T. orientalis (Ikeda group) is transmitted by Haemaphysalis longicornis and has caused anaemia outbreaks in Australia and New Zealand; T. lestoquardi causes malignant ovine theileriosis and is transmitted by H. anatolicum.
Calves are naturally resistant to babesiosis for their first months and receive colostral antibodies from immune dams. Where tick challenge is high enough that nearly every calf is infected young, calves become immune with little disease, and adult cases are rare: endemic stability. If tick control is so intensive that many calves escape infection, the herd becomes unstable and adults infected later suffer severe disease. Moving susceptible cattle into tick areas, or ticks into clean areas, also causes outbreaks.
Control combines strategic rather than intensive acaricide use, live attenuated Babesia and Anaplasma vaccines where available, Theileria vaccination or infection-and-treatment, tick-resistant Bos indicus and crossbred cattle, pasture management, and treatment of cases with antiprotozoal drugs (a diamidine or imidocarb for babesiosis, a hydroxynaphthoquinone such as buparvaquone for theileriosis), used according to label and national formulary. Imidocarb leaves long-lasting tissue residues, so withdrawal periods are long and country-specific. In areas where Anaplasma marginale shares the Boophilus vector, the same endemic-stability reasoning applies to anaplasmosis, and the three tick fevers are usually managed together.
Bluetongue is a non-contagious disease of ruminants caused by an orbivirus (family Sedoreoviridae, formerly Reoviridae) with at least 24 classical serotypes and several atypical ones; immunity is largely serotype-specific. Sheep suffer most: fever, oedema of the face and lips, oral ulcers, a swollen, sometimes cyanotic tongue, coronitis, lameness, wool break and deaths. Cattle are usually infected without signs but stay viraemic for weeks and are important sources of virus for midges; BTV-8 in northern Europe from 2006 and BTV-3 from 2023 also caused disease in cattle. Some strains cross the placenta and cause brain malformations. Bluetongue is WOAH-listed and restricts trade in ruminants and germplasm.
The virus is transmitted biologically and propagatively by Culicoides; contact transmission is unimportant for classical serotypes. Ingested virus must infect the midgut, escape it and reach the salivary glands; this extrinsic incubation lasts days to a couple of weeks depending on temperature, and replication slows and stops in cold weather, so transmission is seasonal. C. imicola is the classical vector in Africa, the Mediterranean, the Middle East and South Asia, C. sonorensis in North America, C. brevitarsis in Australia and C. insignis in Latin America; the northern European epidemics showed that the C. obsoletus and C. pulicaris groups are competent. Wind carries infected midges across water and borders.
Control relies on serotype-specific vaccination (inactivated vaccines are preferred in many countries because live strains can cause viraemia and reassort), movement restrictions and zoning, sentinel and vector surveillance, and seasonally vector-free periods. Housing at dusk and dawn, repellents and pyrethroid pour-ons reduce exposure, but evidence that insecticides alone reduce transmission is limited.
Lumpy skin disease (LSD) of cattle and water buffalo is caused by a capripoxvirus (family Poxviridae) related to sheep pox and goat pox viruses. It causes fever, enlarged superficial lymph nodes and firm skin nodules that may become necrotic, with lesions in the mouth and respiratory and genital tracts, limb oedema, mastitis, abortion, infertility in bulls, hide damage and heavy milk loss; mortality is usually low. Long confined to sub-Saharan Africa, it spread to Egypt and Israel, through the Middle East to Turkey, the Balkans and Russia from 2015, to South and East Asia from 2019 (with a large Indian epidemic in 2022) and to Italy and France in 2025. It is WOAH-listed.
LSD virus is transmitted mainly mechanically by blood-feeding arthropods. Stable flies (Stomoxys calcitrans), mosquitoes such as Aedes aegypti, and hard ticks including Rhipicephalus appendiculatus, R. (B.) decoloratus and Amblyomma hebraeum have been implicated; transstadial and transovarial passage in ticks has been reported experimentally. Spread is favoured by warm, wet seasons with many biting flies, by crowding at water points and markets, and by cattle movement. Direct contact transmission is inefficient, but virus in lesions, saliva, semen and milk allows spread through shared needles and semen.
Vaccination is the most effective control: live attenuated homologous vaccines (such as the Neethling strain) controlled the Balkan epidemic within about two years, and heterologous sheep pox or goat pox vaccines, generally somewhat less protective, have been used in the Middle East and South Asia. Vaccination is combined with movement control, quarantine and, in free countries, stamping out. Insecticides, repellents, stable fly breeding-site management and tick control reduce exposure but alone have not stopped epidemics. Examiners like the contrast: bluetongue is biological transmission by Culicoides; LSD is mechanical transmission by many blood-feeding arthropods.
Ectoparasiticides are applied as dips, spray races and jetting, pour-ons and spot-ons, impregnated ear tags and collars, injections, oral tablets and chews, dusts and environmental sprays. The choice depends on the parasite (surface or blood feeder), host, duration of protection, withdrawal periods, operator and environmental safety, and cost. Good practice: confirm the diagnosis, dose to the heaviest animal in a group, calibrate equipment, replenish dips (they strip out active ingredient), treat all in-contact animals and observe label withdrawal periods, which vary by country.
Organophosphates (diazinon, coumaphos, chlorpyrifos) and carbamates (carbaryl, propoxur) inhibit acetylcholinesterase, irreversibly for organophosphates and reversibly for carbamates. Poisoning causes muscarinic signs (salivation, lacrimation, diarrhoea, miosis, bradycardia), nicotinic tremor and weakness, and central signs. Atropine is the antidote; oximes such as pralidoxime help early in organophosphate poisoning but not for carbamates. Operator safety led many countries to restrict these compounds. Organochlorines (DDT, lindane, dieldrin) persist in fat, milk and the environment and are banned for veterinary use in most countries.
Synthetic pyrethroids (permethrin, cypermethrin, deltamethrin, flumethrin) keep voltage-gated sodium channels open, giving rapid knockdown; type II pyrethroids carry an alpha-cyano group. Several repel sandflies, mosquitoes and ticks. They are highly toxic to fish, and permethrin causes tremors and seizures in cats. Amitraz, a formamidine, is an octopamine receptor agonist in arthropods, used against ticks, mites (including Demodex), lice and keds; in mammals it acts as an alpha-2 agonist (sedation, bradycardia, hyperglycaemia, reversible with atipamezole) and it causes colic in horses, in which it must not be used. Fipronil (phenylpyrazole) blocks GABA-gated chloride channels and is toxic to rabbits. Neonicotinoids (imidacloprid, nitenpyram) act at insect nicotinic acetylcholine receptors; oral nitenpyram kills adult fleas within hours but does not persist. Spinosad acts at a different nicotinic site; indoxacarb and metaflumizone block sodium channels.
Macrocyclic lactones, the avermectins (ivermectin, doramectin, eprinomectin, selamectin) and milbemycins (moxidectin, milbemycin oxime), open glutamate-gated chloride channels of invertebrates, causing flaccid paralysis. Because they kill nematodes and arthropods they are called endectocides. Injected, they control sucking lice, mange mites and warble and bot larvae, but chewing lice and ticks less well; pour-ons also reach chewing lice. P-glycoprotein normally keeps them out of the mammalian brain; dogs with the ABCB1 (MDR1) mutation, common in Collies and other herding breeds, can suffer severe neurotoxicity at mange-treatment doses. Residues in dung harm dung beetles and slow pat breakdown. Milk withdrawal differs between members, so check the label in each country.
Isoxazolines (fluralaner, afoxolaner, sarolaner, lotilaner) block arthropod GABA- and glutamate-gated chloride channels with high selectivity. Given orally or topically to dogs and cats, they kill fleas and ticks for weeks to months; several are licensed in some countries for Demodex, Sarcoptes and Otodectes, and fluralaner in drinking water for poultry red mite. Regulators have warned of neurological adverse events (tremors, ataxia, seizures), so a seizure history must be considered.
Insect growth regulators act on development. Juvenile hormone analogues (methoprene, pyriproxyfen) stop immature stages completing development and flea eggs hatching. Chitin synthesis inhibitors (benzoylphenylureas such as lufenuron, diflubenzuron, triflumuron) disrupt new cuticle formation; lufenuron in the pet's blood reaches fleas and stops their eggs developing. Cyromazine and dicyclanil are applied to sheep before the fly season to prevent strike. IGRs reduce adult numbers slowly, so an adulticide is added for existing infestations.
Non-chemical tools include tick-resistant Bos indicus cattle, pasture spelling, manure management, traps and insecticide-treated targets, the sterile insect technique, screening and housing against midges and mosquitoes, Bacillus thuringiensis israelensis against mosquito and blackfly larvae, dung beetles against horn flies, and the recombinant Bm86 anti-tick vaccine, whose effect varies with tick strain.
Resistance is a heritable reduction in a population's susceptibility to a compound that once controlled it, selected by repeated use of one class, by treatments that leave few susceptible parasites unexposed and by underdosing. Mechanisms are target-site insensitivity (kdr sodium-channel mutations affecting DDT and pyrethroids; altered acetylcholinesterase affecting organophosphates; rdl GABA-receptor mutations affecting cyclodienes and fipronil), metabolic detoxification (esterases, cytochrome P450 monooxygenases, glutathione S-transferases), reduced cuticular penetration and behavioural avoidance. Cross-resistance is resistance to several compounds through one shared mechanism; multiple resistance is separate mechanisms to several classes in one population.
Resistance is well documented in Rhipicephalus (Boophilus) microplus, which in parts of Latin America, Australia, Africa and Asia resists organophosphates, pyrethroids, amitraz, macrocyclic lactones and fipronil; in horn flies to pyrethroid ear tags; in house flies to most farm classes; in Lucilia cuprina to organophosphates and increasingly to strike-preventive IGRs; in sheep lice to pyrethroids; and in Psoroptes ovis to pyrethroids and, in some reports, macrocyclic lactones.
Tick resistance is measured with bioassays: the larval packet test (the FAO standard), the larval immersion test, and the adult immersion test, in which dipped engorged females' egg output is compared with untreated controls. Results are given as the LC50 and the resistance ratio (LC50 of field strain divided by LC50 of a susceptible strain); molecular tests detect known mutations. Management aims to slow selection: treat only when needed, dose correctly, keep refugia (unexposed parasites that dilute resistance genes), rotate between classes with different modes of action, usually annually, avoid long tails of low drug concentration, and integrate non-chemical control.
Learn each arthropod as a set: identifying features, life cycle stages and where they live, number of hosts, direct damage, pathogens transmitted and the route (mechanical, transstadial, transovarial, ingestion), and the drug classes that work. Practise identification in the laboratory with a hand lens and microscope: tell a sucking louse from a chewing louse, C. felis from C. canis, Ixodes from Rhipicephalus and Boophilus, and Sarcoptes from Psoroptes, Chorioptes and Demodex. Learn to take a deep and a superficial skin scraping, an acetate tape impression and a trichogram. Link every ectoparasiticide to its target site so that toxicity and cross-resistance questions become logic, not memory.
Diagnose pruritus systematically: flea combing, skin scrapings, tape impressions and trial treatment before steroids. Explain the flea life cycle to owners so they treat every pet and persist long enough. Check a dog's breed and ABCB1 status before high-dose macrocyclic lactones, never dispense permethrin dog products to cat households without warning, and avoid amitraz in horses. For farm clients, identify ticks to genus, time acaricide treatments to the tick's seasonal peaks, protect endemic stability in tick-fever areas, vaccinate against lumpy skin disease and bluetongue where schemes exist, and give a written plan for strike, lice and scab control with withdrawal periods.
Build ectoparasite control into herd and flock health plans that include nutrition, breed choice, biosecurity for purchased stock and housing design. Run resistance testing (larval packet tests through a reference laboratory, or treatment-efficacy checks on farm) before recommending a class change, and keep records of classes used on each client farm so rotation is deliberate. Advise cooperatives and dairies on tick-fever vaccination and on outbreak response to vector-borne notifiable diseases, including movement controls. Train paraprofessionals in correct dosing, dip management, operator safety and residue avoidance. Report suspected product failures and adverse events to the regulator.
Open research questions include how vector species adapt to new pathogens and climates, as with bluetongue in northern Europe and the northward return of New World screwworm; the role of ticks in mechanical and biological spread of lumpy skin disease; overwintering of arboviruses; molecular markers and field tests for resistance in Rhipicephalus microplus, Lucilia and Psoroptes; and durable anti-tick vaccines beyond Bm86. Useful methods include vector competence studies, entomological surveillance and trap networks, modelling of vectorial capacity and R0 under climate scenarios, population genomics of resistance, and randomised field trials of integrated control. Supervise students to report negative trial results and to separate label claims from independent evidence.
No product doses, concentrations, treatment intervals or withdrawal periods are given, because they differ by product, formulation, species and country; drugs are discussed by class and mode of action only. Identification keys are simplified to the features examiners use; full keys to species, detailed mite leg and sucker arrangements, and larval identification of myiasis flies are not reproduced. Triatomine bugs, bed bugs, Pentastomida, fish lice and bee and wildlife parasites are mentioned briefly or not at all. Tick-borne diseases other than babesiosis and theileriosis are listed by vector only; their clinical detail belongs to microbiology and medicine subjects. Trypanosomosis and leishmaniosis are covered here only as vector relationships; the parasites belong to protozoology. Notifiable status and regulatory rules for sheep scab, screwworm, bluetongue and lumpy skin disease vary by country and change often, so current national rules must be checked. Recent events (2023–2025 bluetongue, lumpy skin disease and screwworm spread) are summarised at the level of reliable reports and may be out of date. No images are included yet.
Original practice questions written to the syllabus and pattern of the exams named in each question's examTags. They are not past papers and do not reproduce any board's questions.
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