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Nematodes > Cattle > Flashcards

Cattle Flashcards

1
Q

What are the nematodes of veterinary significance of cattle?

A

Ostertagia ostertagi
Cooperia oncophora
Dictyocaulus viviparus
Thelazia

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2
Q

What is the superfamily of ostertagia ostertagi?

A

Trichostrongyloidea

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3
Q

What is the life cycle of Ostertagia ostertagi?

A

Eggs are passed into the faeces, here they hatch and moult from L1-L3.
L3 migrates onto pasture where they are ingested by the host.
L3 can overwinter.
L3 exsheaths in the rumen and develops to L4 in the gastric gland of the abomasum.
L4 is the adult and lies within the abomasal lumen. The female lays her eggs here.

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4
Q

What is the pre-patent period of Ostertagia ostertagi?

A

21 days

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5
Q

How long may developing larvae undergo hypobiosis?

A

<6 months

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6
Q

What are the size and shape of the eggs of Ostertagia ostertagi?

A

Medium.
Elliptical shape with barrel shaped walls.
Thin shell.
Filled with many blastomeres.

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7
Q

What is the shape and colour of an adult Ostertagia ostertagi?

A

Small and slender.

Red/brown.

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8
Q

How can a male Ostertagia ostertagi be identified?

A

6-8mm.

Small bursa, spicules have small branches at the end.

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9
Q

How can a female Ostertagia ostertagi be identified?

A

8-11mm.
Vulval flap.
Double ovijectors.

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10
Q

What is the pathology associated with Ostertagia ostertagi?

A

The developing stages are within the gastric gland. So a reduction in the gastric gland mass is to be expected.

Parietal cells are replaced with poorly differentiated cells.

pH increases from 2 to 7. So pepsin cannot be activated from pepsinogen. This looses the bacteriostatic effect in the abomasum.

Increased permeability of the epithelium and increased protein in the lumen increases the production of albumin and Ig. This is at the expense of muscle and fat deposition.

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11
Q

What are the clinical signs of Ostertagia ostertagi?

A 
Diarrhoea
Dehydration
Anorexia
Weight loss
Submandibular oedema
High plasma pepsinogen
Death
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12
Q

What is the epidemiology of type I Ostertagia ostertagi?

A

Calves in first grazing season.
Ingestion of large numbers of overwintered L3.
Mid-July onwards.

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13
Q

How can type I Ostertagia ostertagi be prevented?

A

If the pasture is rested for a grazing season, then most of the L3 will die.

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14
Q

What is the epidemiology of type II Ostertagia ostertagi?

A

Late winter/spring following first grazing.

Maturation of larvae emerging from hypobiosis, which were ingested in the previous autumn.

Arrestment of larvae at early L4 stage.

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15
Q

What diseases are caused by type I ostertagia ostertagi?

A

High morbidity, low mortality.
Diarrhoea, which is green and watery. Also contributes to poor weight gain.
High faecal egg counts.

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16
Q

What diseases are caused by type II ostertagia ostertagi?

A 
Low morbidity, high mortality.
Intermittent diarrhoea.
Hypoalbuminaemia anaemia.
Weight loss.
Faecal egg count may be low during PPP.
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17
Q

How can infection by ostertagia ostertagi be diagnosed?

A 
Weight loss, diarrhoea.
Seasonality and grazing history.
Plasma pepsinogen levels.
Faecal egg counts 
ELISA for adults - use serum and milk
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18
Q

How can ostertagia ostertagi be controlled?

A

Antihelmintic 2-3 times in the spring/summer - type I

Dose and move in July - type I/II

Dose at housing over winter to prevent hypobiosis - type II

Alternate grazing/rotational grazing

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19
Q

What is the superfamily of cooperia oncophora?

A

Trichostrongyloidea

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20
Q

What is the lifecycle of cooperia oncophora?

A

Eggs hatch in faeces. L1 -> L3.
L3 migrates from the faeces onto the pasture and ingested by the host.
L3 exsheaths in the rumen and moults to L4 in the mucosal crypts of the small intestine.
L4 moults to adult stage on the surface of the small intestine mucosa lumen.
Females lay eggs which pass out in faeces.

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21
Q

What is the pre-patent period of cooperia oncophora?

A

14-21 days

22
Q

When in it’s lifecycle can cooperia oncophora become arrested in development and for how long?

A

Early L4 stage. For a period of <6 months.

23
Q

What is the size and shape of cooperia oncophora eggs?

A

Medium size.
Thin shell - parallel walls.
Filled with blastomeres

24
Q

What is the shape and colour of cooperia oncophora adults?

A

Small and slender.

Red/brown colour.

25
Q

How can a male cooperia oncophora be identified?

A

5-9mm.
No gubernaculum.
Spicules have wing like expansion in the middle region.

26
Q

How can a female cooperia oncophora be identified?

A

6-8mm.

Long tapering tail.

27
Q

What is the pathogenesis of cooperia oncophora?

A

Mildly pathogenic in calves.
Exacerbated pathology of co-infection with Ostertagia ostertagi.
Heavy infection -> catarrhal enteritis, localised villous atrophy and oedema.

28
Q

What are the clinical signs of a cooperia oncophora infection?

A

Inappetence.
Weight loss.
Diarrhoea in heavy infections.

29
Q

What is the epidemiology of cooperia oncophora?

A

Overwintering by hypobiosis (similar to ostertagia ostertagi)

30
Q

How can cooperia oncophora be diagnosed?

A

Faecal egg counts. The eggs can be cultured to L3 to confirm/differentiate.

31
Q

How can cooperia oncophora be controlled?

A

Antihelmintic 2-3 times in spring/summer.
Dose and move in mid-July
Dose at housing over winter to prevent hypobiosis.
Alternate grazing/rotational grazing.

This is a dose limiting species and anthelmintic resistance is an issue.

32
Q

What is the superfamily of dictyocaulus viviparus?

A

Trichostrongyloidea

33
Q

What is the lifecycle of dictyocaulus viviparus?

A

Adults are in the lungs.
Eggs in the trachea are coughed up and swallowed.
Hatch to L1 in GI tract.
L1-L3 in faecal pat.
L3 can overwinter.
L3 moves through fluid and via pilobolus fungi to grass where it is ingested.
L3 through intestine to lymph nodes to moult to L4.
L4 carried via blood or lymph to lungs.

34
Q

What is the meaning of ovoviviparous?

A

They lay their eggs within larvae.

35
Q

What is the pre-patent period of dictyocaulus viviparus?

A

25 days

36
Q

What is the role of the pilobolus fungi?

A

On pasture, the larvae of dictyocaulus viviparus is dispersed.
L3 migrates to sporangium where they are dispersed a distance of 3m

37
Q

What are the identifying features of L1 of dictyocaulus viviparus in the faeces?

A

300-450um
Intestinal cells contain numerous brown granules
Rounded head.
Tail is a blunt point.

38
Q

How can male and female worms of dictyocaulus viviparus be distinguished?

A

Males: 4-5.5 cm
Females: 6-8 cm

39
Q

What is the pathogenesis of the pre-patent phase of dictyocaulus viviparus?

A

8-25 days.
Larvae in alveolvi leads to alveolitis, bronchiolitis and bronchitis.
This happens as larvae moults and moves up the bronchi.
In heavy infections, death may occur from severe interstitial emphysema and pulmonary oedema.

40
Q

What is the pathogenesis of the patent phase of dictyocaulus viviparus?

A

26-60 days.
Bronchitis with 100-1000s of adults in frothy mucus in lumina in bronchi.
Parasitic pneumonia caused by egg and L1 aspiration. Dark red collapsed areas of lung around collapsed bronchi.

41
Q

What is the pathogenesis of the post-patent phase of dictyocaulus viviparus?

A

61-90 days.
If the calves recover, the damage caused make take weeks-months to heal.
25% develop a fatal flare characterised by lung fibrosis and epithelialization, which was caused by dissolution of dead worms or a superimposed bacterial infection.

42
Q

What is the pathogenesis of the re-infection husk of dictyocaulus viviparus?

A

Immune animals exposed to large L3 challenges can develop lymphoid nodules in the bronchioles.
This causes coughing.

43
Q

What are the clinical signs of dictyocaulus viviparus?

A

Mildly affected -> cough intermittently.

Moderately affected -> coughing frequently at rest, tachypnoea and hyperpnoea.

Severly affected -> severe tachypnoea, dyspnea, deep cough.

44
Q

What are the clinical signs of dictyocaulus viviparus in young cattle?

A

Sometimes death within the PPP.
Severe dyspnoea.
Death within 24-48 hours.

45
Q

What is the epidemiology of dictyocaulus viviparus?

A

Most commonly affects calves in their first grazing season.
Older animals are infected if they have not been exposed previously.
Overwintered larvae and carrier animals may persist in the airwats.
Disease usually occurs late summer/autumn. Can be earlier if there is high contamination.

46
Q

What diseases are caused by dictyocaulus viviparus?

A

Severe bronchitis and pneumonia.
Coughing.
Respiratory distress.
Death.

47
Q

How can dictyocaulus viviparus be diagnosed?

A

Time of year, history of grazing, clinical signs.

L1 only in faeces in PPP.
More likely to identify when a large amount of faeces is used from animals which first showed signs or are recovering.

ELISA. Seroconversion at 4-6 weeks and lasts for 4-7 months.
This is useful for cases of re-infection husk.

48
Q

How can dictyocaulus viviparus be controlled?

A

Treat with anthelmintic in early stages.
Severe cases may require antibiotics.
Lungworm vaccine from live attenuated larvae can prevent the disease. This does not prevent pasture contamination, so there will be a low level of infection.
Can prophylactically give anthelmintics, but this does not allow for the development of immunity.

49
Q

What is the superfamily of thelazia?

A

Spiruroidea

50
Q

What is the lifecycle of thelazia?

A

Adults reside in the conjunctival sac of the direct host and shed L1 larvae.
L1 is ingested by muscid flies (intermediate host), when they feed on tears.
L1-L3 in the muscid fly.
L3 migrates to the fly’s mouthparts, where they remain until the fly feeds on the tears of the direct host.
L3 - adults after around 1 month.

51
Q

What diseases are caused by thelazia?

A

Conjunctivitis.

Cloudy ulcerated cornea in heavy infections.

Nematodes (6 decks)

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