Equine Nematodes

Question 1

Strongylidae Family

Answer 1

Cyathostominae (small strongyle, small “red” worms (not all are red))

Strongylinae (large strongyles, large red worms)

Question 2

Cyathostominae- Key facts

Answer 2

Small stongyles

>50 species, c. 10 comon– biology considered largely the same

Highly prevalent- assuming all grazing horses in temperate climates

Direct, non-migratory life cycle (PPP 5-12 weeks)- infects horse directly via pasture

Propensity for prolonged duration (inhibited development).

Variable but low host immunity

Principle parasitic pathogens of equidae in the DEVELOPED world

Question 3

Cyathostomin Life Cycle

Answer 3

Adults in the LI–> eggs in feces–> L1, L2, L3 on pasture–> L3 is infective stage, gets ingested–> develop within the LI wall (caecum and colon)

Some L3 arrested in LI mucosa–when in EL3, not susceptible to ABX

If unarrested or after arrest–> moult to L4–> emerge from LI wall–> moult to L5–> adults in the large intestine

Question 4

Cyathostomin development on pasture

Answer 4

Horse excretes egg in feces, on pasutre moults from egg–> L3

Question 5

Worms in refugia

Answer 5

those that are free-living on pasture, or those worms in untreated animals (i.e. those not exposed to drug tx)

Question 6

Cyathstomin development in host

Answer 6

EL3 (arrested/inhibited larval stage- look quite coiled up)–> LL3–> DL4 (larger red blobs are developing/emerging)–>L5 and adults in intestinal lumen–> eggs

Question 7

Cyathostomin inhibited development

Answer 7

AKA hypobiosis/arrested development

In ruminants i.e. ostertagiosis arrest is a couple/several months long. In horses, hypobiosis is MUCH longer.

NB: dewormers DO NOT work on hypobiotic stages

In horses, hypobiosis can last for months-years of 100 or 1000s of larvae

Hypobiosis reflects (incomplete) immunity

Age: (1-3 years)- after 3 years prett y good immunity but horses have life-long variable immunity for cyathostomins

Size of the larval challenge

Negative feedback of luminal stages (L4 and adult)

Question 8

Negative feedback of luminal stages

Answer 8

Immunity may or may not be affected by chemical negative feedback of luminal stages. Basically, the presence of L5 and adults basically tells EL3 to stay in hypobiosis. Therefore, if you deworm and remove all the L5s and adults, L3s re-enter life cycle/exit hypobiosis.

Question 9

Cyathostomin inhibited development continued

Answer 9

resumption of larval development reflects decreasing immunity

Larval emergence may result in disease

Question 10

Cyathostominosis

Answer 10

Protein losing enteropathy

Diagnosis: fecal larvae, NOT eggs- pathogenic stages don’t produce eggs- have to look for larvae in feces.

Seasonal- late winter/spring- not as seasonal as in something like ostertagiosis

Sometimes occurs post anthelmintic dosing for control programme

Clinical signs: preputial oedema

oedematous mucosa- when hypobiotic larvae start to develop again in synchrony, protein losing enteropathy–> mucosa becomes like a seive.

Question 11

Host susceptibility to cyathostomins

Answer 11

“80% of worms in 20% of animals”

The majority of the parasites are often present in the minority of the host population

Host susceptibiltiy varies markedly

most (adult) horses have low levels on infection

No 100 percent immunity, such that horses may need to receive life long periodic anthelmintic doses–> confers anthelminitic resistance.

Question 12

Strongylinae Family- key facts

Answer 12

Strongylinae (large strongyles)- 6 species

Low prevalence in developed world- sensitive to anthelmintics

Direct migratory life cycle (cf. cyathostomins= non-migratory)

PPP=6-10 months (MUCH longer than cyathostomins)

Migratory larval stages are highly pathogenic

Adult stages are plug feeders- feed on mucosal surface, pathogenic but not as much as larvae

All host-stages susceptible to modern anthelmintics (incl. larvae and adult)

Variable but reasonable host immunity.

Question 13

Large strongylse- 3 main species

Answer 13

S. vulgaris, S. equinus and S. edentatus

also, triodontophorus species

Question 14

Strongylus vulgaris life cycle

Answer 14

Adults in LI–> eggs in feces–> L1–>L2–>L3–>L3 (sheathed)–Ingested. After ingestion, L3s exsheath in small intestine and penetrate the intestinal mucosa and moult to L4s. L4s penetrate submucosal arteries and migrate to the caecal and colic arteries and then to the root the cranial mesenteric artery and its main branches. After a period of development of 3-4 months, larvae moult to L5s, but retain cuticle as external sheath. Return to the intestinal wall via arteries. Nodules formed around L5s in wall of caecum and colon. Subsequent ruptue of these nodules release young adult parasites into the lumen of the intestine where they mature in another 6-8 weeks.

Can cause colic by causing infarcts

Question 15

Strongyle Biology summary

Answer 15

Large strongyles: long (PPP c. 6months) migratory life cycle; larval stages are pathogenic; larval stages extremely sensitive to modern anthelmintics

Small strongyles: Short (PPP c. 8 weeks), non-migratory life cycle; propensity for prolonged (>2 years) arrested developemnt; arrested larval stages are refractory to anthelmintic

Question 16

Strongyle epidemiology

Answer 16

All ages of horses potentially contaminate pasture

Many temperate regions have year-round pasture larval infectivity

UK: peak pasture infectivity mid/late summer- similar to rumen parasites

Prolonged, dry heat lethal to pasture larvae

They like warm and moist

NB: the nearer the fecal pats they graze, the more worms they get.

Question 17

Background to equine parasite control

Answer 17

Lifelong susceptibility to certain parasites

Host susceptibility: markedly varies, most adult horses have low levels of infection NB: 80% of parasite in 20% of hosts

Frequent on-movement of horses–> take worm burden with them as they move i.e. boarding properties etc.

Body weight of individual horses is often NOT known- can use a weight tape (not accurate in minis or draughts) for accurate dosing.

Question 18

Conventional parasite control

Answer 18

Conventional wisdom, up until 5 years ago-ish: intensive, interval anthelmintic dosing of all grazing animals regardless of age, infective status

Assumes that one size fits all; simplistic strategies for owner convenience; aggressive marketing by manufacturers

This resulted in a MASSIVE decrease in prevalence of strongylus vulgaris, but also results in widespread anthelmintic resistance in cyathostomins.

Question 19

Anthelmintic resistance in equine parasites

Answer 19

Widespread prevalence: up to 100% for benzimidazoles

Detection difficult: particularly in horses

Awareness is low: both vets and horse owners

Question 20

Anthelmintic resistance continued

Answer 20

Benzimidazoles (i.e. fenbendazole)- cyathostomins

Pyrantel- cyathostomins

IVM (macrocylic lactone)- ascardis? apparent resistance to IVM

Moxidectin (macrocylic lactone)- newer drug, much more efficaicious for cyathostomins 13 weeks duration of efficacy- combined with tapeworm tx

Virtually 100% resistance to BZM

Question 21

Parasite refugium

Answer 21

the proportion of parasites NOT exposed to anthelmintic chemical compound at points when animal is dosed is said to be “in refugia”

i.e. no kill-out of all susceptible worms.

Question 22

Cyathstomin refugia

Answer 22

Eggs, L1, L2, L3 on pasture (i.e. any life stage that’s free-living)

EL3- larvae in hypobiosis

Question 23

Anthelmintic resistance in cyathostomins- key facts

Answer 23

Irreversible

GENETIC feature of parasite populations

in brazile and UK- multi-drug resistance in cyathostomins to all 3 major anthelmintic classes (BZM, pyrantel salts and macrocylic lactones)

Question 24

Detecing anthelmintic resistance

Answer 24

fecal egg count reduction test: <90% reduction in groups of worms indicative of resistant worms

do FWEC day 0 and then day 10-14

but: 1) FWEC repetability is poor
2) sample numbers are often small i.e. don’t have huge herds of horses
3) overdispersed cyathostomin populations

likely, resistance is underdetected.

Question 25

Equine parasite control: best practice 1

Answer 25

cyathostomins tapeworm ascardis (foals and weanlings) bots (fly stages that infect horses on skin- not v. pathogenic, only certain products work against them) Large strongyles There is no blue-print- must custom-design programme on basis of mgmt. conditions

Question 26

Equine parasite control: best practice 2

Answer 26

Targeted selective dosing (to control cyathostomins) ideally, monthly FWEC all animals Anthelmintic dose to known body weight and only FWEC positvie (\>200 epg) DO NOT ROTATE ANTHELMINTICS Monitor anthelmintic resistance Mixed species co-grazing: use sheep to graze shared pasture- sheep ingest horse worms and has no effect on sheep Caution with harrowing: pulls out old grass and levels off paddock- can scatter worms and fecal pats everywhere Practice pasture hygiene

Question 27

Pasture hygiene

Answer 27

generally encouraged as an "add on" possibly sole means of parasite control- lifting feces before eggs have time to hatch Removing refugia also can possibly increase the parasite burden Parasites in refugia don't have genes for anthelmintic resistance i.e. they're still susceptible to anthelmintics. the more refugia there is in a population, the more dilute the resistance genes will be. when an entire group is dewormed, we eliminate all the refugia and the only worms that survive are resistant.

Question 28

Tapeworm control

Answer 28

either target dose on basis of serology OR, annual inclusion of praziquantel dose (combo products)

Question 29

Bot control

Answer 29

IVM during winter, combine with tapeworm dosing

Question 30

When best-practice is likely to fail

Answer 30

poor owner/mgmt compliance frequent "on movement"- boarding facilities, public studs groups of young foals/weanlings "serial" use of moxidectin If/when S. vulgaris regains high prevalence.

Question 31

Equine Nematodes II

Answer 31

parascaris equorum- ascaridoidea oxyuris equi- Oxyuroidea (pinworms) strongyloides westeri- rhabditoidea Summer sores

Question 32

Parascaris equorum

Answer 32

worldwide, common in foals and yearlings Age resistance Infection rates decrease from 6 months onwards cause unthriftiness Typical ascarid lifecycle Large worm: chunky, 40 cm Site: small intestine, primarily duodenum and proximal jejunum.

Question 33

Parascaris equorum life cycle (similar to T. canis)

Answer 33

Adults in SI --\> eggs in feces--\> L1 in egg--\>L3 in egg is infective Nb: minimum of two weeks from egg to L3 in egg L3 in egg hatches after ingestion--\> L3 travels to liver via portal circulation--\> liver--\> travel in blood to lungs--\> travel up bronchial tree and swallowed--\> L4 and adult in SI PPP=10-15 weeks

Question 34

Parascaris equorum pathogenesis

Answer 34

Migrating larvae cause damage to: liver: focal hemorrhage and fibrosis (if a lot of larvae) Lungs: focal hemorrhage, lymphocyte infiltration, nodules (form round larvae as they penetrate) Adult worms in intestine: little pathology, very rarely in heavy worm burdens can cause impaction, perforation, peritonitis.

Question 35

Parascaris equorum- clinical signs

Answer 35

Ill thrift: due to adult worms in SI, common in foals and yearlings, can develop to emaciation if left untreated, adult horses show age immunity- unaffected Respiratory signs: due to migrating larvae; Foals: coughing +/- greyish nasal discharge + runny nose Symptoms seen occasionally, usually with concurrent ill-thrift

Question 36

Parascaris equorum

Answer 36

Impaction, perforation, peritonits occurs occasionally with very heavy worm burden Can occur post-treatment with anthelmintics- in one study, 72% of 25 horses with SI obstruction had been treated with drugs 24 hours previously.

Question 37

Diagnosis of parascaris equorum

Answer 37

Clinical signs/history FEC (tens of thousands eggs/gram)- VERY sensitive d/t fecund female ascarids corprophagia can lead to fals positives Eosinophilia- transient in migratory phases of infection Always consider other causes of ill-thrift/concurrent disease typical ascarid eggs: unlarvated, brown, thick pitted shell Larvated: clear egg, shell has lost pitted appearance

Question 38

Parascaris equorum- epidemiology

Answer 38

Adult horses not a major source of contamination but can act as carriers Foal to foal diseae (season to season) Female worms have very high biotic potential- just a few females can produce loads and loads of eggs Eggs very resistant (survive several years) and sticky Eggs tend to build up on pasture towards the end of summer- just as foals are being turned out to graze.

Question 39

P. equorum treatment/control

Answer 39

Control measures aimed at small strongyle control should effectively control parascaris IVM resistnace an increasing problem Several reports of macrocylic lactone resistance in UK, netherlands, germany, denamrk, canada, USA one report that pyrantel less effective but still senstive to BZ compounds.

Question 40

Strongyloides westeri- rhabditoidea

Answer 40

Worldwide distribution Adult worms are very small \<1cm Only females are parasitic- no males in horse reasonably common in foals less than 6 months old

Question 42

Strongyloides westeri life cycle

Answer 42

Adult females in SI via parthenogenesis (eggs don't have to be fertilized by sperm) produce larvated eggs--\> L1--L2-L3--L4-free living male and female adults L3 can get ingested or penetrate through skin. After ingestion/penetration, L3 can either: 1) go to lungs via bloodstream--\> L4-adult in lungs--\> adult females in SI or 2) L3s lie dormant in muscle--\> can give rise to transmmary infection (no migration) to lungs--\> adult females in small intestine PPP=8-14 days

Question 43

Strongyloides westeri- clinical signs

Answer 43

Only seen in very young animals (a few weeks old) requires heavy worm burden diarrhea, anorexia, dullness, reduced weight gain

Question 44

Diagnosis of strongyloides westeri

Answer 44

clinical signs larvated egg in feces (small than strongyle egg) high egg count can be seen in healthy animal

Question 45

Strongyloides westeri: epidemiology

Answer 45

free-living L3 not very resistant, not sheathed Thrive in warm and wet conditions/ poor hygiene Transmammary route is important- successive progeny of same dam often show heavy infections.

Question 46

Oxyuris equi

Answer 46

pinworms, found in LI, L3 in egg is infective, very common parasite. nb: human pinworm= enterobious vermicularis- common in children, domestic animals are NOT a reservoir for human pinworms

Question 47

oxyuris equi adult appearance

Answer 47

male= 1cm female= up to 10 cm with a long, pointy tail

Question 48

Oxyuris equi life cycle

Answer 48

Adults in colon--\> female lays egg at anus--\> L1 inside egg--\> L2 inside egg--\> Infective L3 inside egg--\> Egg ingested and hatches--\> L3 penetrates colonic mucosa--\> L4--\>re-emerge from mucosa as L4--\> adults in colon PPP=5 months

Question 49

Oxyuris equi- clinical signs

Answer 49

Adults in intestine rarely produce clinical signs Egg laying activity can cause: intense perineal irritation, rubbing, alopecia/inflammation over rump and tail head

Question 50

Oxyuris equi- diagnosis

Answer 50

Clinical signs +/- eggs around the perineal region (usually not in feces) scraping + microscopic examination of eggs adult worms in feces- sometimes egg: 80-95 microns in length, by 40-45 microns wide yellow, ovoid, one side flattened, mucus plug at one end.

Question 51

Oxyuris equi-epidemiology and control

Answer 51

infective L3 in egg can develop on perineal skin usually flakes of skin with eggs get rubbed off little immunity to re-infection heavy burdens can build-up in infected stables. Susceptible to many broad spectrum anthelmintics May be some resistance to ML compounds keep environemt clean

Question 52

Habronema microstoma

Answer 52

host: horses, donkeys IMH: muscid flies Site: adults in stomach L3 from housefly usually swallowed by horse and adults develop in stomach

Question 53

Summer sores

Answer 53

instead of fly being swallowed, cutaneous infestiation by L3 of habronema or related parasite draschia L3 deposited on skin, often around eyes No further development L3 break out of fly mouthparts when stimulated by temperatures within 1-2 c of body temp Associated with warm weather, often on dark coated horses WIll seen eosinophils on biopsy.