Endoparasitism Flashcards
Equine endoparasites
Cyathostomins
Parascaris
Tapewrom
Large strongyles
Strongyloides
Gasterophilus
Features of Cyathostomins
Small redworms
Ubiquitous
Minimal clinical effects in most horses - but occasionally large burdens can be fatal
Lifecycle of Cyathostomins
Eggs in faeces onto pasture
Mature into larvae under suitable climate
Infective L3s consumed
Larvae mature in fibrinous cysts in the horses large intestine and caecum
Young adults emerge from cysts and produce eggs into lumen of intestines
Larval syathostomosis
Young horse disease
Severe inflammation of the LI and caecum
Clinical signs of cyathostomosis
Ill-thrift, very thin, dullness, inappetance, often develop diarrhoea
Pathogenesis of cyathostominosis
Larvae emerging induces inflammation
Leakage of fluid and protein causes hypoalbuminaemia
Lack of normal intestinal functions: weight loss, diaarhoea, lethargy
If chronic can cause anaemia
Intestinal dysbiosis can lead to shedding salmonella
Low colloidal oncotic pressure -> dependent oedema
Diagnosis of cyathostominosis
Process of elimination of other causes (faecal analysis etc.)
Presence of red worm in diarrhoea
Hypoalbuminaemia
Treatment of cysthostominosis
Replacement of albumin losses with plasma transfusion
Treat intestinal inflammation with steroid medication (dexamethasone)
Eradication of redworm with larvicidal dewormer
- Fenbendazole at day 5 or Moxidectin
Epidemiology of cyathostominosis
Pasture factors: larger burden on apsture by end of summer/autumn
Prevention of cyathostominosis
No good way as interval worming (preventative) accelerates resistance
Test before treat
Define low, medium, or high shedders
Target the few horses that are contaminating the pasture
Resistance detection of cyathostominosis
Faecal egg count reduction test detects resistant
Features of parascaris
Young horse problem
Worldwide resistance to dewormer drugs and elimination of eggs from the pasture is difficult (thick walled eggs)
Most common pahtogenic parasite in foals
Strong protective immunity after first year of life
Lifecycle of parascaris
PPP = 75-90 days
Eggs pass out in faeces onto pasture
Horses consume thick-walled eggs whilst grazing
Eggs hatch and larvae migrate from the intestine- lymphatics - liver (1-2 weeks)
Circulation to pulmonary vsacular bed - L3s penetrate the alveolar capillaries, travel up to the brochi to the trachea
Larvae coughed up and swallowed back into SI for fial L$-L5 adult worm moults
Clinical signs of parascaris
Non-specific signs or vague syndromes
- diarrhoea, constipation, colic, lethargy, rough coat, pot-bellied, weight loss, poor growth
- grey/white nasal discharge
Ascarid impactions
- 4-8mo
- risk factor recent dewormer with drug targeting NM funciton (colic 24-48hrs later)
- paralysis of worms en masse
- moderate to severe colic + reflux + fluid (and worm) distended SI
Diagnosis of parascaris
Faecal egg count to identify its present - not linear with worm burden
Transabdominal U/S to grade burden
Control of parascaris
Elimination of burden in non-wormed herds
Detect high burdens for treatment - strategic treatment
Focus on non-pharmaceutical controls - pasture hygiene , low stocking density
Parascaris spp. resistance
High prevalence of ML resistance, lowest resistance shown in fenbendazole
Features of tapeworm
Require an intermediate host
Species of oribatid mites, ubiquitous in forage
3 species of tapeworm in horses
Anoplocephala perfoliata - most common, found at ileocaecal valve
A. magna - SI
Anoplocephaloides - SI
Clinical disease of tapeworm
Inflammation, necrosis, hyperaemia
Thickening or area around ileocaecal valve
Increased risk of intussusception, ileal impaction, and ileal and caecal rupture
Diagnosis of tapeworm burden
ELISA - shows exposure not infection
Post-treatment (24hr) faecal analysis
Prevention of tapeworm-related disease
Properly timed single tapeworm dewormer once a year
Tapeworm ELISA negative might suggest when no treatment required
3 species of large strongyles
Strongylus vulgaris
Strongylus edentatus
Strongylus equinus
Features of large strongyles
Mandatory parenteral migration in larval stages
Pasture associated - eat L3
S. vulgaris migrates along arteries and congregate at root of mesentery
