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Parasitology > Equine Nematodes > Flashcards

Equine Nematodes Flashcards

1
Q

Strongylidae Family

A

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

Strongylinae (large strongyles, large red worms)

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2
Q

Cyathostominae- Key facts

A

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

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3
Q

Cyathostomin Life Cycle

A

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

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4
Q

Cyathostomin development on pasture

A

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

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5
Q

Worms in refugia

A

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

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6
Q

Cyathstomin development in host

A

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

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7
Q

Cyathostomin inhibited development

A

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)

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8
Q

Negative feedback of luminal stages

A

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.

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9
Q

Cyathostomin inhibited development continued

A

resumption of larval development reflects decreasing immunity

Larval emergence may result in disease

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10
Q

Cyathostominosis

A

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.

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11
Q

Host susceptibility to cyathostomins

A

“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.

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12
Q

Strongylinae Family- key facts

A

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.

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13
Q

Large strongylse- 3 main species

A

S. vulgaris, S. equinus and S. edentatus

also, triodontophorus species

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14
Q

Strongylus vulgaris life cycle

A

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

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15
Q

Strongyle Biology summary

A

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

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16
Q

Strongyle epidemiology

A

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.

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17
Q

Background to equine parasite control

A

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.

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18
Q

Conventional parasite control

A

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.

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19
Q

Anthelmintic resistance in equine parasites

A

Widespread prevalence: up to 100% for benzimidazoles

Detection difficult: particularly in horses

Awareness is low: both vets and horse owners

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20
Q

Anthelmintic resistance continued

A

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

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21
Q

Parasite refugium

A

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.

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22
Q

Cyathstomin refugia

A

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

EL3- larvae in hypobiosis

23
Q

Anthelmintic resistance in cyathostomins- key facts

A

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)

24
Q

Detecing anthelmintic resistance

A

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.

25
Q

Equine parasite control: best practice 1

A

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

26
Q

Equine parasite control: best practice 2

A

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

27
Q

Pasture hygiene

A

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.

28
Q

Tapeworm control

A

either target dose on basis of serology

OR, annual inclusion of praziquantel dose (combo products)

29
Q

Bot control

A

IVM during winter, combine with tapeworm dosing

30
Q

When best-practice is likely to fail

A

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.

31
Q

Equine Nematodes II

A

parascaris equorum- ascaridoidea

oxyuris equi- Oxyuroidea (pinworms)

strongyloides westeri- rhabditoidea

Summer sores

32
Q

Parascaris equorum

A

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.

33
Q

Parascaris equorum life cycle (similar to T. canis)

A

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

34
Q

Parascaris equorum pathogenesis

A

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.

35
Q

Parascaris equorum- clinical signs

A

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

36
Q

Parascaris equorum

A

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.

37
Q

Diagnosis of parascaris equorum

A

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

38
Q

Parascaris equorum- epidemiology

A

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.

39
Q

P. equorum treatment/control

A

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.

40
Q

Strongyloides westeri- rhabditoidea

A

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

41
Q
A
42
Q

Strongyloides westeri life cycle

A

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

43
Q

Strongyloides westeri- clinical signs

A

Only seen in very young animals (a few weeks old)

requires heavy worm burden

diarrhea, anorexia, dullness, reduced weight gain

44
Q

Diagnosis of strongyloides westeri

A

clinical signs

larvated egg in feces (small than strongyle egg)

high egg count can be seen in healthy animal

45
Q

Strongyloides westeri: epidemiology

A

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.

46
Q

Oxyuris equi

A

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

47
Q

oxyuris equi adult appearance

A

male= 1cm

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

48
Q

Oxyuris equi life cycle

A

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

49
Q

Oxyuris equi- clinical signs

A

Adults in intestine rarely produce clinical signs

Egg laying activity can cause: intense perineal irritation, rubbing, alopecia/inflammation over rump and tail head

50
Q

Oxyuris equi- diagnosis

A

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.

51
Q

Oxyuris equi-epidemiology and control

A

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

52
Q

Habronema microstoma

A

host: horses, donkeys

IMH: muscid flies

Site: adults in stomach

L3 from housefly usually swallowed by horse and adults develop in stomach

53
Q

Summer sores

A

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.

Parasitology (12 decks)

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