Parasitology

Parasites of Importance

• Sheep

• Cattle

• Deer

Sheep:

1. Teladorsagia circumcincta

2. Haemonchus contortus

3. Nematodirus spp.

4. Trichostrongylus colubriformis

5. ± Long-tails (Bunostomum and Chabertia)

6. Muellerius capillaris

7. Toxoplasma gondii

8. Cestodes: Taenia ovis

9. Fasciola hepatica

11. Lice: Bovicola ovis

12. Chorioptes bovis

13. Flystrike

Cattle:

1. Ostertagia ostertagi

2. Dictyocaulus viviparis

3. Cooperia oncophora

4. Trichostrongylus axei

5. Fasciola hepatica

6. Trichomonas foetus

7. Coccidia

8. Cryptosporidium

9. Neospora caninum

10. Theileria orientalis strain IKEDA (see “Systemic Diseases”)

11. Haemaphysalis longicornis

12. Lice: Bovicola bovis and Linognathus vituli

Deer:

1. Trichostrongylus askivali

2. Trichostrongylus axei

3. Dictyocaulus eckerti

4. Oesophagostomum sikae

5. Ostertagia-like

6. Haemaphysalis longicornis

4 Types of Helminths

• Phylum

• Common name

• Distinctive features

• Examples

1. Nematode = Roundworm

   • Examples: Strongylida

     1. Trichostrongyloidea = Ostertagia, Teladorsagia, Haemonchus, Trichostrongylus, Cooperia, Nematodirus

     2. Metastrongyloidea = Dictyocaulus viviparus

2. Cestode = Tapeworm

   • Features: Indirect lifecycles

     • Adult lives in DH small intestine

     • Eggs infect IH

   • Examples: Taenia ovis

3. Trematode = Fluke

   • Features: Indirect lifecycles with sexual and asexual phases → Increase biopotential

   • Examples: Fasciola hepatica and Calicophoron calicophorum

4. Acanthocephalans = Thorny-headed worms

Describe the general lifecycle of Strongylida (type of Nematode)

Pre-patent period = Time from ingestion of [L3] larvae to eggs being shed in faeces

• PPP = ~21d for most nematodes

Lifecycle: SIX stages

Parasitic Phase

1. DH ingests [L3] and exsheaths into L3 within GIT

2. L3 enters mucosal glands to moult to L4 → Adult

3. Sexual reproduction to produce eggs

Free-Living Phase

4. Female nematode produces eggs (or larvae) which are deposited on pasture within faeces

5. Eggs hatch L1 which feeds on bacteria in faeces

6. → Moult to L2 then [L3]

   • ~2 - 3w for development into [L3] in-field (5 - 7d in lab)

   • [L3] cannot feed → Moves away from food scour and onto pasture of infect DH

Describe optimal conditions for nematode development

• Development in faeces (3)

• Survival of [L3] (3)

Faeces (Egg → L2):

1. Oxygen

2. Warm faeces (optimum 25 - 27˚C)

   • No development when <10˚C → Exponential increase in rate of development BUT fewer larvae develop to [L3] due to mortality

   • >40 - 50˚C = Lethal

3. Moist conditions = Required for feeding, movement and to avoid desiccation

   • L1 and L2 more susceptible to desiccation than eggs and [L3]

   • Larval desiccation and death does NOT occur in NZ due to lack of severe enough droughts

Survival of [L3]:

1. Moisture

   • Insufficient droughts in NZ to spell pasture

2. Temperature (optimum 10˚C)

   • <10˚C → Quiescent

   • Haemonchus: Winter too cold → Cannot overwinter on pasture (survives year-to-year in animals)

3. Relies on stored metabolites (higher temperature = More active BUT faster use of metabolites)

Describe distribution of larvae on pasture

95% of parasite population within pasture (5% within animals)

• Close to bottom 2 - 3cm of sward (eggs + L1 - L3)

• Longer pasture dilutes larval load

• Avoid over-grazing

Alternative Forages for Parasite Prevention

• 3 Advantages

• 2 Disadvantages

+ve:

1. Process of establishing crops → Kills larvae and reduces contamination

   • eg. Ploughing/turning over soil and spraying out paddock to let grass die-off before planting crops

   • → Newly sown crops have minimal larval contamination prior to 1st grazing

2. Growth habitat of some crops is NOT supportive of high larval numbers

   • eg. Kale = Tall with long stem (animal does not graze base of sward)

   • eg. Spread out plants with soil in between

3. Some alternative forages contain higher levels of condensed tannins → Reduce larval establishment in host

-ve:

1. Margins of grass along fence lines and around trees/troughs/rocks → Becomes highly contaminated with larvae

   • Lambs will preferentially overgraze grass with parasites before eating new crops

2. Multi-graze crops become very contaminated if farmers do not drench young stock still

Describe the seasonal pattern of parasites on a sheep farm

• Larval contamination and FEC

• Dominant parasites by season

Larval Contamination and FEC:

1. Spring rise of larvae on pasture from TWO sources:

   1. Periparturient rise (PPR) of ewes = Reduce immune response around late gestation → Increased FEC

      • NOT in cattle

   2. Overwintered larvae

2. Larvae from spring rise are ingested by lambs

3. Eggs deposited by lambs = source of ‘autumn peak’ infective larvae

4. These larvae ingested = disease in autumn/winter + some overwinter (source of 1.)

5. A number of eggs deposited in autumn fail to develop (temp.

No PPR in cattle

Seasonality:

• Late spring/early summer = Nematodirus and Teladorsagia

• Summer/early autumn = Haemonchus, Teladorsagia, Trichostrongylus

• Autumn/early winter = Trichostrongylus

When does immunity against parasites begin to develop in calves and lambs

Begin consuming larvae when eating pasture (2w for lambs)

• Immune response begins to develop at 6 - 12m → Full adult immunity at 18m

• Cattle: Immune response reduces female worm fecundity (esp. Ostertagia) → Poor relationship between parasite burden and FEC in calves ≥6m

  • Cattle faeces is more liquid → Dilution effect

  • Adult cattle do NOT contribute to pasture contamination (no PPR)

Parasitism in Beef Cattle

• Why are they less of a problem in extensively managed beef calves (vs. dairy)? (5)

• Main risk period

• When to begin drenching

1. Better nutrition to weaning (milk NOT pasture)

2. Being suckled, calves eat less grass → ingest fewer larvae and put out fewer eggs to contaminate pasture

3. Less heavily stocked

4. Often share grazing with sheep

5. Stay with dams until 6 months = Net removers of larvae on pasture

Risk: Late weaning (May) → Heavily infected pastures as calves are NOT drenched until weaning

Drench: Begin ~6m (may not need to be q28d or at all for low-risk farms)

Clinical effects of nematode parasites

Clinical Parasitism:

1. Inappetence #1

2. Weight loss (PLGE)

3. Diarrhoea (inflammatory response)

4. ± Anaemia and sudden death (Haemonchus)

Subclinical Parasitism: Reduced GR and wool growth

• Young animals take longer to reach target LWT → Lower schedule prices and increased maintenance costs and less likely to reach minimum weight for mating

• Higher GR → Reach target slaughter weight earlier when schedule prices are better

Describe the general principles of parasite control on-farm (7)

“FARMED”

ONE: FEEDING

1. Good nutrition enhances an animal’s ability to deal with worms (effective immune response)

2. Growing out young stock → Less time “worm factories” are on farm

   • Trade off with reduced slaughter weight

   • Avoid unnecessary retention of young stock (difficult in lamb/calf finishing farms or pedigree farms)

TWO: AVOID = Avoid exposing susceptible animals to high pasture contamination

1. Provide safe feed

   1. Crops/alternative forages/new grass (difficult on steep hill country farms)

   2. ± Resting/spelling pasture? NOT practical (≥3m required)

   3. Silage/hay → Removes larval contamination from paddock AND kills parasites within conserved forage

2. Cross-grazing to remove larvae

   1. Sheep with cattle/deer = Dead-end host

      • Uncommon as farmers reserve SAME areas for specific stock classes (eg. lamb paddocks)

      • Avoid goats and alpaca with sheep

   2. Older (immune and well-fed) animals of same species = Net removers of larvae from pasture

      • CAN contribute to larval contamination if immunocompromised

3. Maintain higher post-grazing residuals >1400 - 1500kgDM/ha

   • Do NOT force young animals to graze larvae

4. ZERO grazing systems eg. cut and carry in goat farms

5. Select for genetic parasite resistance/tolerance

   • Moderate heritability (0.23 - 0.35)

   • Resistance (FEC), CARLA and resilience (high worm burden with little effect)

6. Quarantine protocols to avoid introducing resistant worms

THREE: REFUGIA = Deliberately retaining a gene pool of susceptibility by allowing some parasites to reproduce without exposing them to anthelmintic

• Only from worms that are ingested by sheep, mate and produce eggs that contribute to subsequent generations

• To keep the prevalence of the resistance worms low (susceptible worms breed with resistant worms to reduce AR)

• Outcome: AR is constant or not worse

FOUR: MONITORING

1. Evaluate post-drench GR and clinical signs

2. Drench check

3. FECRT

FIVE: EFFECTIVE DRENCH

• Regular drench checks and monitoring

• Avoid long-acting anthelmintics → Increase rate of AR

• Drench programmes differ between cattle farms (more individualised)

  • High drench use = Run-off or finishing block

  • Moderate drench use

  • Low drench use

3 Methods of Monitoring for Parasitism

• Method

• Advantages

• Disadvantages

1. Evaluate Post-Drench GR and Clinical Signs

   • +ve: No cost

   • -ve: Highly inaccurate (drench efficacy can be as low as 65 - 80% before farmer sees problem)

2. Drench Check

   • Method: Assess x10 FEC 7 - 10 after drenching (should be ZERO)

     • FEC ≠ 0 → Ar parasites or poor drenching practice

   • +ve:

     1. Cheap ($60 - 100)

     2. Very easy → Good farmer compliance

     3. Rapid results

     4. Excellent starting point for conversation with farmer about anthelmintic efficacy (may lead to FECRT)

   • -ve:

     1. Must assume animals had worms pre-drench

     2. No quantitative assessment (yes/no)

     3. Only tests ONE anthelmintic product

     4. Assumes farmer drenches accurately

3. FECRT

   • Method: January = Good mix of nematode genera

     1. Measure FEC pre-drench (≥500epg required)

        • Individual FEC and pooled sample for larval culture

     2. Test EACH drench on separate group of 12 - 15 lambs

     3. Measure FEC post-drench 7 - 14d later

     4. Calculate % reduction = Overall drench efficacy

        • [(pre-treatment average) - (post-treatment average)]/(pre-treatment average) x 100

          • BOTH Strongyles and Nematodirus

     5. Larval culture to determine which genera are resistant to the drench

        • Multiply % by average number of eggs to extrapolate number of eggs in faecal samples that were produced by each genera

   • +ve:

     1. Most accurate

     2. Evaluate efficacy of multiple anthelmintics

     3. Big investment → Farmer pays attention to results

     4. Good motivation to follow-up with thorough parasite control plan

   • -ve:

     1. Expensive ($1500 - 4500)

     2. Single point in time → Not reflective of exactly what is happening on-farm

     3. Time-consuming (monitor FECs until high enough → 2 visits required)

     4. 12d to obtain results from larval cultures

Calculate the efficacy and individual genera efficacy of the drench “Matrix”

Drench Efficacy:

• [(pre-treatment average) - (post-treatment average)]/(pre-treatment count) x 100

• Strongyles: (1230 - 205)/1230 x 100 = 83%

• Nematodirus: (216 - 58)/216 x 100 = 73%

Reduction at the Genera Level:

Multiply % by average number of eggs to extrapolate number of eggs in faecal samples that were produced by each genera

Label the following eggs

1. Strongylid egg = Thin-shelled, non-operculate, ovoidal egg with 8 - 64 morula

2. Strongyloides spp. egg (Rhabditida)

3. Trichuris spp. egg

4. Nematodirus spp. egg = 2x size of normal strongylid egg

5. Strongylid egg + coccidial oocyst (top right)

6. Moniezia expansa (tapeworm) egg

List 11 ways to reduce/delay AR development (sources of refugia)

1. 28-day drenching interval (PPP = 21 days, leaves 7 days for new susceptible eggs to develop)

2. Leave some lambs undrenched (healthiest lambs)

3. Graze undrenched ewes after (and before) lambs

   • Eggs from ewe faeces will be from non-drenched larvae (later consumed by lambs)

4. Run some un-drenched ewes with lambs (eg. low BCS ewes)

   • Ewes put non-drenched eggs into the pasture to be consumed by lambs AND gain BCS in the process

5. Avoid anthelmintic treatment of adult stock

6. Avoid underdosing

7. Avoid use of long-acting drenches (eg. moxidectin)

   • Continues to kill ALL larvae for awhile, allowing AR larvae to persist

   • Conc. of drug decreases overtime and eventually drops below MIC = sublethal dose allowing parasites to persist

8. Purchase lambs from farms with proven excellent drench efficacy

   • Do NOT give quarantine drench, then graze in areas where home-bred lambs have been → Introduce susceptible worms and refugia

9. Combination drenches

   • Avoid single active drenches

10. Avoid drenching and moving onto clean pasture with no larval contamination

    • Clean pasture: Crops, newly sown grass, silage or hay paddock post-harvesting, grazing different species for a long time (no sheep larvae)

    • Only AR larvae would be present on the paddock

11. Avoid repeatedly grazing young animals on same area

    • Lamb finishing system is NOT sustainable (ONLY young lambs grazing and increasing parasite burden)

    • eg. Pedigree farms with ram lambs (retention of young rams and repeated drenching until sales to maintain weights)

    • eg. Finishing cattle (eg. intensive bull beef), heifer rearing for dairy and ram breeders

Possible Conflict: Farmer focus = Parasite control NOT selecting for AR

How to select which young stock to leave undrenched as a source of refugia in cattle

Leave some heifers undrenched depending on age class (caution when <7 months of age) and mark to ensure they are treated next time

• Sufficient immunity to leave some undrenched → 6 - 7 months of age

  • No drench selection criteria:

    1. BCS

    2. FEC (impractical)

    3. LWT gain

• ≥12 - 14 months → Good immunity and do NOT require drenching

• Small number given high efficacy of drench

• Lower efficacy of drench: More must be left untreated as more resistant larvae will be present on pasture

9 Anthelmintic Options

• MoA

• Examples

• Spectrum of action

• Pharmacokinetics

1. BENZIMIDAZOLES (BZ)

   • MoA: Bind helminth β-tubulin protein, preventing their incorporation into microtubules → Interfere with cell nutrition/division → Starvation and ovicidal

   • Examples: Albendazole, oxfendazole, fenbendazole

   • Spectrum:

     1. Nematodes

     2. Giardia

     3. ± Tapeworms (albendazole/fenbendazole)

     4. ± Fluke (albendazole)

   • Pharmacokinetics: Water-insoluble → Slow absorption in rumen over several days

2. LEVAMISOLE (LEV)

   • MoA: Bind nicotinic ACh receptors → Paralysis

     • Narrow safety margin

   • Spectrum: Nematodes ± immune stimulant (added to 5in1)

   • Pharmacokinetics: Water-soluble → Fast elimination

3. MACROCYCLIC LACTOMES (ML)

   • MoA: Acts on glutamate-gated Cl- channels at NMJ → Paralysis

   • Examples:

     1. Avermectins: Ivermectin, abamectin, doramectin, eprinomectin, selamectin

     2. Milbemycins: Moxidectin, milbemycin

   • Spectrum:

     1. Nematodes

     2. Arthropods (lice and mites)

   • Pharmacokinetics: Fat-soluble → Slow absorption (eg. MOX depot injection)

   • Heavily used in cattle in NZ, $$$, but easy pour-on

4. TETRAHYDROPYRIMIDINES

   • MoA: As for LEV

     • Higher safety margin

   • Examples: Morantel (pyrantel and oxantel SA)

   • Spectrum: Nematodes ± Cestodes?

   • Pharmacokinetics: Soluble and well-absorbed

5. MONEPANTEL

   • MoA: As for LEV

   • Example: Zolvix Plus = MON + ABA (2009)

   • Spectrum: Nematodes (good for AR)

   • Licensed for sheep AND cattle

6. DERQUANTEL

   • MoA: Nicotinic ACh antagonist (cannot use with LEV or MON)

   • Example: Startect = DER + ABA (2010)

   • Spectrum: Nematodes (good for AR), nasal bot and mites

   • Only licensed for sheep

7. PRAZIQUANTEL

   • Spectrum: Tapeworms #1

     • Highly effective against Echinococcus granulosus

     • BZ and pyr/mor have some activity

   • Standard dose NOT effective against ALL tapeworms

8. TRICLABENDAZOLE

   • MoA: Unique structure = Chloride halogenated BZ

   • Spectrum: Flukes (immature and adult) #1

     • Albendazole has some activity (also closantel) BUT only later stages

9. OTHER

   1. Closantel = Fluke and Haemonchus

   2. OP = Triple combination against Haemonchus (AUS) and ectoparasites

Best route of anthelmintic administration

• ORAL combinations #1

  • Best pharmacokinetics + highest efficacy

  • Cheapest

  • Can be trained

• Pour-on: Assume reliable absorption through skin and bloodstream in high enough conc. to kill parasites (most absorbed by licking off other herd mates)

  • NOT an option for sheep (fleece)

  • Influenced by coat length and rain

  • If oral not feasible: Injection next best (better chance of absorption)

  • If farmer insists pour-on: Ensure it is combination

Describe AR in:

• Sheep

• Cattle

• Goats

• Alpaca

Anthelmintic resistance = Failure to remove ≥95% of worms

Sheep: ~1/3 of farms with triple-resistance

• Esp. Teladorsagia and Trichostrongylus

• No AR in Haemonchus in NZ (vs. AUS)

Cattle: Very rarely discussed

• Triple-resistant Ostertagia reported

• ALL farms have ML-resistant Cooperia (well-marketed and easy to use pour-on)

• BZ resistance widespread

• LEV still effective

Goats: Resistance a HUGE issue (improper dosing and rapid metabolism of drug)

• Triple combination resistance very common (MON and DER resistance also reported)

Alpaca: Similar resistance pattern as sheep

8 Considerations for drench selection

1. Efficacy against different parasites of interest

2. Potential impact on selection for anthelmintic resistance

3. Persistent activity

4. Frequency of administration

5. Route of administration

6. Which animals are receiving the drench (and what are we trying to achieve by giving it)

7. Withholding period (WHP)

8. Price

Describe the anthelmintic protocol for sheep

Preventative Drenching Programme (Lambs): Limit number of [L3] larvae on pasture (avoid autumn peak) → Reduce clinical and subclinical parasitism in summer and autumn

• Start: Based on climate when eggs will likely develop to [L3]

  • North Island = Early December at weaning

  • Lambs begin to ingest larvae at 2w of age

• Stop: Depends on climate, grazing management of efficiency of parasite control over summer/autumn

  • Colder areas stop drenching earlier than warmer areas

  • Mid- to late autumn

  • Drench at 28d interval for 1st 4 - 5 drenches → Spread out drenching until stopping in April - July

• Programme: ≥5 drenches q28d

  • 28 days = Allows 21 days for PPP and additional 7 days for newly established worms to shed eggs for refugia

    • 21 days = Suppressive drench (BUT selects quickly for resistance as worms surviving are resistant)

    • ≥28 days → Excessive larval contamination

  • May have issue if conditions are optimal (PPP 18 days) allowing 10 days of susceptible larvae to be produced

• Do NOT give anthelmintics to MA sheep (can consider at key times such as pre-tup and pre-lamb)

Describe 4 features of the quarantine protocol for parasite control

1. Keep new stock off pasture for 72 - 96hr

   • Takes time for nematode eggs to pass through the GIT and shed in faeces

   • Provide with supplementary food (hence not typically done as sheep are fussy eaters)

2. Quarantine drench

   • Sheep: 4 drug combo = Zolvix plus (MON/ABA) or Startect (DER/ABA) + BZ + levamisole

     • 1/3 of farms have triple-resistance

   • Cattle: Zolvix plus OR Startect

     • Limited data on AR in cattle as FECRT rarely performed

       • FEC lower after 7 - 9 months due to immunity (poor correlation with worm burden)

       • Should be performed in YOUNG stock

     • Triple resistant Ostertagia and Cooperia have been reported

3. Drench check ~10d later = 10 - 15 animals tested to ensure drench was effective (FEC should be ZERO)

4. Place on pastures known to be contaminated with susceptible larvae to dilute resistance ones remaining

4 Features of parasitism in goats

1. Lower tolerance to parasites (evolved as browsers in small herds over an extensive area) → Young goats AND adults need drenching

   • Do NOT develop the same level of immunity as sheep

2. Agents shared with sheep (Teladorsagia, Trichostrongylus and Haemonchus)

   • No cross-over with cattle

3. No USEFUL anthelmintics are on-label for goats AND they require higher dose rates than sheep

4. Highly susceptibility to toxicity

5 Methods of parasite control in goats

1. Allow goats to graze NORMALLY (i.e. do not force to graze grass like sheep)

   • ≤60% of diet is browsing (weeds, trees, thistle) → Cut and carry

   • High pasture residuals (1500 - 2500kgDM/ha)

2. Cross-graze with cattle (NEVER adult goats as net CONTRIBUTORS of pasture contamination)

3. Consider ZERO-grazing (eg. many dairy goat farms)

   • Eliminate need for off-label drenches (eg. dairy goats with standard WHP)

4. Cull goats which require lots of drenching

5. Anthelmintics = CHALLENGING for goats

   • Drug: Licensed for goats (oxfendazole, ivermectin and triclabendazole) → NOT useful

     • Almost always off-label → 91d meat WHP

     • Triple combination resistance very common (MON and DER resistance also reported)

   • Dose: 1.5 - 2x higher dose rate than sheep (rapid metabolism)

     • Higher susceptibility to toxicity (oesophageal groove retained → Drug bypasses rumen)

     • Ensure accurate weighing (eg. bathroom scales) to avoid toxicity (eg. levamisole toxic at 3x sheep dose rate)

4 Features of parasitism in alpaca

1. Little known about alpaca parasites but share with sheep AND cattle

   • Haemonchus → Clinical disease (esp. young alpaca after weaning)

2. Drench young alpaca ± adult alpaca based on FEC

3. No licensed alpaca anthelmintic → ALL off-label

4. Recommend 1.5x sheep dose rates due to rapid metabolism

Teladorsagia circumcincta

• Localisation

• 6 Pathological effects

Localisation: Abomasum of sheep

Pathology: Also Ostertagia in cattle

1. Larvae enter gastric glands and surrounding mucosa responds with nodular hyperplasia

2. Parietal/chief cells replaced by goblet cells → Neutral pH and more mucus

3. Inflammation and oedema

4. Morocco leather appearance of mucosa

5. Villous atrophy of small intestine

6. PLE

Haemonchus contortus (Barber’s pole)

• Localisation

• Seasonality

• Pathogenesis

• 3 Clinical Signs

• Treatment

• Prevention

Localisation: Abomasum of sheep, goats, alpaca ± cattle

Seasonality: Summer - autumn

Pathogenesis: Blood-sucking → Severe anaemia

• Overwinters as eL4 in sheep (eggs killed in winter environment)

• Prolific egg-layer (10,000 eggs/female/d)

Clinical Signs: No diarrhoea

1. Anaemia (FAMACHA colour chart → Drenching?)

2. Bottlejaw (PLE)

3. ± Sudden death

Treatment: Anthelmintic (no AR in NZ) eg. ML

Prevention: Barbax? = Somatic Ag from gut of worms collected from donor sheep

• When worms feed on vaccinated animals, Ab binds to gut lining of worms to prevent Hb digestion

• Short-lived immunity with regular boosters required

Importance of Muellerius capillaris

Non-pathogenic lungworm of sheep with indirect lifecycle (IH = mollusc)

• Pathogenic in goats

• PM: Worms deeper in lung tissue and surrounded by nodule of tissue reaction → Grey lesions on the dorsal surface of the lungs

Taenia ovis (Cysticercus ovis)

• Importance

• 4 Management recommendations

Importance: Aesthetic defects in sheep meat (no public health risk) → Downgrading of carcass

• No clinical signs in DH or IH

Recommendations:

1. Appropriate dog feeding (adequately frozen at -10˚C for 10d) → No longer covered by legislation

2. Praziquantel q1m for dogs

3. Prevent dogs scavenging carcasses containing cysts

4. Dog control: Farm dogs, visiting dogs and town dogs should not be allowed on property unless treated with praziquantel

Do NOT recommend farmer treat sheep for metacestodes (results in calcified lesions that do not disappear) OR prevent dogs from defaecating in paddocks

Fasciola hepatica

• PPP

• Signalment

• Seasonality

• Lifecycle

• IH

• 4 Requirements

• Pathogenesis

• Clinical signs

• 3 Methods of diagnosis

• 3 Methods of prevention

PPP: ≥8w

Signalment: Sheep, cattle and goats

• Adult infection just as common as young animals

• Cattle more resistant than sheep and goats

• Northland #1

Seasonality: Metacercariae build in Jan (>10˚C) and drop to zero by July

• Higher risk in East coast = DRY with green grass in swampy areas only

Lifecycle:

1. Adult liver fluke located in the bile ducts of the DH lays eggs

2. Eggs shed in DH faeces and enter water

3. Eggs develop in water and hatch to release the miracidium (L1)

4. Miracidium penetrates the snail integument and a mother sporocyst (L2) develops

5. 5 - 12 daughter rediae (L3) develop within the mother sporocyst (asexual reproduction) and burst out to travel to the hepato-pancreas (digestive gland) of the snail

6. Further asexual reproduction leads to cercariae (L4) production within the daughter rediae (up to 40) and are released in water via a birth pore in the rediae

   • Occasionally, 2nd generation of rediae

   Mother sporocyst > daughter rediae > cercariae = huge proliferation by asexual reproduction in the snail

7. Cercaria released in water swim to the edge of the water and onto vegetation

8. Tail is shed and a cyst wall is secreted to become encysted on vegetation as metacercariae (200µm)

9. Metacercariae ingested by ANY DH on herbage and excyst

10. Young fluke are released from cysts within the DH small intestine and develop into adults

11. Immature fluke burrows out of the small intestine and crosses the peritoneal cavity

12. Penetrate liver capsule (at 1 - 2mm long)

13. Within the parenchyma for 5 - 6 weeks

    • Immature flukes are very destructive to liver tissue: Burrow around feeding in the liver parenchyma

    • Can observe immature liver fluke tracts under the liver capsule during sheep/cattle necropsy (mid - late Summer)

    • Clostridia: Causes black disease induced by F. hepatica which creates an anaerobic environment in the liver for the C. novyi to develop

14. Enter bile ducts (1cm long) and take 3 - 4 week to mature

IH: Lymnaea spp. = Freshwater snail

• Lymnaea tomentosa (indigenous to NZ) and Lymnaea columella (more widespread and introduced)

Requirements:

1. Egg development (and larvae in snail) requires ≥10˚C (optimum 25˚C)

2. Development of miracidium within egg also requires O2 (more that what is in faeces) and water

3. Development in snail affected by snail nutrition (better fed, less infected = more rediae from each miracidium)

4. Water/marshy areas that are permanently wet (prevent egg desiccation, facilitate miracidium/cercaria swimming, penetration of aquatic snail and metacercaria must be kept moist to survive on vegetation)

Clinical Signs:

• Sheep

  1. Acute: Sudden death

     • MANY immature fluke migrating through liver parenchyma for first 5 - 6w → Liver failure

     • Late summer/early autumn

  2. Subacute: Death 8 - 12w ± Jaundice

     • Liver damage and blockage of biliary system

     • Late summer/early autumn

  3. Chronic: Anaemia, bottlejaw, weight loss, increased GGT

     • Adult fluke feed from bile duct lining and blood

     • Late autumn and winter

  4. Black Disease: Clostridium novyi Type B = Infectious necrotic hepatitis → Acute death from toxaemia

• Cattle = Chronic disease as for sheep (+ calcified bile ducts which persist when fluke no longer present)

  • Black disease and acute disease very rare

Diagnosis: GGT (DDx: FE)

1. Faecal sediment → ID eggs

2. Blood/milk ELISA Ab pooled from 10 animals

   • Becomes negative 3m after treatment

3. Faecal Ag (overseas)

Prevention:

1. Triclabendazole #1 = Drench or pour-on for ALL stages of liver fluke in ruminants

   • 1 - 3x over late summer - early winter

     • Most farmers treat ONCE in winter and rely on there being no overwintering to metacercariae or infected snails

   • Treatment with nematocidals (eg. albendazole) as some effect but not for immature fluke

   • Potential for eradication as entire fluke population within animals over winter (August)

2. Drainage (permanent solution but impractical)

3. Fencing to prevent sheep grazing marshy areas? Impractical except for small areas

Molluscicides not an option for NZ due to environmental impact

Ostertagia ostertagi

• Localisation

• 2 Types of disease

  • Signalment and seasonality

  • Pathogenesis

  • Diagnosis

• Clinical signs

Localisation: Abomasum of cattle

• Most pathogenic worm of cattle

Type I Ostertagiosis:

• Signalment: Calves in mid - late winter

• Pathogenesis: High larval intake/high worm burden

• Diagnosis: FEC

Type II Ostertagiosis:

• Signalment: Yearling or 2yr cattle in spring

• Pathogenesis:

  1. Cattle graze highly contaminated pasture in autumn

  2. Accumulation of inhibited eL4 in gland crypts of the abomasum heading into winter (worsening climate) = Hypobiosis → No clinical signs

  3. Larvae resume development in early spring → En mass emergence

  4. Clinically affected cattle due to damage to abomasal mucosa

• Diagnosis: Plasma pepsinogen assay (cannot diagnose with FEC as L4 cause disease NOT adults)

Clinical Signs: Diarrhoea, dehydration, bottlejaw, inappetence, weight loss and death

Cooperia oncophora

• Importance

• Signalment

• Localisation

• Resistance

Importance: Less pathogenic than Ostertagia (does not kill, but causes decreased GR)

Signalment: Immunity develops quickly (solid by 12 months)

Location: Small intestine

AR: Very frequent resistant to ML anthelmintics

• Poor-on drenches very common: just single ML

• Most commonly-used anthelmintics in cattle

Nematodirus

• Localisation

• Lifecycle features

Localisation: SI of ruminants

Lifecycle: Develop into [L3] within egg

• Slow development rate and survive at low temperatures

• Requires chilling before hatching

Pathogenesis: Bigger issue in cold climates in spring (eg. Southland) as overwinters in high numbers (eggs resistant to cold)

Lungworm

• 2 Examples

• Lifecycle

• PPP

• 2 Methods of diagnosis

Examples:

1. Dictyocaulus viviparus (cattle)

2. Dictyocaulus eckerti (deer)

Lifecycle:

1. Adults mate in bronchioles and trachea

2. Females produce embryonated eggs which hatch L1 within the lungs → Pharynx → Swallowed

3. L1 exits faeces → L2 → [[L3]]

   • 4 days

   • [[L3]] NOT very mobile and hence lots in one place on pasture

4. [[L3]] = infective stage and ingested by cattle/deer

5. [L3] exsheaths and burrows through SI to undergo lymphatic-pulmonary migration (lymphatics → thoracic duct → heart → lungs)

PPP: 4w

Diagnosis: History and clinical signs →

1. PM exam = Trachea full of worms with thickened mucus and exudate

   • Powerful way to show farmer evidence → Prompt treatment

2. Baermann’s faecal larval count = Count L1 in faeces

   • Method:

     1. Wrap faeces in double gauze swab and place into glass funnel with water

     2. Leave overnight to allow larvae to migrate out of faeces and drop into red tube

     3. Release clamp to allow larvae to fall into container

     4. Count larvae under dissecting microscope

   • 2g faeces with 50 larvae = 25 larvae/g

   • -ve: Counts may not represent parasite burden

Dictyocaulus viviparus

• Signalment

• Seasonality

• 4 Clinical signs

• Treatment

• Prevention

Signalment: Calves <10m (esp. dairy calves)

• Less common due to widespread use of anthelmintics to treat GI parasites

• Infection common, disease uncommon due to strong immune response to migrating parasites

Seasonality: Late summer and autumn

• Sporadic outbreaks of disease due to unique epidemiological factors that allows naive animals to be suddenly exposed to huge numbers of infective [[L3]]

Clinical Signs: 3w post-infection of [L3] → Verminous pneumonia

1. Coughing, tachypnoea and dyspnoea (“Husk”)

2. Weight loss

3. Death

4. ± 2˚ bronchopneumonia

Treatment: ALL common drugs (no AR)

• LA ML injectables #1

Prevention: NONE! Farmer does not think about D. viviparus as killed with more important GI nematodes

• Huskvac vaccine = Irradiated L3 PO x2 doses 4w apart before being turned onto pasture in UK

Dictyocaulus eckerti

• Signalment

• Seasonality

• 3 Clinical signs

• Treatment (+ risk)

• 3 Methods of prevention

Signalment: Weaners <1yr (adults immune)

• Higher risk in intensive, single-species grazing (sheep or cattle) with no alternative crops/forages

• No drench or larval flotation history

Seasonality: Autumn and early winter = Warm and wet conditions to facilitate [L3] survival on pasture

Clinical Signs: ≤20% mortality rate with sudden death

1. Scruffy weaners with reduced GR

2. ± Soft cough with stress/exercise/yarding (mask clinical signs vs. cattle)

3. ± Slight increased moist lung sounds on auscultation

Treatment: Some products licensed for deer

• ML = Highly effective but persistent activity

• Lev = NOT good for deer lungworm

• BZ = Shorter drench interval

• Cervidae = Triple combination in deer

• Risk: High burden → Death after treatment (dead worms block trachea)

  • WARN farmer of this risk

Prevention:

1. Preventative drench program x5 q28d

   • Start: PRIOR to weaning in Feb/March to reduce early autumn pasture contamination

2. Cross-grazing with sheep, cattle OR older deer

3. Alternative forages

Oesophagostomum sikae

• Signalment

• Localisation

• Pathogenesis

Signalment: Young deer in autumn

Location: Large intestine

Pathogenesis: Simultaneous emergence as for Type II ostertagiosis → Reduce GR in autumn

4 Types of protozoan (+ examples)

1. Amoebae

2. Ciliates = Rumen commensals

3. Flagellates

   1. Trichomonas foetus

   2. Giardia spp.

4. Apicomplexan = Highly evolved obligate parasites

   1. Coccidia (Eimeria and Isospora spp.)

   2. Cryptosporidium spp.

   3. Toxoplasma gondii (see “Sheep”)

   4. Neospora caninum

   5. Theileria orientalis strain IKEDA (see “Systemic Diseases”)

Trichomonas foetus

• Agent

• Prevalence

• Source of infection

• Transmission

• Clinical sign

• 3 Methods of diagnosis

Agent: Trichomonas foetus = Flagellate protozoan with 3 forward-facing flagella and 1 posterior

• Reproduce via binary fission

Prevalence: Uncommon in NZ, but historical outbreak on East Coast

Source: Bull genital tract (no disease but infected for life) → Cull

Transmission: Naive cow infected by bull during coitus (esp. heifer)

• T. foetus multiplies in vagina causing vaginitis

• Travels through cervix to uterus and destroys the placenta

Clinical Sign: Abortion 6 - 8w after natural mating → Late return to service

Diagnosis:

1. Flush prepuce with saline or growth media for PCR (also foetus and vaginal discharge)

2. Ab detected in vaginal.cervical mucus

Treatment: Cows spontaneously clear infection

Coccidiosis

• Agents/clinical signs

  • Cattle

  • Sheep

  • Goat

  • Pig

• Signalment

• 5 Risk factors

• Lifecycle

• 2 Methods of diagnosis

• 3 Treatments

Agent/Clinical Signs:

• Cattle = Eimeria bovis/zurnii

  • Often complicated by BVD

  • Large bowel diarrhoea (± mucosal strips in faeces and fresh blood), tenesmus

  • 11 other non-pathogenic Coccidia spp.

• Sheep = E. ovinoidalis

  • Often concurrent with other enteric infection

  • Rare clinical disease in NZ as lambs exposed to low level of infection → Immunity without disease

• Goat = 1 - 2 highly pathogenic

  • Often complex with nematodes and Yersinia

• Pig = Cystoisospora suis

  • Pasty diarrhoea (no haemorrhage)

  • NOT fatal, but reduced GR

Signalment: Young animals

• Calves <6m

• Lambs <2 - 4m

• Goats young AND old

• Piglets 1 - 2w

Risk:

1. High density of young animals

2. Warm and moist conditions (eg. leaking water trough with defaecation and pugging)

3. Underfeeding

4. Poor hygiene in calf pens

   • Normal conditions with good management: Young animals exposed to few oocysts and develop effective immunity within 1 - 2 weeks with NO clinical signs

5. Coccidiostats in milk replacer → No immunity → Post-weaning coccidiosis

Lifecycle:

1. Oocyst passed in faeces (unsporulated)

   1. NOT infective when first shed

   2. Contains a sporont = single-cell zygote state

   3. Environmental resistance with thick wall

2. Sporulation (SPOROGONY) = Sporont develops into sporocysts which contain sporozoites → Infective oocyst

   1. Cystoisospora = 2 sporocysts each with 4 sporozoites

   2. Eimeria = 4 sporocysts each with 2 sporozoites

3. Ingestion of sporulated oocyst and liberation of sporozoites which penetrate intestinal epithelial cells

4. 1st PHASE OF SCHIZOGONY = Asexual reproduction and host cell ruptures to produce numerous schizozoites

5. 2nd PHASE OF SCHIZOGONY = Asexual reproduction

6. GAMETOGONY = Sexual phase. 2nd gen schizozoites invade cells and differentiate into:

   1. ONE macrogametocytes (female)

   2. Many motile microgametocytes (male) which leave the host cell to seek the macrogamete

7. FERTILISATION = Oocyst formation which contains a zygote

8. Unsporulated oocyst released from host

Diagnosis:

1. Very high oocyst count in faeces (cattle > 100,000/g)

2. PM and mucosal scraping to ID schizonts, gametocytes and oocysts in large numbers

Treatment:

1. Supportive care (fluids and electrolytes)

2. Remove animals from contaminated environment

3. Coccidiostat/coccidiocide

   1. Polyether ionophores (eg. Lasalocid or monensin) = Milk replacer/calf meal

   2. Amprolium = Avian drinking water or oral drench

   3. Sulphonamides ± pyrimidine for synergism

   4. Fluoroquinolones

   5. Toltrazuril (Baycox) = ONLY curative option (coccidiocide)

Cryptosporidium parvum

• Signalment

• Seasonality

• Lifecycle

• Oocyst structure

• Clinical signs

• 3 Methods of diagnosis

• Treatment

Signalment: Calves <10d AND humans

Seasonality: Spring peak in humans associated with calving (summer peak associated with C. hominis)

Lifecycle:

1. Calf ingests oocyst which liberates sporozoites

2. Sporozoites invade microvillus brush border of GIT to carry out:

   1. 2 cycles of schizogony

   2. Gametogony

   3. Sporulation while oocyst still in microvillus

3. Oocyst becomes immediately infective to another/SAME host

Oocyst: 4 free-floating sporozoites with acid-fast cell wall

• Immediately infective (infective dose only requires 1 - 10 oocysts due to autoinfection)

• Highly resistant in environment (accumulate in calf shed)

Clinical Signs: Atrophy and fusion of intestinal villi → Neonatal diarrhoea

Diagnosis:

1. Ziehl-Neelsen stain on faecal float to ID oocysts

2. Faecal PCR

3. PM histopathology ASAP (brush border deteriorates rapidly)

Treatment: Supportive care ONLY and remove animal from infected environment

• Anti-cryptosporidials??? eg. Beta-cyclodextrin, paramomycin (aminoglycoside) or halofuginone (Halocur)

Neospora caninum

• Lifecycle

• 2 Methods of transmission in cattle

• 3 Clinical outcomes in cattle

• Diagnosis

• Prevention

Lifecycle: DH = Dog (HL paralysis in puppies) and IH = Cattle

1. Dog (DH) passes unsporulated oocysts in faeces

2. Oocysts sporulate to produce sporozoites

3. Sporozoites liberated when cow (IH) ingests pasture contaminated with dog faeces

4. Sporozoites infect GI cells →

   1. Tachyzoites invade ALL tissues (esp. CNS and myocardium)

   2. Bradyzoites

5. Tachyzoites invade the placenta and foetus → Placentitis and inflammation

6. Abortion

7. Dog infected by ingestion bovine placenta containing bradyzoite cysts

Transmission:

1. Horizontal transmission = Ingestion of oocysts from dog faeces (epidemic neosporosis)

2. Vertical transmission = Congenital infection via immunosuppression late gestation → Bradyzoite reactivation (endemic neosporosis = maintain infection in herd without dog)

Cattle: Abortion

1. No clinical signs in cow and no gross lesions

   • Early gestation infection (<5m) = Abortion

   • Late gestation infection = Calf born clinically normal, but infected

2. Infected cows repeatedly give birth to congenitally infected calves (70 - 80% of pregnancies)

3. Congenitally infected heifers have higher chance of abortion during 1st pregnancy

Diagnosis:

1. Serology IFAT/ELISA Ab (titres decline after 2 - 3m, but cows with recent abortion have high titres)

2. Histopathology of placenta, foetal brain and myocardium

3. PCR on fresh foetal stomach

Prevention: None? No vaccination available

Haemaphysalis longicornis

• 6 Effects on deer/cattle

• Structure

• Location on host

  • Cattle

  • Sheep

  • Deer

  • Dogs/cats

• Distribution in NZ

• Lifecycle

• Habitat of ticks

• Diagnosis

• 3 Methods of prevention

Deer/Cattle:

1. Mortality of newborn fawns (adult ticks at highest numbers in summer = same time fawns hide in pasture)

   • Death by exsanguination/anaemia

2. Hide damage (~10% wet blue hides with tick damage → 1/4 downgraded)

3. Velvet antler damage by adults (late November)

4. Reduced growth and production

5. Papulonodular lesions, variable pruritus and pain

6. Transmission of Theileriosis

   

Structure: 3 lifestages = Larvae, nymph, adult (only nymph and adult transmit Theileria)

• Larvae = 6 legs

• Nymph = 8 legs

• Adult = 8 legs

Location: Areas with thin coat and skin close to ground

• Cattle = Ventrum, udder and head

• Sheep = Non-fleeced areas of axilla, groin, face ad ears

• Deer = Ears and antlers

• Dogs/Cats = Ears, interdigital areas and under jaw

Distribution: Northern parts of North Island (unfed nymph best adapted to overwinter and require mild conditions to survive)

• Annual mean temp > 12˚C

  • July max > 12˚C and July min > 2˚C

• < 50 ground frosts/yr

Lifecycle: Three-host tick = Each stage of lifecycle (larvae, nymph and adult) feeds on separate host animal

1. Nymph climb onto host and engorge on blood (August - October)

2. Nymph drops to ground when full and moults to adult stage

3. Adult climbs onto another host and engorges on blood (November - January)

4. Adult drops to ground to lay eggs in sheltered and moist spot

   • ONLY females in NZ → Reproduce via parthogenesis

5. Larvae emerge from egg and climb onto host (February - March)

6. Larvae engorge on blood for ~5d

7. Larvae drop to ground and moult to nymph stage which overwinters unfed

Habitat: Dense grass, scrub, rushes, long grass = same habitat as fawn hiding places

Diagnosis: Easy to see adult ticks on PE

• Assess pastures with towel or “indicator animal” eg. sheep or light-coloured dog grazed through pasture

Control:

1. Pasture management = Reduce “tag” and dead matter which nymph live in over winter

2. Chemical

   1. Pour-on bayticol (1% flumethrin) = 21d protection with repeat treatment q3w during 3 waves of ticks

      • Begin before calving

   2. Ear tags impregnated with synthetic pyrethroids (some transfer from hinds to fawn)

3. Reduce paddock burden with sheep as “cleaners”

Lice

• 2 Types (+ genera examples)

• Lifecycle

• Seasonality

• Transmission

• Aim of treatment

Types:

1. Biting louse = Head wider than thorax with ventral mouthparts

   1. Bovicola spp.

   2. Trichodectes canis

   3. Felicola subrostratus

2. Sucking louse = Head narrower than thorax with anteriorly projecting mouthparts

   1. Haematopinus spp.

   2. Linognathus spp.

   3. Solenopotes spp.

Lifecycle: Can complete entire lifecycle on ONE host

1. Males and females mate

2. Nits = Operculate eggs cemented to hair shaft (easily seen with naked eye)

3. 1st nymph stage hatches after 1 - 3w

4. TWO more nymphal stages via gradual metamorphosis

Seasonality: Winter peak (thick coat with more stable environment and temperature)

Transmission: Direct contact

Treatment: Kill ALL lifestages ASAP during treatment (may require 2nd treatment if 1st treatment cannot penetrate eggs)

Sheep Lice

• 3 Agents

  • Prevalence

  • Location

  • Type of louse

• 3 Effects

• Diagnosis

• Treatment

Species:

Species	Prevalence	Location	Type
Bovicola ovis	Very common (#1 species)	Body louse	Biting louse
Linognathus pedalis	Uncommon	Feet and legs	Sucking louse
Linognathus ovillus	Rare	Head	Sucking louse

Effects:

1. Pruritus (movement of lice over skin)

2. Damage to fine wool breeds (eg. Merino)

   • Broken fibres, change in colour (increased yolk/lanolin)

3. Cockle = Small hard nodules on partly processed pelt (recurrent type I hypersensitivity to B. ovis)

Diagnosis: Assess if sheep have lice by looking for stringy pulls of wool hanging from the animal or off fencing where they have been scratching

Treatment:

1. Shearing along can remove up to 80% of lice

2. Eradication possible with modern insecticides (low biotic potential and ONLY found on host)

   • Treat BEFORE winter (difficult to coordinate with shearing) to prevent peak

Cattle Lice (Pediculosis)

• 2 Agents

  • Signalment

  • Seasonality

  • Type of louse

• Location

• 4 Effects

• Treatment

Species:

Species	Signalment	Seasonality	Type
Bovicola bovis	Beef cattle	August - September	Biting louse
Linognathus vituli	Dairy cattle	June - July	Sucking louse

Effects: Anaemia uncommon and seldom clinically apparent

1. No significant effects of growth rates

2. Welfare and aesthetic problem (pruritus, alopecia, poor hair coat)

3. Hide damage

4. Bulls kept in paddocks with electric fencing → Forced to rub on each other → Fighting

Location: Above withers

Treatment: No economic benefit

• Autumn (before numbers build in winter) q14 - 21d to kill newly hatched lice which were not killed within egg on 1st treatment

• ML common due to GI nematode control

Pig Lice

• Agent

• Effects

• Treatment

Species: Haematopinus suis = Sucking louse

• Largest domestic louse species

• Pig hairs are coarse and far apart

Effects: Irritation and anaemia proportional to numbers present

• Symptom of poor husbandry in backyard piggeries and lifestyle blocks

Treatment: Repeat treatment q10 - 14d (very hard to get drug to persist on sparsely haired pig skin)

Mites

• Lifecycle

• Main mite of livestock

  • Host

  • Prevalence

  • Location

  • Clinical effects

  • Diagnosis

• Treatment

Lifecycle: Entire lifecycle on animal with gradual metamorphosis

• Egg → Larvae (6 legs) → Nymph 1 - 3 (8 legs) → Adult (8 legs)

Agent: Chorioptes bovis → Chorioptic mange

• Host: Horse, cattle, sheep, goat

• Prevalence: 72%

• Location: Legs, tail, scrotum, udder

• Clinical Effects: Reduced fertility in rams (>1/3 of scrotum affected) with hypersensitivity reaction

  • Rare disease of cattle (housed ONLY in winter) → Pruritus, crusting and alopecia

  • Few mites required to cause disease due to allergic reaction

• Diagnosis: Scratch affected area with gloved hand and assess if ram nibbles with mouth

Treatment: Injectable ML (oral ineffective)

Flystrike

• Prevalence

• Seasonality

• Importance (3)

Prevalence: Common even with preventative methods (~1 - 2%/yr)

• Some farms ≤10%

Seasonality: Warm and wet conditions

• North Island = Oct - May (Dec - Mar #1)

• South Island = Nov - Apr

Importance:

1. Production cost

2. Welfare cost = Code of Welfare for Sheep and Cattle section 15

   • All reasonable steps must be taken to prevent, or identify and manage the risk of flystrike in sheep

     • Sheep cannot control flies due to wool → Rely on humans to protect them

   • Affected sheep must receive appropriate treatment at the earliest opportunity

3. Increased pressure from international markets and NZ public to reduce/rationalise use of ectoparasiticides BUT less tolerance for cases of flystrike

TWO types of Strike Flies (+ examples and appearances)

Agents: Family = Calliphoridae (Blowflies)

1. PRIMARY Strike Flies (1y) = Initiate strike through intact skin (OR act as 2y)

   1. Lucilia sericata = Greenbottles

   2. Lucilia cuprina = Australian blowfly

      • Can adapt to live almost exclusively on sheep (cannot compete with other flies for carrion)

   3. Calliphora stygia = Black body with fine brown hairs

2. SECONDARY Strike Flies (2y) = Require pre-existing wound

   1. Chrysomya rufifacies = Hairy maggot fly

      • Greenbottle with black bands

      • ONLY in North Island

   2. Other Calliphora spp. = Bluebottles

Lifecycle of Calliphoridae (Blowflies) → Flystrike

Generation interval: 7 - 10d in optimal conditions

1. Adult blowfly feeds on organic material and reproduce via sexual reproduction

2. Female lays eggs in shaded/moist areas

   • eg. Carrion, live animals, decaying vegetation

   • Eggs and larvae prone to desiccation

3. Eggs hatch in 1d and L1 larvae begin to feed on surrounding nutrition

4. → L2 which penetrates skin allowing wound to expand rapidly

5. → L3 fall to ground to pupate within the soil

6. Complete metamorphosis in puparium (3 - 4w)

   • OR overwintering as pre-puparium = Diapause

7. Adult emerge from puparium and feed on protein source

   • Sexually mature in 2d

Flystrike

• Pathogenesis

• 5 Areas commonly affected

• 6 Risk factors

Pathogenesis: Wool provides perfect microclimate for fly eggs and maggots

1. Risk factors = Dags, wounds and footrot → Olfactory trigger to attract flies

2. Maggots bite sheep causing inflammatory response resulting in leakage of fluid (electrolytes and protein) which attracts more flies

3. Fluid runs down sheep and causes lesions to spread

Areas:

1. Crutch/breech #1 (reliably contaminated with faeces ± urine in ewes) ~80% of flystrike

2. Dorsum

   • Fleece rot = Pseudomonas aeruginosa

     • Release proteolytic enzymes → Dermatitis → Localised serum ooze → Olfactory cue and nutrient source for L1 larvae)

   • Dermatophilus congolensis in rain/humid conditions → Dermatitis → Serous exudate and scab formation → Nutrient source for L1 (even when skin has healed)

3. Feet (footrot)

4. Pizzle (rams)

5. Head (fighting rams)

Risks:

1. Dags

2. Footrot

3. Wounds (eg. head-butting or shearing wounds)

4. Fleece length >4w → Moist and protected

5. Fleece conditions causing extra smell (eg. bacterial/fungal disease)

6. Genetic predisposition

Clinical signs of flystrike in sheep

• 8 Clinical signs

• 3 Clinical signs after treatment

Clinical Signs: Death due to dehydration or toxaemia

1. Brown staining of wool → Deranged and falling out

2. Irritation = Stamping feet, looking at self and quickly running forwards a few steps then stopping, nibbling at affected area

3. Maggots visible on close inspection of the area

4. Depression and shade-seeking

5. Reduced BCS (not eating)

6. Dehydration due to fluid, electrolyte and protein loss

7. ± Recumbency

8. Distinct flystrike smell

AFTER Treatment:

1. Sunburn of affected area (scarring)

2. Medium-term production loss (eg. severe effect on lamb GR)

3. Affected ewes non-pregnant that breeding season

8 Flystrike treatments

1. Remove affected wool (NOT at skin level as sunburn is a common sequelae)

2. Remove maggots by manual removal

3. Application of ectoparasiticides licensed to kill maggots (OPs)

4. Rehydration with access to high quality feed and water

5. Access to shade

6. NSAIDs for anti-inflammatory and analgesia

7. ± Antibiotics due to 2˚ bacterial infection → Bacteraemia (fever and depression)

8. Euthanasia if depressed or extensive lesions

List 3 ways to control for flystrike

1. Monitoring = Knowledge of risk periods via local knowledge, monitoring climatic conditions and fly activity through fly traps

2. Non-chemical control methods

3. Chemical control

   • Even with careful use of non-chemical control methods, it is very difficult to control flystrike in most areas of NZ without use of ectoparasiticides

     • Key is strategic and effective use

   • → Apply dip chemical ~4 weeks after shearing = Sufficient fleece to bind the chemical and retain it for longer BUT fleece still short enough that flystrike should not occur before the chemical is applied

8 Examples of non-chemical control method for flystrike

1. Ensure lamb tails are docked to correct length = Long enough to cover the vulva of ewe lambs and equivalent length in ram lambs

   • +ve: Reduce build up of faecal matter (dags) = Important risk factor for flystrike as smell attracts flies and the daggy area itself is humid and moist → Perfect maggot conditions

   • Docked too short →

     1. Exposure of the perineum to sunlight and sunburn

     2. Nerve damage and neuroma

   • Docked too long → Defeats the purpose of docking

2. Crutching and dagging to remove soiled wool

3. Shearing at strategic times = Early summer

   • Ensures 4 weeks of flystrike protection during high-risk period AND application of chemical at optimum time to an optimum fleece length

   • May NOT be feasible or desirable time depending on farm

     • Also issues with shearer availability during this busy period

4. Control footrot and rapidly treat other wounds

5. ID areas of farm with high challenge (warm, sheltered areas eg. bush margins, gullies and avoid grazing those areas during periods of high risk)

   • Areas of lower risk = Exposed and windy paddocks

6. Limit fly populations by disposing of dead carcasses ± use of large fly traps

7. Shedding sheep (eg. Wilshire, “easy care”) or hair sheep breeds → Reduce requirement for shearing and less prone to flystrike

8. Genetic selection for low dag score (linked to resistance and resilience to internal parasites)

2 Types of ectoparasiticide MoA

1. Target arthropod nervous system → Uncoordinated movement/paralysis and eventual death

2. Interfere with growth/moulting → Eggs cannot hatch and larvae cannot moult or pupate

   1. Interferes with growth hormones OR

   2. Interferes with chitin synthesis

6 Ectoparasiticides

• Advantages

• Disadvantages

Drug	Advantages	Disadvantages
Organophosphate (OP)	Cheap Kills maggots → Treat existing flystrike	Toxic Widespread resistance → Short period of protection (avoid for prevention) Unlikely to remain on market long-term
Insect growth regulators (IGR) Benzyl phenyl ureas (BPUs) = Diflubenzuron and triflumuron Triazine and pyrimidine derivatives = Cyromazine and dicyclanil	Not known to be toxic to vertebrates Wide range of options with potentially very long periods of protection Available as low volume/spray-on OR saturation/jetting products → Range of application methods Current chemical option of choice for flystrike control	Not effective against existing flystrike Some resistance to BPU chemicals → Shorter period of protection
Ivermectin	No recorded fly resistance Kills maggots → Used for treatment of existing flystrike	Only available in combination formulation
Synthetic pyrethroid (SP)	Cheap	Most are ineffective against flystrike Short period of protection Resistance
Spinosyn	No recorded fly resistance Kills maggots → Used for treatment of existing flystrike Nil meat WHP	Very short period of protection against fly (mainly use for lice control)
Neonicitinoid	Included in some combinations to provide treatment of existing flystrike	NOT useful for flystrike prevention on their own (occasionally used in combinations to kill maggots) Toxic to aquatic invertebrates and some vertebrates

5 Methods of Ectoparasiticide Application

• Advantages

• Disadvantages

Method	Advantages	Disadvantages
Plunge dip (rare in NZ)	Full saturation of whole sheep	Environmental impact = Large amounts of left-over dip material must be discarded AND run-off from fleece Require infrastructure or hire dipping contractor with mobile plunge dip Highly stressful for sheep Labour intensive and high exposure to dip chemical for staff Dip water becomes contamination → Strip active chemicals from some dips NOT suitable for wool > 8 weeks
Shower dip (infrequent in NZ)	Full saturation of whole sheep if performed correctly Quicker than plunge dipping and less labour intensive	Large volume of drug per sheep required for full saturation (4 - 7L) Environmental impact = Large amounts of left-over dip material must be discarded AND run-off from fleece Labour intensive and high exposure to dip chemical for staff Require infrastructure and must be maintained (otherwise reduced efficacy eg. blocked shower nozzles) Dip water recycled and contaminated with time → Strip active chemicals from some dips
Automated jetting races (#1 in NZ)	Lower volumes (1 - 2L) required → Less chemical use and run-off Only clean water and chemical applied (no recycling or contamination) Easy set up and fast to dip Targets at-risk areas of sheep (backline and breech)	Some do not apply sufficient volumes of drug (rate being pushed through race) → Reduce efficacy Difficult to apply adequate volume onto longer wool Aerosol droplets → Workers must take care Relatively expensive to purchase
Hand jet	Low volume applied to at-risk areas Clean water and chemical (no recycling or contamination) Achieve good saturation if done correctly Best method for ensuring saturation of longer fleece	Slow and hard work Exposure to chemicals for staff Must use correct applicator Unused dip wash must be disposed
Low volume pour-on/spray-on (Common (esp. lambs) around breech/crutch at docking)	Very low volumes of chemical (eg. 10 - 50mL) and no run-off No aerosol droplets → Less risk to human health Targets at-risk areas (backline and breech) No infrastructure/expensive equipment required	Slow application when correct Risk of poor application (eg. sheep jumping on each other) Dip formulations more expensive on per head basis

9 Factors which influence protection periods of ectoparasiticdes

• Label claim for protection periods are NOT always accurate as influenced by many factors

  1. Application method

  2. Correct mixing/concentration and appropriate dosage applied for size of sheep and wool length

  3. Correct applicator with label-recommended application pattern

  4. Stock class

  5. Wool type and length

  6. Stock cleanliness

  7. Wet fleece at time of application

  8. Rainfall after treatment

  9. Resistance to the chemical → Reduced protection periods

EXAMPLE: Hamilton early February with 1500 ewes and 1300 lambs (plus cattle)

• 12 ewes and 50 lambs with active flystrike and several of each age group dead

• Sheep were dipped with products purchased from the vet clinic

• Lambs received spray around crutch after docking in late-October with Clik Extra Spray on (dicyclanil = IGR))

  • Protection for 14 - 26 weeks

  • Applied at dose rate as per label instruction and lambs were dagged and weaned in mid-December but yet to be shorn

• Ewes shorn in late December and dipped a week later in early January with Zenith (diflubenzuron = IGR) with Electrodip (automatic jetting race)

  • Protection for ≤12 weeks

Questions:

1. Good aspects of flystrike prevention

2. Bad aspects of flystrike prevention

3. Reasons for flystrike

4. Describe an appropriate flystrike control programme

Good Aspects:

1. Lambs dagged in mid-December → Reduce risk of dags accumulating which is a risk for flystrike

2. Lambs sprayed around crutch at docking (open wound)

3. Ewes shorn in risk period

4. Appropriate dip method for ewes

Bad Aspects:

1. Lambs not yet shorn in February and did not receive a dip → Longer fleece and high flystrike risk

2. Dagged shortly after drug application to crutch → Removal of product

3. Interval between shearing and treatment of ewes with ectoparasiticides is too short (ideal ~4 weeks) to ensure there is sufficient fleece growth for drug to adhere to the wool for longer duration of action

4. Lack of monitoring (ideally q3d)

Reasons for Flystrike:

1. Waning drug protection during highest risk period of flystrike

2. Drug resistance (esp. Zenith)

3. Protection UP TO…

4. Extremely high risk farm: Early February in Hamilton = Warm and humid

5. Lack of monitoring

6. Lack of lamb flystrike prevention

Appropriate Flystrike Control Programme:

1. Spray lamb crutch at docking with shorter-acting drench (will dagging in a few months time)

2. Pre-wean crutch or dag for ewes

3. Weaning → Dagging (consider drafting out and dagging dirty sheep only)

4. Ewe shearing during risk period and dip 4 - 6 weeks later

5. Dip ± shear lambs early January (after weaning to prevent stress)

6. Rotation of chemicals to avoid resistance developing?

7. Monitor q3d