parasitology (strongyles, Ancylostomatoidea)) Flashcards
general characteristics of strongyloide
Mostly parasites of the GI tract
Generally have a large buccal capsule (cavity)
Plug feeders
adults in cecum and colon
Horses
cyathostominae (small stronglyes)
up to 2cm
subfamily of strongylidae
About 50 similar species
Cannot tell eggs or immature stages apart
usually in horses
strongylinae
large stronglyes (up to 5cm)
subfamily of strongylidae
migrate in host
small strongyles inside the host body
- Enter crypts of Lieberkuhn, penetrate mucosa for period of larval development
- Return to lumen to mature
- Minimum prepatent period 2-3 months
- Larvae in wall may become hypobiotic (L3 or L4)
- Dynamic relationship - as adults lost from lumen, new larvae move in - maintain population of adults
- Seasonal effects on arrest also seen
- larvae are pathogenic when they all reactivate after death of adults
small strongyles infection/clinical importance
Not highly pathogenic parasites
Low to moderate numbers in healthy horses - no apparent effect
Clinical importance
* Most pathogenic stage is larvae, as emerge from intestinal wall cause inflammation
type 1: Chronic cyathostominosis
Gradual inflammation and thickening of gut wall
Possible protein losing enteropathy
- Clinical signs:
- Intermittent diarrhea
- Mild to moderate colic
- Poor condition
- Hypoproteinemia
Acute larval cyathostominosis (Type II)
- Rapid onset
- Occurs when large number of arrested larvae synchronously emerge
- Fever
- Diarrhea - Dehydration
- Edema, hypoproteinemia
- Drug treatment of horses with high worm burden
- Seasonal: late winter or early spring
diagnosis of cyathostominosis
Chronic cyathostominosis
* Large number of strongyle eggs in feces is supportive
**Acute **cyathostominosis
* May not be many eggs in manure
Typical for strongylid nematodes, most normal adults can control worm population (subclinical)
Immunity
* <3-4 years most susceptible
large strongyle life cycle
Adults in large intestine: 3-5 cm
Complex larval migration:
* Following infection, molt, L4 migrates through arteries
* Reaches junction of cranial mesenteric artery and aorta
* Return to large intestine about 4 months after infection
* Occasionally larvae migrate to other locations
Prepatent period: 6 months
Strongylus vulgaris pathogenesis
large strongyle
* Causes verminous arteritis/aneurysm
* Larvae damage arterial vessels leading to thrombus formation
* Thrombus can reduce blood flow
* Portion of thrombus may break off (embolus), block blood flow distally, ischemia
* In severe cases necrosis of portions of bowel occurs
* Lesion regresses after worm leave or treatment
Clinical signs:
* Colic: thromboembolic colic
* Abdominal pain
* In severe cases: death
* Diagnosis difficult, not common
Ancylostomatoidea
Hookworms
order strongyloida
Small intestine of many animals and humans
Blood feeders via plug feeding
1-2 cm
Teeth or cutting plates
DOGS
Ancylostoma caninum life cycle
Superfamily Ancylostomatoidea, order strongylida
External: same development from egg to L3
Best in moist, shaded, slightly sandy soil
Dogs infected from environment by:
* Ingestion of L3
* Skin penetration by L3: more important
Following skin penetration, larvae can:
1. migrate to heart/lungs and then either coughed up, swallowed and develop in small intestine (prepatent 3-4 weeks)
2. OR travel to tissues and become dormant (hypobiosis called somatic reservoir larvae) then become active at end of pregnancy, migrate to mammary gland OR reactivate when adults die
Ancylostoma caninum - Pathogenesis
Low worm numbers asymptomatic
Young animals very susceptible; also heavy exposure or immunocompromised
* Hookworms are blood-suckers and switch sucking sites at a few hours’ interval
* Diarrhea, melena
* Anemia, hypoproteinemia
* Skin lesions
Immunity
* Like large animal strongylids
* Develops following exposure
Ancylostoma caninum - Diagnosis
Fecal exam
Only common strongylid eggs: we can call them hookworm eggs
Ancylostoma tubaeforme
Superfamily Ancylostomatoidea, order strongylida
feline hookworms
Lower prevalence than A. caninum
Not as pathogenic as A. caninum
Little if any perinatal transmission
