Farm 6 - Parasites Flashcards
What is an endoparasiticide?
Internal antiparasitics - kill parasites living inside the animal include anthelmintics (agents lethal to worms) and antiprotozoal (agents lethal or suppressive to protozoa)
What are ectoparasiticides?
External antiparasitics - kill parasites living on the outside of an animal, including fleas, ticks, mites, and lice
What are endectocides?
Combine the activity against internal and external parasites
What are group 1 anthelmintics in ruminants?
benzimidazoles, white drench, lots of resistance , still useful for nematodirus
What are group 2 anthelmintics in ruminants?
levamisole, yellow drench, increasing resistance
What are group 3 anthelmintics in ruminants?
the macrocyclic lactones (the avermectins and milbemycins), clear drench
What are group 4 anthelmintics in ruminants?
monepental (trade name Zolvix), orange drench, no resistance yet
What are group 5 anthelmintics in ruminants?
Derquantel, purple drench, dual active product 50% ML abermectic 50% spiroindol
Is there any scientific proof that drug rotation delays or enhances the development of resistance?
No, there is no evidence that drug rotation stops drug resistance.
What anthelmintics are used in horses?
1.Benzimidazoles: (eg. fenbendazole)
2. Tetrahydropyrimidines (eg. pyrantel embonate)
3. Macrocyclic lactones (eg. Iver/aver-mectins)
And for tapeworm ONLY 4. Praziquantel
What anthelmintics are used in cats and dogs?
- Benzimidazoles: (eg. fenbendazole)
- Tetrahydropyrimidines (eg. pyrantel embonate)
- Macrocyclic lactones (eg. Iver/aver-mectins)
And for tapeworm ONLY 4. Praziquantel, Epsiprantel, Dichlorophen
What is the mode of action of benzimidazoles?
Bind to b-tubulin – inhibition of polymerization, causing abnormal microtubule formation and disrupts intracellular homeostasis
What is the mechanism of resistance to benzimidazoles?
A single nucleotide (SNP) change changes the target protein so changes the affinity of the drug to the target
What is the mechanism of action for imidazothiazoles (levimidazole)?
Affect NICOTINIC acetylcholine (nAch) receptors agonists
By mimicking Ach action they change permeability of the post-synaptic membrane, leading to depolarisation and spastic paralysis of the worms
What other effects do imidazothiazoles have?
Immuno-stimulant in some species - was used as a growth promotor
Toxicity in some dogs
What are tetrahydropyrimidines (pyrantel and oxantel) active against?
Active against larval & adult forms of nematodes, but are not active against migrating/arrested larvae, and no action on cestode
How are tetrahydropyrimidines (pyrantel and oxantel) usually formulated?
Usually formulated as tartrate or embonate salts (aka pamoate salt).
Pyrantel tartrate is more water soluble and better absorbed from the GI tract.
The embonate (pamoate) salt is less water soluble and more poorly absorbed, and thus less toxic to the host, and is considered safe to administer to young, sick or pregnant animals
What are macrocytic lactones?
Endectocides
Made up of 2 groups:
- Avermectins
- Milbemycins
What are macrocytic lactones active against?
Arthropods and nematodes
Cestodes, trematodes and adult heart worms are insensitive
Moxidectin effective against strongyles in encysted larval stage
What is the mechanism of action of macrocytic lactones?
Causes permanent opening of Cl channels leading to hyperpolarisation and paralysis of the pharynx, somatic muscle and uterus
How does resistance form against macrocytic lactones?
P-glycoprotein transmembrane transport pump pumps foreign substances out of cells into the GI lumen
(this is also how vertebrates are not affected by this drug)
What is the mechanism of action of mopepental?
Targets MPTL-1 receptors, a unique kind of Ach receptor, so it can co-ordinate its movement.
What is the mechanism of action of spiroindoles?
Ach antagonist causing flaccid paralysis and expulsion of parasites.
What is the mechanism of action of emodepside (a cyclo-octadepsipeptides)?
Acts on a specific class of transmembrane G-protein coupled receptors (GPCR) causing flaccid paralysis of pharynx
Which anthelmintic targets cestodes?
Praziquantel
What is the mechanism of action of praziquantel?
Binds to b-subunit of voltage gated calcium channels leading to spastic and tetanic muscle contractions and vacuolation of the tegument.
Some helminths do not have this subunit – Fasciola spp are not susceptible
Why do we control parasites?
To minimize the risk of parasitic disease
To control parasite egg shedding
To maintain efficacious drugs and avoid further development of resistance
What should be considered before using anthelmintics?
Talk to the client (want to know the history and clinical signs)
Choice of anthelmintic (spectrum, effectiveness, thereputic index, ease of administration, price, residues drug interactions)
Side effects
Which anthelmintics should not be used together?
Pyrantel with piperazine – opposite modes of actions
Which anthelmintic can cause severe reactions in foals?
Moxidectin
What are the toxicity signs of imidazothiazoles?
Salivation, respiratory distress, seizures, vomiting and anaphylaxis, and are related to stimulation of mammalian nicotinic cholinergic receptors
What are the toxicity signs of praziquantel?
Anorexia, vomiting, salivation, diarrhoea, and lethargy in less than 5% of animals
What are the toxicity signs of dichlorophen?
Vomiting, salivation and diarrhoea may be seen after dichlorophen administration.
What are the toxicity signs of benzimidazoles?
Albendazole: Bone marrow suppression has been reported following treatment of dogs and cats and has teratogenic effects if given during pregnancy
Mebendazole and oxibendazole: have been associated with an idiosyncratic hepatotoxic reaction in some dogs
Which breed of dog should ivermectin not be given to?
Collies as they are deficient in P-glycoprotein
How can you deal with resistance to anthelmintics in horses?
FWEC testing
Avoid overuse of one particular active ingredient
Rotate the active ingredient used for each grazing season
Target specific worms with an effective product at the correct time of year
Weigh or weigh tape before dosing
Use pasture management techniques
What pasture management techniques help to reduce worm burden?
Remove dropping regularly (daily – twice a week)
Don’t spread horse manure on pasture
Don’t overstock pastures (1-1.5 acres per horse)
Graze similar ages horses together
Sub-divide grazing areas and rotate
Harrow during dry conditions to expose soil borne larvae
Graze paddocks with other livestock
Worm horses that graze together at the same time with the same product if the FWEC indicates (>200 eggs/g)
What should you advise horse owners about worming?
Record the horses worming activity i.e. FWEC date and result and products and dose used
Discuss worming protocol
Ensure they have an effective fly repellent
Check skin and coat regularly for signs of disease
Do not give moxidectin to foals <6.5 months
Don’t rotate blindly between wormers
Don’t treat at frequent fixed intervals all year round
What can cause lack of efficacy of anthelmintics?
Resistance
Interactions with another drug or health condition in the patient that diminish the drug efficacy
Patient immunodeficiency
Failure to diagnose and treat mixed infections of parasites or other infectious agents
Re-infection/infestation due to contaminated environment
Failure to deliver the correct dosage/form of product, such as compliance failures, usage of out of date products
Unrealistic objective
What are the 3 most important neurotransmitters in nematodes?
ACh – excitatory
GABA – inhibitory
Glutamate – inhibitory
What are some novel strategies for new anthelmintics?
Ovijection (Ovijector ganglion contains many different types of nicotinic Ach receptors)
New neurotransmitters
New ion channels / transporters
Enzymes unique to parasites
Absence of de novo synthesis of purines in protozoa
Trypanosomes depend upon glycolysis of host glucose
Inhibition of protein or DNA synthesis
What are the most common farm animal parasites?
(in order of clinical importance)
- GI Nematodes (Trichostronyles, Nematodirus battus, Haemonchus, Teladorsagia, Ostertagia, Cooperia
- Trematodes (Fasciola hepatica and Oesophagostomum)
- Coccidia (sheep and cattle)
- Lungworms (Cattle and sheep)
- Ectoparasites (Lice and Mites)
- Tapeworms (sheep)
What parasites can sheep and cattle develop immunity to?
Trichostrongyles, Nematodirus battus, Teladorsagia, Ostertagia, Cooperia, Coccidia, Lungworm – requires trickle exposure over time
They will NEVER develop immunity to Fasciola hepatica and Haemonchus contortus
What is trickle challenge?
A low infectious challenge over time which allows immunity to develop without clinical signs of disease
Avoiding all challenge will mean the animals are naïve and susceptible to infection
When in the year is nematodirus most commonly seen?
April-May
Transmitted from lamb crop to the next lamb crop the following year
Occasional cases seen in autumn
What do nematodirus eggs require to hatch?
Eggs passed the previous year need a period of cold over winter to prime them and then they hatch all together over a short period of time in the spring when the weather gets warmer i.e. infecting lambs when they start to graze
Warmer spring = earlier peak
How do nematodirus affect the host?
Large numbers of immature larvae attack the small intestinal wall causing dehydration and rapid death
Larvae attack = NO EGGS FOUND on FWEC
What anthelmintics are nematodirus susceptible to?
Almost all
BZ commonly used although some resistance now being seen
What are the clinical signs of nematodirus?
Dirty back ends, weight loss, ‘open fleece’ dehydration, sudden death
What is unique about the development of L1-L3 of nematodirus?
It occurs inside the egg – eggs are very tough and viable for up to 2 years on pasture
When in the year is coccidiosis most commonly seen?
January – May
When are lambs most at risk of coccidiosis?
Intensive systems (high levels of contamination in buildings and on dirty pasture around creep feeders and water troughs)
3-12 weeks old
Lambs born in the second half of the lambing season – higher challenge leading to infection rather than immunity
Why is coccidiosis rare in older lambs?
Develop immunity after exposure to low numbers of oocysts
What are the clinical signs of coccidiosis?
Scouring, diarrhoea, retarded growth due to damaged villi
Why is a high oocyst count not proof of coccidiosis?
Only 2 of the 11 Eimeria species in sheep are pathogenic.
When in the year do you see coccidiosis in cattle?
All year round
When in the year is it most likely to see teladorsagia and trichostrongylus?
June – January
When does the pasture become infected with teladorsagia and trichostrongylus?
Infectious larvae can only hatch when conditions are warm and wet enough so ewes lambing in March-May contaminate the pasture with eggs which hatch in time to infect their lambs when they start grazing.
What are the clinical signs of teladorsagia and trichostrongylus?
Disease can be clinical or subclinical depending in infectious dose
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 e.g. mastitis
Why are lambs most commonly affected with teladorsagia and trichostrongylus?
Adults become immune with age and exposure
What is the most important factor in worm control with teladorsagia and trichostrongylus?
Lambing period – determines if the susceptible lamb crop will overlap with the pathogenic level of infectious larvae.
Earlier lambing means ewes are generally indoors so when lambs are moved outside there is a lower level of challenge.
When do ewes shed teladorsagia and trichostrongylus?
In spring the hypobiosis larvae are activated and shed by ewes that are stressed by lambing.
What happens in periparturient rise?
Ewes under nutritional stress around lambing lose some of the immunity they have acquired to the parasite allowing hypobiosed early L4 larvae to develop to adults and also new infections to become patent.
Ewes under more stress (e.g. triplets) will lose more immunity and contribute more to pasture contamination
As ewes pass peak lactation and the nutritional stress declines they recover their immunity and kill off the parasites so their FEC falls
Why is periparturient rise important?
Causes pasture contamination which will lead to the lambs becoming infected.
What causes parasitic gastroenteritis (PGE) in cattle and sheep?
Ostertagiosis & Cooperiosis in cattle and Strongylosis & Haemonchosis in sheep
When in the year is type 1 parasitic gastroenteritis (PGE) most common?
August – November
What is the cause of type 1 PGE?
Wet summer cause eggs to hatch and infect stock early causing disease in the same season.
What are the clinical signs of type 1 PGE?
scour, weight loss, low DLWG, poor feed conversion efficiency
When in the year is type 2 parasitic gastroenteritis (PGE) most common?
February – May
What is the cause of type 2 PGE?
Rare compared to type 1
Dry summers cause eggs to remain unhatched until autumn wet conditions
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
What are the clinical signs of type 2 PGE?
severe disease, dehydration and death (Ostertagia) and anaemia (Haemonchus)
Which species does Haemonchus contortus affect in the UK?
Sheep
What are the clinical signs of Haemonchus contortus?
Anaemia, weakness, weight loss and sub-mandibular oedema in chronic cases.
Fertility, fecundity, milk yield may also be affected
Do sheep build immunity to haemonchus contortus?
No
How can haemonchus contortus be treated?
Closantel, BZ, LV and ML
When in the year are peracute, acute and subacute infections of fasciola hepatica seen?
October - January
When in the year are chronic infections of fasciola hepatica seen?
January – June
What determines the severity of infection with Fasciola hepatica?
Dose – higher infectious dose leads to more sever disease
What are the clinical signs of Fasciola hepatica?
PerAcute / Acute – sudden death – diagnosis by post mortem exam (PME)
Sub-acute - rapid deterioration, dull, depressed, sometimes anaemia, dead – diagnosis by serology/biochem and PME
Chronic – weight loss, anaemia, poor productivity, sometimes submandibular oedema only die after a long slow decline – diagnosis by FEC, coproantigen ELISA
What is the life cycle of Fasciola hepatica?
Infected sheep drop fluke eggs onto pasture which then infect mud snails
The parasite develops in the snail and emerges to contaminate the grazing pasture for the next sheep
Once a sheep has ingested the parasite it migrates from the gut to the liver and completes its development. Migration through the liver destroys liver tissue due to the immune reaction to foreign protein. The more parasites the more damage and the worse the clinical signs
In the bile ducts the adults suck blood and starts producing eggs that are passed in the faeces.
What drugs can be used to treat liver fluke?
Oxyclozanide Albendazole Clorsulon (cattle only) Nitroxynil Closantel Triclabendazole
When are oxyclozanide, albendazole and clorsulon most effective?
50-70% 10-12 weeks after ingestion
80-99% 12-14 weeks after ingestion
When are nitroxinil and closantel most effective?
50-90% 7-10 weeks after ingestion
91-99% 10-14 weeks after ingestion
When is triclaendazole most effective?
90-99% 2-4 weeks after infection
99-100% 4-14 weeks after infection
Triclaendazole is the only product active against the immature fluke so should be preserved.
When in the year are lungworm infections most likely to be seen?
July – October
But can cause disease at any time in the grazing season
What are the clinical signs of lungworm?
Couching after exercise, death in naïve cattle
How can we prevent lungworm infection?
Vaccination Anthelmintic bolus (pulse release or continued release
What are the aims when treating parasitic infection?
Good productivity / profitability
Good immunity when possible rather than treatment
Sustainability – continued efficacy of anthelmintics
How is parasitic infection diagnosed?
Clinical signs Related outcomes e.g. production loss Prediction based on climate models Faecal egg count Serology
What samples are need for serology of fluke?
Blood and milk
What samples are needed for serology of roundworms?
Milk
What should be considered when using serology to test for parasitic infection?
Indicates exposure rather than infection
Of more use in younger animals
With which parasites do you get pre patent disease?
Nematodirus, acute and subacute liver fluke and type 2 PGE
How is prepatent parasitic disease diagnosed?
Can’t rely on finding eggs or antibodies!
Nonspecific biochemical tests such as albumin, fibrinogen, GLDH and plasminogen are supportive evidence
PME
What is the traditional approach to timing worm treatments?
Treating once you get visible disease
How should we time worming treatments?
Use faecal egg counts to predict the point at which treatment is required before there are any visible signs.
What are the faecal egg count thresholds for poor growth and feed conversion efficiency, obvious clinical disease, and death?
Poor growth and feed conversion efficiency >300/350epg
Obvious clinical disease >500 epg
Deaths >900 epg
Which parasite would you suspect if lambs had a very high FEC but are not scouring?
H.controtus – because it is a very fecund worm and will produce many more eggs per adult
How much daily live weight gain (DLWG) would you expect per lamb?
> 300 g/d pre-weaning
200-300 g/d post weaning until the winter.
150 g/d over autumn/winter
How can DLWG be used to advise anthelmintic treatment?
Work out which lambs are underperforming and treat
How can pooled FEC be used to advise anthelmintic treatment?
Weekly/fortnightly FECs are used to track the rise in FEC and predict when treatment is required.
What should be considered when prescribing anthelmintics to a farm?
Efficacy – e.g. immature fluke and BZ+LV resistant nematodes Withdrawal period Administration route Owner compliance Resistance and long term effects
How can we limit anthelmintic resistance?
Target treatments to animals that need it – limiting the number of selection events
Maintain an in-refugia population (untreated population) to dilute the eggs produced by AR worms
Quarantine treatment for purchased stock
Dose for the heaviest in the group to avoid underdosing
Use a narrow spectrum product
Use non-chemical means of control
How can anthelmintic treatment be tested for?
FECRT on lambs with a high starting FEC (>500epg)
Individual samples
Drench accurately the three groups each with a different group
Resample at 7days (LV) and 10-14 days (BZ,ML)
Less than 95% reduction in FEC = resistance
Less than 50% reduction in FEC = obvious drench failure
What are the main drivers of anthelmintic resistance?
Buying in resistant worms.
Under dosing individuals.
Over treating the population.
Allowing resistant worms the chance to dominate.
What non-chemical methods can be used to control the worm population?
Rotational grazing
Use different grazing crops that change the grazing behaviour e.g. kale, stubble turnips, forage, rape
Enhance ability to fight infection – good nutrition, use crops with anthelmintic control properties (chicory and sainfoin), reduce reliance on grazed dry matter i.e. provide creep
What do we need to know before making a parasite treatment plan?
Susceptibility of the animals on the farm
Parasite status of farm (species present, resistance)
Risk assessment of the pasture
What methods of monitoring parasites are available?
FEC
Larval count (lungworm)
Antibody and coproantigen ELISA
How do you make a parasite control plan for a flock?
History of flock management
Identify disease threats and the options for monitoring and control of those threats
Rank the parasites in order of priority and chronology
