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Y4 Equine - GI > Equine gastrointestinal parasites > Flashcards

Equine gastrointestinal parasites Flashcards

1
Q

GI arasites in the horse

A
  • Habronema spp.
  • Parascaris equorum
  • Anoplocephala perfoliate/magna
  • Large strongyles
    – Strongylus vulgaris
    – Strongylus equinus
    – Strongylus edentatus
  • Small strongyles – Cyathostominosis
    – Previously called cyathastomosis
    ▪Oxyuris equi
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2
Q

Which GI parasite has the most clinical relevance for dz in adult horses?

A
  • Small strongyles -> cyathostominosis
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3
Q

Shape of adult small strongyles

A
  • small and red (when beed feeding on blood meal) or white
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4
Q

GI predilection site for small strongyles

A
  • LI
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5
Q

CS of small strongyle infestation

A
  • ill thrift +
  • colic +
  • d+++ (early L3)
  • weight loss +++ (early L3)
  • severe SIRS (early L3)
  • death (early L3)
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6
Q

Shape of large strongyles

A
  • a bit bigger than small strongyles but still quite small and red or white
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7
Q

GI predilection site for large strongyles

A
  • LI
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8
Q

CS of large strongyle infestation

A
  • ill thrift
  • blood vessel wall damage, haemorrhage and infarction
    – S.vulgaris ++
    – Others +
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9
Q

Shape of adult round worms

A
  • large (up to 10cm), fat and white
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10
Q

Equine GI roundworm

A
  • Parascaris equorum
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11
Q

GI predilection site of Parascaris equorum

A
  • SI
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12
Q

Shape of adult Oxyuris equi (pinworm)

A
  • up to 5cm, white, pointy tail like a beansprout
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13
Q

GI predilection site of Oxyuris equi

A
  • rectum
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14
Q

CS of Oxyuris equi infestation

A
  • itchy bottom (perineal region)
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15
Q

Equine GI tapeworms

A
  • Anaplocephala magnum and perfoliata
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16
Q

Shape of adult tapeworms

A
  • small flat white, look like someone has stood on them
  • no hooks, but very large suckers that attach to the intestinal mucosa
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17
Q

GI predilection site of tapeworms

A
  • ileocaecal area (perfoliata)
  • SI (magna)
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18
Q

CS of tapeworm infestation

A
  • ill thrift
  • colic
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19
Q

What is Habronemiasis mainly associated with?

A
  • skin sores (‘summer sores’) and occasionally conjunctivitis
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20
Q

When is Habronemiasis seen?

A
  • in all ages of horses during June-September
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21
Q

Where do adult worms that cause Habronemiasis live and reproduce?

A
  • in the stomach (mostly no dz)
  • those deposited in conjunctiva or in wounds can’t migrate and so cause dz locally
  • occasionally horses mount a response agains the worms causing nodules of granulation tissue which also contain eosinophils (in the stomach)
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22
Q

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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23
Q

Prevention of 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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24
Q

Parascaris
equorum lifecycle

A
  • Ascarids (lifecycle almost identical to Ascaris suum)
  • involves migration through the liver, vena cava, alveoli, bronchi, trachea, so eggs are coughed up and swallowed
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25
Q

Which horses are usually affected by Parascaris suum? Why?

A
  • usually causes dz in horses less than 2y/o
    – immune response more developed in older animals
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26
Q

Prevalence of Parascaris equorum

A
  • 10-50%
  • quite common
  • but clinical dz is rare
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27
Q

Which GI parasite is regarded as the up and coming parasite and we should watch due to emerging resistance?

A
  • Parascaris equorum
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28
Q

Reservoirs of Parascaris equorum

A
  • adult horses
    – small numbers but shed enough eggs to infect foals/young stock
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29
Q

Are foals infected in utero or via milk with Parascaris equorum?

A
  • no
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30
Q

Parascaris equorum - clinical signs and diagnosis

A
  • Coughing and nasal discharge
    – often ‘mini- outbreaks’ on farms
    – when parasites in the lungs
    – some of this is hypersensivity to worm
  • Should be on ddx for young horses that are coughing
  • Poor coat and weight gain, dull, anorexic
    – adults compete for nutrients in the intestinal lumen and for micronutrients so commonly presents with poor coat & weight gain
  • Occ colicking incl bowel obstruction
    – can get complete SI obstruction due to the size of the parasite
    – present with signs of acute colic, systemic inflammation, and this presentation can be fatal
  • Disorders of bone and tendons as the parasites consume lots of Ca, P, Zn, Cu
  • Diagnosis can be difficult – very distinct eggs when present
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31
Q

Tx of Parascaris suum

A

▪ MDR – Avermectins
▪ 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. 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
– drug of choice

32
Q

Signalment of horses affected by Anoplocephala perfoliata/magna

A
  • usually young horses but can be any age
33
Q

Prevalence of Anoplocephala perfoliata/ magna

A

~60%

34
Q

A. perfoliata - clinical signs

A

Colic
▪Ileal impaction – often very painful
▪ Intussusceptions
▪Caecal impactions and motility disorders ▪Spasmodic (gas) colic
▪ (Diarrhoea)
▪Functional and physical blockages

35
Q

Egg shedding of A. perfoliata

A
  • irregular
  • sometimes released from segments in LI
  • sometimes released after excreted from horse
36
Q

What are A. perfoliata eggs infective too? What is the relevance of this?

A
  • Oribatid mites (intermittent host)
  • Mites live on the ground and overwinter in the soil
  • horses are infected in spring (grass) -> mite ingestion
  • only equine parasite that has an indirect life cycle
37
Q

PPP of A. perfoliata

A
  • 6-10w
  • can then shed large numbers of eggs
38
Q

When is dz from A. perfoliata most common?

A
  • in Oct/Nov
39
Q

A. Perfoliata - Diagnosis

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

  • Blood test (approx £30) numerous labs run
  • Salivatest (Approx.£18)
    ▪ These are antibody tests – values are historic
    ▪ Currently <25% of horses tested require treatment

Diagnosis based on antibody detection

40
Q

A. perfoliata - treatment & prevention

A

▪Two drugs – high dose pyrantel (double dose required for other worms) and praziquantel – treat in Autumn/Winter
▪Prevention – stable horses for 48 hours after worming to prevent increased pasture contamination. Can’t kill the mites

41
Q

Parascaris equorum eggs

A
  • ascarid eggs are unique
  • round and lumpy
  • look like desiccated raison
  • reports that they can survive for up to 10y on pasture
42
Q

Which is the most clinically important large strongyle and why?

A
  • Strongylus vulgairs
  • causes verminous arteritis
    – basically am immune response in the wall of the blood vessels
  • lifecycle involves dissemination through the mesenteric arteries
  • was very important cause of surgical colic that was frequently fatal
    – mainly larvae that cause dz
43
Q

Prevalence of S. vulgaris

A
  • fallen since use of wormers containing ivermectin as worm very sensitive
  • 20y ago was ~60%
  • now ~6%
44
Q

S. vulgaris immunity

A
  • get some immunity but never complete to stop re-infection
45
Q

Which individuals are usually most affected by S. vulgaris?

A
  • young/unexposed animals
46
Q

Signalment of S.vulgaris

A
  • seen in all ages
  • worse in weanlings and yearlings
47
Q

Reservoirs of S.vulgaris

A
  • asymptomatic horses that shed large numbers of eggs
48
Q

S. vulgaris (& S. edentatus & S. equinus) - diagnosis

A

▪Difficult as this is a pre-patent disease – disease caused by larval stage
▪May be able to feel thrombi (in the mesenteric arteries) when perform rectal examination
▪Faecal analysis –not always useful and can’t tell from other Strongyle eggs
▪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

49
Q

S. vulgaris - disease

A

▪ 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
- as affects/reduces blood supply to major arteries of the hindlimbs
▪ Occasionally migrate aberrantly and end up in the brain, kidneys, lungs, liver and can form granulomas

50
Q

When do we usually see dz from S.vulgaris?

A
  • Autumn/winter
  • high numbers on pasture in spring/summer, often in arteries in autumn/winter, which is when dz is seen
51
Q

S. vulgaris - treatment

A

▪Drugs
– benzimidazoles and avermectins – larvae and adults
– Pyrantel – adults only
▪All drug groups still OK for use but same as for small strongyles when it comes to identifying horses requiring tx
▪Avoid overgrazing (eggs often on ground)
▪Pick up faeces regularly

52
Q

What kind of strongyle is S.edentatus?

A
  • hepatoperitoneal strongyle
53
Q

PPP of S.edentatus

A
  • 11 months
  • long as goes through over and peritoneal cavity as part of lifecycle
54
Q

What kind of strongyle is S.equinus?

A
  • hepatopancreatic strongyle
  • they don’t enter blood vessels like the other 2 strongyles
    – therefore, less likely to cause infarction and mesenteric dz
55
Q

PPP of S.equinus

A
  • 9 months
  • goes through liver and pancreas as part of lifecycle
56
Q

Disease caused by S. edentatus

A
  • colic due to liver dz or peritonitis
57
Q

Disease caused by S. equinus

A
  • mild colic
  • some associated with pancreatic dz and primary DM
    – both of these conditions are extremely rare in horses
58
Q

Which is the most important equine parasitic dz currently in terms of prevalence and severity of CS

A
  • Cyathostominosis
59
Q

CS of cyathostominosis

A
  • severe acute d+ & colic
  • chronic d+
60
Q

Prevalence of cyathostominosis

A
  • 80%
61
Q

Are cyathostomin encysted hypo biotic larvae affected by anthelmintics?

A
  • no, they are largely unaffected by any anthelmintic
62
Q

What % of the larval population of cyathostomins are hypo biotic?

A
  • 50%
63
Q

When do cyathostomin larvae emerge?

A
  • in spring
  • often loads at once
64
Q

PPP of cyathostomins

A
  • 6-14w if no hypobiosis
65
Q

When are most cyathostomin larvae on the pasture?

A
  • in autumn
66
Q

Immunity to cyathostominosis

A
  • do see it but takes a long time an never complete
  • younger horses more likely to have higher burdens
67
Q

Diagnosis - Cyathostomins

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 cyathostominosis

▪ The future - ELISA for cyathostomin larvae – current ELISA for IgG antibodies against specific cyathastomin antigens looks at probabilities of total worm burdens but not at likelihood of clinical disease

68
Q

Disease- Cyathostomins

A

▪First syndrome – seen in SPRING
▪ACUTE LARVAL CYATHOSTOMINOSIS
▪Due to mucosal damage caused by emergence of the late L3
- Colic
- Weight loss
- Diarrhoea – acute and chronic
– can be very profuse and watery
– sometimes slightly haemorrhagic
- Wasting and death either acutely or chronically
- Often affected by the loss of mucosal integrity
– often have bacteraemia, severe SIRS, protein loss (particularly albumin) across the gut so can get ventral and peripheral oedema due to loss of oncotic pressure

69
Q

Clinical signs- Cyathostomins

A

▪Autumn syndrome – when larvae entering intestinal wall – less common than that seen in the Spring
▪Colic
▪Diarrhoea due to inflammation

70
Q

Signalment of O. equi

A
  • affects any age
  • parasite of stabled horses (eggs don’t survive well outdoors)
71
Q

Reservoirs of O. equi

A
  • other infected horses and immediate environment
72
Q

CS & diagnosis of O. equi

A

▪Anal pruritus and skin excoriation and/or myiasis
▪Eggs in the perianal region on examination
▪Sellotape test – put on slide and examine under the microscope

73
Q

O. equi - treatment and prevention

A

▪All anthelmintics should be effective – some resistance
▪ Anal application as a paste
– way to target anthelmintic at the area of likely highest burden
– but most important thing is hygiene to manage these
▪Can use topical or systemic anti-inflammatories to decrease pruritus and keep area clean with disposable material
▪Good stable hygiene – water troughs, mangers etc

74
Q

What environment do Cyathostomins love?

A
  • high stocking densities
  • mild wet winters
75
Q

Where do L3 cyathostomin larvae encyst?

A
  • in the wall of the large colon and caecum

Y4 Equine - GI (25 decks)

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