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Parasitology > Ovine GI nematodes continued > Flashcards

Ovine GI nematodes continued Flashcards

1
Q

Ovine Hemonchus Pathogenesis

A

3 types
Hyperacute hemonchosis (up to 30K adults)
- sudden death due to severe hemorrhagic gastroenteritis
Acute hemonchosis (2K-20k)
- clinical signs two weeks post infection
- regenerative anemia followed several weeks later by non-regenerative anemia if not treated
Chronic hemonchosis (several hundred)
- Weight loss, weakness, inappetance

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2
Q

Clinical signs of hyper acute hemonchosis

A

Sudden death

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3
Q

Clinical signs of acute hemonchosis

A 
anemia (pale mm)
submandibular edema
ascites
dark faces (diarrhoea not usually a feature)
drooping wool
inappetance
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4
Q

Clinical signs of chronic hemonchosis

A

Weight loss
Weakness
Inappetance

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5
Q

How to diagnose hemonchosis

A 
Clinical signs 
- Anemia (pale mm)
- Both ewe and lambs affected
- Lowland flocks (high stocking density)
Fecal Egg Counts
 - Typical trichostrongyle egg
- 1K-20K epg
PM
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6
Q

Discuss pathological lesions in hemonchosis

A

Adult worms on mucosa, focal lesions where feeding (hemorrhagic)
Pale carcass/liver/gelatinous bone marrow

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7
Q

What is FAMACHA and what is it used for?

A

Assess clinical anemia
Used to decided which animals in flock to treat
Place in eye and assess anemia (PCV) based on colour of conjuctival membrane

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8
Q

Discuss the epidemiology of hemonchosis

A

Parasite best in warm climates (temp is key to egg development)
- high temp/humidity
Cant overwinter in UK, so survive by hypobiosis
Epidemiology varies on region
-Tropical w/o severe dry season
-Tropical w/ severe dry season
-Temperate

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9
Q

Discuss the epidemiology of hemonchosis: tropical w/o severe dry season

A

East Africa

  • hypobiosis unimportant
  • high parasite burdens all year round
  • high fecundity
  • often year round deworming
  • # s of L3s on pasture depend on rainfall
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10
Q

Discuss the epidemiology of hemonchosis: tropical w/severe dry season

A

Australia/Brazil

  • Dry season: L3s can’t survive on pasture
  • High levels of hypobiosis during dry season
  • Dz outbreak at start of wet season
  • -> reactivate arrested L4s
  • -> rapid increase in pasture L3s
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11
Q

Discuss the epidemiology of hemonchosis: temperate

A

UK

  • Aided by arrested development in winter (L4)
  • Peak of abundance late in the year
  • Gradual build up of infective stages thru the summer
  • Don’t survive overwinter (no overwintered larvae)
  • Reactivate in spring (don’t know the signal) –> adults –> pasture contamination with eggs –> develop to L3s
  • Lambs ingest L3s in summer
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12
Q

Nematodirus species in sheep

A

N. battus: Small Intestinal
- Specific syndrome in lambs,
N. ficollis + N. spathiger = contribute to PGE in mixed infections

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13
Q

Life cycle of N. battus

A

Atypical - free living stages are different.
L3 still infective form

Eggs laid –> L1 to L3 development in egg –> infective L3 hatches–> ingested

PPP = 2 weeks

Overwinters as L3 in egg on pasture

Hatching requirements: prolonged chill followed by mean day/night temp of 10C
–> Thus eggs passed during grazing season do not hatch that year

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14
Q

What is different or atypical in the life cycle of N. battus

A

Free living stage development all occur within the egg shell (thus egg is 2x larger than other trichostrongylus species)

Egg is not infective, L3 that hatches from it is. Overwinters as L3 in egg on pasture. Hatches in spring

Hatching requirements: prolonged chill followed by mean day/night temp of 10C
–> Thus eggs passed during grazing season do not hatch that year

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15
Q

Hatching requirement for N. battus

A
  • Hatching requirements: prolonged chill followed by mean day/night temp of 10C
  • -> Thus eggs passed during grazing season do not hatch that year
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16
Q

Host age resistance in N. battus

A

Lambs more than 3mo = non-permissive host
Ewes very resistant to infection (no periparturient rise)
Resistance is physiological and not immunological
Lambs dont graze a lot in early life, so only susceptible from 3wk to 3mo = very narrow window of infectivity

17
Q

Epidemiology of N. battus

A

Ewes have little role (age resistant)
“Lamb to Lamb dz”
Large #s hatch in spring from eggs passed on to pasture from previous years lambs
L3s die off quickly in warmer conditions

  • For dz to occur, emergence of L3s must coincide with presence of susceptible lambs (3wk-3mo)
    Thus varies year to year on weather and lambing period = PREDICTABLE
    use weather forecasts

Cattle are permissive host - could be source of infection to lambs (calves on pasture one year followed by lambs the next) - consider rotational grazing

18
Q

High disease risk factors: N. battus

A

Lambing just before it temperature rises and is maintained

19
Q

Low disease risk factors: N battus

A

1) mild spring = L3s hatch early +/- late lambing

2) late spring = L3s hatch late +/- early lambing

20
Q

N. battus Pathogenesis

A

Pathology due to larval stages –> severe disruption of SI mucosa
Most damage 10-12d post infection (during L4 moult to adult) (PPP =14d)
Large #s synchronous L3s
Enteritis + villus atrophy

21
Q

Clinical signs: N battus

A
  • Rapid onset
  • Profuse diarrhea
  • Dehydration, congregate around water
  • Lambs affected, ewes fine
22
Q

Diagnosis: N battus

Control: N battus

A

FEC not reliable since clinical sings due to larvae
Grazing history
Clinical signs
PM

Avoid grazing on pasture used for lambs the previous year

23
Q

Nematodirus eggs vs other Trichostrongylus eggs

A

Nematodirus:
large eggs with large blastomeres and prominent parallel sides

Trichostrongylus:
large eggs with large blastomeres, NO parallel sides

24
Q

Other Nematodirus species

A

Develop to L3 in egg, but no hatching requirements
Mixed infections
Contribute to PGE

25
Q

Small Intestinal Trichostrongylus species

A

T. virtinus - sheep/goats
T. capricola - sheep/goats
T. colubiformis (all ruminants/cattle)

26
Q

Trichostrongylus in sheep

A

Primary pathogen in temperate regions (UK)
part of PGE as mixed infection (often T. circumcinta)

ACUTE PGE in lambs in autumn/early winter
- dark faces/foul smell/mucous
Poor growth and chronic wasting dz - affect economic viability

Occur later in grazing seasons (fall/winter)

27
Q

Pathology of Trichostrongylosis

A

Larvae + adults burry beneath surface epithelium –> enteritis and mucus/mucosal hypertrophy

lamina propria infiltrated with inflammatory cells

Shortened villi

  • Lesions localized as resistance develops
28
Q

Cooperia curticei: Basic info

A
  • SI of sheep
  • Not very pathogenic, dose limiting species
  • Typical lifecycle of Trichostrongylus
  • Adults 1cm with large bursa
  • Watch spring appearance (coiled anterior and straight posterior)
29
Q

Bunostomum trignocephalum: Basics

A
  • Strongyloidea
  • SI
  • Sheep/goat hookworm
  • Adult = 1-3 cm w/ hooked anterior
  • Infective L3
  • Percutaneous route = pulmonary migration
  • Oral route = no pulmonary migration

PPP = 1-2mo

30
Q

Chabertia ovina: basics

A
  • Large mouthed bowel worm
  • LI
  • 1.5-2.5cm w/ large buccal capsule
  • -> no cutting plates, just pull off parts of mucosa
  • Very common, disease important in winter rainfall areas
  • Low levels of infection
  • PGE
31
Q

Chabertia life cycle

A

Eggs in feces –> L1 to L3 in pasture, L3 ingested + enters SI or LI mucosa –> Moult to L4 in one week and emerge and migrate to cecum (can arrest here)–>immature adults cecum –> migrate to colon –> adult in colon –> eggs

  • *Most pathology due to adults
  • *Hypobiosis for transmission over dry season
32
Q

Pathogenesis of C. ovina

A

Contribute to PGE

  • 200-300 worms to cause dz
  • Mucosal damage (pull of chunks - no cutting plates –> haemorrhage)
  • Protein losing enteropathy
  • Diarrhea +/- anemia
33
Q

Esophagastomum species

**More in pigs

A

O. columbianum
- Nodule formation from L3s in intestinal walls (pathogenic)
O. venulosum
- no nodules

**adults = 1-2cm
Clinical problems: diarrhea/weight loss

34
Q

True or false: goats more susceptible to GI nematodes than sheep

A

TRUE, esp new kids and debilitated animals

  • acquired immunity less effective
35
Q

T/F: Goats require 1/2 as much deworming as sheep

A

FALSE: require 2x as much - different pharmacokinetics, resistance develops faster

36
Q

Discuss fecal egg counts

A
  • Indirect measure of adult parasite burden
  • Useful for flock/herd dx
  • Don’t sample from individual and apply to herd
  • NOT a linear relationship of adult worm burden
37
Q

Number of parasites in faces is dependent on:

A
  • # of adults
  • Level of host immunity
  • age of host (mainly young)
  • species of parasite (fecundity varies)
  • *most fecund: hemonchus
  • *least fecund: nematodirus
  • stage of infection
    • some dz caused by pre patent parasites (no eggs in feces yet)
  • *Type II osteragia in cattle
  • *Nematodirus in sheep
  • parturition/lactation
  • constancy of feces
38
Q

How to collect an FEC sample

A

Sample sufficient animals from group

  • At least 10 in large groups
  • All in small groups

Sample from severely affected, moderately, and normal animals

Parasitology (3 decks)

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