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GIL 2 > equine GI parasites > Flashcards

equine GI parasites Flashcards

1
Q

which equine parasites affect the stomach

A
  • gasterophilus spp
  • habronema spp
  • trichostrongylus axei
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2
Q

outline the lifecycle of gasterophilus

A
  • L 1 develops in mouth tongue and gums
  • morph into L2 in pharynx and base of tongue
  • migration to stomach, L3 attaches to gastric mucosa along margo plicatus or dorsoproximal part of the duodenum
  • L3 survive there 10-12 month before dropping off to pupate in feces
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3
Q

describe how L3 larvae of gasterophilus look

A
  • 2 cm long
  • cylindrical with rows of strong spines/tips
  • mouthpieces have 2 stong hooks
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4
Q

can gasterophilus pupate in litter?

A

no- require soil, only occurs in fields

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5
Q

how is gasterophilus diagnosed

A
  • gastroscopy or post mortem - not fecal analysis
  • rarely causes disease, may cause some chronic gastritis
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6
Q

how is gasterophilus prevented/controlled

A
  • cant control fly
  • mechanical removal of eggs using bot knife
  • topical insecticides
  • very sensitive to treatment with dewormers contatining ivermectin and moxidectin (L2 and L3 only)
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7
Q

outline the lifecycle of habronemiasis

A
  • adult worms in the stomach
  • eggs hatch shortly after being deposited and L1 is passed into the feces
  • L1 ingested by maggots in which develop into L2 and L3
  • infectious L3 larvae migrate to the oral parts of the fly
  • flies feed on horse secretions (L3 deposit on lips, nostrils, around eyes)
  • L3 ingested and migrate through tissues to mature in stomach
  • L3s that settle on conjunctiva or wounds can not migrate through to stomach and only cause disease locally
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8
Q

summer sores are cuased by which parasite

A

habronema

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9
Q

discuss epidemiology of habronema

A
  • PPP 6-8 weeks
  • reservoid = infected horses and flies
  • seen in all ages of horses June - sept
  • not very common with a low rate of infection - depends on the cleanliness of the yard and number of flies
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10
Q

how is habronema diagnosed

A
  • most of the time no disease
  • difficult to diagnose during fecal analysis (eggs very fragile and break while still in feces
  • horses can build up a response against worms causing granulation tissue nodules containing eosinophils
  • gastric nodules seen using gastroscopy
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11
Q

how is habronema prevented

A
  • good fly control
  • muck pile management
  • frequent replacement of bedding
  • regular removal of excrement in paddocks
  • harrowing fields
  • cover wounds and treat eye diseases to stop discharge
  • avermectins and benzimidazoles
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12
Q

what is trichostrongylus axei and why is it important to be aware of the egg morphology

A
  • mainly an abomasal nematode of ruminants
  • sometimes seen in horses grazed with cattle
  • rarely causes disease, sometimes diarrhea in foals
  • infection transmitted by mother
  • eggs look identical to equine strongyles!!!
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13
Q

outline the lifecycle of parascaris equorum

A
  • when temp rises (20-25) and humidity increases, development occurs in 2 weeks at L2
  • L3 protected in shell and infect horse by ingestion
  • L3 pass through intestinal wall and migrate to liver via hepatic portal vein
  • L3 reminas in the liver for a week then enters vena cava and moves to the pulmonary alveoli
  • morph into L4 coughed up and swallowed
  • return to stomach and SI to mature into adult
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14
Q

parascaris equorum causes disease in which age group and what are the clinical signs

A
  • usually in horses under 2 (older animals developed immunity)
  • largest horse worm
  • enteritis
  • colic
  • intestinal obstruction
  • poor coat
  • poor growth
  • dull
  • anorexic
  • bone and tendon disorders (parasites consume Ca, P, Zn, Cu)
  • cough, runny nose when parasites impacting resp system (cuased by hypersensitivity reaction)
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15
Q

list parasite affecting the small intestine of horses

A
  • parascaris equorum
  • strongyloides westeri
  • anoplocephala perfoliata
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16
Q

how is parascaris equorum diagnosed

A
  • clinical sigsn (notspecific and difficult due to long PPP period of 10-16 weeks)
  • repeated fecal analysis
  • tracheal washes/BAL reveals eosinophils
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17
Q

how is parascaris equorum treated/controlled

A
  • adults and larvae have some resistance to benzimidazoles and avermectins
  • deworm mares just before or after foaling
  • keep foaling stalls very clean
  • remove feces every day
  • 3 year rotation of pens for young animals
  • deworm foals regularly
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18
Q

outline the lifecycle of strongyloides westeri

A
  • larvae go to lung and migrate to trachea to be coughed up then swallowed
  • enter intestine in adulthood within a few days
  • some migrate through other tissues (mammary glands)
  • larvae in mammaory glands pass into colostrum and milk to infect newborn
  • PPP = 5-7 days
19
Q

what are the clinical signs of strongyloides westeri

A
  • abundant and non fetid diarrhea without fever
  • foals get sick quickly
  • one of the causes of foal heat diarrhea
  • sometime coughing
20
Q

how is strongyloid westeri diagnosed

A
  • fecal analysis in foals
  • fecal not useful in adults because will generally be negative (immunity)
21
Q

how is strongyloid westeri prevented

A
  • regular collection of feces in paddocks
  • benzimidazoles at 2 or 3 recommended normal doses. ivermectin good for larval and adult stages
  • need to derwom on the day of partuition and 12 hours later to prevent passage into milk (not practical?)
22
Q

outline the lifecycle of anoplocephala perfoliata

A
  • reproduce via hermaphrodism
  • oribatid mites are intermediate hosts
  • PPP=6-10 weeks
23
Q

what is the immune response to anoplocephala perfoliata

A
  • immunity is more pronounced in older horses (therefore more likely to clear infection)
  • immune response of antibodies is used as the basis of a serological ELISA test for diagnosis
24
Q

how is anoplocephala perfoliata diagnosed

A
  • difficult fecal analysis because segments are lost intermittently and in small numbers so they can be missed
  • detection improved by using flotation and sedimentation methods
  • ELISA
25
Q

what are the clinical signs of anoplocephala perfoliata

A

colic
- ileal impaction
- ileal intussusception
- disorder of caecal impaction and motility
- spasmodic colic
- diarrhea
- functional and physical blockages

  • mucous lesions
  • asymptomatic infection in the majority of horses
26
Q

how is anoplocephala perfoliata treated/prevented

A
  • pyrantel as a double dose
  • praziquantel treatment in the fall
  • high risk horses benefit from june tx
  • stable horses for 48 hours after deworming to avoid further contamination of pastures
  • no environmental control (cant kill mites)
27
Q

list parasites that affect the large intestine of horses

A
  • oxyuris equi
  • strongylus vulgaris
  • strongylus equinus
  • strongylus edentatus
  • cyathostomes
28
Q

outline the lifecycle of oxyuris equi

A
29
Q

what are the clinical signs of oxyuris equi

A
  • anal pruritis
  • skin excoriation and/or myiasis
  • can cause colic if you have a huge intestinal load
  • rat tail appearance
30
Q

how is oxyuris equi diagnosed

A

eggs in perianal region collected with sellotape - put on slide and examine under microscope

31
Q

outline the lifecycle that occurs outside of the horse in all strongyle species

A
32
Q

outline the lifecycle of strongylus vulgaris

A
  • L3 passes through the intestinal wall, morphs into L4
  • migrates via blood to form thrombus in cranial mesenteric artery
  • morphs into L5, leaves thrombus (causing hemorrhage) and returns to the large intestine to mature into adult
  • eggs excreted in feces, L3 ingested
33
Q

what is the clinical impact of strongylus vulgaris

A
  • most clinically important dzz
  • causes arteritis thrombosis at the aortoiliac junction and colic (fatal)
  • mainly larvae that cause diarrhea
  • adult worms cause protein losing enteropathy, diarrhea and anemia
  • very painful - tongue biting
34
Q

outline the life cycle of strongylus equinus

A
  • L3 invades the wall of the caecum and colon to morph into L4
  • L4 passes through the visceral peritoneum to the liver and moutls to L5
  • L5 returns to the large intestine via the pancreas
35
Q

what are the clinical signs of strongylus equinus

A
  • mild colic
  • can cause pancreatic disease and primary diabetes mellitus (rare)
  • hemorrhagic nodules in the large intestine
36
Q

outline the lifecycle of strongylus edentates

A
  • L3 passes through the intestinal wall ad travels through the blood to the liver moulting into L4
  • L4s migrate to the peritoneum adjacent to the liver and moult to L5
  • L5 returns to caecum and colon
37
Q

describe the disease caused by strongylus edentates

A
  • colic due to liver disease or peritonitis
  • cup shaped mouth/oral capsule without teeth so doesnt suck blood, just grazes on mucus debris
38
Q

how are equine strongyles diagnosed

A
  • difficult to diagnose because pre-patent disease
  • period prior ro the patent stage is 6-11 months
  • may be able to feel thrombus during rectal exam
  • fecal analysis still useful but cannot differentiate strongyle eggs
  • can do fecal culture which may reveal infectious L3 larvae
  • recurrent colic as hx may help diagnose
39
Q

how are equine strongyles treated/controlled

A
  • benzimidazoles and avermectins treat larvae and adults
  • pyrantel treats adults
  • avoid overgrazing (eggs often on ground)
  • rotation of fields after treatment to reduce risk of reinfection
  • collect feces regularly
40
Q

what is the most important equine disease in terms of prevalance

A

cyathostomosis (small red worms) 40-70% mortality rate ion affected animals even with aggressive treatment

41
Q

outline the life cycle of cyathosomins in the intestine of horses

A
  • L1 to L3 same as other strongyles
  • ingestion of L3 on grass
  • L3 exsheaths in the stomach and passes through the small intestine to invade the mucosa (still in L3) and submucosa of the colon and caecum
  • moult to L4 and return to intestinal lumen and moutl to L5 then adults

alternatively, L3 stage can become dormant (hypobiosis) for several months to years (cant be affected by anthelmintics or immunity)
- L3 can then emerge in large quantities at certain times
- stimuli for emergence usually seasonal
- synchronous death and low number of adult worms in intestinal lumen as result

42
Q

what are the clinical signs of cyathosomins

A
  • late winter or spring syndrome = due to mucous leasions caused by the emergence of L3 encysted: colic, diarrhea, weight loss and death
  • autumn syndrome = when larvae enter the intestinal wall: colic and diarrhea due to inflammation
43
Q

how is cyathosotomiasis treated/controlled

A
  • intestive care for animals with acute larval cyanthostomiasis including steroid and anthelmintics effective against L3 and L4
  • single dose moxidectin and then 5 day course of fenbendazole (larvicides)
  • not all horses are sensitive to worms and should not be treated in the same way (80% of eggs come from 20% of horses on farm)
  • treat during the autumn using a larvicide drug
  • pick up feces
  • keep different ages of horses separated
  • avoid overgrazing (pick up from dirt)
  • rotate pastures

GIL 2 (113 decks)

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