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VMS 2003 > Parasitic Gut Diseases I > Flashcards

Parasitic Gut Diseases I Flashcards

1
Q

What is the typical lifecycle of gut nematodes in ruminants?

A
  1. Adults mate in the GIT
  2. Eggs are then passed out in the faeces
  3. Eggs then hatch out and develop into L3 larvae
  4. Larvae are ingested, and 2 moults occur
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2
Q

What are the important sheep abomasum parasites?

A
  • Haemonchus contortus
  • Teladorsagia circumcinta
  • Trichostrongylus axel
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3
Q

What are the important small intestine sheep parasites?

A
  1. Nematodirus battus
  2. Trichostrongylus spp.
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4
Q

What is the important cattle abomasum parasite?

A

Ostertagia ostertagi

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5
Q

What is the important small intestine cattle parasite

A

cooperia oncophora

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5
Q

What are the key notes for osteratagia ostertagi?

A
  • Has a worldwide distribution
  • larvae develop in the gastric glands of the abomasum and mature on the mucousal surface
  • The prepatent period is 3 weeks
  • requires up to 2 grazing seasons to acquire immunity
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6
Q

What is the pathogenesis for type 1 bovine ostertagiosis?

A
  • Occurs in calves in the first grazing season
  • they ingest larvae and then it develops 3-4 weeks later
  • Occurs from mid July
  • there is profuse watery diarrhoea (green), weight loss, mortality is rare if it is treated early
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7
Q

What is the pathogenesis for Type II bovine ostertagiosis?

A
  • Occurs in yearlings in the late winter/ spring following the first grazing season
  • the larvae are ingested in the autumn and then arrest *hyperbiosis *
  • larvae emerge together in late winter months
  • has a high mortality rate
  • diarrhoea, anorexia and thirst
  • poor treatment response
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8
Q

What is hyperbiosis?

A

development arrests around the L3/L4 stage
metabolic rate decreases

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9
Q

What are the initiating factors of hypobiosis?

A
  • Host immune responses
  • seasonal influences
  • overcrowding
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10
Q

What is the biological importance of hypobiosis?

A
  • allows them to survive in hostile environmental conditions
  • larvae may be less susceptible to some antithelmintics
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11
Q

What does ostergiosis do to the body?

A

There is a loss of the parietal cells in the abomasum
This increases the pH of the abomasal contents
This causes a failure to convert pepsinogen to pepsin
therefore protein digestion is impaired and there is a bacterial accumulation in the GIT
you also dont have the acid ph preventing bacterial growth

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12
Q

What is the epidemiology of ostertagiosis?

A

1) Overwintered L3 infect calves after turn-out → sub-clinical infection, eggs deposited
2) Overwintered L3 die during spring
3) Eggs develop to L3, become infective by mid-June, can → type I disease in July-Oct
4) As temps↓ larvae arrest at EL4. By late autumn calves can harbour 1000s of EL4
5) Maturation of EL4 larvae in winter & early spring → type II disease

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13
Q

What is the epidemiology of ostertagiosis in spring-calving herds?

A
  • Immune adults graze alongside calves & ingest larvae
  • Little ostertagiosis, egg production by adults is low
  • Overwintered L3 die before suckling calves ingest much grass
  • Low numbers of L3 available on pasture later in the year
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14
Q

What is the epidemiology of autumn/ winter calving?

A
  • Ostertagiosis in following grazing season if grazed on contaminated pasture &
    insufficient immunity as young calves
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15
Q

What does cooperia oncophora cause?

A
  • inappetence/ poor weight gain in calves
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16
Q

Where do cooperia oncophora develop?

A

The adults develop on the surface of the intestinal mucosa

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17
Q

What are the four main gut nematode diseases in sheep?

A
  1. Nematodirosis
  2. Ostertagiosis
  3. Haemonchosis
  4. Trichostrongylosis
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18
Q

What are the key features of nematodirosis?

A
  • Important in lambs
  • Development to L3 takes place in eggshell
  • Hatching requires prolonged chill, then mean temp >10oC (late spring)
  • L3 larvae penetrate mucosa of small intestine, 2 moults then enter lumen
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19
Q

What is the pathogenesis of nematodiresis?

A
  • Due to larvae
  • It causes severe damage to the villi and erosion of the mucosa -> villous atrophy and fusion
  • there is an impaired ability of the intestine to exchange fluids and nutrients
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20
Q

What are the clinical features and diagnosis of nematodiresis?

A
  • Yellowy-Green Diarrhoea
  • dehydration and inappetence, reduced growth rate
  • mortality is high if left untreated
21
Q

What is the unique epidemiology of nematodiresis transmission?

A
  • Eggs survive on pasture for long periods
  • Lots of L3 appear on pasture at same time
  • Disease outbreak if hatching coincides with grazing of lambs (often May &
    June)
  • Cool, wet summers prolong L3 survival – may get outbreaks in older lambs later
  • Lamb-to-lamb transmission, one generation of parasites each year
  • Adult sheep play little role in transmission
22
Q

What causes ostergiosis in sheep?

A

Teladorsagia circumcincta

23
Q

What are the clinical signs of ostertagiosis in sheep?

A

weight loss & intermittent diarrhoea, poor protein & fat deposition,
particularly in lambs

24
Q

What is the epidemiology of ovine ostertagiosis?

A
  • Highest larval numbers on pasture July-Oct
  • Derived from:
    1. Eggs passed by ewes during periparturient period (2 wks prior to – 6 wks
    after lambing)
    2. Eggs passed by lambs after ingesting overwintered larvae
    3. Eggs passed by lambs infected in July
  • If ingested prior to Oct, larvae develop to adults → type I disease
  • Later ingestion, larvae arrested, may get type II disease
25
Q

What causes Haemonchosis?

A

Haemonchus contortus

26
Q

What is the appearance of Haemonchus?

A

In females it has a “barbers pole” appearance

27
Q

What do the Haemonchus contortus larvae do?

A

Larvae exsheath in rumen & moult 2x in gastric glands

28
Q

What does acute haemochiosis look like?

over 2000 worms

A
  • Anaemia, ↓↓ packed red cell volume, loss of iron & protein to GI tract
  • Oedema e.g. submandibular & ascites
  • Inappetence, lethargy, dark coloured faeces, falling wool
  • Mortality
29
Q

What does chronic haemonchosis look like?

100s of worms

A

Continual loss of blood -> weight loss, weakness and inappetence
particularly in areas where the pasture is deficient in nutrients

30
Q

What is the epidemiology of haemonchosis?

A
  • Larval development depends on high temp and humidity
  • High egg output so rapid pasture contamination
31
Q

What is the epidemiology of haemonchosis in temperate areas

A
  • Ewes deposit eggs in spring, L3s ingested by ewes & lambs in early summer,
    most arrest development → disease following spring
  • Some do not arrest → disease in lambs in late summer
32
Q

What parasites cause Trichostrongylosis in sheep?

A
  • Trichostrongylus axei (abomasum) & Trichostrongylus spp. (small intestine)
33
Q

What are the clinical signs of Trichostrongylosis?

A
  • Rapid weight loss & diarrhoea (dark, foul-smelling)
  • Inappetence & poor growth rates (lower levels of infection)
34
Q

What is the epidemiology of Trichostrongylosis?

A
  • Eggs/L3 larvae survive in environment under adverse conditions
  • Larvae on pasture ↑ in late summer/autumn → clinical problems in lambs in
    Nov-Dec
  • Occasionally disease in spring due to survival of eggs & L3, also hypobiosis
35
Q

What do you need to consider when diagnosing gut nematodes?

A
  • Host species
  • Host age
  • Season
  • Grazing history
  • History of parasite infection
  • Clinical signs
36
Q

What is the difference between battus and strongyle eggs?

A

N.battus eggs are 160 μm long, Strongyle eggs are ~80 μm long

37
Q

What are some other tests you can do for parasites?

A
  • Plasma pepsinogen levels
  • Anti-Ostertagia ostertagi (T. circumcincta) antibody
    levels can measured in milk
  • Blood haemoglobin, packed cell volume & red blood
    cell count ↓ in haemonchosis
38
Q

What causes rumen fluke?

A

paramphistomes e.g. Calicophoron daubneyi

39
Q

What does rumen fluke cause?

A

Disease - heavy infestations of immature fluke in intestine
* Diarrhoea, anorexia, anaemia, ill-thrift

40
Q

Where are rumen fluke parasites found?

A
  • Young flukes in duodenum, adults in forestomachs
41
Q

What is the lifecycle of rumen fluke?

A
  1. Eggs
  2. Miracidia
  3. galba trunculata (snail)
  4. cercariae
  5. metacercariae
42
Q

What are Moniezia benedeni & M. expansa?

A
  • Cestode parasites – tapeworms
  • they are adults in the small intestine
  • not highly pathogenic but a solid mass of tapeworms could occlude the intestinal lumen in lambs
43
Q

What are tapeworms common in?

A

They are common in calves and lambs, there is seasonal fluctuation due to active periods of forage mites

44
Q

What is the lifecycle of the Moniezia species?

A
  • Definitive host is infected when it eats an infected mite, adult tapeworm in the hosts small intestine may be several metres long
  • eggs then pass through in faeces
  • eggs are ingested by orbitid mites
  • Cysticercoid develops in mite
45
Q

What is the SCOPS principle?

A
  • Make sure that treatment is fully effective
  • Reduce reliance on anthelmintics using management options and monitoring
  • Avoid bringing in resistant worms by following a robust quarantine protocol
  • Minimise selection for worms that are resistant to anthelmintics when treating
    sheep
46
Q

How can farmers impliment the SCOPS principle?

A

Make sure that the treatment is fully effective
* Dose at rate for heaviest sheep (weigh biggest sheep!!)
* Calibrate drench gun
* Make sure correct dosing technique is used
* Chose the right product for the parasites on farm
* Test for resistance (Faecal Egg Count Reduction Test)

47
Q

What are some parasite management options?

A

o Pasture risk assessment
o Wean lambs at 12 weeks and move to less contaminated grazing
o Grazing by mature ewes – reduces contamination on pastures
o Mixed grazing (sheep and cattle) and reduced stocking densities
o Rotational grazing

48
Q

How can nutrition assist in the prevention of parasites?

A
  • Sheep under nutritional stress less able to withstand challenge
    from internal parasites
    Bioactive forages (chicory, birdsfoot trefoil and sainfoin)
49
Q

What do Haemonchosis Contortus Develop?

A

a ‘piercing lancet’ this allows them to take blood from mucousal vessels

VMS 2003 (33 decks)

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