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Paras - Sheep Nematodes > Trichostrongyloidea - sheep > Flashcards

Trichostrongyloidea - sheep Flashcards

1
Q

What are some general features / characteristics of Trichostrongyloidea in sheep?

What are the major spp, and where are their sites of infection?

A
  • It’s the most important group of nematode pathogens in grazing ruminants
  • Direct LC, L3 is infective
  • Mainly GI nematodes (Dictyocaulus is the exception)
  • PPP ~21 days
  • Teladersagia (Ostertagia) - abomasum
  • Haemonchus - abomasum
  • Trichostrongylus - abomasum and SI
  • Nematodirus - SI
  • Cooperia - SI
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2
Q

What is the life cycle of Teledorsagia (Ostertagia) circumcincta?

A
  • Direct, L3 is infective
  • Ingested L3 on pasture
  • Adults in abomasum pass eggs
  • Eggs hatch in feces on pasture
  • Development to L3 on pasture
  • Ingestion of L3 and penetration of abomasal gland
  • Development ot L4 in abomasal gland and either EL4 (hypobiosis) or continued development into adults
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3
Q

Ovine Ostertagiosis is caused by what spp?

How many types of Ostertagiosis are there, and which one is most common?

Describe the difference between the different types.

A
  • Teledorsagia
  • Two types, type I is the most common
  • Type I is due to eggs being released onto pasture from July to October. Ewes are an important source of contamination. Also, 1st generation worms lay eggs in lambs that contribute to contamination.
  • Type II disease is less common and due to overwintered EL4’s. (didn’t discuss much in lecture with regard to sheep).
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4
Q

What are some clinical signs of Ovine Ostertagiosis?

A
  • Weight loss, failure to gain weight
  • Intermittent diarrhea (less dramatic than bovine Ostertagiosis)
  • Appetite loss
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5
Q

What causes pathology in ovine Ostertagiosis?

A
  • Larva emerging from abomasal glands
  • Similar to bovine Ostertagiosis
  • Destruction and loss of numbers of parietal cells
  • Decreased HCl production
  • Increased pH from ~2 to ~7
  • Loss of bacteriostatic environment and bacterial overgrowth
  • Rupture of intercellular junctions
  • Elevated plasma pepsinogen
  • Hypoalbuminemia / hypoproteinemia
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6
Q

How is diagnosis made for ovine Ostertagiosis?

A
  • Clinical signs
  • Predominant dz in lambs (but increasing reports of dz in older animals)
  • Time of year and grazing history
  • FEC
  • PM
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7
Q

Is immunity fast or slow to develop for Teledorsagia circumcincta in sheep?

A
  • slow to develop
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8
Q

What are the important factors in the epidemiology in Ostertagiosis in sheep?

A
  • Ewes are very important
  • 2 weeks before and 6 weeks after lambing ewe’s fecal egg output increases. Due to:
  1. Inhibited EL4’s reactivate
  2. Overwintered larva on pasture a source as well
  3. Female worms have increased fecundity

The buildup of L3’s on pasture are from ewes during the periparturient rise (described above), and from eggs passed from LAMBS by 1st generation parasites established from overwintered larva. Mainly from ewes though.

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9
Q

How is ovine Ostertagiosis different from bovine?

A
  • In ovine, ewe’s are a major source of pasture contamination. In bovine, overwintered larva on pasture is a major source, as well as egg production in calves. Adult cattle usually have a low worm burden
  • Anthelmintic resistance seems to be a more serious problem in sheep than cattle.
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10
Q

What is a diagnostic feature of the adult Haemonchis spp?

A

Barbers Pole worm

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11
Q

What is the Life cycle of Haemonchus contortus?

What is important about this spp with regard to immunity?

A
  • Typical trichostrongylid (Direct, L3 infective, abomasal gland site of infection, EL4 possible, inhibited larval stage on pasture possible, PPP ~21 days)
  • Ewes remain susceptible to dz.
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12
Q

Is pathogenesis from Haemonchus contortus due to the larva or adults?

A
  • Adults - voracious blood feeders
  • Hyperacute Haemonchosis (30,000 worms) = sudden death due to severe hemorrhagic gastritis
  • Acute Haemonchosis (2,000 - 20,000 worms) = regenerative anemia then non-regenerative anemia several weeks later
  • Chronic Haemonchosis - weight loss, weakness, inappetence (anemia is absent or slight)
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13
Q

What are some clinical signs of Hyperacute, Acute, and Chronic Haemonchosis?

Is diarrhea usually present?

A
  1. Hyperacute
    • sudden death
  2. Acute
    • anemia
    • submandibular edema (“bottle jaw”)
    • ascites
    • dark feces
    • dropping wool
  3. Chronic
    • Weight loss
    • Weakness
    • Inappetence
  • Diarrhea is NOT usually present
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14
Q

How is diagnosis made for Haemonchosis?

A
  • Clinical signs - anemia (pale MM), ewes and lambs both affected, predominantly lowland flocks
  • FEC - 1,000 - 20,000 epg (much higher than for Teledorsagia, etc…)
  • PM
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15
Q

How is the life cycle of Haemonchus spp slightly different in tropical areas without a severe dry season compared to tropical areas with a severe dry season?

A
  • No severe dry season - worm burden all year round, hypobiosis unimportant, often year round anthelmintic usage, # of L3’s on pasture dependent on rain
  • Severe dry season - during the dry season: hypobiosis, inhibited larva on pasture, parasites survive predominantly in host, dz outbreaks at the start of the wet season
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16
Q

Nematodirus, Cooperia, and some Trichostrongylus spp infect which site of the sheep?

What is the major Nematodirus spp in sheep? What is atypical about this spp compared to other Trichostrongyles?

A
  • SI
  • Nematodirus battus
  • Atypical LC, atypical epidemiology
17
Q

Describe the life cycle of Nematodirus battus.

What is atypical about this cycle?

A
  • PPP 14 days
  • Adults in SI pass eggs
  • Larva develop INSIDE eggs to the L3 stage on pasture
  • Hatching of L3 in spring after 8-9 months of inactivity
  • L3’s ingested
  • Atypical:
    • larva develop to L3 inside egg
    • overwinters on pasture as L3 inside egg (very resistant)
    • Very specific hatching requirements - prolonged period of chill followed by a mean day/night temperature of 10c
    • Because of the special hatching requirements: eggs passed during the grazing season do not hatch that year, they hatch simultaneously the following spring
18
Q

Due lambs play a role in epidemiology of Nematodirus battus?

Is the epidemiology therefore more like Bovine Ostertagiosis or Sheep Ostertagiosis?

A
  • Ewes do not play a significant role in dz. It is a lamb to lamb dz. “Age Resistance”
  • Therefore it is more like bovine Ostertagiosis, in that spread of dz is from young animal to young animal
19
Q

For Nematodirus battus disease to occur, what must coincide with the hatching of L3’s?

Why is this information valuable?

A
  • Susceptible age of lambs. Only lambs grazing under 3 months of age will be highly susceptible. Since they start grazing around 3 weeks of age, emergence of L3’s must coincide with the presence of lambs from ages 2 weeks to 3 months.
  • This makes outbreaks predictable:
    • Climate
    • Lambing period
    • Farmers can read the disease risk forcast based on climate conditions.
20
Q

Name some scenerios for high disease risk and low disease risk (2) for Nematodirus battus.

A
  1. High dz risk
    • susceptible lambs grazing coincides with hatching of L3’s
  2. Low dz risk
    • mild spring and/or late lambing
    • in a mild spring L3’s hatch early, and they die relatively quickly on pasture
  3. Low dz risk
    • long winter/late spring and/or early lambing
    • in a later coming of spring, L3’s will hatch after susceptible lambs are grazing (i.e. the lambs will be older than 3 months)
21
Q

Why should rotational grazing systems be concerned with Nematodirus battus?

A
  • Cattle are permisive hosts and dz occasionally occurs in calves
  • It is relatively common for calves to carry N. battus
22
Q

Is pathology due to larva or adult Nematodirus battus parasites?

A
  • Larva
  • Mostly due to L4 to adult moulting in the SI
  • Causes disruption of the SI mucosa
  • Enteritis and villus atrophy
  • Remember, PPP for this spp is ~14 days. L4 to adult moulting takes place around days 10-12
23
Q

What are the clinical signs of Nematodirus battus?

How is diagnosis made?

What is the best method of control?

A
  • Lambs affected, ewes perfectly normal
  • Rapid onset (10-12 days post infection)
  • Profuse diarrhea (different than Haemonchus contortus which doesn’t cause diarrhea. Ostertagiosis shows intermittant diarrhea)
  • Dehydration (polydipsia)
  • Grazing history, Clinical signs, PM
  • FEC not used since clinical signs often due to larva
  • best method for control is to avoid grazing the same pasture used the previous year (or ideally the previous two years)
24
Q

What are two other genera of Trichostrongyloidea that contribute to PGE as part of a mixed infection?

A
  • Trichostrongylus (can also be a common primary pathogen in the UK)
  • Cooperia
25
Q

What is unique about Trichostrongylus infection compared to Nematodirus and Teledorsagia (Ostertagia) with regard to time of year?

A
  • Trichostrongylus infection tends to occur later in the grazing season (late Autumn to Winter - October to December)
  • Nematodirus occurs the earliest (Spring - April to June)
  • Teledorsagia (Ostertagia) occurs in the middle (Summer to Autumn - June to November)

Paras - Sheep Nematodes (4 decks)

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