Clinical Manifestations of Equine Parasites Flashcards

1
Q

Write a list of common parasites in the horse

A
  • Gasterophilus spp. or ‘bots’
  • Habronema spp.
  • Parascaris equorum
  • Strongyloides westeri
  • Anoplocephala perfoliata
  • Dictyocaulus arnfieldi
  • Strongylus vulgaris
  • Strongylus equinus
  • Strongylus edentatus
  • Small strongyles – Cyathostomosis
  • Oxyuris equi
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2
Q

Name the parasite

A

Gasterophilus

Lay whitey cream and yellow eggs on legs

Flies look like bumble bees

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3
Q

What is the diagnosis and significance of Gasterophilus?

A
  • See using gastroscopy NOT faecal analysis
  • Rarely cause disease even in large numbers – cause a mild chronic gastritis by ‘grazing’ on the mucosa - ? poor performance, eat slower when in mouth, ? Colic
  • Recent paper suggesting association with ulcers and perforating ulcers – data however ‘inconclusive’
  • Owners dislike the L3 larvae in the faeces
  • Owner dependent disease rather than something that will cause bad signs in horses
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4
Q

What is the prevention and treatment of gasterophilus?

A
  • Can’t control fly as short lifespan (2-3 weeks) and don’t feed and really short life span. Need to NOT be using anthelmintic agents inappropriately
  • Remove eggs in the summer months using a bot knife/ topical insecticides
  • Very sensitive to treatment with wormers containing ivermectin (all stages) and moxidectin (L2 and L3)– contributing to anthelmintic resistance
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5
Q

What is Habronemiasis mainly associated with?

A

Mainly associated with skin sores (‘Summer sores’) and occasionally conjunctivitis - adult worms live and reproduce in the stomach

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6
Q

With habronemiasis, what happens to those deposited in conjunctiva or in wounds?

A

Those deposited in conjunctiva or in wounds can’t migrate so cause disease locally

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7
Q

What age of horse is habronemiasis seen in and what months of the year?

A
  • Seen in all age of horses during June to September
  • Some horses prone to re-infection
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8
Q

What gastric disease does habronemiasis cause?

A
  • Mostly no disease
  • Occasionally horses mount a response against the worms causing nodules of granulation tissue which also contain eosinophils
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9
Q

What is the diagnosis of habronemiasis?

A
  • Often hard to diagnose on faecal analysis as eggs are very fragile and rupture
  • Identify gastric lesions using gastroscopy
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10
Q

Which parasite?

A

Habronemiasis

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11
Q

What is the prevention for Habronemiasis?

A
  • Good fly control and muck heap management
  • Frequent replacement of bedding
  • Collection/removal of droppings in paddocks
  • Cover wounds and treat ocular diseases causing ocular discharge
  • Will be killed in horse with worming for other parasites (Avermectins/Benzimidazoles to lesser extent)
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12
Q

What is Parascaris equorum?

What age of horse does it cause disease in?

A
  • Wasn’t a very big problem years ago – similar to ascaris suum
  • Ascarids – if ever stuck with life cycle almost identical to Ascaris suum
  • Usually causes disease in horses less than 2 years old – immune response more developed in older animals (thought, so not seen as often) -equine specific
  • Prevalence – 10-50% - quite common – probably bit higher in younger horses
  • Regarded as the up and coming parasite and one to watch
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13
Q

What is the longest worm in horses?

A

Parascaris equorum - largest worm of horses – up to 4cm in length, cream and round

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14
Q

Parascaris equorum

  1. What does the life cycle involve?
  2. Can foals be infected through uterus or milk?
A
  • Life cycle involves migration through the liver, vena cava, alveoli, bronchi, trachea so eggs are coughed up and swallowed
  • Reservoirs – adult horses – small numbers but shed enough eggs to infect foals/young stock
  • Foals NOT infected in utero or via milk
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15
Q

Parascaris equorum - what are the clinical signs?

A
  • Coughing and nasal discharge – often ‘mini-outbreaks’ on farms – when parasites in the lungs – some of this is hypersensivity to worm
  • Poor coat and weight gain, dull, anorexic
  • Occ colicking incl bowel obstruction
  • Disorders of bone and tendons as the parasites consume lots of Ca, P, Zn, Cu

–Can see if enough adults worms nicking all electrolytes and minerals

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16
Q

Parascaris equorum - what is the diagnosis?

A
  • Difficult – long PPP (10-14 weeks)
  • Repeated faecal analyses – eggs distinctive when present – can be useful in some cases
  • Endoscopy down to duodenum. Occ get worms when stomach tube and reflux
  • Eosinophils on tracheal washes/ BAL – can sometimes see this when they are on their wander through the lungs, but don’t often see them in the peripherak blood
  • The future – TA ultrasound
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17
Q

Parascaris equorum - what is the treatment?

A
  • MDR – Avermectins – DO NOT USE! THEY DO NOT WORK! This is why the VDS has so many claims at the moment
  • Only ascarid with MDR – none in pigs, dogs and people

–likely relates to the treatment regimes we have and use

  • Drug rotation DOES NOT prevent resistance. In fact, it selects for MDR parasites. Stick to drugs that work!
  • Can see colic if treat lots of adult worms with paralytic drugs – (avermectins and pyrantel)
  • PYRANTEL – this works on 50% of yards (probably a bit higher for Ascarids, but might be facing yards where no drugs are going to work and will have to be much more reliant on pasture management)– very important to undertake FECRT annually or every other year
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18
Q

Parascaris equorum - what is the prevention?

A
  • Hard to prevent pasture contamination – deworm mares just before or just after foaling and keep foaling stalls very very clean. Problem with young foals is that they test their whole environment with their mouths – can be ingesting Ascarid eggs!
  • Remove faeces three times per week in Summer and once weekly in Winter
  • 3-year rotation of paddocks for young animals
  • De-worm foals regularly
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19
Q

What disease does S. Westeri cause?

A
  • V. mild pathogen
  • Dermatitis (frenzy behaviour)
  • Enteritis - profuse, non-fetid diarrhoea in foals with no temperature
  • Occasionally associated with a cough – much rarer than with P. equorum
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20
Q

S. westeri – What is the prevention?

A
  • Pick up faeces regularly in paddocks
  • Anthelmintics

–Benzimidazoles at double or triple normal recommended dosages – they don’t really work for very much, best use we have for fenbendazole

–Avermectins –ivermectin good for larval and adults stages

–Need to worm dam day of parturition and 12 hours later to prevent passage in milk –not always practical OR needed

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21
Q

What parasite is Anoploephala perfoliata?

Which age of horse most commonly affected

A
  • Equine tapeworm – cestode
  • Disease seen frequently in horses associated with this – usually young horses, but can be any age
  • These parasites have no hooks, but very large suckers that attach to the intestinal mucosa
  • Prevalence – ~60%
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22
Q

What parasite?

A

Anoplocephala perfoliata

They hang out at ileocaeco colic junction

They do drug avoidance

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23
Q

According to Gayle, what are some Key clinical notes regarding A. perfoliata?

A
  • Egg shedding irregular (can make it tough when trying to use FEC to confirm diagnosis) and sometimes released from segments in LI and sometimes after excreted from horse
  • The eggs released are infective to ORIBATID MITES, (Intermediate Host). Don’t want to kill this mite as they are useful for good pasture health. These mites bury themselves in the soil and can over winter
  • Mites live on the ground eating plant debris and lichens - overwinter in the soil
  • Horses infected in Spring (grass) -ingest mites as they are at the top of the grass as the grass is short
  • PPP – 6-10 weeks –can then shed large numbers of eggs
24
Q

What creature is this and what parasite lifecycle is it involved in?

A

ORIBATID MITES

Part of the A. perfoliata life cycle

  • The eggs released are infective to ORIBATID MITES, (Intermediate Host). Don’t want to kill this mite as they are useful for good pasture health. These mites bury themselves in the soil and can over winter
  • Mites live on the ground eating plant debris and lichens - overwinter in the soil
  • Horses infected in Spring (grass) -ingest mites as they are at the top of the grass as the grass is short
25
Q

At what time of year is A. perfoliata most common?

What is disease largely triggered by?

A
  • Disease most common Oct/Nov
  • Disease largely triggered by adult tapeworm
26
Q

A. perfoliata

  1. What is the immune response like?
  2. Is faecal analysis for diagnosis possible?
A

•Immune response - worms within the intestine – more pronounced in older horses -more likely to clear the infection

–Basis of a semi-quantitative serological test

–ELISA for diagnosis IN POPULATIONS – BUT NOT FOR INDIVIDUAL DIAGNOSIS

–LOTS of false positives

–Long way from salivary test being useful – need to do on blood

•Faecal analysis difficult – shed intermittently/ low numbers can be missed

–Improved sensitivity using flotation methods

27
Q

A. perfoliata - what are the clinical signs?

A

•Colic

–Ileal impaction – often very painful

–Intussusceptions

–Caecal impactions and motility disorders

–Spasmodic (gas) colic – can lead to displacement

–(Diarrhoea)

–Functional and physical blockages

28
Q

A. perfoliata - what is the treatment & prevention?

A
  • Two drugs – high dose pyrantel (double dose required for other worms, high dose) and praziquantel – treat all horses in Autumn/Winter (Nov) in order to reduce population that over winters so when they go out to grazing in the spring they aren’t putting more eggs onto the pasture
  • Prevention – stable horses for 48 -72 hours after worming to prevent increased pasture contamination. Can’t kill the mites…nature’s dustman
29
Q

What is the most clinically important large strongyle in horses?

A

Strongylus vulgaris

Most clinically important large strongyle – causes ‘verminous arteritis’

30
Q

What parasite?

A

Strongylus vulgaris

Adult worms on surface of LI mucosa

31
Q

S. vulgaris - what is the epidemiology?

A
  • Get some immunity but never complete to stop re-infection
  • Disease often most severe in those young/unexposed animals
  • See in all ages – worse in weanlings and yearlings
  • Reservoirs-asymptomatic horses that shed large numbers of eggs
32
Q

S. vulgaris - what is the diagnosis?

A
  • Difficult as this is a pre-patent disease – disease caused by larval stage
  • May be able to feel thrombi when perform rectal examination
  • Faecal analysis –not always useful and can’t tell from other Strongyle eggs
  • Faecal culture may reveal infective L3 larvae
  • History and recurrent colic
33
Q

What are the diagnostic tests and clinical disease for S. vulgaris?

A
  • Larval culture for S. vulgaris and edentatus and egg counts for P. equorum high PPV, but very low NPV (0.37-0.66)
  • No correlations with Strongyle egg counts and luminal worm counts!
  • Thus increased egg counts DOES NOT mean large worm burdens
  • What we also don’t know is whether the worm burden (which we can’t easily measure) correlates with disease
  • However reducing pasture contamination can only be beneficial

If you find them – more likely they associated with clinical disease but if you don’t find them, doesn’t mean they aren’t associated with the clinical disease

34
Q

What is the diagnosis for S. vulgaris?

A
  • Due to high numbers on pasture in Spring/Summer, often in arteries in Autumn/Winter - when see disease
  • Adults – protein-losing enteropathy and anaemia
  • Colic, diarrhoea, anorexia
  • Ischaemic, dying gut=sick, colicking, dying horse – need surgery for resection if possible
  • Can form thrombi at aorto-iliac junction – can lead to lameness and poor performance
  • Occasionally migrate aberrantly and end up in the brain, kidneys, lungs, liver and can form granulomas
35
Q

S. vulgaris - what is the treatment and prevention?

A

•Drugs

–Avermectins and maybe benzimidazoles– larvae and adults

–Pyrantel – adults only – only works on 50% premises – do WECRT

  • Avoid overgrazing (eggs often on ground)
  • Rotate fields after treatment to decrease risk of re-infection
  • PICK UP FAECES REGULARLY
36
Q

How are these different - Strongylus edentatus and S. equinus?

A
  • Less significant than S. vulgaris but still important in some forms of clinical disease
  • Prevalence now similar to S. vulgaris for same reasons
  • S. edentatus - hepatoperitoneal strongyle

–PPP=11 months

•S. equinus - hepatopancreatic strongyle

–THEY DO NOT ENTER BLOOD VESSELS LIKE THE OTHER TWO STRONGYLES DISCUSSED

–PPP=9 months

–Likes to go into pancreas, could cause fibrosis and then early diabetes mellitus

37
Q

What has happened here - which parasite?

(i know its a stupid question, but may help us to remember it as so random)

A

S. edentatus

Parasite eroded through one of the main hepatic portal vein and into cranial vena cava and this animal bled out through its nose

38
Q

What parasite?

A

S equinus

Little holes where parasite/larvae has exited on its way to the liver

39
Q

S. edentatus and S. equinus - what is the epidemiology?

A
  • As for S. vulgaris, worse in young animals, but can affect all ages
  • Clinical signs seen in Winter and with stress
  • Reservoirs are asymptomatic horses shedding large numbers of eggs
40
Q

S. edentatus and S. equinus - what disease does it cause?

A
  • S. edentatus – colic due to liver disease or peritonitis
  • S. equinus – mild colic. Some association with pancreatic disease and primary diabetes mellitus– both of these conditions EXTREMELY rare in horses
  • Diagnosis, prevention and treatment – as for S. vulgaris
41
Q

Cyathostominosis - what disease does it cause?

A
  • This is still currently just about the most important equine parasitic disease in terms of prevalence and severity of clinical signs seen
  • Severe acute diarrhoea and colic; chronic diarrhoea
  • 50 different species of equine small strongyle
  • 80% prevalence
42
Q

What parasite?

A

Cyathostominosis

43
Q

According to Gayle, what are some Key clinical facts about Cyathostomes?

A
  • Encysted, hypobiotic larvae unaffected by any anthelmintic
  • Hypobiotic population (unaffected by any anthelmintic) makes up 50% of the larval population, which is 90% of the total population (10% adults)
  • For various reasons, larvae emerge in Spring, often many many at once – one is a reduction of adults in the lumen!!
  • PPP-6-14 weeks if no hypobiosis
  • Do see immunity to cyathostomosis, but takes a long time and never complete
44
Q

What is the epidemiology for Cyathostomes?

A
  • All ages affected – more common in young or unexposed horses
  • Egg shedding highest in Spring and due to rapid cycle will get re-infection in June and all the way to Sept/Oct if not too dry
  • Larvae at maximum number in horse in Autumn
45
Q

What is the diagnosis for Cyathostomes?

A
  • Very difficult as PPP disease
  • History and clinical signs – young animals, poor worming history or change
  • May see larvae in faeces or on glove after rectal examination in animals with acute larval cyathostomiasis
  • The future - ELISA for cyathostomin larvae – this is looking positive for worm burden assessment – LAUNCH SOON
46
Q

What disease does Cyathostomes cause? Due to what?

A
  • First syndrome – seen in SPRING
  • ACUTE LARVAL CYATHOSTOMIASIS
  • Due to mucosal damage caused by emergence of the LL3

–Colic

–Weight loss

–Diarrhoea – acute and chronic

–Wasting and death either acutely or chronically

47
Q

What are the clinical signs of Cyathostomes?

A

•Autumn syndrome – when larvae entering intestinal wall – less common than that seen in the Spring

–Colic

–Diarrhoea due to inflammation

48
Q

What is Oxyuris equi?

What is the PPP?

A
  • 15 years go, was only got if the client was not managing to administer some form of anthelmintic – relatively common and benign and just from a poor worming protocol
  • Pinworm
  • Common and relatively benign – presence indicative of poor worming protocol, although is some resistance
  • Specific to horses – prevalence of 25% ?
  • PPP= 5 months
49
Q

O. equi - what is the epidemiology?

A
  • Affect any age
  • Parasite of stabled horses – eggs don’t survive well outdoors
  • Reservoirs – other infected horses and immediate environment e.g. walls of stables, feed buckets, water troughs etc.
50
Q

What is the clinical disease of O. equi?

Differential Diagnosis?

A

•Anal pruritus and skin excoriation and/or myiasis

–DD – sweet itch

•Rarely colic if have HUGE intestinal burden

51
Q

What is the diagnosis of O. equi?

A

Diagnosis – easier than other parasites

  • Eggs in the perianal region on examination
  • Sellotape test – put on slide and examine under the microscope
52
Q

What is this?

A

O. equi

An adult female worm coming out to lay her eggs around their anus. Once they have come all the way from distal part of LI, they then die – they don’t migrate back into the LI – becomes important when we think about some of the random treatments recommended!

53
Q

O. equi - what is the treatment and prevention?

A
  • All anthelmintics should be effective – some resistance
  • DO NOT administer per rectum!
  • Can use topical or systemic anti-inflammatories (usually steroids) to decrease pruritus and keep area clean with disposable material
  • Good stable hygiene – water troughs, mangers etc. – thorough cleaning!!
54
Q

Which drugs are cyathostomes, large strongyles and ascarids resistant/working to?

A
55
Q

How can we prevent and manage anthelmintic resistance?

A

•Side resistance:

–Massive problem in sheep with avermectins – no data in horses currently

–NO reversion in horses (like happens with sheep) with the benzimidazoles – a worry – if you don’t use a drug for a period of time, it becomes back effective to some populations – NOT seeing this is in horses!! BAD

–No new classes planned in the short to medium term

•NEW APPROACH

S – Stop anthelmintic overuse – for things like habronema, gastrophilus etc. – cause minimal to no clinical signs

M – Minimise pathogenic stages

A – Avoid increasing worm burdens in individuals

R – Rely on environmental control

T – Target for stage and shedding

  • Adjuncts are needed - cannot just continue relying on giving drugs all of the time
  • We know that young horses and certain horses have a propensity to carry increasing worm burdens –
  • 10-20% horses excrete 80% eggs – what do we do with these high shedders to reduce contamination on pasture?
56
Q

What is the anthelmintic approach in adults in terms of controling parasite burden and trying to reduce resistance to drugs?

A

•Surveillance AND strategic treatments

–Pick up faeces – once a week in winter when temp under 10, 2-3 weeks in spring summer and autumn when temp over 10 – as this is likely when eggs will develop

–Do faecal worm egg counts

  • Spring EPG> 200 Pyrantel – not about treating disease in the horse but reducing pasture contamination
  • June/Jul EPG>200 Pyrantel
  • Sept/Oct EPG>200 – Ivermectin
  • Nov/Dec - Moxidectin/praziquantel – 1 post treatment FECR – to try to minimise over wintering, primary of tapeworm and Cyathostomes Provides an annual yard saving of £300 based on WEC at £7
  • Poo-picking does work and hand-picking better than poo hoover which is better than paddock sweeper. Harrowing and paddock sweeper spreads poo and eggs all over the pasture and not to be recommended – means horses cannot even avoid it. Leaves eggs all over the pasture rather than selective sections

PROTOCOL BASICALLY: 2 yearly treatment in nov/dec and other treatments throughout year Is FEC say to do so

57
Q

What is the anthelmintic approach in foals in terms of controling parasite burden and trying to reduce resistance to drugs?

A

•No selective therapy recommended in foals

–NO EBM

–More susceptible animals

–P. equorum – different susceptibility

•Want to use diagnostic tests

–FEC

  • Hard to know when ascarids disappear and strongyles take over
  • What is the tapeworm burden on the farm? But mainly that is more important when we get to 6-9 month marl – when their parasite burden type switches (?)
  • Should we worm mares prior to foaling – controversial and lacks EBM, but if so 2-3 months
  • <6 months - Ascarids – use Benzimidazoles/Pyrantel based on WECRT
  • At 6 months – use a faecal sample to decide if have Ascarids or Strongyles – choose drugs accordingly
  • Did the therapy work? Check in two weeks
  • Could do 5d fenbendazole at weaning
  • 9 months (Spring) – Primarily Strongyles – use efficient drugs – Avermectins/ ? Pyrantel
  • 12 months (Spring/Summer) – As above plus tapeworm
  • FOUR-FIVE TREATMENTS which when they are younger will probably be pyrantel and when they are older with large strongyles, will be avermectins