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== Introduction ==
 
== Introduction ==
Parasitic gastroenteritis (PGE) is a disease complex associated with a number of nematode species (mostly strongyles), either singly or in combination. It is characterised by:
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Parasitic gastroenteritis (PGE) is a disease complex associated with a number of nematode species (mostly strongyles), either singly or in combination. It is characterised by
*diarrhoea
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*Diarrhoea
*less than optimum productivity (sub-clinical disease)
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*Less than optimum productivity (sub-clinical disease)
*seasonal appearance
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*Seasonal appearance
*hypoalbuminaemia.
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*Hypoalbuminaemia
 
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PGE is of considerable economic importance in grazing livestock. It is a potential welfare problem, particularly on organic farms. Losses are associated with the cost of:
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*replacement stock
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*disruption of breeding programme
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*impaired productivity, e.g. weight-gain, wool clip, milk yield, etc.
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*treating clinically affected stock, e.g. drugs, labour, veterinary bills
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*prophylaxis (prevention), e.g. drugs, labour, pasture management.
      +
PGE is of considerable economic importance in grazing livestock. It is a potential welfare problem, particularly on organic farms. Losses are associated with the cost of
 +
*Replacement stock
 +
*Disruption of breeding programme
 +
*Impaired productivity e.g. weight gain, wool clip, milk yield etc.
 +
*Treating clinically affected stock e.g. drugs, labour, veterinary bills
 +
*Prophylaxis (prevention) e.g. drugs, labour, pasture management
    
== Aetiology ==
 
== Aetiology ==
Strongyle nematodes are the main cause of PGE in grazing animals and, in particular, those found in two superfamilies, i.e. '''Trichostrongyloidea''' and '''Strongyloidea'''. Non-bursate nematodes are rarely responsible for PGE, although ''Strongyloides'' species (a member of the family Rhabditoidea and NOT a strongyle) may sometimes contribute to the disease.
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Strongyle nematodes are the main cause of PGE in grazing animals and, in particular, those found in two superfamilies; '''Trichostrongyloidea''' and '''Strongyloidea'''. Non-bursate nematodes are rarely responsible for PGE, although ''Strongyloides'' species (a member of the family Rhabditoidea and NOT a strongyle) may sometimes contribute to the disease.
 
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Normally, only a few of the many roundworm species that are found in the alimentary tract of grazing stock are important as causes of PGE, e.g. in first season calves in northern Europe, ''Ostertagia'' species (an abomasal nematode) is the primary pathogen with ''Cooperia'' and ''Nematodirus'' species (intestinal nematodes) acting as contributory factors; other worms are rarely of clinical significance.
      +
Normally, only a few of the many roundworm species that are found in the alimentary tract of grazing stock are important as causes of PGE. In first season calves in northern Europe, ''Ostertagia'' species (an abomasal nematode) is the primary pathogen with ''Cooperia'' and ''Nematodirus'' species (intestinal nematodes) acting as contributory factors; other worms are rarely of clinical significance.
    
== Epidemiology ==
 
== Epidemiology ==
 
=== Introduction ===
 
=== Introduction ===
The epidemiology and pathogenesis of many strongyle infections of grazing animals are very similar. Infection by ingestion of an infective larva (L3), development to L4 and adult stages is generally restricted to gastric or intestinal mucosa (although a few species migrate around the body), adult worms eventually emerge to lie on the mucosal surface. The prepatent period is normally 2weeks, though may be 6+months for certain species or if development is "arrested".
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The epidemiology and pathogenesis of many strongyle infections of grazing animals are very similar. Infection by ingestion of an infective larva (L3), development to L4 and adult stages is generally restricted to gastric or intestinal mucosa (although a few species migrate around the body), adult worms eventually emerge to lie on the mucosal surface. The prepatent period is normally 2 weeks, although it may be >6 months for certain species or if development is "arrested".
 
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'''Risk of disease''' depends on the balance between:
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*'''rate of infection''' if the host; and
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*'''host immunity'''.
      +
'''Risk of disease''' depends on the balance between
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*'''Rate of infection''' of the host
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*'''Host immunity'''
    
=== Rate of Infection ===
 
=== Rate of Infection ===
The rate of infection of the host by infective L3 depends upon:
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The rate of infection of the host by infective L3 depends upon
*host appetite (under normal circumstances this is fairly constant, increasing with host liveweight); and
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*Host appetite (under normal circumstances this is fairly constant, increasing with host liveweight)
*numbers of infective larvae (L3) on pasture (there are marked fluctuations in the number of L3 on pasture grazed by livestock during the year which help to explain the seasonal occurence of PGE).
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*Numbers of infective larvae (L3) on pasture (there are marked fluctuations in the number of L3 on pasture grazed by livestock during the year which help to explain the seasonal occurrence of PGE)
 
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Development from L1 → L2 → L3 is temperature dependent. Also, the L3 cannot feed as it is ensheathed (i.e. enclosed in the shed L2 cuticle). Its life-span therefore depends on how quickly its food stores are used up, and this too is temperature dependent as it is more active in warm weather.
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a) ''Infective larvae (L3) overwinter on pasture'':
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*if infected stock grazed pasture previous year
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*longer lifespan in colder weather
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b) ''Larval numbers decline in the spring'':
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*heavy mortality of overwintered L3 (food reserves soon depleted as temperatures rise)
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*diluted by spring grass growth
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''Host infected at turnout, patent infections develop and pasture contaminated'':
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*stock ingest remaining overwintered L3
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*strongyle eggs passed out with faeces onto pasture
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c) ''Development from egg to L3'':
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*strongyle eggs passed in host faeces for most of the grazing season
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*development of egg to L3 depends on dung-pat microclimate and requires:
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**'''high relative humidity''' (nearly 100%) - dungpat acts as a "buffer" against drought; and
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**'''warmth''' (optimum temperature 25°C) - dungpat cannot buffer against changes in macroclimate temperature.
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*development is therefore influenced largely by '''macroclimate''' and '''temperature'''. Net result = concertina effect.
      +
Development from L1 → L2 → L3 is temperature dependent. Also, the L3 cannot feed as it is ensheathed (i.e. enclosed in the shed L2 cuticle). Its life-span therefore depends on how quickly its food stores are used up, and this too is temperature dependent as metabolism is faster in warm weather.
   −
d) ''Translation of infective larvae'':
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''Infective larvae (L3) overwinter on pasture''
*movement of larvae from dungpat onto grass in order to infect final host
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*If infected stock grazed pasture previous year
*L3 must cross a zone of repugnance around the dungpat (up to 45cm) - normally left ungrazed
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*Longer lifespan in colder weather
*L3 cross zone by swimming in a film of moisture. Also, beetle and earthworm activity, rain splash, soil migration, etc.
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''Larval numbers decline in the spring''
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*Heavy mortality of overwintered L3 (food reserves soon depleted as temperatures rises)
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*Diluted by spring grass growth
   −
e) ''Autoinfection peak in infective larvae'':
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''Host infected at turnout, patent infections develop and pasture contaminated''
*due to larvae reaching L3 stage simultaneously ("concertina" effect) and translation of L3 onto pasture
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*Stock ingest remaining overwintered L3
*factors affecting either egg - L3 development or translation will influence the timing of the peak, e.g. cold spring, dry summer
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*Strongyle eggs passed out with faeces onto pasture
*decline in L3 after autoinfection peak due to a combination of (a) shorter lifespan in warmer weather; and (b) autumn flush of grass growth
      +
''Development from egg to L3''
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*Strongyle eggs passed in host faeces for most of the grazing season
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*Development of egg to L3 depends on dung-pat microclimate and requires
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**'''High relative humidity''' (nearly 100%). The dungpat acts as a "buffer" against drought
 +
**'''Warmth''' (optimum temperature 25°C). The dungpat cannot buffer against changes in macroclimate temperature
 +
*Development is therefore influenced largely by '''macroclimate''' and '''temperature'''
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**Net result = concertina effect; later developing eggs will require less time to become L3 due to increased temperature. The majority of larvae will therefore reach L3 stage simultaneously
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f) ''Overwintering of larvae'':
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''Translation of infective larvae''
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*Movement of larvae from dungpat onto grass in order to infect final host
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*L3 must cross a zone of repugnance around the dungpat (up to 45cm) which is normally left ungrazed
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*L3 cross zone by swimming in a film of moisture. Also by beetle and earthworm activity, rain splash, soil migration etc.
   −
In temperate climates, some species can overwinter on the grass, while others cannot. In either case, nematodes may survive inside the host for long periods of time, not as normally developing adult worms (that would be expelled within a few weeks), but as larval worms that have become temporarily arrested in their development and may remain inside the host 'asleep' for many months.
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''Autoinfection peak in infective larvae''
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*Due to larvae reaching L3 stage simultaneously ("concertina" effect) and translation of L3 onto pasture
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*Factors affecting either egg → L3 development or translation will influence the timing of the peak e.g. cold spring, dry summer
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*A decline in L3 after the autoinfection peak is due to a combination of
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**Shorter lifespan in warmer weather
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**Autumn flush of grass growth
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''Overwintering of larvae''
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*In temperate climates, some species can overwinter on the grass, while others cannot
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*Nematodes may survive inside the host for long periods of time, not as normally developing adult worms (that would be expelled within a few weeks), but as larval worms that have become temporarily arrested in their development and may remain inside the host 'asleep' for many months
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'''Arrested Larval Development''' (synonyms: inhibited development, hypobiosis, diapause):
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====Arrested larval development====(synonyms: inhibited development, hypobiosis, diapause)
*Long lifespan - several months (c.f. adult worms - a few weeks).
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*Long lifespan of several months (c.f. adult worms; a few weeks only)
*Larvae become arrested at an early stage in their development, e.g. ''Ostertagia'' as EL4 (i.e. early fourth stage), equine cyathostomes as L3.
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*Larvae become arrested at an early stage in their development e.g. ''Ostertagia'' as EL4 (i.e. early fourth stage), equine cyathostomes as L3
* Mechanism for ensuring the survival of the parasite when climatic conditions adverse. Note seasonal pattern of arrested development, e.g. ''Ostertagia'' only need to arrest over winter.
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*Its a mechanism for ensuring the survival of the parasite when climatic conditions become adverse
*Stimulus for arrested development varies, e.g. falling temperatures - ''Ostertagia''; drought - ''Haemonchus''.
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*There is a seasonal pattern of arrested development e.g. ''Ostertagia'' only need to arrest over winter
*Termination of arrested development - spontaneous (i.e. a genetic alarm clock). Previously arrested larvae then resume their development and grow to adult worms.
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*Stimulus for arrested development varies e.g. falling temperatures - ''Ostertagia''; drought - ''Haemonchus''
 
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*Termination of arrested development is spontaneous (i.e. a genetic alarm clock). Previously arrested larvae then resume their development and grow to adult worms
    
=== Host Immunity ===
 
=== Host Immunity ===
 
Acquired host immunity affects both the establishment of recently ingested infective larvae as well as the course of infection of developing worms. When considering the effects that host immunity has on a worm burden, remember that animals grazing at pasture are continuously exposed to infection and not just challenged by a single large infection.
 
Acquired host immunity affects both the establishment of recently ingested infective larvae as well as the course of infection of developing worms. When considering the effects that host immunity has on a worm burden, remember that animals grazing at pasture are continuously exposed to infection and not just challenged by a single large infection.
      
'''Worm Population Dynamics - Continous Infection''':
 
'''Worm Population Dynamics - Continous Infection''':
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