2. Arachnoentomology

Oral part - Study of Arachnids - spiders, mites etc. and insects. (VS, lecture - intro, insects, mites). pink = fant ikke i pres.. men er fra notes.

1.General Morphology and Classification of ARTHROPODA

Arthropods: Largest in Animal kingdom, 3 major classes are of medical importance: Insecta, Arachnida + crustacea. Over 1mill. known species.

• Ecto- or endoparasites of animals & humans, vectors of pathogens, poisonous animals + household and storage pests.

Classification:

Phylum: Arthropoda (Arthropods)

subphyl:Trilobitomorpha

subphyl: Chelicerata

1. Class: Arachnida (octopoda: ticks, mites, spiders, scorpions)

subclass: Acari - mite, tick (distribution according to localization of stigmata):

• Order: Ixodida (metastigmata)

• Order: Gamasida (mesostigmata)

• Order: Trombidiformes (prostigmata)

• Order: Sarcoptiformes (astigmata)

• Order: Oribatida

Subphylum crustacea:

2. Class: Crustacea (cyclops, crabs)

Subphylum Tracheata:

3. Class: Insecta (hexapoda: mosquitoes, flies, bugs, lice, fleas)

• Order: Heteroptera (true bugs)

• Order: Phthiraptera (lice)

• Order: Diptera (flies)

• Order: Siphonaptera (fleas)

Morphology of Arthropods:

• Body structure: segmented (tagmata)

  • Insects → head, thorax + abdomen

  • Arachnids (spiders) → cephalothorax/gnathosoma (head + chest fused) + abdomen/idiosoma

• Exoskeleton (outer): hard outer covering of chitin, prevents drying out, must moult to grow. Antenna is here.

• Jointed limbs → can move easily, segmented (6), ends in claws. parts + segments are joined by flexible membranes.

• Open vascular system/circulatory - dorsal bv. Fluid - haemolymph inside body (haemocoel)

• NS: ventral nerve cord, sensory organs - anterior ganglia, paired nerve cords, antennae (in insects) - which may/not have receptors

• Digestive system: Mouth → intestine → anus. Mouthparts vary (biting/sucking), salivary gl. make enzymes + toxins.

• Respiratory: gills, trachea or absent (resp. through skin). Air enters through spiracles/stigmata - openings in abdomen/thorax.

• Reproduction: separate sexes - sexual or parthenogenesis (no mating → clones). Most lay eggs. (some are ovoviviparous/viviparous)

• Sensory system: compound eyes → many lenses (sees movement well) or simple eyes → one lense for detecting light

Development by Incomplete & Complete Metamorphosis:

2.Veterinary significance of arthropods as vectors of pathogens

Arthropods can be intermediate hosts for various parasites. They can be vectors of bacteria, virus, parasites and other pathogens. They are very adaptable organisms.

As ectoparasites, they can cause direct harmful effect: blood loss (as bloodsuckers), myasis, skin inflammation, pruritus (skin reactions), their saliva can lead to allergic reactions, and they may produce venom that can be toxic.

Or indirect harmful effect: Disturbance/social nuisance - large amounts can lead to stressed animals/affects behavior/interactions → immunosuppression over time, Self-wounding from trying to get rid of them → causing wounds that attract new flies.

Arthropods as VECTORS of pathogens:

1. Viruses, bacteria - Mechanical vector (passive carrier, no development of pathogen inside vector)

2. Protozoa, tapeworms (cestoda), round worms (nematoda)

• Biological vector - undergoes specific stages of their LC - development and/or reprod. of pathogen before it becomes infective

Common arthropod vectors - for pathogens:

• Malaria: Anopheles mosquito

• Leishmaniosis: sand fly (phlebotomus, Lutzomyia)

• Trypanosomosis: Glossina, kissing bugs (triatoma), horse flies (tabanidae)

• Babesiosis: ticks (rhipicephalus sanguineus, dermacantor reticulatus)

• Moniezia & Anoplocephala spp. (oribatid mites)

• Dirofilarial immitis heart worm

• Myiasis: infestatiuon with insect larvae that develop in tissues of live vertebtrates, ex. botflies like hypoderma bovis.

Can cause severe tissue damage to the host like anemia.

Vector-disease concept: Disease occur when all connect - vector + host + pathogen + environment → transmission.

• Interacts bw. each other, vector takes up pathogen, pathogen develops inside vector → transmitted to host → cause disease → cycle repeats

Types of pathogen development in vectors:

• Propagative transmission: pathogen multiplies only, ex. yellow fever, eastern equine encephalitis (EEE)

• Cyclodevelopmental: pathogen develops, but does not multiply, ex. in filaria - single microfilaria eaten by culex mosquito

• Cyclopropagative: pathogen changes form + multiplies ex. malaria (plasmodium in mosquito, chagas disease)

Transmission

• Direct contact: Host contact with bedding, clothing contaminated with eggs/pupae.

• Adults: actively seek host to feed or lay eggs, mosquitoes (fly to host), fleas jump onto passing host, eggs

• Eggs: contaminating shared environment

  • larvae emerge and feed on hosts tissue.

Parasitic stages:

1. Flies and mosquito – adult stage and larvae

2. Lice – eggs cling to hair/feather

3. Ticks – epidermal parasites, adults feed on blood

4. Mites – adults feed on skin, suck lymph

5. Fleas – larvae are not parasitic but feed on debris associated with bedding. Adult stages are parasitic, feed on host blood. 

3.Parasitic Nematocera 

Nematocera = suborder. Order: Diptera (flies), Class: Insecta

• Families: Culicidae (mosquito), Psychodidae (drain flies), Simuliidae (blackflies), ceratopogonidae (biting midges, culicoides)

General - Nematocera:

• Typical antennae (6 and more segments)

• Slim body (except - simuliidae) + long limbs

• Hematophagous LC (sucks blood). Only females feed on blood.

• Found in aquatic/semiaquatic habitat, LC depend on moisture

• Animals - protected by antiparasitic drugs, repellents, spot-on, collars

1) Culicidae (Mosquitoes)

• 3-6mm (small)

• Subfam: anophelinae (genus: anopheles) & Culicinae (genus: aedes, culex - vectors for avian pox, filarial worms, equine encephalitis)

2) Psychodidae (Drain flies)

• Genus: Phlebotomus, Lutzomyia - Vectors of Leishmania

3) Simullidae (Black flies)

• genus: Prosimulium, simulium

• Clinical signs: Combined effect of anaphylactic reaction, blood loss, inhalation of flies + pulmonary edema → rapid death of animals.

  • Toxins in saliva → subcutaneous edema, pruritus, vascular damage, hypersensitivity reaction.

• Simuliotoxicosis - vectors of: leucocytozoon, viruses of stomatitis, trypanosoma, dirofilaria. onchocerca spp.

4) Ceratopogonidae (Biting midges)

• Genus: Culicoides with species like: C. obsoletus, C. oulicaris, C. pulicaris

  • Biting midges (culicoides) are vectors of trypanosoma, Haemoproteus, Hepatocystis, Leukocytozoon: Mansonella, Onchocerca, viruses like Blue tongue virus

  • Clinical signs: cause chronic lesions of lichenification and alopecia in horses with Culicoides hypersensitivity. Use antihistamine and corticosteroids for treatment.

4. Parasitic Brachycera 

Order: Diptera

Suborder: Brachycera (Tabanids - horse flies, deer flies)

Family: Tabanindae – Horse flies, livestock pests but do not often bite humans

Subfamily: Tabanidae (horse fly, livestock biters), Chrysopinae (deer fly, licestock and people biters)

Main genus - coloration of wings used to differentaite

Tabanus spp (horse fly, klegg) – Surra disease
Chrysops (dark transverse band)

Haematopota (mottled)

Morphology: Large flies, over 25mm, may be brown-gray-yellowish, vary in color. Robust blood sucking flies with thick but short antennae (3 segments), large compound eyes, two-winged and has a wide head. Females have adapted mouthparts to pierce and cut skin, and then feed on blood. They belong to order diptera and have the same morphology as the rest: open respiratory system, 3 segmented body, nervous and circulatory system, 3 legs…

Life cycle: Complete metamorphosis with min 6 larval stages. Female lays batches of eggs on underside of vegetation or on stones in muddy areas. Eggs hatch within 12 weeks ->  larvae drop into water. Larval development takes 3 months in optimal conditions but may extend up to 3 years. Pupa is subcylindrical and brown. Pupate for 1-3 weeks.

Vector for: Active during hot, sunny weather. Found worldwide. Vectors for many diseases like Surra, Q fever, anthrax, hog cholera, equine infectious anemia, California encephalitis ect. Can be a serious irritation to the livestock animals, may cause stress and self-harm.

Treatment: Important to use insecticides and repellent during summer when the weather is warmer. 

5. Hypodermosis of cattle.

Class: Insecta

Order: Diptera

Family: Oestridae

Cattle hypodermosis is caused by warble fly infestation, specifically: Hypoderma bovis (common cattle grub) and Hypoderma lineatum (northerns cattle grub). The larvae cause a subcutaneous myiasis.

 

Morphology:

Larvae – mature larvae are thick and barrel-shaped. 2.5-3cm and most segments bears short spines. They appear white when newly emerged, but rapidly turns into dark brown.

Pupa is almost black.

Adult – bee-like, hairy. Without functional mouthparts. It has hairs on head and anterior part of thorax. Yellowish-white in H. bovis, and greenish-yellow in H. lineatum.

The female is long ovipositor, which is telescoped into the abdomen at rest.

Geographical distribution: Worldwide.

Life cycle: H. bovis. They never fly into stables, only affect grazing cattle.

Female deposits eggs on the hair on the distal part of the body of cattle during June-september. The larvae hatch within 24h, burrow into the skin and migrate through facial and perineural tissue to nerve fibers and spinal canal. Stay in epidural fat for a long time, until march next year. Larva comes back to the skin and form a warble. Larva then molts to L2 and L3. They penetrate the skin, pupate and pupa fall on the ground and adult emerges, ready start next generation.

H. lineatum – Similar but eggs are laid in batches, L1 penetrate to submucosa of esophagus, stay in esophageal wall and come back via diaphragma to subcutaneous tissue of the back.

 

Pathology and clinical signs: Warble flies laying eggs causes irritation to the cattle which can lead to injuries, cattle may stump legs. Larval migration is not usually noticed clinically, but heavy infestations may reduce growth and milk production. Occasionally, pressure of larvae on spinal cord can cause paralysis.

Diagnosis: Presence of larvae under skin of back. ELISA.  

Treatment: Ivermectin, moxidectin, cydectin, make sure they don’t conflict with each other. But only treatment in March-October. During winter, the larvae are in spinal cord or esophagus, killing the larvae can cause problems with removing the dead larvae, like paralysis, ataxia and death 

6. Oestrosis of sheep and rhinoestrosis of horses.

Class: Insecta

Order: Diptera

Family: Oestridae

Oestrosis is nasal myiasis, caused by Oestrus ovis (sheep nasal bot fly) – “head maggot”

Morphology:

Larvae – young ones are white or light yellow in color. When mature, a dark transverse band develop on dorsal segments. Full grown larva is 3cm. They have large, black, oral hooks, connected to internal cephalopharyngeal skeleton. Ventral surfaces bears rows of small spines.

Adult – greyish, 10-12mm. Ornamented with numerous black spots, especially on thorax. Not as hairy as bot flies or warble flies.

Geographical distribution: Worldwide.

Life cycle: female is viviparous and released larvae in the nostrils or mouth edges by squirting. L1 migrate through nasal passages and attach by hooks which causes irritation. -> moulting into L2 which migrate into frontal sinus and develop into L3 -> (takes long time) migrate back to nostrils and fall to ground by coughing or actively, where it moults into pulpa and pupate into adult.

Larvae can stay in nose/frontal sinus during winter and complete migration when the weather gets warmer in spring. Males die after copulation. June to April.

 

Pathology and clinical signs: Nasal discharge, rubbing, sneezing, weight loss, circling and lack of coordination. Larvae and thickening mucosa cause impaired respiration – inflammation and mechanical damage. Abnormal migration can cause pneumonia and death.

Diagnosis: Clinical signs assist, but may need to be differentiated from other conditions with similar symptoms. Can confirm with endoscopy. ELISA. Necropsy is needed.

Treatment: Macrocylic lactones – ivermectin, doramectin and moxidectin + closantel.

Rhinoestrosis of horses.

Caused by larvae of flies belong to genus Rhinoestrus.

Rhinoestrus purpureus and Rhinoestrus usbekistanicus parasitise horses, donkeys and zebras.

Morphology: Adults are yellowish to gray/brown and quite hairy. Mouthparts are rudimentary.

Geographical distribution: worldwide

Life cycle: Similar to sheep.  

Clinical signs: Same as in sheep.

Diagnosis: Same

Treatment: Same

7. Gasterophilosis in horses.

Family: Oesteridae

Gasterophilus intestinalis – most common type, found in duodenum

G. haemorrhoidalis – Stomach and rectum

G. pecorum – stomach and rectum

G. inermis – found in esophagus and stomach

G. nigiricornis – duodenum

 

Morphology: Adults are robust dark flies, 1-2 cm.

Larvae – yellowish-brown, narrowed anteriorly. Prominent oral hooks and 11 visible segments. 2 rows of blunt spines on all segments except the last. 

Life cycle: Adult bot flies lay eggs on the horses hair coat in late June-august. Eggs hatch only if horses licked and eat them. Moisture, warmth and friction stimulate larval hatch. Larvae migrate to mouth and burrow in the gap between molars and premolars for 1 month -> L2 which migrates to its predilection site in GIT -> L3. It stays in its specific location until April and are then released with feces. They pupate in the environment. Takes 2 months for adults to emerge.
Pathology and Clinical signs: Burrowing L1 and L2 stages in tongue and mouth may result in lesions and tunnels which may become infected. Inflammation and ulceration of stomach and intestine. Formation of ulcers present as irritation, colic, anemia, inappetence, and may lead to necrosis and sever inflammation.

Diagnosis: Endoscopy show clusters looking like many grapes.

Treatment: Ivermectin.

8. Myiasis.

Myiasis is a parasitic infestation of organs and tissues by dipterous larva (maggots), they grow inside the host while feeding on living or dead tissue. Hosts are usually mammals, humans and occasionally birds, reptiles and amphibiens.

Main families:
Oder: Diptera

Family: Oesteridae – Warble flies (highly specific species. Accidental or pseudomyiasis). Most advances myiasis adaption. Adults live only for 1 week. Mouthparts are non-functional, they do not feed.

• Hypoderma spp (under skin)

• Dermatobia spp (under skin)

• Gasteriphilus spp (GIT)

• Oestrus spp (nasal cavity) + rhinoestrus

Family: Sarcophigidae (permanent myiasis, flesh flies). Accidental or pseudomyiasis.

·       Sarcophaga spp

·       Wohlfarthia spp (wound, meat, primarily infests humans)

Family: calliphoridae – blow and screw flies. They develop in animal flesh. Facultative and obligatory.

• Cochliomyia spp – Screw-form myiosis. Cochliomyia hominivorax and Chrysoma bezziana in humans invade nose, mouth ad eyes, cause severe pain.

• Chrymosoma spp

• Lucilia spp –  Blowfly-strike myiasis. Destroy the skin and cause inflammation. Flies are attracted to lay eggs on warm wet skin, especially urine and fecal stained areas and wounds. Burrow deep into the skin and muscle.

• Phormia spp

• Calliphora spp

Life cycle: Obligate require living host to deposit larvae. Facultative and accidental can use carcasses and living hosts. Eggs are deposited on the host, either my eggs in hair, squirted into nasal passage, penentrate and or being licked up. Larvae usually hatch within 24h, migrate to tissue and molt twice. They feed and leave the host, pupate in the environment and emerge as an adult. Egg deposition is often done in open wounds. Botflies and warble flies have long larval development, 8-10 months.

Pathology and clinical signs: The parasites can cause mechanical damage of tissues. They release proteolytic enzymes which dissolves tissues, and suffer deep and extensive damage and strong exudate formation. Can cause bacterial infection, inflammation and the animal may die. Clinical signs are dull, lethargic, anemic, irritated, secondary bacterial infections. Often cause weight loss.

Diagnosis: Tunnelling lesions, suspicious wound yielding larvae, necropsy findings

Treatment: Subdermal warble forming larvae should be removed surgically.

Cutaneus myiasis, larvae should be removed and wound cleaned and disinfected. Ivermectin, eprinomectin, moxidectin and doramectin may also be effective against cutaneous myiasis, but are particularly effective against nasopharyngeal, subdermal and gastrointestinal myiasis.
Wounds should be properly dresses to prevent infection. In areas with many flies – avoid branding, dehorning and ear marking during fly season. 

9. Melophagosis. (in sheep)

Family: Hippoboscidae (louse flies)

Melophagosis is known to occur in sheep, caused by melophagus ovinus (sheep ked).

Capable of transmitting bluetongue virus, can also carry other diseases like Border disease virus (BDV).

Morphology: Brown, hairy fly that resembles a tick. Host specific, permanent ectoparasite. It is wingless, has a small head. Dorsoventrally flattened. Very strong legs and tipped claws. They have 6 legs (true ticks have 8). Small compound eyes. When the ked is released for its pupa they have wings, but break when they attach to the host (exception is Hippobosca equina). Found worldwide.

 

Life cycle: Live their whole lives in the wool of sheep. Hematophagus (blood sucking). They stay in the fleece of chest and neck area or abdominal wall.  They have complete metamorphosis.

The uterus of the females are adapted to develop larvae, so they release larvae not eggs. Female produces one single larvae at a time. It is retained inside the body for 1 week before it pupates. The pupae is glued to the wool. Females live for about 4 months and only produce 10-13 puparia. Population increase in winter due to longer wool and spread by contact.

Clinical signs: heavy infestation present with itching, dirty wool with feces from flies, wool loss, inflammation of skin via allergic reactions, small nodules on skin surface with hemorrhages. Cause high economic losses in some areas. Populations increase during winter due to longer wool.

Diagnosis: adults and pupa on surface and fleece.

Treatment: pour on with pyrethroids (deltamethrin), dipping method. There are no repellents to prevent louse fly infestations. Frequent change in the bedding of stables will eliminate deposited pupae.

10. Lice of mammals (Anoplura).

Lice are insects belonging to order Phtiraptera. Includes four suborders:

-        Anoplura (sucking lice)

-        Amblycera and Ischnocera (biting or chewing lice)

They are highly adapted to parasitic life, permanent ectoparasites and are highly specific to animals. Humans cannot get lice from pets, and pets not from humans, species specific!!

General characteristics: They are small 0.5-8mm, dorsoventrally flattened, have no wings but strong legs with one or two terminal claws. They live attached to the hair of their host. Feed either on skin debris, sebaceous secretions or blood. Lice can either be chewing, with chewing mouthparts and wider head than thorax or sucking, with piercing-sucking mouthparts, head more narrow than thorax and more distinct claws on legs. Eyes are rudimentary.

Order: Phtiraptera

            Suborder: Anoplura (sucking lice, only mammals)

                        Family: Pediculidae (can carry diseases, like salmonellosis and typohoid fever)

                                   Haematopinidae (main one of veterinary importance)

                                   Linognathidae

                                   Hoplopleuridae (mainly in rodents)

Morphology: Piercing-sucking mouthparts. Head elongated and narrower than thorax. Thorax has 3 segments, fused together. Abdomen is relatively large, segments often bear at their sides.  Legs have distinct claws (1 on each leg in mammals), 6-legged, adapted for clinging to hair/fur. They are not very mobile. Transfer by contact with maximum populations in winter. Variable size and color. Most are blind, only a few species have primitive eyes (photosensitive spots). All developmental stages suck blood.

Life cycle: Incomplete metamorphosis. Both sucking and chewing lice have similar life cycle. Life span is around 1 month. Female lay 200-300 eggs, usually white and is glued to the hair (or feathers). The eggs hatch in 1-2 weeks, goes through 3 nymph stages before becoming adults. Whole life cycle takes about 2-4 weeks. Can be vectors of Rickettsia and borelia.

Ruminants and pigs

Haematopinous eurysternus – Cattle

Linognathus vituli – Cattle

Solenoptes capillatus – Cattle

Linognathus ovillus – Sheep

Linognathus pedalis – Sheep

Linognathus stenopsis – Goat

Haematopinus suis – Pigs

Sucking lice in ruminants are typically found on the head, neck and shoulders, base of tail, back and rump. Heavy infestations often reduces productivity and causes scratching, hair loss and self-inflicted trauma. In cattle and sheep, an hypersensitivity reaction to allergens present in the feces or saliva of the lice could be responsible for these clinical signs. Heavy infections of sucking lice can cause anemia.

In pigs, we can find sucking lice by the ears and neck. Cause itching, skin lesions and can survive off its host for 3 days.

Dogs and cats

Linognathus setosus – dogs

Pruritus may be variable, some animals can be asymptomatic carriers, other present with seborrhoea. It is important to differentiate from other possible diagnosis with similar clinical signs like flea allergy dermatitis, cheyltiellosis, scabies, dermatophytosis and allergy.

Diagnosis: History and clinical signs. Identification from samples of skin and hair, adult and eggs seen under microscope. Acetate tapes or superficial skin scrapings. Sucking lice are slow to move, easy to catch. Eggs can be stuck to hairs.

Treatment: Drugs used to treat mange are usually effective against lice too. Can use pyrethroids and treatment must be repeated after 10 days. Can use different pour on formulations and avermectins in ruminants. In dogs and cats we use insecticidal shampoo or leace on dips 3 times in 14 days. Fipronil, imidacloprid, pyriprole, metaflumizole and selamectin are effective.

Pediculidae

Pediculus capitis – Humans. head louse (all have had them).

Pediculus humanus–  Humans likes to live in clothing, body louse, spread infection.

11. (Biting lice of mammals) Ischnocera of mammals

Lice are insects belonging to order Phtiraptera. Includes four suborders:

• Anoplura (sucking lice)

• Amblycera and Ischnocera (biting or chewing lice)

They are highly adapted to parasitic life, permanent ectoparasites and are highly specific to animals. Humans cannot get lice from pets, and pets not from humans, species specific!!

General characteristics: They are small 0.5-8mm, dorsoventrally flattened, have no wings but strong legs with one or two terminal claws. They live attached to the hair of their host. Feed either on skin debris, sebaceous secretions or blood. Lice can either be chewing, with chewing mouthparts and wider head than thorax or sucking, with piercing-sucking mouthparts, head more narrow than thorax and more distinct claws on legs.

Order: Phtiraptera

            Suborder: Anoplura (sucking lice, only mammals)

            Suborder: Ischnocera (chewing lice, mammals and birds)         

Morphology: Dorso-ventrally flattened and wingless. Head not pointed, more somewhat broadened. Mouthpart adapted for chewing. Very mobile. Thorax is segmented. Legs are not adapted for clinging. Host specific, transfer by contact. Feed on keratin.

Life cycle: Same as sucking lice. Incomplete metamorphosis. Both sucking and chewing lice have similar life cycle. Life span is around 1 month. Female lay 200-300 eggs, usually white and is glued to the hair (or feathers). The eggs hatch in 1-2 weeks, goes through 3 nymph stages before becoming adults. Whole life cycle takes about 2-4 weeks.

Ruminants and pigs

Dalmalinia (bovicola) bovis – cattle

Dalmalinia (bovicola) ovis – sheep

Dalmalinia (bovicola) caprae – goat

Dalmalinia equi - horse (only species of lice normally in Norway)

Sucking lice in ruminants are typically found on the head, neck and shoulders, base of tail, back and rump. Heavy infestations often reduces productivity and causes scratching, hair loss and self-inflicted trauma. In cattle and sheep, an hypersensitivity reaction to allergens present in the feces or saliva of the lice could be responsible for these clinical signs. Heavy infections of sucking lice can cause anemia.

Dogs and cats

Trichodectes canis – dog

Heterodoxus spiniger – dog

Felicola subrostratus – cat

Pruritus may be variable, some animals can be asymptomatic carriers, other present with seborrhoea. It is important to differentiate from other possible diagnosis with similar clinical signs like flea allergy dermatitis, cheyltiellosis, scabies, dermatophytosis and allergy.

Diagnosis: History and clinical signs. Identification from samples of skin and hair, adult and eggs seen under microscope. Acetate tapes or superficial skin scrapings. Eggs can be stuck to hairs.

Treatment: Drugs used to treat mange are usually effective against lice too. Can use pyrethroids and treatment must be repeated after 10 days. Can use different pour on formulations and avermectins in ruminants. In dogs and cats we use insecticidal shampoo or leace on dips 3 times in 14 days. Fipronil, imidacloprid, pyriprole, metaflumizole and selamectin are effective. 

12. Biting lice of birds (Amblycera + Ischnocera). 

Lice are insects (class: INSECTA) belonging to order Phtiraptera. Includes three suborders:

-        Anoplura (sucking lice)

-        Amblycera and Ischnocera (biting or chewing lice)

They are highly adapted to parasitic life, permanent ectoparasites and are highly specific to animals. Humans cannot get lice from pets, and pets not from humans, species specific!!

General characteristics: They are small 0.5-8mm, dorsoventrally flattened, have no wings but strong legs with one or two terminal claws. They live attached to the hair of their host. Feed either on skin debris, sebaceous secretions or blood. Lice can either be chewing, with chewing mouthparts and wider head than thorax or sucking, with piercing-sucking mouthparts, head more narrow than thorax and more distinct claws on legs.

Order: Phtiraptera

            Suborder: Amblycera (chewing lice, birds)

            Suborder: Ischnocera

Morphology: Dorso-ventrally flattened and wingless. Head not pointed, more somewhat broadened. Mouthpart adapted for chewing. Very mobile. Thorax is segmented. Legs are not adapted for clinging. Host specific, transfer by contact. Feed on keratin.

Life cycle: Same as sucking lice. Incomplete metamorphosis. Both sucking and chewing lice have similar life cycle. Life span is around 1 month. Female lay 200-300 eggs, usually white and is glued to the hair (or feathers). The eggs hatch in 1-2 weeks, goes through 3 nymph stages before becoming adults. Whole life cycle takes about 2-4 weeks.
 
Most pathogenic: Lipeurus and Menacanthus

Lipeurus caponis (wing lice) - ischnocera

Menacanthus stramineus (body lice) - amblycera

Menopon gallinae (quill lice) - amblycera

Goniocotes gallinae (very small) - ischnocera

Goniodes gigas (bighen lice) - ischnocera

Columbicola columbae - Ischnocera

Pathogenesis and clinical signs: Picking of feathers, damage and droppings. Reduction of tooth. Weight loss, anemia, young birds may die, restlessness. Heavy infestations decrease reproductive potential in males, egg production in females and weight gain in growing chickens. Skin lesions are sites for secondary bacterial infections

Diagnosis: History and clinical signs. Identification from samples of skin and hair, adult and eggs seen under microscope. Acetate tapes or superficial skin scrapings. Sucking lice are slow to move, easy to catch. Eggs can be stuck to hairs/feathers.

Treatment: Drugs used to treat mange are usually effective against lice too. In dogs and cats (and birds) we use insecticidal shampoo or leave on dips. Preparations based on cypermethrin and permethrin. Repeat treatment after 14 days. 

13. Fleas (Siphonaptera) of mammals and birds.

Class: Insecta

Order: Siphonapteria

Morphology: Laterally flattened, covered with bristles, simple eyes, mouthparts are hard and adapted to piercing and sucking blood. Wingless, strong and large legs adapted for jumping. Abdomen is bigger. Thick, dark brown chitinous covering.

 

Life cycle: Fleas are NOT species specific. Fleas can live for months without a blood meal, but during that time it is aggressively using all its powers to locate the host. Once it finds a host, it will never purposely leave it.

Complete metamorphosis. Female lays white eggs loosely on hairs, in feather or in habitat of host. Eggs fall off hosts onto the ground, floor, bedding or furniture. They hatch into larvae. Larvae are maggot-like, brownish head and coat of bristles. They have chewing mouthpart and feed on debris and feces from adult fleas which contain blood and give larvae a reddish color. Larvae moults twice and then makes a cocoon, 1 week later an adult emerges.

 

Pathogenesis and clinical signs: Cause itching, erythema papules on surface. Saliva have different enzymes, with proteolytic, cytolytic, and anticoagulant properties. Lysis of tissues, inhibition of blood coagulation, inflammatory skin reaction. Special antigens in flee saliva (haptens), together with dermal collagen can cause allergic reaction Flea allergy dermatitis (FAD) is the most common skin disease in dogs, military dermatitis in cats. Repeated flea infestations can sensitize the host to allergens in flea saliva. Should always be considered a differential diagnosis in many cases of pruritus. Most commonly 3-5 years of age. Non-allergic animals tolerate fleas and develop minimal dermatolgical signs. But they can have anemia, mild skin irritation, tapeworms, acute moist dermatitis (hot spots), alopecia and hyperkeratosis.

Acutely pruritic crusted papules with erythema, areas of acute moist dermatis.

Diagnosis: History and clinical signs. Identification of fleas or flea “dirt”. Intradermal allergy or in vitro allergy testing with flea allergens. Response to strict flea control programme. Biopsy.

Treatment: Use topical spot on or spray therapy with fiprinol, imidacloprid, sedamectin for prevention. Minimize flea infestation of all animals in household. Break the flea life cycle, control the allergic reaction of flea bite. Treated with mechanical approach of chemical treatment with insecticides. Topical spot on or spray therapy (frontline). Glucocorticoids may be given to help control itching. Antibiotics should be given for secondary pyoderma, if so glucocorticoids should not be given.

14. Hard ticks - morphology, life cycle, significance

Order: Ixodida (hard and soft ticks)

Family: Ixodidae (hard ticks)

Morphology: They are dorsoventrally flattened when not engored, round/oval shape, more posterior rounded. Their body is covered by very hard chitin shell – the scutum. On females, the scutum only covers 1/3 of the idiosoma, while in males it covers the whole body and they are therefore unable to suck blood. Nymphal stages and females suck blood. The gnathosoma has chelicera, hypostome, and one pair of palps. The chelicera cut the skin, then the hypostome is used to pierce the skin and has teeth that fixe it inside. The palpa have hairs that serve as sensory organs. On the base of the gnathosoma, there is basis capitula with sensitive cells – area porosae. The position of area porosae is species specific and used for species identification. The most important sensory organ is the Haller’s organ on the first tarsus (first leg). It detects odors and hosts. Some species have festoons at the caudal end of the idiosoma. They have 4 pairs of legs, 6-sigmented. Some have colored enamel-like area on the body called ornate ticks.

The internal organs are located in the caudal part of the idiosoma. Genital opening is in ventral midline and anus is posterior. Mouthparts adapted for piercing and sucking, salivary glnads which can secrete toxins.

Eyes are present in some species and are reduced.

Life cycle: Ticks can have one, two or three hosts (all stages in different hosts). They are found in grass ect and hang on animals when they touch grass. Incomplete hemimetabolous. Egg -> Larvae -> Nymph -> Adult. They are not permanent parasites.

Life cycle has 4 stages. Adult females feed on blood for 5-10 days, males don’t suck blood but are on the host to find mates. Engorged females lay eggs on the ground. The eggs hatch and release larvae. Ticks require blood in each stage in order to survive, so the larvae must find host, often a small mammal or a bird. After a blood meal, the larvae molt into a nymph. The nymph must also feed. They have 4 legs (only larvae have 3). Members of Ixodidae have one nymphal instar, but Argasids have 2-8. Nymphs molt again into adult. The adult feed on larger mammals until it is time to lay eggs.

 

Three-host: Dermacentor, Haemaphysalis, Ixodes

Two host: Hyalomma, Rhipicephalus

One-host: Amblyoma, Anocentor (Boophilus)

Why is does ticks have high vector potential? They have a relatively slow feeding time, which allows time for pathogens to transfer and they have a wide host range. Feeding on blood makes them able to take up various pathogens. They have few natural enemies and a high reproduction potential, producing up to 18 000 eggs in some species. They also have transovarial and transstadial transmission of some pathogens.

Significance – Medical importance of ticks

• Dermatosis – inflammation, itching, swelling at site of bite

• Anemia can result from heavy infestation

• Otoacariasis – auditory canal infestation, post. Secondary infections

• Predispose to myiasis and infection

• Tick paralysis (enveomization)

• Pathogen transmission (virus, ricketta, bacteria, spirochaete, protozoa, filarial worms)

Pathogenesis and clinical signs: Ticks cause a first local lesion at site of bite, erythema and itching. Ulceration can occur and invite secondary bacterial infections and myiasis. Some can release neurotoxins (eg. Hyalomma and Rhipicephalus), that block neuromuscular function and form paralysis.

Diagnosis: Engorged females easily recognized under microscope.

Treatment: Acaricides (chemical that kills ticks), used in forms of sprays, spot-on, collars and dips.

Ixodes Ricinus – Ixodes is the largest genus of hard ticks. Most prevalent species in Europe and worldwide. Wide host range, over 200 different species of mammals and birds.

Ixodes hexagonus (hedgehog tick) is usually found in hunting dogs. All stages are active through the year. Can transmit borelia.

Haemaphysialis – Occur most in Africa, South Asia and western and central Europe. Most important in Slovakia. Have a red-brown color.

H. punctata (red sheep tick)

H. concinna

H. inermis

Rhipicephalus sanguineus (brown dog tick, kennel tick). Ca 80 species, found in Africa and Europe. All stages affects dogs.

 

Dermacentor (ornate ticks)

D. marginatus (omate sheep tick)

D. reticulatus

D. variabilis

D. andersoni

Ca 35 species, found in Asia, Europe, Africa and America. Main vector of babesia canis canis.

Hyalomma They have striped legs and are bigger.

H. anatolicum – Vector of Theileria annulate, T. equi, T. lestoquardi

H. marginatum – 2 host tick. Babesia occultans, T. equi

H. aegyptian – 3 host tick

25 species, found in Africa, Asia, Southern Europe

 

Amblyomma (large ornamented ticks)

A. hebraeum

A. variegatum

A. Americanum

A. maculatum

140 species, found in Sub Saharan Africa, America, NOT in Europe

15. Soft ticks (Argasid ticks) – the most important species. 

Differences from hard ticks: Scutum is missing. Cannot see gnathosoma from dorsal view, more rounded bodies. Life cycle is shorter than hard ticks and they have 2-8 nymphal stages. Adult males also suck blood during their life. Blood feeding lasts 20-30 minutes (several days in hard ticks). They lay fever eggs. Nymphal stages feed several times (hard ticks only once).

Order: Ixodida
Family: Argasidae (soft ticks)

Genus: Argas, ornitodoros, Otobius

Argas reflecus (pigeon tick) – Bite at featherless sites on inner surface of thighs, under the wings and at neck. Pigeons are restless at night, devitalized, poor flight performance. Repeated infestation can lead to life-threatening anemia and death in nestling and young animals.

Diagnosed by inspection of nesting and resting places and the presence of ticks.

Treated with acaricides.

A. persicus (chicken tick) – cause toxicosis, release neurotoxins and form severe paralysis. Cause high loses due to painful bites and heavy blood consumtion.

Otobius spp.

O. lagophilus (rabbits)

O. megnini (larvae and nymphs a found inside the ear. Adults are difficult to find as they breed in hidden cracks of barns, fences and trees)

Only larvae and nymphs infest hosts! Can cause digestive and nervous disturbance. Secondary bacterial infections may extend with serious result. Ulceration, may clog ears and cause deafness, waxy or oily material is discharged from ear.

Diagnosed: Visual sighting of the tick on the outer part of the ear canal or inside the canal

Treatment: manually removing the tick, dipping or spraying the animal and treating the environment. Treated with acaricide.

Ornitodoros spp.

O. lahorensis

O. moubata (feed on pigs, birds and reptiles) Transmit African swine fever.

O. moubata porcinus

O. savignyi

Cause blood loss and local reactions, severe irritation and toxicosis

16. Sarcoptosis and notoedrosis of mammals.

Order: Sarcoptiformes /Astigmata

Family: Sarcoptidae

Genus: Sarcoptes

Sarcoptosis is one of the mites that cause mange/scab. Burrowing mite! = Skabb

Sarcoptes scabiei var. – Zoonotic! Seen in dogs, pigs, cattle and small ruminants. Host specific!

Morphology: Small, round, 0.2-0.5mm. Gnathosoma is short, short legs. 1^st and 2^nd pair of legs are significantly separated from 3^rd and 4^th pair. Gnathosoma is very short. Chewing function. Form tunnels under the skin. Missing eyes and stigma. They have triangular scales and transversial striations. Varying number of ambulacrum. 

Life cycle: Typically start at the head around ears and eyes. As they develop and reproduce, they migrate to other parts of the body. Females burrow under the skin deeply, form tunnels, irritating keratocytes which start to reproduce. Only one female in each tunnel. They release 3-5 oval eggs each days. 2 days later the larva hatch, with 3 pairs of legs. They form tunnels and moult to protonympha. Protonympha - deutonympha - tritonympha go back to skin surface and burrows its own tunnel - adult - male fertilizes and they are fertilized for life due to semen pouch.

They prefers skin without hair – head, neck, auricle, and later migrate to other regions.

Pathogenesis and clinical signs: Incubation period is 1-3 weeks. Starts off with severe itching, erythrema, formation of papules, hyperkeratosis and hard crusting of the skin. Vertical skin folds occur due to allergic reactions, alopecia, scratching, rubbing. Can cause chronic disease with weight loss, abnormal behavior and unthriftiness, may even cause death. Depress growth rate and feed efficiency.

Diagnosis: based on history and clinical signs. Skin scrapings (until capillary bleeding) under microscopical examination, but difficult to find - skin biopsies. Serology – ELISA, raised allergen-specific IgE and IgG. Many other differential diagnosis (flea allergy dermatitis, Malassezia dermatitis, atopic dermatitis ect).

Treatment: Selamectin, moxidectin or amitraz (not in horses). Infested bedding should be disposed and antiparasitic sprays should be used in environment, permethrin. Glucocorticoids may be useful in severe pruritus.

 

Notoedric mange (feline scabies, of rabbits and rodents)

Notoedres cati

N. cuniculi

N. muris

N. musculi

Morphology: Similar to S. scabei, but it is smaller.

Life cycle: Similar to S. scabei. Transmission by direct contact.

Pathogenesis and clinical signs: Start with itching, first lesion on the edge of ears, rapid spread to forehead, neck. Cause thick skin and wrinkles. Cause self-mutulation - excoriations and alopecia.

Diagnosis: Same as S. scabei.  

Treatment:Amitraz, selamectin, fipronil, lime sulphur. Glucocorticoids may be useful in severe pruritic animals. Pyoderma can occur as a rare secondary complication, treated with antibiotics

17. Cnemidocoptosis and cytoditosis

Order: Sarcoptiformes /Astigmata

Family: 

Cnemidocoptidae  (chewing mites)

Cnemidocoptes mutans – keratinization of legs, scaly leg

C. gallinae – loss of feathers

C. pilae – scaly face, tassel foot

C. prolificus

Morphology: Similar in general to S. scabiei but there are rounder. Gnathosoma is short and legs are shorter. Chewing mouth parts. Legs with pedunculated ambulacrum, sometimes reduced.

Life cycle: Fertilized (viviparous) female burrowing in upper layers of epidermis -> give birth to live larvae. Larvae crawl to skin surface and burrows in superficial layers and create moulting pockets where they moult into protonymph and then tritonymph before they become adults. 2 nymphal stages.

Pathogenesis and clinical signs: Localized in the corneal layer of the skin on legs. Irritate, exudate dries on surface and forms hard calcierous mass on surface. On exotic birds it is typical with beak formation (C. pilae), difficult to eat and drink, also sometimes breathing, mites can migrate and cover the eyes. Pruritus is severe. Long lasting disease -> weight loss.

Diagnosis: Identified under microscope by skin scraping

Treatment: removing the scales with glycerine. Acaricides (Ivermectin, amitrax, pyrthroids), supportive vitamin A. Treatment repeated for 8-10 days.

Cytoditosis

Family: Cytoditidae

Cytodites nudus – Cause acarinosis of the respiratory organs and subcutaneous tissue

Morphology: Oval. Gnathosoma small and rounded. Legs are longer.

Clinical signs: Often without clinical signs, but can show breathing difficulties, granulomatous bronchitis. Transmissable through coughing or contaminated water.

Diagnosis: only post mortem

Treatment: not known

18. Demodicosis mange of animals

Order: Trombidiformes /Prostigmata

Family: Demodecidae – burrowing mites

Demodex canis – Inhabits hair follicle, sebaceous duct and gland

D. injai – Inhabits hair follicle, sebaceous duct and gland

D. cornei – inhabit stratum corneum

D. cati – rare in cat

D. gatoi

D. phylloides – pig

D. foliculorum – man

D. bovis

D. equi

D. ovis

D. caprae

Morphology: Elongated body, wormlike. Capitulum is horse-shoe shape with short and wide mouthpart. 4 pairs of short legs, situated behind gnathosoma. Thick in the fronts of body. Transverse ridges, setae. Body is 0.2mm. They feed on cells, sebum and epidermal debris. Located in hair follicles and sebaceous glands with “upside down” position. Very species specific.

Life cycle: Eggs hatch into 6-legged larvaes, which moult into 8-legged nymphal stages x2. -> adult

Most species spend their whole life in follicles with their heads down.

Pathogenesis and clinical signs: Often seen as a part of normal skin flora. Can become pathogenic in animals with depressed immune system. Mites start to proliferate in the hair follicles which cause inflammatory reactions and can cause secondary bacterial infections and destroys the hair follicles. Present in 3 forms in dogs: 

Localized form – Starts around eyes, nose and ears. Cause scaly excema, alopecia, erythema, folliculitis, wrinkles, skin thickening. Most young dogs recover spontaneouslu within 1-2 months. Does not itch. Less than 5 patches.

Generalized form – often begins on head and forelimbs, then spread to hind legs and trunk. Juvenile onset. More dry reaction, little erythema, but have alopecia and thickening of skin or more severe form, bacterial invasions of lesion, thickened, wrinkleded and small postules which are smelly.

Pododemodicosis – on feet in dogs

Worldwide distribution. Cattle: outbreaks are observed mainly in tropical areas. Start as small nodules on the neck, containing thick yellowish substance. Normally not itchy. Rare in horses and pigs, if occurs, clinical picture similar as cattle.

Diagnosis: Deep skin scraping is necessary to reach into hair follicles and sebaceous glands. Squeeze skin to extrude the mites from the follicles before scraping. Hair plucking and biopsy can also be done.

Treatment:Amitraz dips, ivermectin, milbemicin. Whole dog must be treated, over a longer period. In livestock, treatment is not always necessary, can use organophosphates, many cases spontaneously resolve after 6-8 weeks. 

19. Psoroptosis of animals.

Order: Sarcoptiformes /astigmata

Family: Psoroptidae

Non-burrowing mites!

Psoroptes ovis – Sheep scab, cattle

P. cuniculi – rabbit

P. equi

Morphology: Their mouth part is pointed for piercing and sucking exudate. Oval body, 0.75mm. Long and hairy legs and funnel shaped suckers (ambulacrum). 3 segmented pedicula (before the sucker). Rounded abdominal tuberkules in male.

Life cycle: female lay eggs on the skin -> larvae -> protonymph -> tritonymph -> adult. Around 10 days.

Pathogenesis and clinical signs: Sheep scab, most severe ectoparasitic infection of sheep. Extremely contagious for sheep. Transmitted by direct contact and especially during cutting season through equipment. Starts at neck, shoulder and flanks, forming papules, serous exudate, dry yellowish crusts and inflammation of the skin, releasing wool - alopecia and thikcneing of the skin. Cause itching and rubbing, restlessness, impaired growth or weight loss.

Diagnosis: Clinical signs of sheep scab provide a good indication that sheep scab is present. Diagnosis require visualization of lesions and confirmation of presence of the scab – superficial skin scrape WITHOUT capillary bleeding.

Treatment: Dipping or by use of macrocyclic lactone injectables – ivermectin, moxidectin and doramectin. Control of environment is also important. 

20. Chorioptosis of animals.

Order: Sarcoptiformes /astigmata

Family: Chorioptidae

Genus: Chorioptis

Non-burrowing mites! = Fotskabb

Chorioptes bovis

Ch. Ovis

Ch. Equi

Ch. Caprae

Morphology: Resembles Psoroptes, but body is smaller, but larger than Sarcoptes. Long legs. Do not pierce skin, but feed on skin debris. Cup-shaped suckers (ambulacrum). Non-segmented pedicula. Rounded mouthpart. Square abdominal tuberkules in male.

Life cycle: Same as Psoroptes. Lasts 3 weeks. Release exudate, feed on debris.

Pathogenesis and clinical signs: Infest woolless eareas, particularly lower parts of hindlimbs and scrotum. Can decrease fertility by causing inflammation of the scrotal skin. Does not pierce skin but feed on debris leading to a yellow-brown lesion with hemorrhaging fissures resulting from allergic reactions to the mite or mite by-products. Cause intensive itching, foot stomping and biting. In horses they cause sticky scales, restlessness, stining and limb cracking. Foot mange starts as excema, dry scales and form small nodules and postules. Then they lose a layer of skin and form granulomas on the surface, and the skin become very hard. This may be a cause of laminitis.

Diagnosis: Skin scrapings under microscope.

Treatment: Ivermectin is effective at reducing mite populations, but cannot eliminate them. Effective topical treatment include a series of 3 whole-body baths, 5 days apart. In horses – careful clipping of long hair, removal of scabs followed by scrubbing of affected areas with appropriate insecticidal shampoo or powder. Oral ivermectin paste or moxidectin paste. But, Chorioptes may live in the environment for up to 69 days. Topical washes are main approach.

21. Otodectosis and cheletiellosis of carnivores.

Order: Thrombidiformis /prostigmata

Family: Cheylettiellidae

Genus: Cheyletiella

Non-burrowing mites!  = walking dandruff. All species zoonotic!

C. Yasguri – dogs

C. Blakei – cats

C. Parasitovorax – rabbits

 

Morphology: Ovoid with a narrow neck. Palps are enlarged, looks like extra legs, each palp has claws. Mouth adapted for piercing and sucking. Ingest keratin debris and fluids. Worldwide distribution. They move fast and are very active

Life cycle: Strong claws allow them to cling to fur and migrate quickly to epidermis. Egg - Larva - 2 nymph stages - Adult.

Pathogenesis and clinical signs:  Cause scaling, pruritic dermatitis, most severe on the dorsum. Occurs in overpopulation and poor sanitation.  

Diagnosis: Use transparent adhesive tape (for fast-moving parasites) or glue on a slide. Visual examination of hair coat, presence of walking dandruff.

Treatment: Lime-sulphur rinse for cats, puppies and rabbits, Pyrethroids for dogs. Topical treatment with amitraz and ivermectin. Environmental treatment, cleaning and insecticide sprays, important for eliminating infestation.

Otodectosis

Order: Sarcoptiformes /astigmata

Non-burrowing mites! = ear mite          Potential zoonosis!

Otodectes cynotis

Morphology: Short pretarsi and bell-shaped pulvilli. Long and thick legs. Localizd in external ear canal.

Life cycle: Egg  larvae  2 nymph stages  Adult. Lasts 3 weeks. Eggs are attached to skin of ear.

Pathogenesis and clinical signs: A common disease in dogs and cats, especially kittens. Highly contagious between animals, not species specific. Cause puritic erythematous otitis, with a dark dry exudate. Commonly found in ears but can also bee seen on other parts of the body. Clinical signs are head shaking, itching and one can see dried blood in the ear canal.

Diagnosis: Direct otoscopic examination, demonstration on smear, no stain needed. Skin scraping or scotch tape impressions

Treatment: Regular examination of ear canal, cleaning, application of acaricidal preparation and special ear drops. Amitraz, selamectin, ivermectin, moxidectin. 

22. Dermanyssidosis

Order: Gamasida (mesostigmata)

Family: Dermanyssidae (Dermanyssus, Liponyssoides)

Dermanyssus gallinae – birds.

Morphology: Transient form between ticks and mites. They are hairy. Long limbs for active moving. Stigma between 3^rd and 4^th leg. Larval stages do not have stigma, they breath through cuticle. They are temporally hematophagous ticks, and night feeders.

 

Life cycle: same as others. Egg – larva – 2 nymphal stages– adult. Males and females suck blood. Lasts 7-10 days.  

Pathogenesis and clinical signs: Cause anemia, decreased production of birds. birds, mammals. Infection of chickens – high infestation may cause mortality. Biting – painful, itching, skin irritation, anemia, weight loss, cachexia. Transmit cholera, spiroketosis, dengue fever, psenudomor, and other pathogens of poultry. Humans have allergic reactions. Chicken decreased egg quality.

Diagnosis: Finding mites on surface

Treatment: Synthetic pyrethroids (carbamates and organophosphates are forbidden in EU). Cleaning with boiling water and acaricides. Individual treatment with acaricide. 

23. Trombiculosis.

Order: Trombidiformes (prostigmata)

Genus: Trombicula (neotrombibula)

Neotrombilua autumnalis

Morphology: Only larval stages are parasitic! Nympha and adults are non-parasitic. Very small <0,2 mm, yellow, long haired legs, legs have 3 large claws, head has hard hypostome.

 

Life cycle: egg – larva (parasitic) – nympha - adult.

Pathogenesis and clinical signs: Cause dermatitis, vectors of various pathogens (rickettsia spp.)

N. autumnalis has extra-intestinal digestion, larval hypostome penetrates skin and release cytolytic enzymes that digest the tissues. The larvae sucks up digestied tissues (lasts 3-4 days).

Infect cats, dogs, humans. Predilection sites are areas with thin skin (paws, inguinal region, around eyes, around ear canal). Mild to severe skin reactions, dermatitis, irritation, itchings, eurythrema, blisters, crusts, secondary alopecia. In humans they form papula with crust in the middle and form brown color pigments around (sensitivity reaction to release of cytolytic enzymes).

Diagnosis: Anemia, according to clinical signs. Can find larva, but they are very small. 

Treatment and control:Synthetic pyrethroides, repellents. There is seasonal problem – larva suck blood middle august to September, start repellent or prophylaxis treatment accordingly