Parasitic gastroenteritis Flashcards
Parasitic causes of diarrhoea (& their main risk periods)
- Coccidiosis/Cryptosporidium (protozoal causes of diarrhoea)
– Jan-June - Nematodirus
– April-July - Teladorsagia & Trichostrongylus
– June-November
Can sometimes see them all year round but tend to be seasonal
Coccidiosis
- Eimeria (protozoan parasite)
- Many species but only 2 are pathogenic in sheep (E.ovinoidalis and E.crandallis) NB oocyst counts
- Host specific.
- Timing of infection risk related to seasonality of lambing rather than seasonality of parasite (in housed dairy calves can see infection almost any time of year)
Which lambs are most at risk of coccidiosis?
- Lambs 3-12 weeks old are most at risk from infection.
- Typically lambs born in the first half of the lambing period exposed to a low level of challenge and develop immunity
- However, these early lambs multiply up the oocysts in the shed or field whilst they develop immunity and the later born, youngest lambs then encounter a high challenge of infectious oocysts and suffer with clinical disease (scouring, dehydration) before they develop immunity
- More common in indoor systems, but can affect lambs at grass too
Coccidiosis life cycle
Source of coccidia oocysts:
- ewes pass low numbers
- some overwinter on pasture
Lambs:
- immunity increases with exposure
- naive lambs at risk of severe dz
Multiplier effect:
- lambs shed millions more oocysts than they eat
Coccidiosis risk factors
- Mixing age groups of lambs
- Moving young lambs to shed/pasture where older lambs were kept
- Intensively stocked systems
- Faecal contamination in/around feed/water troughs
Coccidiosis pathogenesis and CS
- Damage to gut lining causes straining, abdominal pain and diarrhoea +/- mucus and blood
- Leads to dehydration and death in severe cases (young lambs exposed to high challenge)
- Affected animals may also show ill thrift and poor growth rates
- Concurrent infection with Nematodirus or Cryptosporidium can exacerbate clinical signs.
Coccidiosis control measures
- Ensure adequate colostrum intake, maintain good hygiene and prevent faecao-oral transmission
- Raising feed and water troughs may help to prevent faecal contamination, and troughs in fields can be moved regularly to prevent build-up of oocysts in one area
- Grazing later born lambs where earlier lambs haven’t already been might also help if possible.
Coccidiosis effect on growth
- stunted growth
Cryptosporidium parvum
- Protozoal parasite that can cause disease in young lambs (usually <10d old) and calves
- It is zoonotic.
- Faeco-oral transmission
- Oocysts persist in environment and resistant to many disinfectants = infection levels build up over time.
Cryptosporidium parvum CS
- diarrhoea
- inappetence
- abdominal pain
- mild pyrexia
- In mild infections may see reduced growth rates and general poor performance
- May get mixed infections with E.coli/Nematodirus = severe clinical signs
Cryptosporidium parvum diagnosis
- faecal sample
- PM
Cryptosporidium parvum control measures
- Ensure adequate colostrum intake, maintaining good hygiene and preventing faecao-oral transmission (e.g. raising feed and water troughs)
- Can be transmitted in water courses so could consider fencing these off.
- Older animals tend to shed the parasite which then causes disease in younger animals, so mixing animals of different ages should be avoided where possible.
- Check that any disinfectants used are effective against Cryptosporidium
Parasitic gastroenteritis (PGE)
- Major production limiting disease of sheep – estimated to cost UK sheep producers £42.2 million/year.
- Anthelmintic resistance a real concern.
- Sustainable and holistic parasite control integral to flock health planning
- Issue for cattle and sheep but focus on sheep as majorly production limiting
Relative importance in sheep, cattle and pet ruminants
Sheep
- Internal parasites are the most important production limiting disease in UK sheep systems
Cattle
- In beef and dairy calves (<18 months old) they are important
- In dairy cows they are rarely important except occasionally lungworm and liver fluke
In ‘pet’ ruminants such as goats & camelids they are the cause of very severe disease because of the inherently highly susceptible nature of these species to both sheep and cattle parasites.
Endoparasites of cattle and sheep
GI nematodes (roundworms), PGE:
- Sheep: Trichostrongylus, Teladorsagia, Nematodirus battus, Haemonchus
- Cattle: Ostertagia ostertagi, Cooperia oncophora, Trichostrongylus axei
Trematodes
- Sheep: Fasciola Hepatica
- Cattle: Fasciola Hepatica, rumen fluke (Calicophoron daubneyi)
Coccidia/Cryptosporidia
Lungworm
- Sheep: D.filaria & M.capillaris
- Cattle: Dictyocaulus vivparous
Tapeworms
Immunity
After the first grazing season both cattle and sheep will develop immunity to most endoparasites
The exceptions to this are;
- Fluke (sheep and cattle)
- Haemonchus (sheep)
- (Lungworm – immunity in cattle is short-lived)
Trickle challenge vs clinical disease
- A trickle or low infectious challenge over time allows immunity to develop without clinical signs of disease
- A high, abrupt infectious challenge encountered over a short period of time exceeds the ‘threshold’ and causes clinical/sub-clinical disease
- Avoiding all challenge means animals are naïve and susceptible to infection; important to remember this when you are devising a parasite control plan for a client
- Worm control programme is about reducing the worm burden (this is not the case with fluke)
- Reducing not eliminating worms – aim to limit production losses. Balance requires adjustment regularly, not one blueprint you can follow every year.
Nematodirus
- pre parasitic phase (L1-L3) occurs within egg shells
- eggs extremely tough and resistant to freezing and drought, viable up to 2y on pasture
- hatching is stimulated by cold period followed by a mean day/night temperature of ~10C, but L3 are susceptible to climate and need to be ingested quickly
- Therefore, this is usually the 1st species to peak on pasture in spring
- Large number of larvae simultaneously burrowing into the gut cause the pathology (larvae not adult)
Very seasonal, transmitted from lamb crop to the next lamb crop the following year.
Eggs passed the previous year require cold over the winter to prime
Eggs hatch when weather conditions consistently >10C
This results in a high seasonal peak of larvae on pasture in spring (timing dependent on geographical location)
Warm spring = earlier peak
Climate modelling (NADIS & SCOPS websites) to predict risk period
Note: A few cases of autumn disease are reported each year indicating that some populations of the parasite have evolved to hatch without needing a winter cold period to prime them but these are still uncommon – but keep in mind just in case
Nematodirus – signs and control
Clinical disease: huge numbers of immature larvae attacking the gut wall causing dehydration and rapid death.
Pre-patent disease: this happens before they reach adulthood so often NO EGGS FOUND on faecal egg count during an outbreak of clinical disease.
Control: Nematodirus is still susceptible to almost all of the anthelmintics (use BZ - benzimidazole)
Rare cases of BZ resistance have now been reported in Nematodirus
BZD highly efficacious against larval stages of N.battus and has high safety index (important as dosing young animals)
Teladorsagia and Trichostrongylus
- Main GI nematodes in lambs (adults develop immunity – note PPRI)
- Contaminated: eggs and larvae; development to L3 (temperature)
- Infective: L3 present & climatic conditions suitable (rainfall allows L3 to get away from the faeces, therefore increasing the likelihood of it being ingested)
- Hypobiosis is the main way H. contortus survives the winter in the UK
PPRI = peri parturient reduction in immunity
Teladorsagia and Trichostrongylus CS
- Disease: Clinical or sub-clinical depending on the dose of infectious larvae ingested:
– Clinical = scouring, weight loss, poor fleece quality, dull depressed, dehydrated, death
– Sub-clinical = slower weight gain (DLWG), reduced feed conversion efficiency and reduced immunity to other infections - Can see clinical and sub-clinical disease any time of year but it peaks in late summer/autumn
- Get reduction in DLWG before get increase in FEC
Teladorsagia and Trichostrongylus epidemiology
- Eggs deposited early spring: 10 – 12 weeks for L3 to develop
- Eggs deposited summer: 1-2 weeks for L3 to develop
- Therefore high infectivity mid-summer
- L3 are most active during warm weather and, if they are not ingested, consume their energy stores and suffer high mortality rates
- In autumn and winter, L3 can survive longer and some will over-winter on pasture
- Some worm species are better at winter survival than others – Haemonchus larvae do not survive well in freezing temperatures but Nematodirus eggs can survive prolonged cold temperatures
- Over-wintering L3 provide a source of infection to grazing sheep in late winter and early spring but do not survive long on pasture after ambient temperatures rise
- Pasture infectivity tends to decline rapidly to low levels in late April or early May
- Teladorsagia and haemonchus can also overwinter by hypobiosis.
