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Parasitology > Sheep Nematodes > Flashcards

Sheep Nematodes Flashcards

1
Q

Important disease syndromes caused by sheep GI nematodes

A

PGE: ostertagia teladorsagia (similar to ostertagia ostertagi in cattle) and trichostrongylus (axei, colubiformis etc)

Nematodirus battus: very specific in lambs

Hemonchosis: caused by hemonchus contortus- possibly most important in sheep globally (tropical disease)

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2
Q

Trichonstrongyloidea

A

Most important group of nematode pathogens in grazing ruminants

Direct life cycle, L3 infective stage

Mainly GI nematodes except dictyocaulus

PPP=21 days (approx)

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3
Q

Lifecycle of teladorsagia circumcincta

A

Adults in abomasum–> produce eggs which hatch in feces–> L1, L2–> sheathed L3

Sheathed L3 ingested–> penetrate abomasal glands–> emerge d18 post infection (emergence causes pathology)

L4s can go into hypobiosis.

Lifecycle almost identical to bovine ostertagiosis

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4
Q

Ovine ostertagiosis -clinical signs (Brown stomach worm)

A

Type 1 disease: common- very important in sheep

Type II disease- not as common

Clinical signs: weight loss/failure to gain weight; intermittent diarrhea; appetite loss

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5
Q

Pathology of ovine ostertagiosis

A

identical to bovine ostertagiosis

rupture or intracellular junctions, destruction of parietal cells, decrease HCL secretion, increase abomasal pH, bacterial overgrowth, elevated serum pepsinogen. larvae emerging from glands cause pathology.

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6
Q

Diagnosis of ostertgiosis

A

Clinical signs

Predominantly lamb disease but increasing reports of disease in older animals

time of year (autumn) grazing and anthelmintic history

fecal egg counts

PM

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7
Q

Immunity to teladorsagia

A

slow to develop

worm burdens and fecal egg outputs low in adult ewes except during periparturient period

around 2 weeks before lambing, MASSIVE increase in egg production

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8
Q

Periparturient rise in fecal egg output from ewes

A

occurs from approx. 2 weeks pre- lambing

due to:

  1. increased establishment of overwintered larvae acquired from pasture
  2. inhibitied L4s reactivating and developing to adults
  3. female worms have increased fecundity
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9
Q

Epidemiology of Ovine Ostertagiosis

A

As with type I ostertagiosis in cattle, there’s a build-up of L3s on pasture from July to October. Source of build-up due to:

  • eggs passed by ewes during periparturient rise
  • eggs passed by lambs from 1st generation parasites established from overwintered larvae

EWES are important in the epidemiology of ovine ostertagiosis

Need to tx lambs and ewes

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10
Q

Control of ostertagiosis (ovine)

A

need to tx lambs and ewes with anthelmintics

but anthelmintic resistance is a major problem

control is based on not grazing potentially heavilty infested pasture with susceptible lambs.

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11
Q

Hemonchus spp. in sheep

A

Hemonchus contortus (barber’s pole worm)

very important pathogen in tropics and subtropics- also occurs and causes disease in UK

hemonchus similis: predominantly cattle but can infect sheep in tropical regions.

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12
Q

Hemonchus contortus

A

largest parasite in abomasum (Adult=2-3cm)

sucks blood– cause of pathology

barber’s pole worm

Causes hemorrhagic anemia- 5000 adult worms can cause 250 ml of blood loss daily

very pathogenic nematode (poor immunity)

high degree of anthelmintic resistance

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13
Q

Life cycle of hemonchus contortus

A

typical trichostrongylid

best adapted to tropical climates

development L1-L3 rapid under optimal conditions (5 days)

Adults in absomasum produce eggs–> hatch in feces–> L1->L2->L3 (sheathed in L2 cuticle) ingested–> penetrate abomasal gland–>L4–>immature adult–> emerge 18 days post-infection–> adults in abomasum

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14
Q

Pathogenesis of Ovine Hemonchosis

A

Hyperacute (up to 30,000 adults): sudden death can occur due to severe hemorrhagic gastritis

Acute (2000 to 20,000 adults): clinical signs seen 2 weeks PI; regenerative anemia followed several weeks later by a non-regenerative anemia (if un-treated)

Chronic (several hundred adults): weight loss and inappetnace (anemia absent or slight)

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15
Q

Clinical signs of hemonchosis

A

Hyperacute: sudden death

Acute: anemia, submandibular oedema, ascites, dark feces, dropping wool, inappetance

Chronic: weight loss, weakness, inappetance.

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16
Q

Diagnosis of Hemonchosis

A

Clinical signs: anemia! pale mm; ewes and lambs often both effected; predominantly seen in lowland farms with higher stocking densities

FEC: typical trichostrongyloid egg

1000-2000 epg (i.e. much higher than for teladorsagia)

PM

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17
Q

Pathology of hemonchosis

A

Adult worms present on mucosa- often dark brown fluid in abomasal lumen

Hemorrhagic lesions on abomosal mucosa: large focal lesions

on PM: pale carcasses, organs, pale gelatinous bone marrow.

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18
Q

FAMACHA-system for assessing clinical anemia

A
  1. optimal PCV >30
  2. acceptable PCV of 25
  3. borderline PCV of 20
  4. dangerous PCV of 15
  5. fatal PCV of 10
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19
Q

Epidemiology of Hemonchosis

A

Parasite is best adapted to warm climates- larval development in environment requires high temp and humidity

Inhibited development occurs to a varying degree depending on climate- hypobiotic development allows transmission from season to season.

20
Q

Epidemiology of hemonchosis- tropical areas without severe dry season

A

hypobiosis is unimportant

high parasite burdens year round

high worm fecundity

often year round anthelminitic usage

number of L3s on pasture dependent on rainfall

21
Q

Epidemiology of hemonchosis- tropical areas with severe dry season

A

Dry season: L3s don’t survive on pasture

high levels of inhibited larval development occur during dry season

parasite survives predominantly in host

disease outbreaks at start of wet season

  • reactivation of EL4
  • rapid increase in pasture L3s.
22
Q

Epidemiology of hemonchosis in temperate regions

A

gradual build-up of infectious stages right thorough summer.

larvae generally don’t survive over winter- overwintered larve NOT important

Parasite survives winter inside host- many as inhibited L4

Reactivate in spring- develop to adults- pasture contamination with eggs- development to L3s

Lambs ingest L3s in summer

Inhibition of larvae UK= 50% in july to 100% in october

23
Q

Small intestine sheep nematodes

A

nematodirus, trichostrongylus and cooperia: all trichostrongyloidea superfamily

bunostomum- strongyloidea superfamily

strongyloides- rhabditoidea superfamily

24
Q

Nematodirus spp in sheep

A

Nematodirus battus: causes specific syndrom in lambs; epidemiology different to other causes of PGE

Nematodirus filicolis and nematodirus spathiger both contribute to PGE

25
Q

Life cycle of nematodirus battus

A

Adults in small intestine–> produce eggs which exit in feces. L1, L2 and L3 all develop in within egg. Infective L3s hatch in spring after 8-9 months of inactivity. Hatched L3s ingested.

Normally, eggs hatch before L1. Eggs are diagnostic/characteristic

pasture stages L1-L3 occur IN eggs.

Hatch in synchrony on pasture.

Atypical trichostrongylid life cycle.

PPP=14 days, cf. 21 days in most trichostrongylids.

26
Q

Effects of Nematodirus battus life cycle

A

Larva develops to L3 inside the egg. Very resistant and overwinters in large numbers.

Very specific hatching requirements–> prolonged period of chill followed by a mean day/night temp of 10 degrees c (may/june)

Due to special hatching requirements–> eggs passed during the grazing season don’t hatch that year but hatch simultaneously the next spring.

27
Q

Host resistance to nematodirus battus

A

lambs more than 3 months of age are non-permissive hosts– physiological resistance. L3s can’t penetrate intestinal wall. NOT immune, literally physically non-permissive.

ewes are resistant to infection (no periparturient rise)

lambs don’t graze significantly during first few weeks of life

therefore lambs only susceptible between 3 weeks and 3 months of age.

28
Q

Epidemiology of nematodirus battus

A

warmth–> eggs die off if not taken up v. quickly by a host.

ewes play little role in epidemiology– lamb to lamb disease

large numbers of L3s hatch in spring from eggs passed onto pasture from last years lambs. L3s die off reasonably quickly in warmer spring/summer conditions.

for disease to occur, emergence must coincide with presence of susceptible lambs

risk of outbreaks vary from year to year on particular farms depending on climate and lambing period therefore there’s a degree of predictability.

29
Q

Relationship between climate and husbandry for nematodirus battus risk

A

High disease risk: lambing in early spring

low disease risk: mild spring where L3s hatch early and/or late lambing

low disease risk: late spring where L3s hatch late and/or early lambing.

30
Q

Nematodirus and cattle

A

cattle are permissive hosts; disease occasionally occurs in calves

relatively common for calves to carry N. battus

consideration in rotational grazing systems.

31
Q

Pathogenesis of nematodirus battus

A

pathology largely due to larval stages causing severe disruption of SI mucosa– larval stages migrating into tissues and eruption of L4s

Most damage occurs 10-12 days post infection (L4-adult moult)

PPP is about 14 days

enteritis and villus atrophy

large numbers of synchronus L3s penetrating and synchrony of L4 eruption.

32
Q

Clinical signs of nematodirus battus

A

rapid onset (10-12 days PI)

profuse diarrhea

dehydration and increased thirst

lambs affected, ewes perfectly normal

33
Q

Diagnosis and control of nematodirus battus

A

Fecal egg counts not reliable since CS often due to larvae

grazing history

clinical signs

PM

Control: best method is to avoid grazing ewes and lambs on pasture used for lambs the previous year or ideally, the previous two years.

34
Q

Other nematodirus species

A

eggs develop to L3 in egg but NO special hatching requirements

seen as mixed infections with other GI nematodes

contribute to PGE (late summer)

35
Q

Trichostrongylus species in sheep SI

A

trichostrongylus vitrinus (black scour worms) and trichostrongylus capricola- sheep and goats

trichostrongylus colubriformis- all ruminants

36
Q

Trichonstrongylus species in sheep: where and when?

A

Temperate regions (UK), commonly a primary pathogen

Commonly contributes to PGE as part of a mixed infection

Trichostrongylosis: acute PGE in lambs in autumn/early winter. Very dark feces/foul smell/ mucous feces

Chronic wasting disease in hoggs and ewes in early winter

poor skeletal growth and poor wool quality

37
Q

Trichostrongylosis pathology

A

Larvae and adults burrow beneath surface epithelium

Cause enteritis, mucus and mucosal hypertrophy

lamina propria is infiltrated with inflammatory cells

villi shortened/vilus atrophy

lesions become more localized as resistance develops–> “finger-print” lesions.

Sub-epithelial tunnels where larvae have been migrating; can also get ulceration.

38
Q

Cooperia curticei

A

Similar to cooperia oncophora (bovine)

Site: SI of sheep

Not very pathogenic but is a dose limiting species (i.e. need higher dose of anthelmintic to remove this parasite).

typical life cycle of trichostrongyloidea

adults 1cm with large bursa

“watch spring” like appearance.

39
Q

Bunostomum trigonocephalum

A

superfamily strongyloidea

sheep and goat hookworm (sucks blood)

small intestine

adult is 1-3cm with hooked anterior end

life cycle is typical hookworm: infective L3: percutaneous route with pulmonary migration

oral route- no pulmonary migration

PPP=1-2 months

40
Q

Nematodes of sheep LI

A

Chabertia ovina, oesophagostomum spp– strongyloidea superfamily

trichuris ovis–trichuroidea superfamily

41
Q

Chabertina ovina (large mouthed bowel worm)

A

Large intestine

1.5-2cm with large buccal capsule

Very common in temperate regions but disease is important in winter rainfall areas (australia and south africa)

Low levels of infection

contributes to PGE

42
Q

Life cycle of chabertina ovina

A

typical strongyloid

Adults in colon–> eggs in feces–> L1-L3 free living–> L3 ingested and enters SI or LI mucosa–> After 1 week, moult to L4.

L4 emerge and migrate to caecum

L4s can arrest or become immature adults in caecum. migrate to colon and become adults.

43
Q

Chabertia ovina pathology and pathogenesis

A

Immature and mature adults are plug feeders.

contributes to PGE

200-300 worms cause disease–> mucosal damage, hemorrhage, protein losing enteropathy, diarrehea +/- anaemia.

44
Q

Oesophagostomum species in sheep

A

Large bowel worms

Oesophagostomum columbianum- form nodules

Oesophagostomum veulosum- no nodules formed

Adults= 1-2cm

Clinical problems (diarrhea and weight loss) unusual in UK

45
Q

GI Nematodes of Goats

A

generally same species that infect sheep: teladorsagia, trichostrongylus and hemonchus

goats more susceptible to gi nematodes than sheep (browsing animals)

newly kidded goats, kids and debilitated animals most susceptible

acquired immunity less effective than in sheep.

Control more difficult– goats are often zero grazed

Anthelmintic often for all age groups and for most of the year

Goats require 2x dose of anthelmintics than sheep

resistance develops more quickly than in sheep

Parasitology (12 decks)

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