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Parasitology > Equine Strongyles > Flashcards

Equine Strongyles Flashcards

1
Q

What are the 2 groups of equine strongyles?

A 
Large strongyles
- Strongylus vulgaris
- Strongylus equinus
- Strongylus edentatus
Small strongyles (Cyathostominae)
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2
Q

How do you morphologically differentiate among the large strongyles?

A
  • S. vulgaris: ear shaped teeth
  • S. equinus: one large tooth, 2 smaller teeth
  • S. edentatus: no teeth
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3
Q

Strongylus vulgaris - general characteristics

A

Host: horses, donkeys, mules, zebras

  • oval buccal capsule
  • ear shaped teeth at base
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4
Q

Strongylus vulgaris - life cycle

A

Females lay eggs, eggs hatch –> L1 emerges –> L2 –> L3 (ensheathed infective stage) –> L3 exsheath in SI, enter submucousa of cecum/colon and walls of submucosal arterioles –> L4: cecal and colic aortic artery, cranial mesenteric artery, small arteries of intestinal wall, enter tissue (nodules) –> adults in nodules –> nodules rupture –> adults enter lumen of cecum/colon

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5
Q

S. vulgaris pathology - migrating larvae

A
  • arteritis
  • thrombi
  • emboli
  • intestinal nodules
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6
Q

S. vulgaris pathology - adults

A
  • intestinal nodules

- promote granulation, scarring

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7
Q

S. vulgaris pathology - larval damage

A
  • intestinal nodules - minor
  • arteritis - major
  • verminous arteritis
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8
Q

S. vulgaris - arterial system

A
  • inflamed/thickened walls
  • thromboemboli
  • posterior aorta: tracks/debris from migrating L4, damages smooth endothelial surfaces, aneurysms of cranial mesenteric artery
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9
Q

Strongylus vulgaris - clinical signs in adult equid

A
  • anemia/bleeding ulcers
  • confluence of attachment sites
  • diarrhea
  • unthriftiness, weight loss
  • heavy infection with large strongyles: debilitation, weight loss, colic
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10
Q

Strongylus vulgaris - clinical signs in foals

A

Infected with 75-100 adult S. vulgaris = 30 ml of blood lost/day

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11
Q

Strongylus equinus - general characteristics

A

Hosts: horses, donkeys, mules, zebras

  • one large tooth (dorsal, long arrow) and 2 smaller teeth (ventral, short arrows)
  • dark red or black
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12
Q

Strongylus equinus - life cycle

A

Females lay eggs, eggs hatch –> L1 emerges -> L2 –> L3 (ensheathed infective stage) –> L3 exsheaths in SI, migrate to cecum/colon, encapsulate in subserosal nodules –> L4 enters peritoneal cavity, migrates to liver and back to SI thru abdominal cavity (pancreas), forms nodules in gut wall and ruptures into cecum/colon –> adults mature in cecum/colon

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13
Q

Strongylus equinus - pathology

A

Not as pathogenic as S. vulgaris

  • mainly due to larvae
  • hemorrhagic nodules in intestines
  • nodules, fibrotic tracts in liver
  • nodules in pancreas
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14
Q

Strongylus edentatus - general characteristics

A

Hosts: horse, donkey, mules, zebra

  • no teeth!
  • smooth buccal cavity
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15
Q

Strongylus edentatus - life cycle

A

Females lay eggs –> hatch with L1 emerging –> L2 –> L3 (ensheathed infective stage) –> L3 exsheaths in SI, migrate to cecum/colon, right ventral colon, thru gut wall, enter vessels, hepatic portal vv to liver, L3 wander in liver –> L4 exit liver thru hepatic ligaments, tissue under parietal peritoneum to right abdominal flank –> adults via mesentery, return to LI, enter cecum/colon by nodule formation, nodule rupture, mature in cecum/colon

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16
Q

Strongylus edentatus - pathology

A

Mainly due to larvae

  • perivascular thickening
  • subperitoneal cysts
  • nodules and fibrous tissues
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17
Q

Large strongyles - general signs

A
  • anemia
  • poor weight
  • fever
  • depression
  • lethargy
  • colic
  • soft feces
  • rough hair coat
  • death is possible
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18
Q

S. vulgaris - specific signs

A
  • high fever
  • inappetence
  • colic
  • gangrenous enteritis
  • intestinal stasis, torsion or intussusception
  • possible rupture, arteritis
  • especially cranial mesenteric artery
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19
Q

Diagnosis of large strongyle infections

A
  • fecal float: strongyle type eggs
  • L3: strongylus spp.
  • S. vulgaris: palpation of cranial mesenteric artery, arteriography, clinical signs
20
Q

Epidemiology of large strongyles

A 
Southern US
- year round
- max transmission in cooler seasons
Britain/Canada
- max transmission mid-summer to mid-fall
21
Q

Is equine strongyle PPP in weeks or months?

A

Months!

- ruminant strongyles is in weeks

22
Q

Cyathostomes - general characteristics

A 
Family: Strongylidae
Subfamily: Cyathostominae
- horses, donkeys, hinnies, mules, zebras
- cylindrical buccal cavity
- 2 leaf crowns
23
Q

Cyathostomes - life cycles

A

Females lay eggs, eggs hatch –> L1 emerges –> L2 –> L3 (ensheathed infective stage) –> L3 exsheaths in SI, migrate to cecum/colon, encyst in crypts of Liberkuhn, ALD, mucosa or submucosa of cecum/colon –> L4 enter lumen of cecum/colon –> adults mature in cecum/colon

24
Q

Hypobiosis in cyathostomes

A 
Presumed signal received by pasture L3s
- season of year (falling temps) 
- some emergence throughout the year
Hypobiotic early L3s
- stimulated to repopulate cecum/colon
- become adults dependent of season
- influenced by immune status/age of host
25
Q

Larval cyathostomosis

A

Synchronous emergence of large numbers of arrested L4s in early spring

  • hypobiotic larvae can be > 50% total larval population
  • south: summer
  • north: winter
  • number of adults in gut might be influenced by treatment
  • naive horses initial infection
  • results in majority of worms developing without hypobiosis
  • reinfection or frequent exposure (most worms arrest)
26
Q

Hypobiosis may be used by the cyathostomes as a mechanism of ________

A

Controlling the numbers of adult worms in the gut
- treating horses with anthelmintic to eliminate adult cyathostomes from the gut will stimulate development of hypobiotic EL3s to repopulate cecum and colon with adult worms

27
Q

What is the predominant contributor to fecal egg count and pasture contamination?

A

Cyathostomes

  • FEC may not accurately reflect worm burden due to ALD
  • FEC may not reflect number of adult nematodes (animals with high number of adults may have low FEC)
28
Q

Small strongyle pathology

A

Larval cyathostomes in colon wall

  • nodule formation
  • hemorrhagic (black to dark red)
29
Q

Small strongyle clinical signs with adults

A
  • generalized disruption of mucosa
  • superficial ulceration
  • general debilitation
  • intermittent soft feces
30
Q

Small strongyle clinical signs with larvae

A
  • disruption in normal gut motility
  • hemorrhagic, catarrhal, or fibrinous enteritis
  • colic: intussusception, cecal tympany
31
Q

Small strongyles are severe in horses _______

A

Under 2 years

  • inflammation
  • penetration/emergence
  • lymphocytes, plasma cells, eosinophils
  • most pathological event is L4s emerging from tissue!!
32
Q

Protein losing enteropathy

A
  • hypoalbuminemia
  • increased intestinal permeability
  • thickened mucosa/poor absorption
33
Q

Small strongyles are _____ than large strongyles

A

Less severe

  • graze more on surface
  • smaller buccal cavity
  • only serious in large numbers
34
Q

Small strongyle pathology due to all life stages

A
  • intense inflammation possible in response to proteins released from cyst
  • adults attach to large bowel mucosa
  • may cause superficial ulceration
  • leakage of extracellular fluids
35
Q

Larval cyathostomiasis

A

Verminous enteritis

  • acute onset
  • severe diarrhea
  • rapid weight loss
  • pyrexia
  • colic
  • ventral edema
  • L4 in diarrheic feces on gloves
36
Q

Small strongyle infection - diagnosis

A

Strongyle type eggs

- cannot identify larvae, eggs to species

37
Q

Treatment and control of large strongyles

A 
Approved: Fenbendazole, Oxfendazole, Oxidbendazole, Pyrantel salts, Ivermectin, Moxidecin
Pasture management
- remove manure
- alternate grazing with ruminants
- avoid overcrowding and wet pastures
38
Q

Larvae on pasture

A

Only 10% large strongyles, 90% cyathostomes

  • need moisture, shade, relatively low temperature
  • conditions favorable to movement lead to exhaustion and death (non feeding L3)
  • do not live longer than 3 months
39
Q

Maximal transmission of strongylid parasites

A
  • cooler seasons (fall, winter, spring)

- high pasture numbers of L3s

40
Q

Current goals of parasite management

A
  • prevent clinical disease

- reduce level of infection below disease-threatening threshold

41
Q

Approaches to parasite management

A

Targeted selective anthelminic treatment schemes

- only treat animals with high FECs

42
Q

Selective anthelmintic therapy

A

Broadly used in ruminants, makes use of FEC

  • has become important in horses, only horses that exceed a certain FEC are treated
  • interval between FECs as long as possible/as short as necessary
  • high and low shedders are identified
43
Q

Value of SAT relies on stability of ______ over time

A

FEC

- consistency can be estimated measuring repeatability of eggs shedding

44
Q

Recommendations

A
  • targeted anthelminic treatment of high shedders
  • results in reduction of pasture contamination
  • reduces worm burden in whole pasture group
  • lowers risk of developing drug resistance
45
Q

Fecal egg count reduction test

A
  • compare efficacy of anthelmintic
  • detect resistance
  • determine correct interval between anthelmintic treatments
  • ensure low contamination on pasture
46
Q

Delaying resistance

A

Use correct dosing

  • use slow rotation of anthelmintics
  • maintain refugia from treatment
  • limit anthelmintic treatments
  • resistance occurs (benzimidazole and pyrantel pamoate)
47
Q

Pasture management

A
  • collection of feces
  • pasture harrowing, alternate grazing
  • prevalence of resistance increasing
  • cyathostomes need to be considered when designing a control program

Parasitology (28 decks)

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