Equine Nematodes Flashcards
Strongylidae Family
Cyathostominae (small strongyle, small “red” worms (not all are red))
Strongylinae (large strongyles, large red worms)
Cyathostominae- Key facts
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
Cyathostomin Life Cycle
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
Cyathostomin development on pasture
Horse excretes egg in feces, on pasutre moults from egg–> L3
Worms in refugia
those that are free-living on pasture, or those worms in untreated animals (i.e. those not exposed to drug tx)
Cyathstomin development in host
EL3 (arrested/inhibited larval stage- look quite coiled up)–> LL3–> DL4 (larger red blobs are developing/emerging)–>L5 and adults in intestinal lumen–> eggs
Cyathostomin inhibited development
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)
Negative feedback of luminal stages
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.
Cyathostomin inhibited development continued
resumption of larval development reflects decreasing immunity
Larval emergence may result in disease
Cyathostominosis
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.
Host susceptibility to cyathostomins
“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.
Strongylinae Family- key facts
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.
Large strongylse- 3 main species
S. vulgaris, S. equinus and S. edentatus
also, triodontophorus species
Strongylus vulgaris life cycle
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
Strongyle Biology summary
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
Strongyle epidemiology
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.
Background to equine parasite control
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.
Conventional parasite control
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.
Anthelmintic resistance in equine parasites
Widespread prevalence: up to 100% for benzimidazoles
Detection difficult: particularly in horses
Awareness is low: both vets and horse owners
Anthelmintic resistance continued
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
Parasite refugium
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.
Cyathstomin refugia
Eggs, L1, L2, L3 on pasture (i.e. any life stage that’s free-living)
EL3- larvae in hypobiosis
Anthelmintic resistance in cyathostomins- key facts
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)
Detecing anthelmintic resistance
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.
Equine parasite control: best practice 1
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
Equine parasite control: best practice 2
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
Pasture hygiene
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.
Tapeworm control
either target dose on basis of serology
OR, annual inclusion of praziquantel dose (combo products)
Bot control
IVM during winter, combine with tapeworm dosing
When best-practice is likely to fail
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.
Equine Nematodes II
parascaris equorum- ascaridoidea
oxyuris equi- Oxyuroidea (pinworms)
strongyloides westeri- rhabditoidea
Summer sores
Parascaris equorum
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.
Parascaris equorum life cycle (similar to T. canis)
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
Parascaris equorum pathogenesis
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.
Parascaris equorum- clinical signs
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
Parascaris equorum
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.
Diagnosis of parascaris equorum
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
Parascaris equorum- epidemiology
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.
P. equorum treatment/control
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.
Strongyloides westeri- rhabditoidea
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
Strongyloides westeri life cycle
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
Strongyloides westeri- clinical signs
Only seen in very young animals (a few weeks old)
requires heavy worm burden
diarrhea, anorexia, dullness, reduced weight gain
Diagnosis of strongyloides westeri
clinical signs
larvated egg in feces (small than strongyle egg)
high egg count can be seen in healthy animal
Strongyloides westeri: epidemiology
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.
Oxyuris equi
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
oxyuris equi adult appearance
male= 1cm
female= up to 10 cm with a long, pointy tail
Oxyuris equi life cycle
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
Oxyuris equi- clinical signs
Adults in intestine rarely produce clinical signs
Egg laying activity can cause: intense perineal irritation, rubbing, alopecia/inflammation over rump and tail head
Oxyuris equi- diagnosis
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.
Oxyuris equi-epidemiology and control
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
Habronema microstoma
host: horses, donkeys
IMH: muscid flies
Site: adults in stomach
L3 from housefly usually swallowed by horse and adults develop in stomach
Summer sores
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.
