Parasitic gastroenteritis Flashcards
When are you most likely to find parasitic gastroenteritis?
Peak incidence between september and november
What are the main GI nematodes in sheep and cattle?
Sheep
- Trichostrongylus,
- Teladorsagia,
- Nematodirus battus,
- Haemonchus
Cattle
- Ostertagia ostertagi,
- Cooperia oncophora,
- Trichostrongylus axei
What endoparasites are sheep and cattle not able to build immunity to?
- Fluke (sheep and cattle)
- Haemonchus (sheep)
- Lungworm (immunity in cattle is short lived)
What is a trickle challenge?
Low infectious challenge over time allows immunity to develop without clinical signs of disease
Why is nematodirus battus a unique trichostrongyle?
Has an atypical trichostrongyle life cycle
- Preparasitic pahse (L1-L3) occurs within egg shells
- Eggs extremely tough and resistance to freezing and drought, viable up to 2 years on pasture
- Hatching is stimulated by cold period followed by a mean day/night temperature of -1o degrees, but L3 are susceptible to climate and need to be ingested quickly.
- This is usually the first species to peak on pasture in spring
- Large number of larvae simultaneously burrowing into the gut cause the pathology
When are the peaks of nematodirus on pastures? What signs are associated? How can it be controlled?
High seasonal peak of larvae on pasture in spring
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/class 1 wormer/white drench)
Rare cases of BZ resistance have now been reported in Nematodirus
Describe Teladorsagia and Trichostrongylus life cycle. When are they infective? What clinical signs are associated? What time of years are these seen most?
Infective: L3 present & climatic conditions suitable
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 (Daily Live 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
How does seasonality affect the time it takes for L3s to develop?
Eggs deposited early spring: 10 – 12 weeks for L3 to develop
Eggs deposited summer: 1-2 weeks for L3 to develop
High infectivity mid-summer
What is periparturient relaxation in immunity?
All ages of sheep carry roundworms, but with good immunity adult sheep rarely show signs. The exception to this is around lambing time (2-4 weeks pre to 6 – 8wks post).
Ewes under nutritional stress around lambing lose some of the immunity they have acquired to the parasite allowing hypobiosed L4 larvae to develop to adults and also new infections to become patent.
As ewes pass peak lactation and the nutritional stress declines they recover their immunity and kill off the parasites so their FEC falls
This seasonal (peri-parturient) egg count rise is crucial for the parasite as it contaminates the pasture for the lambs to become infected
Ewes under low stress (e.g. adult ewes in good BCS carrying 1 lamb) do not lose much immunity but ewes under high stress (Triplets, Low BCS, young (ewe lambs & shearlings)) are under greatest stress and will generate most of the pasture contamination.
What is the difference between type 1 and type 2 disease?
Type 1 - Wet summers cause eggs to hatch and infect stock early and cause disease in the same season – clinical signs of scour, weight loss, low DLWG, poor feed conversion efficiency…. very common
Type 2 - Dry summers cause eggs to remain unhatched until autumn wet conditions at which point the infectious larvae enter hypobiosis inside the stock rather than completing development to adulthood. All the larvae emerge from hypobiosis at the same time in the spring in the gut of the animal causing severe disease, dehydration and death (Teladorsagia) and anaemia (Haemonchus) – type 2 is quite rare but need to understand the epidemiology
What clinical signs are associated with Haemonchus? How is it controlled?
Different to the other strongyle roundworms of sheep – blood sucker similar to the adult Liver Fluke so causes anaemia, weakness, weight loss and sub-mandibular oedema in chronic cases. Fertility, fecundity, milk yield may all be affected by the infection in the same way as any other debilitating disease.
Immunity not developed (as with other strongyles)
**Control: **Closantel to treat Haemonchus infections as well as other BZ, LV & ML groups
When are cattle most likely to get gut worms? How does the epidemiology vary in the different seasons?
Mid july until housing
Winter (housing):
No new infections acquired
Development of eggs/larvae generally v slow - gradual decline on pasture
Larvae overwinter
Spring:
over-wintered larvae encountered and new infection acquired
Summer: Pasture levels of L3 increase: risk of clinical disease increases without control (same pasture/not treated with anthelmintics
What are we trying to achieve when controlling PGE?
Good productivity / profitability i.e. fast growth, high milk yield, high fertility.
Good immunity where possible rather than relying on treatment
Sustainability = continued efficacy of anthelmintics = delay the development of resistance to the products within the parasite population. Also minimise negative impacts on the environment.
What anthelmintics can we use to control PGE?
Broad spectrum
Cattle and sheep
* BZ (Group 1) (white)
* >85% flocks have resistance – still good for nematodirus on most farms (a few cases of resistance)
* LV (Group 2) (Yellow)
* Increasing resistance rapidly.
* ML (Group 3) (Clear)
* Some resistance found in sheep and a few cattle units.
Sheep only
* AD (group 4) Orange (‘Zolvix’; monepantel)
* Some resistance now reported, useful for extending the life of Group 1,2,3.
* SI (group 5) Purple (‘Startect’) dual active product; spiroindole (derquantel) + abamectin (3-ML).
Narrow spectrum
Closantel (Nitroxynil) - Fluke and Haemonchus
Oxyclozanide (Fluke only)
What non chemical control methods do we have for PGE?
- Genetics (Estimated breeding values – EBVs)
- Useful for breeding flocks
- Grazing management
- Bioactive forage (chicory)
- Combat parasitism or improve nutrition?
