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Sheep parasites - Coggle Diagram

- - - - damged wool and skin and pruritic
      - lives permanently on sheep so shearing helps
      - pour on and dips (rare in UK)
  - - - STRIKE/cutaenous myiasis
      - nibbling at perineum typical sign
        
        extensive skin damage, larvae feed on this and can lead to toxaemia due to skin necrosis and absorption of bacterial toxins
      - Management
        
        Treatment
        
        Clip surrounding hair
        
        Clean tissue, remove visible maggots, apply insecticide
        
        For example Coopers Spot on.
        
        Supportive therapy sometimes indicated in severe cases
        
        Prevention
        
        Tail Docking
        
        Preventative treatment prior to risk periods
        
        Cyromazine
        
        Dicyclanil
        
        Cypermethrin
        
        OP dips
        
        Shearing of sheep
        
        Control of diarrhoea
        
        Worm control
    - - ixodes ricinus
      - disease transmission
        
        lyme disease
        
        tick borne fever
        
        louping ill
        
        tick pyaemia
  - - - macrocyclic lactones (avermectins and milbemycins)
        
        e.g. ivermectin, selamectin
      - Dip all sheep with organophosphate dips
      - injectables ineffective v lice and will increase resistance to products v GIT nemotodes
      - for lice treatment can use pour on insecticides (these are ineffective v mites)
- - - - poor calibration of drenching guns
      - lack of weighing
      - poor dosing/injection technique
      - poor storage and misuse of products
    - - refugia population smallest when on safe/clean grazing, during hot periods, late winter/early spring
- - - - live in abomasum
      - lamb clinical signs
        
        diarrhoea and weight loss
      - egg shedding
        
        around the lambing period (peri-parturient rise)
        
        beginning of grazing season (spring rise)
      - adapted to cold temperatures due to hypobiosis
      - type II ostertagiasis
        
        lambs - late winter/spring
        
        due to emergence of arrested hypo biotic larvae ingested the previous year and inhibited as L4
        
        clinical signs
        
        anorexia
        
        thirst
        
        intermittent diarrhoea
    - - live in small intestine
      - clinical signs
        
        not normally acute disease, generally chronic
        
        weight loss, lower production
        
        possibility of acute diarrhoea in lambs
    - - 'barbers pole'
      - abomasum
      - highly pathogenic --> severe anaemia of lambs --> palour, weakness and death
      - rises in summer (preference for warm climates, does not thrive in cold temperatures)
      - FAMACHA test
    - - clinical signs
        
        pain
        
        stand with head down
        
        ears drooped
        
        sudden and severe diarrhoea
        
        lambs stop eating
      - ewes have no role in transmission
        
        ewes are immune (do not carry worms or contaminate pasture)
        
        lambs can build resistance by 6 months
      - generally lambs only susceptible when 6-12w old
      - majority over winter and hatch in spring after a cold spell when warm
      - damage is from the large no, of larvae burrowing into the gut simultaneously
  - - - female roundworms increase egg production
      - arrested worm larvae can mature
      - ewe immunity is restored at weaning
  - - - Work out a control strategy with your veterinarian or advisor.
        
        include this in flock health plan
        
        informed by FECs and other test results
      - Use effective quarantine strategies to prevent the importation of resistant worms in introduced sheep and goats
        
        treat sheep in quarantine
        
        Assume all bought-in sheep carry BZ, LV and ML resistant worms
        
        Treat with Startect
        
        Hold sheep off pasture for 24-48 hours (90% of eggs shed in 24hrs; 99% in 48hrs)
        
        Turn-out to dirty pasture to dilute the eggs produced by AR worms within purchased sheep
      - Test for anthelmintic resistance on your farm
        
        -->
        
        Post drench efficacy tests
        
        FECRTs
        
        Larval development tests
      - Administer anthelmintics effectively
        
        -->
        
        Dose for the heaviest in the group
        
        Check the dosing gun
        
        Restrict feed (BZ + ML drenches) for 24hrs before dosing
        
        Do not mix products
      - Use anthelmintics only when necessary
        
        based on regional information (forecasts), assessment of risk factors and FECs
        
        investigate other causes of ill-thrift
        
        do not give routinely for set age groups
      - Select the appropriate anthelmintic for the task
        
        -->
        
        Use narrow spectrum products where possible
        
        Avoid ‘off-target’ use
        
        Rotate where appropriate
      - Adopt strategies to preserve susceptible worms on the farm
        
        2 practical options
        
        Part-flock treatment (leave 10-20% untreated)
        
        Proportion left untreated should be higher if anthelmintic less effective
        
        Delay the move after treatment
        
        Allow the flock to be lightly reinfected
        
        Reproductive advantage to AR worms short-lived
        
        4-7 days of grazing post-dose is compromise
      - Reduce dependence on anthelmintics
        
        -->
        
        Use grazing management to reduce the challenge
        
        Avoid exposure to disease-inducing parasite burdens while allowing immunity to develop in sheep to be retained
        
        Forages with anthelmintic properties
        
        Chicory ↓ total worm numbers, ↓ wecs, ↑ live weight gain
        
        Rams bred for resistance / resilience
        
        Strategic prophylactic treatments at potential periods of risk
  - - - eggs shed after a minimum of 12 weeks after infection --> miracidia --> mud snail (galba truncatula)--> cercariae (5-7w)--> metacercariae (on grass)
      - eggs hatch in spring when over 10C
    - - due to liver damage caused by immature flukes migrating through liver (autumn-winter)
      - clinical signs
        
        immature fluke migrating through liver tissue
        
        rapid loss of condition
        
        sudden death
        
        lethargy and liver failure in all ages of sheep (sep-dec)
        
        sudden death due to liver rupture or clostridial disease
        
        no fluke eggs in faeces
      - differentials for sudden death
        
        clostridial disease (pulpy kidney, blackleg, black disease, brassy in unvaccinated stock)
        
        tick diseases (habitats often similar for both snails and ticks)
        
        pasteurellosis or other septicaemic conditions
        
        looping ill
    - - caused by adult flukes in bile ducts from infection picked up 4-5 months previously (winter-spring)
      - 0.5ml blood/fluke/day
      - clinical signs
        
        adult fluke in bile ducts
        
        loss of condition
        
        bottle jaw
        
        associated with low blood protein levels (can occur with chronic fluke, haemonchosis etc)
        
        reduced lambing percentage
        
        livers trimmed or condemned at abattoir
        
        anaemia
        
        terminal diarrhoea
      - differentials for sudden death
        
        inadequate flock nutrition
        
        chronic parasitism including anthelmintic resistant strains
        
        virulent foot rot
        
        johnes disease
        
        poor dentition (esp cheek teeth)
        
        chronic severe lameness
    - - clinical signs
        
        rapid loss of body condition and poor fleece quality despite adequate flock nutrition
        
        severe depression
        
        inappetance
        
        weakness, may be unable to stand
        
        losses typically occur from december onwards, may be much earlier (october) with severe challenge
    - - reduced live weight gains in fattening lambs
      - lowered conception rates
      - twin lamb disease, lower birth weight of lambs, ewes with less milk
      - increased susceptibility to other diseases
      - foetal reabsorption
    - - local knowledge
      - weather conditions
      - post mortem
      - blood samples
        
        acute: elevation of AST and GLDH useful from 2w post infection
        
        chronic: elevation of GGT, AST, GLDH
        
        eosinophilia may indicate recent exposure, but not specific
        
        serology
        
        ELISA to detect antibodies to F.hepatica secretory antigens, >90% specificity
        
        only indicates previous exposure, not present status. There is evidence that sheep will never become immune.
      - no fluke eggs shed in acute or subacute
      - in chronic fasciolosis fluke eggs are in faecal samples and post mortem flukes are demonstrated in bile ducts and gall bladder at necroscopy
        
        special sedimentation technique for fluke egg count as fluke eggs are heavier than roundworm eggs
      - copro-antigen ELISA test on faeces
        
        looks for fluke antigen
        
        will give positive result earlier than FEC as antigen is produced during the pre-patent period
        
        detectable 1-4 weeks post infection
        
        unlike eggs which may be shed intermittently, or may be passed from the gall bladder after the adult fluke is dead, coproantigen is only present for the period of infection