Farm parasitology Flashcards
What is Dictyocaulus viviparus (Dictyocauliosis)? Morphology of adults? What does it cause? Which cattle are affected? When are outbreaks seen in cattle?
Lungworm Adult morphology: - 4-8cm long - Slender, white - Male has reduced bursa - Found in trachea and bronchi Parasitic bronchitis, 'husk' Affected cattle: - All cattle at pasture at risk - Especially first grazing season/previously unexposed cattle - Beef sucklers lower risk Disease usually in August-September Need very few worms to cause disease - 800-1000
How long does cattle lungworm immunity last?
Develops with gradual pasture larval challenge
Immunity to L3: 4 months
Immunity to adults: 2 years
May only have partial immunity - disease at subsequent grazing (reinfection syndrome)
So short lived immunity - needs continual boosting
Clinical signs of cattle lungworm?
Mild: intermittent cough, particularly when exercised
Moderate: frequent cough even at rest, laboured breathing, squeaks and crackles on auscultation
Severe: severe tachypnoea, dyspnoea, air hunger position, mouth breathing, deep harsh cough, salivation, anorexia
Lung pathology caused by lungworm in cattle?
Emphysema - no gas exchange can occur in these areas
Atelectasis?
Diagnostic methods for cattle lungworm? How many to sample? Who to sample?
Baermann test (L1 in faeces) - positive from 25d post infection Serum or milk ELISA for Abs - positive from 28d post infection, bulk milk only positive if 30% herd infected (false negatives) Only sample animals in herd for at least 4 weeks
Treatment and control for cattle lungworm?
Mild/moderate - dose and move, if unable to move dose with product with residual activity (e.g. MLs)
Severe - dose and observe closely (house), NSAIDs, hydrate, antibiotics?
Eprinomectin - only treatment with zero milk withdrawal
House most severely affected calves
Vaccination:
- = huskvac
- = 1000 live attenuated larvae
- calves need to be at least 8 weeks old
- booster 4 weeks apart
- turnout 2 weeks after 2nd dose
- mostly non patent infection
- immunity, no disease (mild cough might be heard)
- turnout on contaminated pasture to maintain exposure and immunity (requires natural boosting to maintain immunity)
Epidemiology of cattle lungworm?
Prolific egg layers
Time between appearance of L1 in faeces and L3 on pasture is 1 week, almost independent of weather
Development of gut worm larvae takes weeks and is more dependent on local temperature/rainfall
Survival on pasture is short, ‘clean’ again after 6 weeks
Gut worm larvae survive months
Most important source of infection are carriers
Gut worm larvae are already present on pasture at turnout
L3 overwinter on pasture
L1 shed by carrier animals
When is clinical disease from lungworm seen in adult cattle?
In a group if they have failed to acquire immunity through natural challenge in earlier years
- infection of non immune cows - introduction of carriers to naive herd
- reintroduction - infection of cows which were immune but were not challenged for 2 years
- reinfection syndrome - high level of infection of cows (with intact immunity to adult worms) when the protection against incoming larvae has waned (5-6 months housing)
Disease is occasionally seen where an individual adult is penned in a heavily contaminated calf paddock
(On farms where disease is endemic only calves in first grazing season are clinically affected as older animals have acquired immunity)
How can lungworm spread between farms?
Pilobolus fungus: L3 moves onto fruiting body of fungus in faecal pat and gets catapulted when fungus spore explodes
Purchase of carriers
Slurry
Deer
Which are the main worms which cause parasitic gastroenteritis in cows? Where found in the cow?
Ostertagia ostertagi - develops in gastric glands of abomasum
Cooperia oncophora - SI
Clincal signs of PGE in cows?
Calves - first grazing season
Loss of appetite (accounts for 60-70% of weight loss)
Scouring
Poor condition
Epidemiology of PGE in cows?
Larvae overwinter on pasture
Energy stores used up and most die in spring
Larvae picked up in spring
Start shedding eggs
Lots produced August
PGE seen Aug-October
Mild winter - more active so use up energy store so more die by spring
Cold winter - larvae don’t use energy, protected from desiccation by frost/snow, more lavage on pasture in spring
Dry summer followed by rain - helps dispersal, see lots of PGE in autumn
Who is affected by PGE in cows?
Dairy calves in first grazing season
Autumn born beef calves in second grazing season
Diagnostics for PGE in cows?
FEC
Plasma pepsinogen
Worm Abs
Performance monitoring
Fasciola hepatica: Life cycle? Features? Intermediate host? Definitive hosts? When are animals at risk?
Definitive hosts = ruminants, camelids, hares, deer, horses, humans
Intermediate host = Amphibious mud snails (mainly Galba truncatula)
Typical trematode:
- Indirect life cycle
- Dorso-ventrally flattened
- Hermaphrodite
- No body cavity
Autumn - risk of acute fluke
Winter-Spring - risk of chronic fluke
Spring-Summer - build up of snails and fluke numbers on pasture over summer
Diagnosis for liver fluke?
Clinical signs, farm history
FEC: low se, high sp, laborious, only detects patent infection (eggs large and yellow)
Ab detection ELISA: milk or bulk tank milk or serum, detects exposure (not necessarily current infection)
Copro-antigen ELISA: no better than FEC
PM/slaughter house feedback
Controlling liver fluke? Problems?
Drug prophylaxis - select according to stage of fluke in animal, clinical need (monitor bulk milk tank tests, FEC, abattoir returns), milk withdrawal
Disease forecasting
Grazing management:
- identify risky pastures
Elimination of snail habitat
Develop annual fluke plan - e.g. avoid flukey pasture in Autumn
Quarantine bought in - test and treat
Drugs that kill worms tend to not kill fluke
Fluke drugs don’t have residual activity
Most flukicides don’t kill all stages of fluke
Flukicides?
Triclabendazole - only one effective for immature fluke (works on all stages 2w+) so use in Autumn but resistance problems
Treat with adulticide at housing to prevent egg shedding:
Closantel (6w+)
Clorsulon (adults)
Nitroxynil (adults)
Albendazole (adults)
Oxyclozanide (adults)
Rumen fluke: Species name? Where found? What causes disease? Appearance of eggs? Clinical signs? Treatment?
Paramphistomes: Calicophoron daubneyi Adults well tolerated on rumen surface Disease invariably associated with large numbers of immatures in intestines Intermediate host = Galba truncatula Eggs similar to F hepatica but grey/green Clinical signs: - Anorexia - Non responsive diarrhoea - Fatal cases reported Treat under cascade with oxyclozanide
Clinical signs of Coccidia in cattle? slides weren’t up - find
Anorexia
Diarrhoea (bloody/watery)
Dehydration
Poor weight gain
Louse control in cattle?
Pour on MLs - Ivermectin, Moxidectin, Doramectin
Synthetic pyrethroids - Deltamethrin, Permethrin (for heavy infestations, give second treatment 2-3 weeks later to kill young lice from eggs)
Chewing and sucking lice of cattle?
Chewing - Bovicola bovis
Sucking - Linognathus vital, Haematopinus eurysternus, Solenoptes capillatus
Mite control in cattle?
MLs - Ivermectin, Moxidectin, Doramectin
What causes PGE in sheep?
Major pathogenic species:
- Teladorsagia circumcincta
- Trichostrongylus spp
- Cooperia spp
Others:
- Nematodirus battus
- Haemonchus cortortus
Teladorsagia circumcincta: where found in sheep? what does it cause? morphology of adults? Life cycle? Egg morphology? PPP?
Adults in abomasum Parasitic gastritis (doesn't involve SI) Adult morphology: - 1cm length - slender, pinky-brown - fine cervical papillae - males have a bursa and spicules Life cycle: - typical trichostrongyle life cycle - direct (no intermediate host) - free living stages on pasture - parasitic stages in host - adults in abomasum -> mate, females produce eggs -> eggs develop in faecal pat -> L1 in egg -> L1 hatches -> feeds on bacteria in faecal pat -> grows and moults to L2 -> L2 moults to L3 -> L3 ensheathed -> L3 released from faecal pat by rain splash - L3 = infective stage on grass - L3 ingested -> L3 swallowed and reaches abomasum -> burrows into gastric glands -> develops to L4 and L5 -> L5 emerges into lumen of abomasum -> matures to adult - leaves swellings/nodules on surface of abomasum when L5 leaving gastric glands Eggs: (typical trichostrongyle eggs) - barrel shaped - undifferentiated - contain undeveloped morula - 90um in length PPP = 3 weeks
What is a pre-patent period?
Time taken from the time of infection (ingesting L3) to the detection of eggs in the faeces
(patent infection = can be detected)
Pathogenesis of Teladorsagia/Ostertagia/PGE in cattle and sheep?
Disease associated with large numbers of developing larvae (L4 and L5) - 40,000+
Damage caused by developing larvae in gastric glands and emerging L5
-> Parietal cells replaced by undifferentiated epithelial cells
-> Loss of acid production
-> Increase in abomasal pH
-> Loss of bacteriostatic effect
-> No conversion of pepsinogen to pepsin
-> increased permeability of mucosa
What are the functions of the gastric glands in the abomasum?
Contain acid producing parietal cells:
- maintains acid pH
- bacteriostatic
- converts pepsinogen to pepsin
Sub-clinical and clinical signs of PGE in sheep and cattle?
Sub-clinical: - poor weight gain - reduced appetite - reduced feed intake - loss of plasma proteins into GIT Clinical: - profuse watery diarrhoea - weight loss - inappetance - dehydration - death
Which sheep are affected by PGE and when? Disease types?
First season grazing lambs
Type I disease:
- mid summer onwards
Type II disease:
- accumulation of L4 larvae in mucosa due to hypobiosis over winter
- trigger in late winter/early spring
- simultaneous resumption of development of hypobiosed larvae (L4 ->L5)
- can have thousands of L5 emerging at same time, causing severe disease
- yearling animals
- late winter
Define hypobiosis
Hypobiosis is the arrested development of larvae within the host, in response to a trigger received by the free living L3
Trigger – drop in ambient temperature in the autumn
Stimulates L3 to hypobiose when ingested
Trichostrongylus axei: morphology of adults? Where found? What does it cause? Life cycle? Pathogenesis?
Morphology of adults: - small (0.5cm) - diagnostic feature = excretory notch Adults in abomasum Contributes to PGE Black scour (leakage of blood causes black diarrhoea) Life cycle: - similar to T circumcincta - hypobiosis - L3 overwinter - next generation of L3 develop on pasture over the summer (takes longer than T circumcincta so disease just associated with T axei seen later, usually autumn) Pathogenesis: - L4 and L5 develop deep in mucosa - sub-epithelial tunnels - villous atrophy - haemorrhage - oedema (leakage of plasma proteins) - diarrhoea Signs: - black scour - weight loss/poor weight gain - poor skeletal growth - summer if mild winter, severe disease in winter/spring
Cooperia: What does it cause? Morphology of adults? Pathogenesis?
Component of PGE
Less susceptible to anthelmintics than other trichostrongyle nematodes (dose defining species)
Adult morphology:
- ‘watch spring’ worm (usually find single worms curled up)
- cephalic vesicle
- male has short, stumpy spicules and bursa
Pathogenesis:
- not very pathogenic
- can affect weight gain
- heavy infections lead to catarrhal enteritis, villus atrophy, oedema of intestinal mucosa
Which worms can be found in the abomasum of sheep and cattle?
Haemonchis contorts Ostertagia ostertagi (cattle)/Teladorsagia circumcincta (sheep) Trichostrongylus axei (tiny)
Which worms can be found in the small intestine of sheep and cattle?
Nematodirus spp
Trichostrongylus spp
Cooperia spp
Which worms can be found in the large intestine of sheep and cattle?
Chaberta spp - large buccal cavity
Oesophagostomum spp - leaf crowns and cervical vesicle, causes nodules in LI wall
Trichuris (whipworm) - not usually pathogenic, very thick tail end, thin head end
What conditions does Nematodirus battus like? Adult morphology? Egg morphology? Life cycle? PPP?
Cold countries, long winters Adult morphology: - 2cm long - often found in groups like tangled cotton wool - cephalic vesicle (male and female) - males have bursa and long thin spicules - females have large eggs within uterus Eggs: - large: 150um Life cycle: - unembryonated eggs shed in faeces - L1-L2-L3 develops in egg - L3 hatches - L3 is infective stage - L3 ingested - L3-L4 in lumen of SI - L4 burrows into mucosa of SI - L4-L5 - L5 emerges and adults mature is SI PPP = 15 days
Pathology caused by Nematodirus battus?
Developing L5 destroy the mucosa Catarrhal enteritis Villous atrophy Fluid and nutrient absorption disrupted 2000 worms can cause clinical disease (fewer worms needed to cause disease)
Clinical signs of Nematodirus battus in sheep? What WEC counts as heavy infestation?
Sudden explosive outbreaks of acute, watery diarrhoea
Inappetence, dehydration (thirsty), abdominal pain, weight loss
Disease in lambs around 4-12 weeks old
Disease often starts in PPP
Mean WEC > 500epg = heavy infestation
Epidemiology of Nematodirus battus?
L3 develops in egg over summer
Overwinters as lariated egg
Requires specific hatching requirements:
- exposure to prolonged period of chill
- exposure to mean day/night temperature of 10C
Emergence of L3 en masse in spring
For disease to occur:
- hatching must co-incide with presence of susceptible lambs
- old enough to graze
- before age immunity develops
May-June in 4-12wo lambs
Strong acquired immunity so ewes unaffected
Lamb-lamb cycle
But not necessarily disease every year (e.g. if eggs don’t hatch one year, might next year if more suitable conditions)
Also now getting outbreaks in Autumn - due to eggs passed that summer, hatching without the need for chilling and warming
Diagnosis of Nematodirus battus in lambs?
Season - May
Grazing history
Age of lambs - 4-12wo
Clinical signs
Control of Nemaodirus battus in sheep?
Grazing management
Prophylactic treatment - April to June
N battus not susceptible to injectable MLs (e.g. Moxidectin)
Disease forecasting
Haemonchus contortus: Where found? Adult morphology? Resistance? Life cycle? PPP?
Tropics and subtropics Abomasum of sheep, goats, cattle Adult morphology: - barbers pole worm (female: white ovaries wrapped around gut) - 3cm (females larger than males) - cervical papillae - male has bursa with 3 lobes - asymmetrical dorsal lobe Resistance to anthelmintics develops rapidly in this species Life cycle: - typical trichostrongyle - larvae develop in mucosa - adults are voracious blood feeders - hypobiosis major feature PPP = 3 weeks
Pathogenesis of Haemonchus contortus? Clinical signs?
Adults = pathogenic stage Adults feed on blood Erosion of abomasal wall Severe haemorrhagic gastritis Clinical signs: - severe anaemia (pale mm) - oedema (lower jaw in sheep, due to plasma protein loss) - weight loss
Epidimiology and diagnosis of Haemonchus contortus?
L3 don’t survive winter in UK
Ewe is main source of pasture contaminationn
Outbreaks of disease in late summer
Diagnosis:
- clinical signs (anaemia, not diarrhoea) - famancha chart
- season
- FEC (very prolific egg layer, eggs same as Teladorsagia etc)
When is PGE of lambs usually seen?
Late summer (August-September)
What affects the severity of disease of PGE in lambs?
Concurrent infection
Nutritional status of sheep
Age
Development of immune response (adults acquire immunity following repeated exposure)
What factors affect the epidemiology/disease outbreak of PGE in sheep and cattle?
Biosecurity Temperature Role of ewe - eggs Stocking density Keeping animals on the same pasture Rainfall/moisture Control measures
What affects the development of the free living stages (L1-L2-L3) of PGE in sheep and cattle?
Temperature >10C
Humidity
Dispersal from faeces
What affects the survival of L3 for PGE in sheep and cattle?
Ensheathed
Temperature <10C
Moisture
(Limited life span as limited food reserves)
What is over dispersion?
Small proportion of the host population carries the majority of the parasite population (e.g. 20% of population sheds 80% of the eggs = negative binomial distribution)
A year in the life of Teladorsagia circumcinta?
Spring:
- overwintered L3 on grass
- ewes turned out with lambs
- ewes contaminate pasture with eggs from the peri-parturient rise
- not enough larvae to cause disease yet
May-June:
- main source of pasture contamination = the ewe
- eggs shed on pasture start to develop
- lambs start to graze and ingest overwintered L3
- PPP = 3 weeks
- eggs shed from lambs onto pasture
June-July:
- day-night temperatures start to increase so development of eggs speeds up
- eggs shed onto pasture in May take longer to develop than eggs shed in June
- by mid-July, large numbers of L3 on pasture
August-September:
- disease seen
When is the peri-parturient rise in egg shedding of ewes for PGE? Why does it happen?
2 weeks before lambing until 6 weeks after
Immunosuppression from milk production and parturition
= main source of infection of lambs
Diagnosis of PGE in sheep?
Clinical signs
Season - type 1/2
FEC: >750epg
Age of animal - normally 4-6mo lambs
Control of PGE in sheep?
Management:
- clean pasture = not grazed by sheep for previous 12 months
- safe pasture = used the previous year but safe by beginning of June (overwintered L3 used up food supply as more active when warmer so die)
- rotation with crops or other stock
- quarantine incoming animals, especially tups
Anthelmintics
- problem with resistance in sheep, increased by repeated blanket treatments
- test for anthelmintic resistance
- administer correctly (e.g. split into weight groups and dose appropriately to heaviest animal and only when necessary
- preserve a population ‘in refugia’
- Use FECs
What are the drug classes of anthelmintics?
White drenches = benzimidazoles
Yellow drenches = imidathiazoles/tetrahydropyrimidines (2-LEV)
Clear drenches = macrocyclic lactones
2 new groups (can only be prescribed by vets):
- Amino Acetonitrile Derivatives: monepantel
- Spiroindoles: derquantel and abamectin combo
What does ‘in refugia’ mean?
A population of parasites not exposed to drugs
Preserves susceptible genes
Anthelmintic plan for a sheep flock with spring lambing?
Ewe and lamb turned out at 5 days
Oral moxidectin to ewes at lambing to kill worms developed from PPR - but leave ewes with single lambs or ewes in good BCS to dilute resistance (Or FEC)
Oral benzimidazole to lambs in late June when overwintered L3 have died so should not get re-infected after treatment
But also need to treat lambs in April/May for N battus
Could move lambs onto safe pasture in June (instead of treating, don’t worm and move)
?????
What to consider when choosing an anthelmintic?
Spectrum of activity - parasite species and stage
Pharmacokinetics - absorption, excretion, residual activity, residues, withdrawals
Formulation and administration
Drug efficacy and drug resistance
Toxicity and specificity vs host
Cost
Benzimidazoles: Examples? Mode of action? Spectrum of activity?
Fenbendazole, albendazole, flubendazole, mebendazole, triclabendazole
Mode of action: bind to microtubule subunit protein, B tubular, to prevent transport and enzyme release
Spectrum of activity:
- not well absorbed systemically (usually oral so just targets gut dwelling stages)
- primarily targets nematodes
- ovicidal: prevents spread from eggs to pasture in faeces
- effective against hypobiosed larvae
