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Parasitic Gastroenteritis (view source)

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== Introduction ==
 
== Introduction ==
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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
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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, less than optimum productivity (sub-clinical disease), seasonal appearance and hypoalbuminaemia.
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*Diarrhoea
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<br>
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*Less than optimum productivity (sub-clinical disease)
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*Seasonal appearance
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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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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, the treatment of clinically affected stock e.g. drugs, labour, veterinary bills and finally, prophylaxis (prevention) e.g. drugs, labour, pasture management.
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*Replacement stock
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<br>
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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
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== Aetiology ==
   
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.
 
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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<br>
 
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.
 
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.
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<br>
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== Epidemiology ==
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=== 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 2 weeks, although it may be >6 months for certain species or if development is "arrested".
 
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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<br>
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Risk of disease depends on the balance between the '''Rate of infection''' of the host and '''Host immunity'''. 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 the 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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Risk of disease depends on the balance between
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<br>
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*'''Rate of infection''' of the host
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*'''Host immunity'''
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=== Rate of Infection ===
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The rate of infection of the host by infective L3 depends upon
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*Host appetite (under normal circumstances this is fairly constant, increasing with host liveweight)
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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 metabolism is faster in warm weather.
 
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.
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<br>
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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.
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<br>
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It is important to remember that a worm burden inside an animal grazing at pasture does not remain static, but is continually changing i.e. as older adult worms are lost, more infective larvae are recruited. A state of equilibrium is reached i.e rate at which L3 establish = rate at which adult worms are lost. In an immune animal, the same equilibrium exists, except that fewer of the L3 ingested become established.
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<br>
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Effects of host immunity on worm burden are reduction in establishment of larvae e.g. fewer L3 establish in an immune adult cow than a parasite-naive calf. There is also expulsion of an existing worm burden ("self cure"), due to immediate-type hypersensitivity reaction to antigen from incoming L3. Arrested development has a minor role only; arrested development is mainly caused by climatic changes e.g. temperature changes (''Ostertagia'')or drought (''Haemonchus'').
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<br>
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Factors adversely affecting host immunity include nutrtion; gross deficiency or mineral/trace element deficiency e.g. cobalt. Also there is a periparturient relaxation in immunity" (PPRI) seen in breeding ewes and sows, which is due to impaired cell-mediated immune response associated with an increase in blood prolactin levels and a shift of [[IgA]] from gut mucosa to mammary gland around parturition. Drug treatment repeated anthelmintic and corticosteroid treatment also affets host immunity, as does concurrent infection; where the pathogenic effects of ''Nematodirus'' infection are exacerbated by concurrent coccidia infection in lambs.
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''Infective larvae (L3) overwinter on pasture''
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<br>
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*If infected stock grazed pasture previous year
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*Longer lifespan in colder weather
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''Larval numbers decline in the spring''
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== Clinical Signs ==
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*Heavy mortality of overwintered L3 (food reserves soon depleted as temperatures rises)
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Diarrhoea, which is often profuse and characteristic depending on the parasite involved, e.g. dark if Trichostrongylus and greenish if Nematodirus. There may also be weight loss, or reduced weight gain plus, oedema in severe chronic cases. In acute cases, the only clinical sign may be sudden death.
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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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<br>
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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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''Development from egg to L3''
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== Diagnosis ==
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*Strongyle eggs passed in host faeces for most of the grazing season
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Clinical signs, seasonal incidence and history are indicative of the condition.
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*Development of egg to L3 depends on dung-pat microclimate and requires
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<br>
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**'''High relative humidity''' (nearly 100%). The dungpat acts as a "buffer" against drought
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Faecal samples should be taken to examine to eggs in the faeces. Only a number above a threshold for eggs to cause clinical disease is a positive diagnostic indicator.
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**'''Warmth''' (optimum temperature 25°C). The dungpat cannot buffer against changes in macroclimate temperature
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*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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''Translation of infective larvae''
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<br>
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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.
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''Autoinfection peak in infective larvae''
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== Treatment and Control ==
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*Due to larvae reaching L3 stage simultaneously ("concertina" effect) and translation of L3 onto pasture
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In an outbreak of PGE on a farm, anthelmintic treatment should be given to all stock. If diarrhoea is very severe then supportive therapy, such as providing an electrolye solution may be given. Affected animals may need to be brought in and housed for a short period of time.
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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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<br>
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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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Clean Pasture would be ideal but this requires no lambs having grazed that pasture the previous year, and so is impractical in many cases.
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*In temperate climates, some species can overwinter on the grass, while others cannot
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<br>
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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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This means in most cases, control strategies work around the presence of a Contaminated Pasture. You will need to dose lambs two or three times at 3-weekly intervals in May or June. Optimum timing may be predicted by a forecasting system based on soil temperatures during March.
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<br>
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Another way to manage worm control is to provide alternate grazing of sheep and cattle. Good worm control is possible by alternating the grazing of fields on an annual basis with each host due to the relative insusceptibility of cattle to sheep nematodes and vice versa.
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<br>
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'''Arrested larval development''' (synonyms: inhibited development, hypobiosis, diapause)
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Tannin-Rich Forages are a new thinking into worm control. Condensed tannins, found in clover, lucerne, trefoil, etc. protect plants against microbial and parasitic attack and have recently been found to protect dietary protein against rumen breakdown and they posses some anthelmintic activity. To date, trials investigating the anthelmintic activity of tannin-rich forages have shown variable results between studies; faecal worm egg output was reduced in most studies and worm numbers in some. Clearly, further research is required, though such forages do offer potential as a long-term epidemiological tool and may reduce farmers' dependence on anthelmintics.  
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*Long lifespan of several months (c.f. adult worms; a few weeks only)
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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
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*Its a mechanism for ensuring the survival of the parasite when climatic conditions become adverse
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*There is a seasonal pattern of arrested development e.g. ''Ostertagia'' only need to arrest over winter
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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
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=== Host immunity ===
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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.
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'''Worm population dynamics - Continuous infection'''
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<br>It is important to remember that a worm burden inside an animal grazing at pasture does not remain static, but is continually changing i.e. as older adult worms are lost, more infective larvae are recruited. A state of equilibrium is reached i.e rate at which L3 establish = rate at which adult worms are lost. In an immune animal, the same equilibrium exists, except that fewer of the L3 ingested become established.
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'''Effects of Host Immunity on Worm Burden'''
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<br>
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*''Reduction in establishment of larvae''
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**e.g. Fewer L3 establish in an immune adult cow than a parasite-naive calf
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*''Expulsion of an existing worm burden ("self cure")''
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**Due to immediate-type hypersensitivity reaction to antigen from incoming L3? Non-specific factor in grass?
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*''Arrested development''
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**Minor role only; arrested development is mainly caused by climatic changes e.g. temperature changes (''Ostertagia'')or drought (''Haemonchus'')
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*''Stunting worm growth''
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**e.g. worm length
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*''Reduction in biotic potential''
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**Host immunity often reduces egg production by female worms. This results in a stereotyped pattern of worm egg output, regardless of the level of infection
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'''Factors Adversely Affecting Host Immunity'''
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== References ==
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*''Nutrition''
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Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004) Bovine Medicine (Second edition), Blackwell Publishing.
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**Gross deficiency or mineral/trace element deficiency e.g. cobalt
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<br>
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*''Reproductive status''
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Blood, D.C. and Studdert, V. P. (1999) Saunders Comprehensive Veterinary Dictionary (2nd Edition), Elsevier Science.
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**"Periparturient relaxation in immunity" (PPRI) seen in breeding ewes and sows
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<br>
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**This is due to impaired cell-mediated immune response associated with
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Fox, M and Jacobs, D. (2007) Parasitology Study Guide Part 2: Helminths, Royal Veterinary College.
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#An increase in blood prolactin levels
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<br>
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#A shift of [[IgA]] from gut mucosa to mammary gland around parturition
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Radostits, O.M, Arundel, J.H, and Gay, C.C. (2000) Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses, Elsevier Health Sciences.
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*''Drug treatment''
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**e.g. Repeated anthelmintic and corticosteroid treatment
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*''Concurrent infection''
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**Pathogenic effects of ''Nematodirus'' infection are exacerbated by concurrent coccidia infection in lambs
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*''Previous experience of a parasite''
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**A hypersensitivity reaction to ''Haemonchus'' occurs in some ewes
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== Pathogenesis ==
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=== Introduction ===
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The pathogenic effects of a worm burden on the host depend on
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*'''Species''' of worm and '''stage''' of life-cycle present (affects feeding, site and host reaction)
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*'''Numbers''' of worms present (or invading)
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*'''Host immunity''' (affects both worm population and pathogenicity)
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*'''Nutrition''' (may affect both host '''resilience''' (ability of an animal to withstand the effects of infection), and host '''resistance''' (ability of an animal to prevent establishment and/or development of infection)
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=== Mechanisms ===
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The nematodes responsible for PGE impair productivity by adversely affecting
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*''Appetite''
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**Very important; the reduction in appetite is the main cause of impaired liveweight gain
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*''Digestion''
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**'''Digestibility'''; this decreases with abomasal infection so there is a compensatory increase in intestinal digestion
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**'''Gut microflora'''; abosomal infection causes a change in flora and increase in numbers
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**'''Gut hormones'''; abosomal infection causes an increase in gastric pH and therefore an increase in gastrin secretion. This is possibly the main cause of the decreased appetite
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**'''Malabsorption of nutrients'''; intestinal infection causes villous atrophy and therefore affects amino acids, fat and mineral absorption
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*''Protein metabolism''
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Normally there is a dynamic equilibrium between dietary protein in the gut, amino acids absorbed into the circulation, protein synthesis in the liver, protein storage in the muscle and protein catabolism. In PGE, this equilibrium is upset
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**Dietary protein intake decreases
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**Dietary protein breakdown decreases
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**Amino acid absorption decreases
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**There is a change in distribution of protein synthesis (reduced muscle synthesis and increased haemoglobin, albumin and immunoglobulins synthesis)
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**Protein leak due to an increase in mucosal permeability
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*''Mineral metabolism''
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**Decreased calcium and phosphorus absorption due to villous atrophy leads to a decrease in bone mineralisation (osteoporosis)
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*''Energy metabolism''
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**Decrease in appetite leads to mobilisation of adipose tissue
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[[Category:To_Do_-_Clinical]]
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[[Category:To_Do_-_Review]]
 
[[Category:Stomach_and_Abomasum_-_Inflammatory_Pathology]][[Category:Intestine_-_Inflammatory_Pathology]]
 
[[Category:Stomach_and_Abomasum_-_Inflammatory_Pathology]][[Category:Intestine_-_Inflammatory_Pathology]]
 
[[Category:Stomach Diseases - Horse]][[Category:Gastric Diseases - Cattle]][[Category:Gastric Diseases - Sheep]]
 
[[Category:Stomach Diseases - Horse]][[Category:Gastric Diseases - Cattle]][[Category:Gastric Diseases - Sheep]]
 
[[Category:Small Intestinal Diseases - Horse]][[Category:Intestinal Diseases - Cattle]][[Category:Intestinal Diseases - Sheep]]
 
[[Category:Small Intestinal Diseases - Horse]][[Category:Intestinal Diseases - Cattle]][[Category:Intestinal Diseases - Sheep]]
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