Flea Allergic Dermatitis
Few flea bites cause severe pruritis, hair loss, papular lesions and miliary dermatitis (cats)
Rasping mouthparts - feed on epithelial scales, scabs and feathers. Species on mammels and birds
Burrowing mite, 1 species with host adapted strains. Cause erythema, papule formation, alopecia, pruritis and self trauma
Serious demodex infection in dogs. Get thickened skin and pustules ooze blood and pus, severe prurits and 2* infection.
Non-burrowing mite, v.contageous, mild in animals - scaly dermatitis, scurf. Severe in humans. Diagnose: scurf on dark paper = walking dandruff
Non-burrowing red mite of poultry. Spend most time off host, visit at night to feed. Eggs laid in crevices, adults survive L/T in unnoccupied wooden poultry houses
Blood sucking poultry mite. Causes irritation, restlessness, drop in egg production, anaemia.
Honeybee mite, notifiable UK. Blood sucking mite, weakens adult bees, damages larval bees, causes disorientation and spreads viral diseases.
Harvest Mite (Neo-trombicula, N.Autumnalis)
any animal, only larval stage parasitic - inject enzymes into skin and feed on partly digested tissue, bright orange, hairy.
Harvest Mite (Neo-trombicula, N.Autumnalis)
On pets affects head, ears, flank. On grazing animals affects face and limbs. Causes irritation and poss. hypersensitivity reaction.
trichostrongyoid in stomach of outdoor pigs. Larve most path. Cause weight loss and death in lactating sows.
Strongyloid that produces nodules LI of indoor and outdoor pigs. Not v.path, decrease growth (young pigs) and milk (sows), piglets may die. Cause thin sow syndrome.
Ascarid in SI of weaner pigs. Inf by ingesting embyonated egg, larvae do hepatotracheal migration, causes milk spot liver (economic loss). Devlop immunity with time.
Affect outdoor pigs, earthworm IH, cause severe lung damage, protective immunity develops quickly
Ascarid in dog SI, vertical transmission to pups - somatic larvae in ***** tissues activated by pregnancy hormones
Ascarid, affects canids and felines. Smooth pale eggs, Inf by ingestion of embryonated egg or paratenic host.
Dogs. Plug feeding hookworm causes PLE. Inf by mouth, no vertical transmission.
Dogs. Hookworm, rare UK. V.path - migration cause alveoli damage, blood sucker - anaemia. Inf mostly percutaneous, transmammary transmission
Dog whipworm. Adult in caecal mucosa causes intermittant diarrhoea. Direct life cycle
Dog metastrongyloid. Adults produce anticoagulants - coagulation disoders. Signs - ascites, cough, vomit, ex.intolerance, wt.loss, anaemia
Dogs. Adults in pulmonary arteries and RHS heart. Eggs - larvae in alveoli - trachea - swallowed - faeces - slug IH, develop to L3 - eaten by dog FH - L3 in mesenteric LN - blood - adults in pulmonary A.
Dogs, zoonotic, in warm humid climate. Adults produce microfilariae in circulation, ingested by IH mosquitos when bite, develop to L3, transmit to next host via saliva when mosquito next feeds.
Atypical poultry ascarid, non-migratory, live in caeca, IH of histomonas meleagridis (causes blackhead in turkeys)
Strongyloidea, "gapeworm," many host birds - pheasants esp. Live in trachea cause resp disease. Feed on blood - cause inflam, haemorrhage, anaemia, death.
Birds - esp. grouse & geese. Live in caeca and intestine epithelium, cause decreased appetite and hypoalbuminea.
Dif species in dif. bird hosts. Non-migratory. Heavy inf - decreased growth rate and egg production, poss intestinal impaction. Aberrant worms can occur in hens eggs
Horse. Large strongle, migrates to root of anterior mesenteric A. burrows into walls causing inflammation = verminous endarteritis. Poss thrombosis - block blood flow to gut - cause colic.
Horse. Plug feeders, large buccal capsule, penetrates deep into LI wall cause small circular bleeding ulcers and poss anaemia
Horse. Non-migratory large strongyle, plug feeder. Small buccal capsule cause superficial damage, but feed in herds causing large ulcers.
Small horse strongyles, Initial inf with L3 causes local inflam. response. L4 are brown specks in LI mucosa = pepper-pot lesions. Can arrest at EL4 anytime of year - if emerge in summer cause wormy horse, if emerge in spring cause severe type 2 disease.
Horse ascarid in SI. Young horses (adults immune). Direct L.C. Inf by ingesting L2 (embryonated egg), larvae - hepatotracheal migration cause eosinophillic tracts and haemorrhage in liver and lungs. Adult worms cause wt.loss, unthriftiness and poss. impaction
Rhabditoid in horse SI. Foals inf by ingesting L3 in mares milk/grass of by skin penetration, cause severe enteritis and diarrhoea. Adults immune, may be carriers.
Horse. Pinworm of caecae, LI, rectum. F lays eggs on perianal hair, cause itchy bum. Inf by ingesting embronated egg containing L3. L4 feed on colon mucosa causing erosions
Horse lungworm, adults in small bronchi cause chonic cough. Donkeys are source of infection
Horse, spiruroid, fairly common, in conjuctival sac/inner aspect of 3rd eyelid. Indirect L.C Musca nusience fly IH
Horse. Worldwide. Spiruroid in stomach. Muscid fly IH. Adults cause mild gastritis. Larvae cause summer sores. Control with ivermectin and covering/turning dung heaps to control IH
Cattle, strongyle, 1cm long. Direct non-migratory L.C. PPP 3weeks, can arrest up to 6months. L3 in abomasum gastric glands
Type 1 disease
Ostertagia disease in dairy calves in 1st grazing season July-Oct. Caused by overwintered L3.
Resumed development of waves of EL4
Cause of type 2 disease ostertagia in dairy yearlings housed after first grazing season. See Feb-May. Signs - diarrhoea, wt.loss, reduced appetite, sub-mandibular oedema, death
Cows. Trichostrongyloidea in trachea and lungs. Cause reduced wt.gain and death in young stock, reduced milk yield in adults. 200-300 worms cause clinical disease. Vacc for 1st season calves born indoors - Huskvacc.
Sheep. In abomasum. High biotic potential esp. in tropics. Blood sucking parasite with piercing lancet on buccal capsule.
Sheep. In SI. Affects lambs 6-10wo in April-June. Cause profuse sudden onset diarrhoea, dehydration and death.
Sheep. Eggs deposited in spring (L3 in egg), hatch after ~12months on pasture.
In sheep abomasum. Cause black scour and wt.loss in lambs at end of 1st grazing season.
Lungworm of sheep and goats. Direct L.C. Causes chronic cough and unthriftiness in young. Sporadic in temperate climate, more disease in warm climates.
Sheep. 1cm long worms in abomasum. Ewes are main source of inf, impaired immunity due to PPRI or if on poor nurtition
Type 1 disease
Ostertagia in lambs in first grazing season July-Sept. Cause wt.loss, reduced appetite and diarrhoea. High faecal egg count
Type 2 disease
Ostertagia in lambs after 1st grazing season Jan-May. Resumed development of arrested larvae in successive waves causes interittant diarrhoea and progressive wt.loss.
Tissue cyst forming coccidia, pigs,dogs,cats. Facultatively heteroxenous. Oocysts 2 sporocysts ach with 4 sporozoites
Pig tissue cyst forming coccidia. Severe enteritis in 6-15do piglets, villous atrophy, some mortality
Pig tissue cyst forming coccidia. Diagnose with IF staining of mucosal smears. Treat with toltrazouril
Piroplasm, blood born tick transmitted protozoa. Multiplies in RBC by budding. Giemsa stain.
Red Water Fever
Cattle disease caused by Babesia B.divergens. Pipestem faeces, neurologic signs, reduced milk yield, fever, anaemia, untreated = fatal.
Associated with high rate of transmission. Freq exposure increases immunity, high herd immunity, low disease incidence.
associated with low rate of transmission. Infreq exposure so low herd immunity. Higher incidence of disease.
East Coast Fever
Lympho-proliferative disease of cattle caused by Theileria T.Parva. Signs-pyrexia, enlarged local LN, loss condition. At PME-pulmonary oedema, mucosal haemorrhage, LN and spleen atrophy
Coccidia in poultry ant.gut. Causes thickening, white lesions, watery exudate and malabsorption
Coccidia in poultry mid gut. Cause white spots, petachaie, haemorrhage into lumen. High mortality.
Coccidia in poultry caeca. Caeca swollen, thick and dark, contain necrotic tissue and blood. High mortality
Rabbit coccidia in bile duct epitelium. Causes wasting disease - liver enlargerd with white nodules, ascites, polyuria, polydipsea, diarrhoea. Prevent-hygiene.
path. bovine coccidia, in CT of lower SI, and epithelium of caecum and colon. Blood stained dysentary and sloughed mucosa in poor condition calves/brought in calves/suckler herds when 1st t/o.
Bovine coccidia, cause diarrhoea in calves after spring t/o as passive immunity from colostrum wanes. High faecal oocyst count but may die before any shed.
Tissue cyst forming coccidia, causes abortion amd decreased milk yield in cattle IH (inf. for life) and lameness in dog FH. PPP 5days.
Tissue cyst forming coccidia. In pups-ascending paralysis, muscle wasting, myocarditis. Successive litters cn be affected.
Tisue cyst forming coccidia, many species. Herbivore IH (2 asexual schizogonys to form bradyzoites in tissue cysts muscle) Carnivore FH (gametogeny occurs)
Widespread, enzootic stability in grazing animals, most asymptomatic, if disease- non-specific, fever, pyrexia, anorexia, salivation, reduced milk etc.
Equine Protozoal Myeloencephalitis
Disease caused by acidental ingestion Sarcocystis Neurona in horses (dead end hosts). Signs - ataxia and pareisis
Cause abortion/mummified lambs/weak lambs in non-immune ewe. White lesions on cotelydons. Vacc.6wks pre-tupping
Produced by acute asexual division of T.Gondii in IH and spread via blood to most tissues.
Slow growing intracellular chronic phase of T.Gondii infection in muscle and nerve tissue of IH
Intestinal protozoa causing diarrhoea in many animals and man. Direct L.C. Auto-inf or faecal oral transfer. Sporulated oocysts passed in faeces.
Protozoa causing diarrohoea in man. Water borne inf. Diagnose by oocysts in faecal smears, ZN stain.
Flagellate protozoan causing diarrohea in animals and man. Direct L.C transfer faecal-oral or water borne. Cysts excreted interrmittantly in faeces, to diagnose must sample 3 consecutive days min.
Flagellate protozoan. Asypmtomatic in chickens, causes blackhead/entero-hepatitis in turkeys. Larvae carried in egg of vector Heterakis Gallinarum. Turkey=yellow droppings.
Venereally transmitted cattle flagellate protozoa. Asymptomatic in bull, cause infertility and abortion in cow. Eradicated UK due to AI.
Cilliate protozoa, normal commensal of pig LI, if mucosa damaged - invasive - causes ulceration and dysentary.
Tropical protozoa. Intracellular parasite of macrophages of humans and canids. Long incubation period. Many dogs assymptomatic. Cutaneous-ulceration. Visceral-chronic wasting, intermittant fever, lymphdenopathy.
Group. Transmitted by tetse fly. Causes chronic wasting disease in cattle and human sleeping sickness.
Triatomid big, tabonid, ked
Vectors for stercararian trypanosoma. Transmit to host by contamination of wound with infected insect faeces.
Eukaryotic, motile, unicellular organisms. Have chromosomes in nuclear envolope. Digestion and nutrition by pino-/phagocytosis. Repro mostly asexual (sporozoa=sexual and asexual)
Nusience flies. Lay eggs in manure, hibernate in winter. Grey thorax with longitudinal stripes and yellow abdomen with 1 black stripe.
Nusience fly. Cause production losses. Transmits enteroviruses, Anthrax, E.Coli, Salmonella, Moraxella Bovis (N.F.Eye)
Nusience horse fly. Blood sucking F active on hot days. Wing is closed discal cell. Vector for anthrax, pasteurellosis, equine inf.anemia, african horses sickness, rickettsial
Nusience horse fly. Eggs laid on leaves overhanging water, larvae drop into water, after 1yr back to land and pupate, adult emerges in few wks.
Glossindae, Tetse Fly
Nusience fly. In Africa. M+F blood sucking. Butchers cleaver cell wings. Transmit trypanosomes that cause fatal disease. Lay single larvae at base of shrubs, pupates in soil, adult emerges 1 month on.
Nusience fly. Blood sucking F. Cause sweet itch in horses, vector for blue tongue, african horse sickness and parasitic onchocerca. Eggs laid on ground near water-larvae into water-pupate-adult, takes 6-12months.
Nusiecnce fly. Biting F sucks blood. Transmit equine encephalitis, myxamatosis and canine heartworm D.Immitis. Eggs laid on water-aquatic larvae and pupae-adult fly, temp dependant 2wks+.
Melophagus, sheep ked
Nusience fly. Wingless, whole life cycle on host. Lay 1 larvae on host-pupates-adult in few wks, temp dependant.
Melophagus, sheep ked
Nusience fly. Hairy, brown, wingless. Biting mouthparts, suck blood, cause anaemia and wool damage. IH for non-path sheep trypanosoma malophagium.
Psychodidae, Sand Flies
Nusience flies in tropics. F suck blood. Transmit leishmania. Egg on gorund/in cracks-larvae-pupate-adult. Takes 4-6wks.
Simulidae, Black Fly
Nusience fly. F sucks blood-painful bites. Vector for viral eastern encephalitis and oncocerca parasite in cattle. Worldwide, active morning and evening on warm cloudy days.
Simulidae, Black Fly
Nusience fly. Eggs laid on plants/stones under flowing water, larvae atttch to submerged rocks, pupate, adult flies emerge en mass, takes~1month. Small black flies, clear wings, arched thorax.
Haematobia, Horn Fly
Nusience fly. Spends most time on host-cattle (back and shoulders), Feed on thin skin, cluster along back and bite, cause skin wounds,then get 2* myiasis producing inf. Cause production loss and annoyance Eggs laid in fresh dung.
Nusience fly, worldwide. Spends most time off host but feed on it. Fly worry causes production losses. Transmit pathogenic bacteria, viruses and trypanosmes. IH for horse worm Habronemia. Eggs laid in rotting hay/straw.
Hydrotaea Irritans, Head Fly
In cattle transmits summer mastitis. In sheep irritation causes self-inflicting damage predisposing to 2* inf, blow fly strike. Eggs laid in decay vegetation/faeces in summer, larvae overwinter, pupate in spring, adult in summer.
Nusience fly, red with yellow spots.On horses and cattle, biting causes irritation. Found on perineum and inner thigh. Mate onhost, deposit 1 larvae-pupate-adults emerge in spring.
Family of myiasis producing flies obligate larval parasites, inc. warble flies, sheep nasal bot fly and horse bot fly.
significant tape worms, scolex w/ 4 suckers (some "armed" w/ hooks), lateral genital pore
mostly in SI, absorb nutrients across body surface, new segments bud off behind scolex, each one ♀ & ♂ (cross-fertilise), gravid segments at end of chain with >100,000 eggs, each immediately infective (contain larva w/ 6hooks - the "onchosphere" w/ a striated shell), 1-2 segments drop off daily
Warble fly, not UK, notifiable. Eradication possible as whole population overwinter in cattle.
F lay white eggs on legs and belly of host, larvae hatch, migrate down hair follicles/skin breaks, migrate S.C. to diaphragm then to winter resting site for 3 months-in spring migrate to midline back-L3 put spiracles through skin . Cause reduced milk yield and wt.gain and hide damage
Sheep nasal bot fly, grey and black spots on abdomen, clear wings. Cause annoyance, poor feeding and reduced wt.gain, nasal discharge and sneezing
Syndrome caused by heavy infestation of Oestrus Ovis, erodes bone in sinus, enter brain causing nervous signs - high stepping gait and in-coordination
F squirt liquid containing larvae up sheep nostrils. Larvae up nasal passages to frontal sinuses and feed on nasal mucosa, mature maggots return to nostrils, sneezed out pupate on ground, adult emerges 1 month later and lives 2-3wks
most common type of horse bot fly in UK. Lays egga on hair of foreleg/shoulder. Larvae in horse stomach in cardiac region.
F lay egg on horse-hatch spontaneously/stimulated by warmth and moisture-larvae migrate to mouth and spend wks in tongue/buccal capsule- then emerged and swallowed, attach to gastric mucosa for 10-12months, passed in faeces, pupate on ground, adults emerge after~1month.
Adluts cause annoyance egg laying. Larvae in stomach cause an inflam. response. If many poss interfere with food passage or sphincter action.
Obligate myiasis producing parasite of tropics, F only mate once so erradicated due to mass release of sterile M.
Family of myiasis producing flies, facultative parasites, inc green bottle, black bottle and blue bottle. Wroldwide affect sheep (mostly unshorn)
F attracted by odour (wounds/soiled fleece/dead animal) - lay clusters of cream eggs - hatch in 24hrs move to skin, moult twice - fully mature maggots after 1-2wks - fall to ground and pupate - adult fly emerges in 1wk (in summer), sexually mature after protein meal.
Calliphoridae flies that cause 2* strike - increase strike damage on already struck animal
causes skin damage, 2* bacterial inf, production losses, irritation, inappetance. Animals affected anoreix, dull, stand alone, smelly/dark/damp fleeces.
metacestode type, pinhead size, only in invertebrates, potential space instead of bladder, scolex not inverted
metacestode of Taenia taeniaeformis (cat tapeworm), single scolex attached to fluid filled bladder by chain of segments
metacestode of Echinococcus granulosus, fluid filled bladder <size of a football, lined w/ germinal epm that buds off "brood capsules" internally, inverted scolices inside brood capsules, in hydatid fluid, forming "hydatid sand". cyst walled off by fibrous tissue (host), "amorphous layer" between this and germinal membrane
metacestode of Echinococcus multioccularis (tropical, v. bad), like hydatid but daughter cysts bud off internally & externally → expands into tissue like a tumour
cestode, adults v short (<0.5cm), few segments, form hydatid cysts, 1 gravid segment per week, eggs half the size of strongyle
zoonotic disease of E. granulosus, FH=K9/fox, large cysts in sheep (liver/lung), cattle (lung), horse (liver), humans (liver>>lung>other), one gravid segment per worm per week (low biotic potential), PPP = 6-7wks, patency = 6months, sheep develop no immunity
E. granulosus: Dog-Sheep strain
E. granulosus in GB not Ireland, K9 infected from offal/scavenging, eggs in faeces (rain/insects spread), sheep infected (at dipping, lambing etc near homestead), cattle and humans (via dog) also infected
E. granulosis: Dog-Horse strain
IH specific E. granulosus strain in GB, hunt kennels important in dissemination
cestode disease, control: define local epidemiology, registration, treatment (praziquantel) and reg testing (serology/copro-antigen detection) of all dogs, education (farmers, K9 owners), no raw offal (boil/freeze), legislation to force compliance
Alveolar hydatid disease
disease of E. multiocularis, not in UK, in man cysts infiltrate liver like an invasive tumour, inoperable. fox=FH, rodent=IH (or man), poss infection in cat/dog. [rabies campaign in EU → ↑foxes, ↑infected rodents]
Pet Travel Scheme
under this legislation dogs must be treated (praziquantel - adults&immature stages) for tapeworm 48hrs b4 entry to UK, to prevent endemics
tapeworm spp. in SI, range from 0.5-15m long, identify by hooks on scolex, segments rectangular w/ one lat genital pore, single eggs (half size of strongyle), adults=little significance, some metacestodes=disease/meat inspection losses
"beef tapeworm", SI, no hooks, FH=man, IH=cattle, ~1cm cysticercus in striated muscle, esp heart & masseter (C. bovis), transmission direct(poo on field)/indirect(sewage on field)/via birds(carry sewage/in droppings)
"pork tapeworm", SI, hooks, FH=man, IH=pig, cysticercus in muscle (pigs - tongue, man - brain/mm) (C.cellulosae), dangerous exotic zoonosis (swallow eggs from environment or tapeworm→eggs→retro-peristalsis)
Taenia sp, FH=dog, IH=sheep, cysticercus in muscle (heart, diaphragm etc) (C.ovis), some localisation in CNS, "sheep measles" in Australasia (vacc in NZ), immunitydeveloped
commenest UK Taenia sp, FH=dog, IH=sheep etc, oncospheres in SI→hepatic portal→ cysticercus (C. tenuicollis)→migrate through liver parenchyma as grow→ peritoneal cavity ~8cm long, often adhere to omentum. traumatic hepatitis. if WHOLE PROGLOTTID swallowed→massive liver damage→death "cysticercosis hepatica", rare
Taenia sp, FH=dog, IH=rabbit, vena cava→liver→perforation of liver capsule→pea-sized cysticercus on omentum (C. pisiformis), if oncospheres migrate through liver, can→death
T. multiceps (aka Multiceps multiceps)
Taenia sp, FH=dog, IH=sheep, hatch in SI, oncosphere→blood→brain→ coenurus in skull (C. cerebralis)→5cm space-occupying lesion→ neuro signs
Taenia sp, FH=dog/fox, IH=rabbit, coenurus in intermuscular CT, (C. cerialis), often → soft subdermal swelling
cestode, 0.5m (short), oval segments, eggs in packets, 2 contralateral genital pores, dog/cat SI, minor significance, poss mild anal irritation, IH = flea, flea control
cestodes, ~5cms, wide short segments, rounded triangular egg, oncosphere contained in "pyriform apparatus", eggs don't float well, use ELISA for Abs in blood, IH=free living pasture mites, horse infected while grazing (caecum ulceration/inflammation)
cestodes, sheep & cattle, v common in UK lambs, ~2m long, segment width>length, spontaneous expulsion late summer, IH= pasture mite, little clinical significance
tiny~ 3mm cestode of poultry, 4-9 segments, hooks around suckers and rostellum, IH=molluscs, deep dwelling, →haemorrhagic enteritis in poultry & pigeons
helminths, typically leaf shaped & DV flattened, no coelom, filled with mesodermal parenchyma, no bvs, simple ladder nervous system
ectoparasites of fish & other aquatic animals, "haptor" organ for attachment w/ suckers and hooks, direct LC
endoparasites of animals, ventral and oral suckers leading to muscular pharynx to pump food into 2 blind ending caecae, integument also active in nutrient uptake. genital pore beween suckers, excretory bladder at other end. most spp hermaphrodite but individuals cross-fertilise
trematode structure that plays an important role in evasion of host immunity, by rapid turnover, molecular mimicry, release of immunomodulatory factors (eg Fasciola), release of enzymes that cleave Ig (eg Fasciola), or antigenic variation during different phases of LC (eg Fasciola)
large egg (2x strongyle), oval, brown, one operculum, contains yolk cells, req high spec gravity flotation fluid, req moisture and 10*C for larvae to develop
1st larval stage of Fasciola, will hatch when correct light intensity and covered w/ a film of water. has cilia for locomotion once hatched.
expelled through redia birth pore, stage of F. hepatica LC that leaves the snail. heart shaped w/ tail for swimming
in F.hepatica LC, cercaria w/out tail having swum onto vegetation, develops protective wall and waits to be ingested
stage in F. hepatica life cycle in final host which migrates SI → liver (burrows through parenchyma)
stage in F. hepatica life cycle, having matured in predilection site, lives in bile ducts, feed on blood & epm→ chronic inflammation→fibrosis of bile duct wall
aka "blood flukes", found in tropics, separate ♀ & ♂, smaller ♀enveloped by ♂, IH = water snail
trematode, adults live in bvs, no metacercaria stage, cercariae enter FH by skin penetration. pathology w/ passage of eggs through liver/bladder/intestine wall
trematodes, rare in UK, plump cylindrical adults, attaches to rumen wall (w/out serious damage), eggs like Fasciola but colourless, IH = water snails, metacercariae on vegetation, disease if ++ eaten, immature fluke migrate from SI towards rumen → enteritis & Dx, serious in ruminants in wet tropics
small trematode (<1.5cm) in bile ducts of ruminants & some other herbivores, migrates directly up common bile duct, much less pathogenic than Fasciola. small dark brown eggs in faeces contain miracidium, IH = land snail→cercariae excreted in smile balls→wood ants→metacercariae→ants eaten with grass
mud snail (Lymnaea truncatula)
IH of F. hepatica, 5-10mm long, brown black spiralled shell (1st spiral = half total length), shell opens on RHs w/ opening upwards, in non-acidy muddy areas, multiply rapidly when lots of green slime to eat, most die in cold British winter, if survive, eggs in spring→hatch in June
trematode, 2-5cm adults in bile ducts, oral & ventral suckers, uterus, ovaries, testes, vitellary glands. eggs twice the size of strongyle, oval, brown, one operculum, req high spec gravity flotation fluid
seasonal trematode disease, more serious some years than others, ppp=8-12wks, in sheep → deaths/clinical disease/subclin disease in all ages, in cattle →clinical disease in younger stock, wet summer→ ↑snail #s, increased disease risk
sheep→ sudden death, Sept-Nov, enlarged pale friable Hx liver w/ >1,000 immature fluke in liver parenchyma, no eggs in faeces. [can →abortion, ascites, abdo pain, dspnoea, necrotic hepatitis etc.] rare in cattle.
sheep→ rapid wt loss over 1-2wks, Oct-Dec, normochromi anaemia, enlarged liver w/ large Hxs, >500 flukes (50:50 immature/adult), sporadic eggs in faeces. [can→ anorexia, eosinophiliia, submandibular oedema]
sheep→ progressive wt loss over wks/months, Jan-March, normochromic→hypochromic anaemia, hypoalbuminaemia→oedema, small distorted cirrhoti liver, enlarged bile ducts, >250 adult flukes, eggs in faeces. in cattle→calcification of bile ducts→"pipe stem liver"
sheep→ poor fleece & fibre quality, liver condemnations. beef cattle→reduced carcass value, dairy→reduced milk yield
trematode disease, large #s of metacercariae ingested quickly → acute disease, small #s ingested slowly → chronic disease. infection → ↓food intake, susceptibility: sheep>cattle>pig, evade immunity by releasing immunomodulatory factors & enzymes that cleave Ig & antigenic variation during different phases of LC
summer fasciola infection of snail
fasciola eggs passed in spring→ hatch June →miracidia infect newly hatched mud snails→ develop & multiply in snail hepatopancreas during summer→cercariae shed late Aug+→eaten by sheep→migration through liver→ ACUTE disease Sep-Nov, CHRONIC disease Jan+
winter fasciola infection of snail
fasciola eggs passed in late summer, halted development when T<10C (flukes trapped in hibernating snails over winter), T >10C development resumes→ cercariae shed from July→disease August+
fluid in body cavity under high pressure, tough elastic cuticle (use structures formed to ID), muscular pharynx to pump food into intestine, nerve ring around pharynx & 4 longtitudinal nerve w/ ganglia coordinating movement, separate sexes, ♀ w/ blunt ending tail, ♂ w/ spicules
in ♂ bursate nematodes, large expansion of cuticle, extends beyong spicules has "rays", acts as a clasping organ
general name for nematodes which suck a plug of mucosa into the buccal cavity→ circular ulcer
basic nematode life cycle
Egg→L1→L2→L3→L4→Adult, moult between each larval stage, many variations depending on spp
egg w/ thick protective shell, some have sticky coat, not immediately infective, L1→infective L2 inside egg
group of bursate nematode superfamilies, produce "typical strongyle eggs", eggs in faeces→infective larvae on ground→eaten by host→larvae in mucosa of stomach/SI→adults in lumen of stomach/SI
bursate group including Trichostrongyloidea, Strongyloidea & Hookworms, contribute to PGE
bursate nematode superfamily, look like short length of cotton, characteristic spicules, PPP=3wks, eggs(faeces on ground)→L1-L3 on ground, L1/2 feed on bacteria, ensheathed L3=infective w/ finite food store for energy, cannot feed→L3 ingested→stomach/SI in gland/crypts→L4→adults on mucosal surface
bursate nematode superfamily incl Ostertagia, Haemonchus, Trichostrongylus, Nematodirus, Cooperia, Dictyocaulus & Hyostrongylus
bursate nematode superfamily, short (1-5cm), stout, characteristic heads, L3→L4→adult usually in LI, larvae penetrate mucosal wall→nodules, some migrate, PPP=3w-6m+
bursate nematode superfamily, q stout, head bent dorsally, large buccal cavity w/ teeth/cutting plates, embed heads deep into SI mucosa, infect by ingestion/skin penetration
bursate nematode superfamily, look like small pieces of string, larvae have S-shaped tails, eggs go up resp tract→swallowed, hatch→L1 out in faeces→infective L3 in IH (=mollusc usually)→paratenic host 1st OR direct to final host→in FH migrate to resp tract/assoc. bv's→lay eggs
bursate nematode superfamily, include Strongylus, Triodontophorus, Cyathostomins, Chabertia, Oesophagostomum & Syngamus
bursate nematode superfamily, incl Metastrongylus, Muellerius, Protostrongylus, Filaroides, Angiostrongylus, Aelurostrongylus
non-bursate nematode superfamily, incl Ascaris, Parascaris, Toxocara, Toxascaris, Ascaridia, Heterakis
non-bursate nematode superfamily, big fleshy worms, typically 5-40cm, 3 lips around mouth, single bulbed pharynx, infection via ingestion of embryonated egg w/ infective L2 inside (can live <5yrs in humid environment), hepatotracheal migration (varies w/ spp, some go via placenta/mammary glands/IH), eggs in SI w/ thick protective shell +/- sticky coat,
L2→intestine→hepatic portal blood→liver→venous blood→heart→lung capillaries→alveoli→trachea→L4 swallowed →intestine→adults
non-bursate nematode superfamily,, double bulbed pharynx, ♀ has long tapering tail, direct LC, non-migratory, in LI, eggs deposited on perineal skin, egga asymetric w/ operculum at one end
non-bursate nematode superfamily, most spp free living, one parasitic genus: only ♀s parasitic (L4)- parthogenesis (repro w/out ♂), penetrate skin/buccal mucosa, ♂ free living, v long pharynx, small (40µm) thin shelled egg, translucent, always embryonated, L4 in SI, vertical transmission
whipworms, stout posterior, long narrow neck - superficially inserted into caecal mucosa. eggs brown, thick shells, barrel-shaped w/ plugs at ends, survive <12y. ♂s only have 1 spicule, sheathed. embryonated egg = infective stage, direct LC. larva forms mucosal nodule b4 emerging into lumen. → inflammation, Hx, Dx, poss anaemia/prolapsed rectum
Trichinelloidea sp, thin, tapering (less than Trichuris), direct/indirect LCs, most important in BIRDS, also in dogs/cats in bladder & liver
"the worm that thinks it's a virus", no exogenous phase, small worms (<4mm), larvae intracellular, use one individual as FH & then IH, each spp adapted to host body T, important zoonosis in PIGS
Trichinella sp, v wide host range: mammals (37-40C), infection by ingestion of encysted larva in striated mm, from SI→migrates via villous lymphatics & blood→ larval cysts in new host mm, muscle cell transforms into "nurse cell" (hypertrophy, encapsulation, infectious after 20days). larva v resistant, can survive in autolytic meat <4m still infectious, smoking & salting don't kill, req >77C to kill
non-bursate nematode superfamily, ♂ has flat coiled tail & unequal spicules. indirect LC, small narrow larvated eggs→arthropod = IH, various sites
non-bursate nematode superfamily, ♂ has corkscrew tail, slender elongated filamentous nematodes <12cm, live in CT, most ♀s produce microfilariae (not eggs, motile)→ blood/tissue fluid→biting arthropod (IH)→L3 released when bites final host→larvae develop & migrate. VIP in man → elephantiasis & river blindness. K9→heartworm
Filaroidea sp, adult in R♥ & pulmonary aa→L1=microfilariae in blood→mosquito→infectious L3→bite→develop & migrate→adults, VIP in DOGS in warm humid climates, high morbidity and mortality
Filaroidea sp, IH=simulidae (black flies), →river blindness in man, surgery finds nodules containing nematodes
egg 100µm, thick shell with albuminous coat (sticky, aids passive spread), brown, thick pitted shell (horse)
Parasitic gastroenteritis (PGE)
disease complec associated w/ a number of nematodes, characterised by Dx/wt loss (clinical), ↓productivity (subclinical), seasonal appearance & hypoabluminaemia
Strongyles, eso Trichostrongyloidea & Strongyloidea, are main cause of this disease in grazing animals, Strongyloides spp also involved. causes ↓appetite, altered digestion, incl villous atrophy, altered protein intake and metabolism, ↓mineral metabolism, ↓energy metabolism
in 1st season calves in N Europe, this abomasal nematode is primary pathogen for PGE, w/ Cooperia & Nematodirus spp (intestinal) contributing to disease
phenomenon where egg development time gets shorter as microclimate of dungpat becomes more favourable (↑RH, ↑T), so larvae reach L3 stage simultneously
phenomenon due to concertina effect and translation of L3 onto pasture, usually Aug-Nov, timing delayed by cold spring/dry summer. followed by decline due to ↓L3 lifespan in warm weather & autumn grass growth
Hypobiosis (arrested larval development)
allows larvae to overwinter INSIDE HOST, as larvae (longer lifespan than adults) whilst climatic conditions are adverse. eg Ostertagia as EL4, stimulated by ↓T, Haemonchus stimulated by drought, equin cyathostomes as L3. resume development spontaneously (genetic alarm clock)
in PGE, this affects establishment of recently ingested larvae and the course of development of worms (considering a constant turnover in worm burden)
in PGE, this can result in ↓establishment of larvae, expulsion of existing worm burden ("self cure), minor effects of arrested development, stunting worm growth & ↓biotic potential of worms (↓eggs laid)
in PGE, this can be adversely affected by: poor nutrition, reproductive status, drug teatment (repeated anthelmentics / CCS), concurrent infection and hypersensitivity reaction from previous exposure (eg w/ Haemonchus in some ewes)
periparturient relaxation in immunity (PPRI)
seen in breeding ewes and sows, due to impaired cell-mediated immune response, poss assoc w/ increased blood prolactin / shift of IgA from gut mucosa to mammary gland
nematode sp, direct non-migratory, young calves weaned early on permanent pasture w/ high stocking densities→ ingest L3→abomasal gastric glands→L4→worms (brown, cotton-like, 1cm), PPP=3ks (5-6m if hypobiosis at EL4), → bovine PGE
Type 1 (Summer) bovine ostertagiosis
disease of calves during 1st grazing season (mid-July - Oct), →Dx, wt loss. high morbidity low mortality
Pre-type 2 phase
disease of calves at end of 1st grazing season (Oct+), accumulation of large Ostertagia worm population at EL4 arrested stage, →usually no clinical signs
Type 2 bovine ostertagiosis
disease of yearlings housed after 1st grazing season (Feb-May), resumed development & emergence of waves of EL4s ingested as L3 last autumn→ Dx, wt loss, submandibular Ox. low morbidity, high mortality
bovine herds where calves are susceptible to ostertagiosis but immune cows pass very few worm eggs
Spring calving beef herds
beef herds least likely to get ostertagiosis, as spring mortality of L3 occurs before calves eat much grass, and immune cows produce few eggs, therefore few L3 on pasture →disease unlikely
Autumn calving beef herds
beef herds, calves graze before spring mortality of L3, pasture contaminated but relatively few calves on pasture (grass needed by immune cows), so relatively few eggs on pasture, →low disease risk
acquired immunity to disease develops slowl over a whole grazing system, may wane during winter housing but re-established at turn out. adults solidly immune.
bovine lungworm, white, thread-like, <8cm, in trachea & larger bronchi, →parasitic bronchitis ("husk"/"hoose"), calves→↓wt gain & deaths, cows→↓milk yield. see L1 in faeces (not eggs)
nematode, LC: adults in trachea/bronchi of cow→ embryonated eggs coughed up & swallowed→hatch→L1 in fresh faeces→L2&L3 in dungpat→L3 ingested→through intestine wall→lymphatics→blood→lungs. PPP=3.5wks
disease in cows carried year to year by low numbers of L3 overwintering on pasture & carrier animals harbouring patent infection (30% yearlings, 5% cows in endemic area)
nematode, epidemiology: calves pick up overwintered L3 from pasture after turnout, L1→L3 in dungpat, translated to pasture by FUNGUS→all calves infected, may cycle several times before disease (July-Sep), larvae may overwinter in lungs→pasture contamination after spring turnout→carrier animals. rapid immunity after heavy exposure (few wks)
filarial nematode (white thread-like <6cm), indirect LC, IHs= Simulium spp & Culicoides spp, gastrosplenic ligament (UK), little significance in UK
bovine & equine "eyeworm", spiruroid nematode (white, thread-like, 1-2cm, in 40% dairy cattle, <30% UK horses), in conjunctival sac / inner aspect of 3rd eyelid / lacrymal duct, indirect LC, IH = Musca spp. ++→lacrymation & conjunivitis in cattle, non-path in horses, normally only see in PM
disease manifestations within this disease complex = 1)Ostertagiosis & Trichostrongylosis, 2)Nematodirosis, 3) Haemonchosis
Ostertagia circumcincta and Haemonchus contortus act as 1* pathogens here in UK sheep, Trichostrongylus axei also found here
(ovine) small intestine
Trichostrongylus spp and Nematodirus battus act as 1* pathogens here in UK sheep
sheep disease, ewes act as main source of pasture contamination on CLEAN pasture (no overwintered L3 so no lamb infection at turnout), ewes & lambs are sources on CONTAMINATED pasture (overwintered L3 on pasture to ewes and lambs at turnout)
Type 1 ovine ostertagiosis
predominant form of PGE in sheep, mainly O. circumcincta, lambs during 1st grazing season (Jul-Sep)→ Dx, wt loss, reduced appetite
Type 2 ovine ostertagiosis
disease of lambs >1yo after 1st grazing season (Jan-May)→progressive wt loss, intermittent Dx
disease of Trichostrongylus axei (abomasum) & other Trichostrongylus spp (SI), lambs <1yo, towards end of 1st grazing season (Nov-Dec)→ black scours (dark smelly Dx), wt loss
ovine disease, epidemiology: mainly breeding ewes, preiparturient relaxation in immunity (PPRI), poor nutrition & winter housing → ↓immunity, → ↑L3 establishment, ↑egg output & resumed development of arrested larvae
causes serious disease of sheep, →susceptible lambs (6-10wo) at beginning of 1st grazing season (late April - june), →acute, profuse Dx (black/green→pale yellow→colourless), rapid dehdration→ FATAL (<30%), PPP = 15days, ewes play no significant role (even during PPRI). ↓disease risk if lambs still suckling / or older and more resistant to challenge
ovine abomasal nematode, 2cm, "barber's pole" appearance when fresh, piercing "lancet" in buccal capsule of L4 & adult worms, high biotic potential (5-10,000 eggs/worm/day), primarily tropical/subtropical but seen in UK (esp SE)
ovine abomasal nematode, in tropical/subtropical areas disease outbreak depends on rainfall, survives drought by arrested development, several cycles on infection seen annually
ovine abomasal nematode, in temperate areas, ewe is 1* source of infection (v few L3 overwinter on pasture), ingested late summer→most L3 overwinter as EL4 in abomasal wall→acute disease following Spring (like Type 2 ostertagiosis); a few L3 ingested by lambs don't overwinter→acute disease if ++ (equiv to Type 1 ostertagiosis), most likely during hot thundery summer. usually only 1 cycle of infection annually.
Dictyocaulus filaria is most important one of these, Muellerius & Protostrongylus spp common w/ high prevalence, survival & patency, and poor host immunity, but not major pathogens
most important lungworm of sheep and goats, sporadic in temperate areas, disease more likely in warmer climates, direct LC, PPP = 5wks, →chronic cough & unthrifty lambs/kids
common ovine lungworm but not major pathogen, indirect LC, IH = mollusc → ingested w/ grass, L3 released by ingestion→lymphatics→lungs, adults in alveoli/parenchyma, PPP = 6-10wks
common ovine lungworm but not major pathogen, indirect LC, IH = mollusc → ingested w/ grass, L3 released by ingestion→lymphatics→lungs, adults in small bronchioles, PPP = 5-6wks
species susceptible to Ostertagia, Haemonchus and Nematodirus spp, mont weaker immune response to GI worms than sheep but more tolerant (less damage) to similar sized worm burdens. req higher doses of anthelmintics (metabolise faster) & develop resistance faster than sheep. don't graze pasture with these before sheep - bad times.
pasture which has never been infected or previous infection has died out & isnt active (no sheep for 12m, or July onwards: cattle since prev Spring/no sheep since prev Autumn)
pasture grazed only by dosed ewes in prev. Autumn; or grazed previous yr by dry yearling ewes dosed prior to entry & during July; or grazed by cattle since prev July (but could still have Nematodirus)
(horses) large intestine
Strongylus spp, Cyathostomins (or trichonemes), Triodontophorus spp and Oxyuris equi found here
Strongylus spp (S. vulgaris, S. edentatis, S. equinus, now uncommon due to worm control programmes, large buccal capsules→ small bleeding ulcers→ anaemia if ++, scars) and Triodontophorus spp (common, smaller buccal capsules, if feed in herds→ large ulcers→ scar) of horses are included in this group
horse nematodes, stout worms 1.5-5cm, large buccal capsule, ♂ bursa visible to naked eye, plug feeders, buccal capsule has double row of leaf crowns, teeth (0,2,3 or more) and dorsal gutter (channel for secretions). L3s infective.
large strongyle of horses, plug feeders, L3→ GIT→ through mucosa→2wks→ anterior mesenteric a. (3-4months)→ burrows back into intestine (6-8wks). q long PPP = 6-7m, can b q. damaging → verminous endarteritis (inflam of artery lining), poss → embolism→ colic. can detect by rectal palpation
large strongyle of horses, plug feeders, no teeth, L3→ GIT→ through mucosa→ bvs→ liver(→forms nodule)→ puncture through liver capsule→ falciform ligament→ peritoneum→ GIT(→forms nodule). long PPP=11-12m
large strongyle of horses, plug feeders, L3→ GIT→ through mucosa(→forms nodule)→ liver→ through capsule→ falciform ligament→ migrates back via peritoneal cavity(→damage). long PPP = 9m
large strongyle of horses, plug feeders, smaller buccal capsule, may feed in herds→ large ulcers, L3→ gut lumen→ into mucosa→ gut lumen. NON-MIGRATORY. relatively short PPP = 2-3m
small horse nematodes <1.5cm, small shallow buccal capsule, double row of leaf crowns, +/- teeth, adults & larvae = plug feeders. ingest L3→ invade mucosa of LI → L4 (or arrest as EL3)→ L4 emerge into gut lumen→ adult worms. PPP = 8-12wks. hypobiosis esp in late Summer/Autumn, may stay arrested for years, resumption in late Winter/early Spring or after removal of adult worm pop
nematode disease of horses. infectious L3→ local inflammation; developing L4s→ "pepper pot lesions" (brown flecks on mucosa, each one is a coiled larva); larval emergence in Summer/Autumn & plug feeding of adults = major contributor to "wormy horse" w/ 1000s of adults and millions of mucosal larvae(→ unthrifty, Dx, poor coat, anaemia); mass emergence of previously arrested larvae in late Winter/early Spring → massive infiltration→ severe Dx +/- wt loss (larval/Type 2 disease_
equine nematode disease in young horses (adults if overcrowding/poor hygiene) on permanent pasture. sources: overwintering L3 on pasture, adults (incl MARES)→ eggs & "spring rise" in faecal egg output
SI nematode of horse, mostly in foals <6m, transmitted from one years foals to next, few in adults. worms stout <0.5m, three large lips around mouth, high fecundity, eggs survive <1yr)direct LC, ingestion of embryonated egg (L2), hepatotracheal migration (liver-heart-lungs-GIT, 3wks), PPP=10-12wks. larvae→tracts & Hx in liver and lungs, poss→coush/nasal discharge. poo-pick every 2wks (2wks to reach L2 stage) & anthelmintics
Rhabditoid of equine SI, mostly in foals <6m, 1st parasite foals are exposed to. <6mm, only ♀ parasitic, long oesophagus (<3d lody length) = ID, parasitic and free-living phases, PPP=1 wk, embryonated egg 50-60µm, infection by skin penetration / ingestion of L3 in grass or MARE'S MILK, hepatotracheal migration. adults normally immune, poss carriers, foals→severe enteritis/Dx if ++
pinworm in caecum/LI/rectum of horses, v common, ♀ <10cm, long white pointy tail; ♂ <1cm. operculate eggs (flattened on one side) on perianal hair→fall to ground→L3 develops inside egg→ingested→L3 invades colonic mucosa→L4 emerges→adult, PPP = 5m. adults non pathogenic but egg laying →irritation and bare patches:"seat itch"; L4 feed on colonic mucosa + nip off epithelium (but not true plug feeders). may see worms in faeces, use anthelmintics & sponge perianal region freq
small trichostrongyle of horse stomach (and ruminant abomasum), typically confined to stomach wall, non-migratory, PPP = 3.5wks. L3 penetrate between gastric glands→nodules & erosions. not usually a 1* pathogen in horse.
Spiruroid sp in equine stomach, worldwide, slender white worms 1-2.5cm long, ♂ has flat spiral twist in tail to grasp ♀, indirect LC, IH= muscid fly, adults under layer of mucus in stomach, elongated embryonated eggs (smaller than strongyle) passed in faeces→L1 ingested by fly larvae→L3 deposited on horse's lips→swallowed→adults, PPP= 2m. adult→mild gastritis, larvae→skin sores. cover/turn over dung heaps to keep flies from breeding sites, ivermectin to kill larvae
Spiruroid sp in equine stomach, tropical/subtropical, slender white worms 1-2.5cm long, ♂ has flat spiral twist in tail to grasp ♀, indirect LC, IH= muscid fly, adults in large nodule in stomach, elongated embryonated eggs (smaller than strongyle) passed in faeces→L1 ingested by fly larvae→L3 deposited on horse's lips→swallowed→adults, PPP= 2m. adult worms→tumour-like nodules, may impair pyloric function. cover/turn over dung heaps to keep flies from breeding sites, ivermectin to kill larvae
equine lungworm, adults in smaller bronchi →chronic cough at rest/during exercise, Autumn/early Winter. embryonated eggs passed in fresh faeces (not L1 like cattle), PPP = 12wks (much longer than cattle), main source of infection = DONKEYS (rarely clinical), remain infected for yrs (patency 5+yrs), infection can cycle in horses (see few worms, often no eggs, patency <8m)
(aka O. reticulata) large filarial nematode of horses (<30cm), ligamentum nuchae (supports weight of head) & limb CT, indirect LC, IH = midge (Cullicoides), limited significance, poss→ localised hypersensitivity or corneal opacity (v rare in UK)
Filarial horse nematode <6cm, subcut nodules & IM CT, found in warmer countries (UK only imports), indirect Lc, IH = horn fly (Haematobia) ingests L1→L3 infection when fly feeds on skin wound. PPP = 8-10m
Filarial nematode<12cm, peritoneal & pleural cavity, non-pathogenic unless randomly migrates→CNS, mosquitoes = IH, PPP = 8-10m
only 4 GI nematodes of consequence in this specied in UK - Hyostrongylus rubicus, Oesophagostomum, Ascaris sum & Trichuris suis
pigs remain susceptible to this group of nematodes throughout life as they do not provoke a strong protective immune response
typical trichostrongyloid of outdoor pigs (ie where faeces not swiftly removed), found in glandular part of stomach, rare in UK, similar to ostertagiosis but no useful immunity developed, →severe wt loss & poss death in lactating sows. produces relatively few eggs, larval culture req to confirm
typical strongyloid of pigs ~1.5cm, in caecum & colon, some PPRI egg rise, relatively prolific egg layers, not very pathogenic but poss →sudden death in piglets, anorexia & Dx in adults, fertilitry problems, abortions etc, ↓milk production. (if anthelmintics too freq, resistance accelerated)
Thin sow syndrome
sporadic condition seen when pig industry is in economic trough, assoc w/ Oesophagostumum, poor nutrition→vulnerabl to infection&eat bedding→++worms→intestinal damage& ++eggs→ ++L3 in bedding→ more damage→excess wt loss during lactation
typical ascarid (buccal cav w/ 3 lips) of pigs, ♀20-30cm, ♂15-25cm w/ coiled tail, contaminated buildings hard to disinfect due to sticky egg coating. larvae undergo hepatotracheal migration→SI. liver damage= "white/milk spot". immunity develops over several months, some adults still have small burdens→carriers→contaminate farrowing house→SOI for susceptible piglets→ingest embryonated egg→L3 hatches. adults produce 200,000 eggs/day which persist in environment, development T dep & thus seasonal
typical whipworm of outdoor/deep-litter pigs, rare in UK, prefers warmer, low burdens = non path, high burdens→severe Dx/dysentery by providing a portal of entry for microbial organisms (anterior part can imbed deep into mucosa)
nematode spp which markedly ↑s T-regulatory activity, thus suppressing some immune-mediated diseases (Th2↑, Th1↓), poss +ve clinical use in human immune-mediated disease (eg IBD, Chrohn's)
Routine (GI nematode control in pigs)
GI nematode control method in pigs, most common, all stock given medicated feed at once, 1st at 3m intervals, omnitor FECs routinely, ↑interval as prevalence/intensity ↓s
Strategic dosing (GI nematode control in pigs)
GI nematode control method in pigs, treat sows b4 enter farrowing house (eliminates shedding by Ascarid carriers, eliminates PPRI egg rise of Strongyles & prevents poor milk production), treat weaners b4 enter fattening house, treat other age groupd when moved to new pens
only lungworm of outdoor pigs (IH = earthworm), mainly piglets, found in bronchioles & smaller bronchi, larvated eggs with a wavy outline passed in faeces→earthworm→eaten→larvae migrate in pig via mesenteric LNs→lungs. v. pathogenic→ severe lung damage, low level infection will check growth. immunity develops fast.
nematode disease of pigs, v v rare in UK but risk, esp free-range, pigs = asymptomatic, serious ZOONOSIS→myositis/myocarditis/encephalitis/facial oedema in humans, sometimes FATAL. other meat animals can also be a SOI for humans.
Trichinella sp of BIRDS (&pigs), req T 40-42.5*C, larvae not encapsulated
in sylvatic cycles of disease, infection transmitted w/in some wildlife pops (eg rats) then ascends food chain to top carnivores/omnivores (eg fox in EU). in domestic cycles, pigs infected by undercooked swill, humans by undercooked pork. one pig eaten by >1000 people (mini epidemic). control by preventing pig scavenging, meat inspection, boiling swill and cooking pork well
"the Gapeworm", birds, esp pheasants, atypical strongyloid, dep red colous, Y shaped (small♂ permanently attached to♀), migrates→ trachea→ resp distress +/- anaemia, esp young birds, PPP = 12-21d. egg like typical strongyle but w/operculum at each end, infective larvae develops inside egg, bird ingests larva/larvated egg/earthworm(transport host). wild birds→earthworms = reservoir of infection
bird trichostrongyloid (similar to ruminant spp), VIP in grouse, in intestice & caeca, hyposiosis poss in winter, on moorland L3 accumulate in heather tips eaten by grouse, worst in Spring (poor condition after Winter)→ reduced egg laying & reduced survival. treat w/ medicated grit.
typical fleshy ascarids of birds, <12cm, smooth shelled ascarid egg, diff spp in diff hosts, in SI, NON-MIGRATORY (atypical), remain in SI/mucosa, ++ reduce growth & egg production. possible to enter oviduct→incorporated into egg! yucky times
atypical ascarid of poultry, lives in caeca, <1.5cm, slender, pointy tail (atypical) but has 3 lips, smooth shelled ascarid eggs. NON-MIGRATORY (atypical), earthworm = transport host. poss vector of Histomonas meleagridis (protozoa→blackhead in turkeys)
Trichinelloidea sp of poultry, various sites, >1cm thread-like worms, front end thinner than tail, eggs typicalled trichuroid (barrel w/ plugs), direct/indirect LCs, some spp v pathogenic→inappetance +/- Dx
Trichostrongyloid in ducks/geese, red, lives under gizzard lining, freq→mortality in ornamental ducks
(dogs) small intestine
Toxocara canis, Toxascaris leonina, Uncinaria stenocephala (and Ancylostoma caninum, rare in UK) found here
typical ascarid, <18cms, slightly bigger than other K9 ascarid spp, SI of dogs / foxes(56-61% in GB) / canids, dark eggs w/ pitted surfaces. zoonotic
SI ascarid of dogs, ubiq in puppies, few = asymptomatic, lots→wt loss, poor growth, pot belly, Dx, Vx, hepatitis (due to hepatotracheal migration), pneumonia, death. PPP=4-5wks., L2 in embryonated egg infective (can survive<5y). in puppies under 3mo, ingest embryonated eggs/larvae→hepatotracheal migration→++ shedding (starts 2-3wo), spontaneous expulsion~6wo. in adults dogs (or warm blooded non-canids, later eaten) →liver→heart→lungs→heart via bvs→somatic tissues (liver/kidney/mm/etc)→granulomatous reactions, "waiting phase"→ dont develop but still metabolically active, immune evasion...→ vertical transmision by 1) somatic (placental) migration, hypobiotic stages reactivated by hormonal changes towards end of gestation, placenta→ to puppy liver , 2) mammary transmission. or faecal transmission, ingestion of L3.
Ascarid nematode of dogs, cats & bears, smooth plae eggs, no prenatal infection, no tranmammary transmission, no hepatocellular migration. transmission mainly by embryonated eggs & predation ("paratenic" hosts, develops to L3 in somatic tissues)
Ascarid nematode of cats, no prenatal infection, transmission via paratenic hosts & transmammary
SI hookworm in dogs, rare in Britain, usually warm/hot climates, teeth around mouth, blood sucking→anaemia, 1-2cm long, typical strongyle eggs, L3 can penetrate skin (percutaneous)→ tracheal migration to SI in PUP, to tissues (waiting phase) then mammary glands in ADULTS (transmammary infection). can→pedal dermatitis. v pathogenic
SI hookworm often in hounds/country dogs, usually cool climates, cutting plates around mouth, infection mostly by ingestion, poss percutaneous(→deaths), →protein leak & Dx, pedal dermatitis. no vertical transmission.
K9 whipworm, ~2cm, adult stages in caecum, L3 inside egg (brown, barrel, plugs), hard to find eggs in faeces, →intermittent Dx
most common feline lungworm, <14mm (♀>♂), infection via slug/snail (mollusc) IH with L3, migrate through lymph/blood →lungs, parasitise bronchi/alveoli→ subplural nodes. few=asymptomatic, lots→severe resp problems, immunocompromised
lungworm of dogs/fox (<40% EU foxes), <24mm (♀>♂), in pulmonary aa & R♥, eggs accumulate in lung capillaries, infectian via eating IHs (=slug/snail/frog) w/ L3, migrate via mesenteric LNs, PPP = 6-7wks, resists>5yrs. →Hx, thrombosis, R♥ dilation, back pressure in parenchyma, ascites, resp distress, Vx, neuro symptoms. detect by bronchial lavage or L1 in faeces. Tx: levimasol/fenbendazol/moxidectin + systemic therapy
Filaroides (Oslerus) Osleri
worldwide lungworm of dogs & cats, <12mm (♀>♂), unusual LC, transmition via sputum (*****→pup during grooming) or coprophagium. horizontal transmission rare. worms in nodules round bifurcation of trachea. PPP = 5-6wks, can live yrs. usually asymptomatic but poss→chronic, dry, debilitating cough
worldwide filamentous nematode of dogs, in warm climates (not UK), long PPP = 180d & lifespan 5-7y, <30mm (♀>♂), IH= mosquito, infected w/ L1 microfilariae in blood→L3 (T dep development, >14*C req)→infective bite w/ L3→migrate through CT (4months)→diffuse eosinophilic reactions in lung parenchyma→adults in pulmonary aa & R♥→microfilariae produced 6-7m p.i. into blood, →ex intolerance, CHF, poss acute collapse, zoonotic risk