Superfamily Strongyloidea Flashcards

(14 cards)

1
Q

Superfamily Strongyloiodea

A
  • Large and small strongyles (equine host)
  • -Large strongyles:
  • –Strongylus vulgaris
  • –Strongylus edentatus
  • –Strongylus equinus
  • -Small strongyles (~40 species)
  • –Cyathostomes
  • Other parasites
  • -Oesophagostomum spp.
  • -Stephanurus dentatus
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2
Q

Large and small strongyles

A
  • Large buccal cavity
  • Leaf crowns (corona radiata)
  • Dorsal gutter
  • +/- teeth
  • Strong and powerful esophagus
  • Worldwide distribution
  • Direct life-cycle
  • -Fecal-oral route
  • -Migration differs between large and small strongyles
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3
Q

Large strongyles

A
  • Subfamily: Strongylinae (4 genera), 1.5-4.5 cm
  • Migrate through various organs before returning to the large intestine
  • Feed on blood; travel through blood vessels
  • PPP is almost a year
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4
Q

Small strongyles

A
  • Subfamily: Cyathostominae (40 species), 0.6-2 cm
  • Migrate through mucosa in the intestine
  • PPP is 2-3 months
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5
Q

Large and small strongyle larval ecology

A
  • Development on pasture is very important in their epidemiology
  • -Development to L3 (infective larvae) occurs in 1-2 weeks
  • -Infective larvae can overwinter
  • -Infective larvae are very resistant to desiccation
  • Horses tend to have many more small strongyles than large strongyles
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6
Q

Strongylus vulgaris

A
  • 1.5-2.5 cm
  • Two ear-shaped teeth in buccal cavity
  • Migrate to the cranial mesenteric artery
  • PPP is 5.5-7 months
  • Most pathogenic
  • Can cut off blood supply as it travels through the vasculature
  • Adults
  • -Active blood feeders
  • -Ingest mucosal plug
  • -Cause ulceration, fluid-loss, and anemia
  • Larvae
  • -Larval migration inflicts greater damage
  • –Damage to cranial mesenteric artery
  • –Interferes with blood flow to the intestines
  • –Thromboembolism, colic, gangrenous enteritis, torsion, intussusception, and rupture
  • —Can cause ischemia –> infarct –> gangrene
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7
Q

Strongylus edentatus

A
  • 2.5-4.5 cm
  • Devoid of teeth in buccal cavity
  • Migrate through the liver - hepatorenal ligament
  • PPP is ~ 1 year
  • More prevalent
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8
Q

Strongylus equinus

A
  • 2.5-4.5 cm
  • Has one large and two small buccal cavities
  • Migrates through the pancreas and liver
  • PPP is 8-9 months
  • Prevalence and pathogenicity is rare
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9
Q

Cyathostomes

A
  • Pathogenic effects are less dramatic than large strongyles
  • -Adults are relatively harmless
  • -No systemic migration of larvae (stay in intestinal mucosa)
  • Most important nematode of horses
  • L3 can undergo arrested development (for up to two years); encyst in fibrous nodules in cecal mucosa
  • -Larval cyathostomiasis
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10
Q

Larval cyathostomiasis

A
  • Mass emergence of encysted larvae (pathology begins)
  • Profuse watery diarrhea, severe inflammation of cecal mucosa, progressive weight loss, anemia, ventral edema, and dehydration (can become fatal)
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11
Q

Large and small strongyle eggs

A
  • Both large and small produce similar eggs - “strongyle-type eggs”
  • -Oval, thin-shelled, multicellular
  • 75-100% of the eggs passed in a naturally infected horse are from small strongyles
  • Readily detected by fecal floatation
  • Larvae may look like pinworms microscopically (but pinworms are MACROscopic)
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12
Q

Large and small strongyle treatment

A
  • Large strongyles: not common in US
  • Small strongyles:
  • -Adult worms - wide range of anthelmintics are effective
  • -Encysted larvae:
  • –Pyrimidines and ivermectin - not efficacious
  • –Moxidectin - variable
  • –Benzimidazoles - effective at elevated doses
  • —Maybe also with ivermectin added in
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13
Q

Nodular and bowel worms

A
  • Oesophagostomum spp. present in sheep, goats, cattle, and swine
  • Direct life-cycle: similar to Trichostrongyles
  • Pathogenicity:
  • -Worse in younger animals
  • -May be markedly pathogenic in sheep, cattle, and primates
  • -Less so in swine
  • Adults in the large intestine:
  • -Catarrhal enteritis, thickened bowel wall, cecal and colonic edema
  • Larval nodules are very large in sheep and cattle; worse reaction with increasing exposure, sensitization; nodules become suppurative, caseated
  • -Interference with motility, digestion, absorption; rupture through serosa and cause peritonitis
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14
Q

Stephanurus dentatus

A
  • Kidney worm of swine
  • Geographically restricted to areas that do not have severe winters
  • Southeastern and south central USA - swine raised outdoors
  • Confinement rearing - reduced incidence of kidney worm
  • Will see eggs in the urine (looks like a Strongylid egg)
  • Not zoonotic, but can still ingest them
  • Routes of transmission
  • -Ingestion of infective L3
  • -Ingestion of transport host (earthworm)
  • -Skin penetration by L3 (migrates to the lungs, then to systemic circulation)
  • Migration through the host
  • -Extensive migration in the liver (3-9 months)
  • -Penetrate the liver capsule - retroperitoneal migration to reach perirenal tissues
  • -Access to ureters - eggs in urine
  • Pathogenesis
  • -Adversely affects growth
  • -Aberrant migration - condemnation of organs and tissues
  • Treatment
  • -Doramectin and fenbendazole
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