Sheep Nematodes Flashcards
Important disease syndromes caused by sheep GI nematodes
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)
Trichonstrongyloidea
Most important group of nematode pathogens in grazing ruminants
Direct life cycle, L3 infective stage
Mainly GI nematodes except dictyocaulus
PPP=21 days (approx)
Lifecycle of teladorsagia circumcincta
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
Ovine ostertagiosis -clinical signs (Brown stomach worm)
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
Pathology of ovine ostertagiosis
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.
Diagnosis of ostertgiosis
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
Immunity to teladorsagia
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
Periparturient rise in fecal egg output from ewes
occurs from approx. 2 weeks pre- lambing
due to:
- increased establishment of overwintered larvae acquired from pasture
- inhibitied L4s reactivating and developing to adults
- female worms have increased fecundity
Epidemiology of Ovine Ostertagiosis
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
Control of ostertagiosis (ovine)
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.
Hemonchus spp. in sheep
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.
Hemonchus contortus
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
Life cycle of hemonchus contortus
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
Pathogenesis of Ovine Hemonchosis
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)
Clinical signs of hemonchosis
Hyperacute: sudden death
Acute: anemia, submandibular oedema, ascites, dark feces, dropping wool, inappetance
Chronic: weight loss, weakness, inappetance.
Diagnosis of Hemonchosis
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
Pathology of hemonchosis
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.
FAMACHA-system for assessing clinical anemia
- optimal PCV >30
- acceptable PCV of 25
- borderline PCV of 20
- dangerous PCV of 15
- fatal PCV of 10
Epidemiology of Hemonchosis
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.
Epidemiology of hemonchosis- tropical areas without severe dry season
hypobiosis is unimportant
high parasite burdens year round
high worm fecundity
often year round anthelminitic usage
number of L3s on pasture dependent on rainfall
Epidemiology of hemonchosis- tropical areas with severe dry season
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.
Epidemiology of hemonchosis in temperate regions
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
Small intestine sheep nematodes
nematodirus, trichostrongylus and cooperia: all trichostrongyloidea superfamily
bunostomum- strongyloidea superfamily
strongyloides- rhabditoidea superfamily
Nematodirus spp in sheep
Nematodirus battus: causes specific syndrom in lambs; epidemiology different to other causes of PGE
Nematodirus filicolis and nematodirus spathiger both contribute to PGE
Life cycle of nematodirus battus
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.
Effects of Nematodirus battus life cycle
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.
Host resistance to nematodirus battus
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.
Epidemiology of nematodirus battus
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.
Relationship between climate and husbandry for nematodirus battus risk
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.
Nematodirus and cattle
cattle are permissive hosts; disease occasionally occurs in calves
relatively common for calves to carry N. battus
consideration in rotational grazing systems.
Pathogenesis of nematodirus battus
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.
Clinical signs of nematodirus battus
rapid onset (10-12 days PI)
profuse diarrhea
dehydration and increased thirst
lambs affected, ewes perfectly normal
Diagnosis and control of nematodirus battus
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.
Other nematodirus species
eggs develop to L3 in egg but NO special hatching requirements
seen as mixed infections with other GI nematodes
contribute to PGE (late summer)
Trichostrongylus species in sheep SI
trichostrongylus vitrinus (black scour worms) and trichostrongylus capricola- sheep and goats
trichostrongylus colubriformis- all ruminants
Trichonstrongylus species in sheep: where and when?
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
Trichostrongylosis pathology
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.
Cooperia curticei
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.
Bunostomum trigonocephalum
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
Nematodes of sheep LI
Chabertia ovina, oesophagostomum spp– strongyloidea superfamily
trichuris ovis–trichuroidea superfamily
Chabertina ovina (large mouthed bowel worm)
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
Life cycle of chabertina ovina
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.
Chabertia ovina pathology and pathogenesis
Immature and mature adults are plug feeders.
contributes to PGE
200-300 worms cause disease–> mucosal damage, hemorrhage, protein losing enteropathy, diarrehea +/- anaemia.
Oesophagostomum species in sheep
Large bowel worms
Oesophagostomum columbianum- form nodules
Oesophagostomum veulosum- no nodules formed
Adults= 1-2cm
Clinical problems (diarrhea and weight loss) unusual in UK
GI Nematodes of Goats
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
