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
2-LEV: imidathiazoles, tetrahydropyrimidines: Examples? Mode of action? Spectrum of activity?
Levamisole, pyrantel, morantel
Mode of action: act on nicotinic acetyl choline receptors
Spectrum of activity:
- not well absorbed systemically
- primarily targets nematodes - gut dwelling stages
- short acting
Macrocyclic lactones: Examples? Mode of action? Spectrum of activity? Toxicity?
Avermectins:
- ivermectin, doramectin, eprinomectin, selamectin
Milbemycins:
- moxidectin, milbemycin oxime
Mode of action:
- acts on nervous system
- potentiators cause hyperpolarisation, target includes invertebrate glutamate-gated chloride channels
Spectrum of activity:
- well absorbed systemically (= longer withdrawal)
- effective against nematodes only: migrating larvae, hypobiosed
- residual activity: 2 weeks for ivermectin
- endectocide
Ivermectin toxic to long nosed dogs (collies)
What is praziquantel effective against?
Potent anti-cestode
Doesn’t target nematodes
What are common combinations of anthelmintics used in cattle and sheep?
Cattle: ivermectin and triclabendazole
Sheep: levamisole and triclabendazole
Which anthelmintic is used for fluke?
Triclabendazole
What are interval dosing, strategic dosing and targeted dosing with anthelmintics?
Interval:
- Treat at regular intervals based on egg reappearance period
Strategic:
- treat when parasite numbers highest to disrupt seasonal cycle of transmission
Targeted:
- treat on the basis of diagnostic indicators
Which nematode parasites affect indoor and outdoor pigs?
Indoor: - Ascaris suum - Strongyloides ransomi - Trichuris suis - Oesophagostomum spp. Outdoor: - Hyostrongylus rubidus (stomach) - Metastrongylus apri (lungs)
Ascaris suum: Adult morphology? Egg morphology? Life cycle? PPP? Diagnosis?
Large worms: 15-25cm Eggs: thick pitted outer wall, 70um Typical ascarid life cycle: - eggs passed in faeces - develop on ground (4 weeks, temp dependent) - L2 in egg - paratenic host = earthworm, L2 hatches - egg or earthworm eaten by pig - L2 migrates to liver, lung (L2-L3) - coughed up, swallowed (L4-L5) in SI PPP = 8 weeks Diagnosis: - abattoir reports - transient respiratory disease - reduced weight gain - eggs in faeces: MgSO4 flotation
Pathogenesis of Ascaris suum?
Hypersensitivity response to migrating larvae - Liver: fibrous reaction ‘milk spot’ - Lungs: transient pneumonia Adults in small intestine: - Poor weight gain - Mechanical blockage in small intestine Major economic costs: - Reduced weight gain - Liver condemnation
Epidemiology and control of Ascaris suum?
Immunity develops rapidly Highly resistant egg Sows contaminate environment Steam cleaning of indoor pens Control more difficult in outdoor units
Which Strongyloides affects pigs? Which pigs? Immunity? Adult morphology? Life cycle? Disease caused? Control?
Strongyloides ransom Typically very young pigs Good immunity Adult morphology: - small: 6mm - hair like - no ovijectors - small eggs (40-50um) Unique life cycle: - free living and parasitic cycle - build up of numbers in dark, warm, moist environment - percutaneous infection - free living males and females in soil and bedding, feed on bacteria - parasitic: only females in SI, reproduce by parthenogenesis, lariated eggs or L1 in faeces, L3 infective, migration via lungs to SI PPP <15d Factors which trigger switch: - genetic? - environmental (temperature) - in host: immunity, over crowding Disease: - piglets: transmammary infection - diarrhoea, weight loss Treat with BZs, Mrs Keep environment clean
Trichuris in pigs: Where found? Morphology of eggs? Infective stage? Disease?
Large intestine Characteristic eggs: lemon shape, highly resistant Egg containing L1 = infective stage Weight loss in pigs Resilient to many anthelmintics
Oesophagostomum spp in pigs: Where found? Adult morphology? Life cycle? Infective stage?
Strongyle nematode in large intestine Adults: - 2cm long - characteristic cephalic vesicle Typical strongyle life cycle L3 is infective stage L3-L4 develop in mucosa, form nodules
Hyostrongylus rubidus in pigs: Where found? What does it cause?
Trichostrongyle nematode found in stomach of pigs
Similar to Ostertagia ostertagi
Hypobiosis
Parasitic gastritis
Metastrongylus apri in pigs: Where found? Life cycle? Adult morphology? PPP?
Metastrongyle lungworm of pigs
Not a typical metastrongyle!
Intermediate host = earthworms
Adult worms in the lumen of bronchi and brochioles
2.5-5cm in length
Life cycle:
- Larvated thick shelled eggs in faeces
- Hatch, L1 infects earthworms
- L1-L2-L3 in earthworm
- L3 survives as long as the earthworm (up to 7 years)
- Earthworm ingested by pig
- L3 released in gut, L3-L4 in mesenteric lymph node
- L4 reaches lung via lymphatics and bloodstream
- Matures to adult in the lungs
PPP ~3-4 weeks
Disease associated with Metastrongylus apri in pigs?
Typical in 4-7 month old pigs Catarrhal and eosinophilic bronchiolitis Coughing, dyspnoea, nasal discharge Reduced weight gain and inappetance Exacerbates other respiratory disease e.g. Staph infections
Trichinella spiralis: Significance? Which animals? Life cycle?
Important zoonosis - eradicated from UK Wide range of hosts - carnivores Humans, pigs, horses Wildlife reservoir Life cycle: - no eggs or larvae in faeces - no free living stages - adults in SI (small, short lived) - Females larviparous - L1 born, pass through the wall of SI - migrate to muscles - Encyst - transmission when muscle eaten - L1 released, adults mature, reproduce, die
Disease caused by Trichinella spiralis? How are people infected?
No disease in domestic animals
Serious disease in humans
Fever, oedema, muscle pains, peri-orbital oedema, myocarditis, meningitis, death
People infected by eating undercooked, contaminated meat (main sources = pigs, horses, game)
Control for Trichinella spiralis?
EU legislation from 2014: all boars, sows and pigs from non controlled housing must be tested at slaughter
Automated muscle digestion systems
Killed by cooking and freezing
Taenia solium: Definitive host? Intermediate host?: What is it? How are humans infected?
Pork tapeworm
NOT IN THE UK
Humans are definitive and intermediate host (adult tapeworms non pathogenic, but metacestode highly pathogenic)
Pigs intermediate host (cysticercus in muscle)
Humans infected by eating cysts in undercooked pork -> develop tapeworm in their SI = definitive host
Humans can also be infected by ingesting eggs -> develop metacestodes in brain -> neurocysticercosis = intermediate host
Human disease:
- epilepsy
- headaches
- sub-cutaneous lumps
Balantidium coli: What is it? Which animals? Where found? Significance? Transmission?
Cilliated protozoa
Large intestine of pigs
Apathogenic in pigs
Important zoonosis, cause of intestinal disease in humans
Faeco-oral transmission, cysts found in faeces
Isospora suis: What does it cause? Transmission? Treatment? Life cycle? PPP?
Severe enteritis in young piglets
Presents as diarrhoea that is unresponsive to antibiotics
Often low or negative oocyst counts
Oocysts (~20um) produced by the sow contaminate the environment
Infects small intestine
Sulphonamides e.g. toltrazuril to treat
Life cycle:
- infection by ingesting sporulated oocysts
- 2 rounds of asexual reproduction in epithelial cells of SI (merozoites in schizonts)
- sexual reproduction: micro and macro gametocytes release microgamets which fertilise macrogamete to produce zygote = oocyst
- unsporulated oocyst leaves host, sporulates in environment (2 sporocysts, each containing 4 sporozoites)
PPP = 5 days
Sarcoptes in pigs: Type of mite? Signs? Transmission? Control?
Burrowing mite, spends entire life cycle on the host
Lesions commonly start around the ears, spread to back, flanks and abdomen
Severe immune reaction, pruritis and erythema
Intense itching, thickened skin, secondary bacterial infections
Sow to piglet transmission
Treat/prevent with MLs
Haematopinus suis: Type of parasite? Where found? Size? Signs? Treatment?
Sucking louse Only louse found on pigs It’s really large!! Common, maybe present at low levels Itching, reduces feeding and growth rates and also affects hide value Treat with MLs
Hypoderma of cattle: Which species? What do they look like? When are they active? What do they do? Life cycle?
Hypoderma bovis (larger) and lineatum
Bee-like, non feeding
Active June-september in UK (warm days, 18C)
Obligate myiasis-producing flies
Short lived - few weeks
Life cycle:
- eggs glued to hairs on legs
- H bovis travels to the spine epidural fat -> L1-L2 in novemebter, migration/development to L3 resumes in Spring
- H lineatum travels to the submucosa of oesophagus by late autumn, migration resumes along connective tissue in spring
- larvae reach skin of backline after approx 9 months -> ‘warble’ forms
- larvae moults to final stage and doubles in size
- H lineatum emerges from lesion in March-May, H bovis in May-June
- larvae on ground, flies emerge 6 weeks later
= approx 1 year life cycle
Disease/economic importance of Hypoderma in cattle?
Perforation of hide - breathing holes
‘Gadding’
‘Butcher’s jelly’ - due to passage of L1 of H lineatum
Diagnosis, treatment and control of Hypoderma in cattle?
Diagnosis:
- palpation of warbles
- ELISA for larval stages
Important to not kill larvae as it’s migrating through - treat in autumn when larvae small and haven’t reached backline
Ectoparasiticides - injectable ivermectin
No longer notifiable, except scotland (been eradicated, but still risk from imports)
Stomoxys calcitrans in cattle: Resting sites? Habitat and life cycle?Feeding sites? Clinical signs? Consequences/disease?
Rest on warm sun exposed surfaces Feed on legs and flanks Lay eggs in batches inside on dung mixed with straw and urine, in silage, on spilt feed etc Build up during summer - spill out onto pasture Clinical signs: - foot stamping - tail swishing - sudden neck movements Consequences/disease: - loss of blood - 10-15% loss of weight gain - milk production 40% - known mechanical vectors of ASF, WN, rift valley viruses (plus poss others)
Lyperosia irritans of cattle: Name? What does it look like? Where found? Significance?
Horn fly Small fly with biting proboscis Found on the back if cows Cows only A true pasture fly Semi permanent ectoparasite Fresh dung Can cause anaemia when 1000s present
Tsetse fly: Species name? Where found? Features? Life cycle? Significance? Control?
Glossina spp
Restricted to sub-saharan Africa
Both sexes require large frequent blood meals
Body 6-14mm
Yellowish/dark brown
Wings held like scissor blades
Life cycle:
- One egg produced at a time which hatches inside female
- Larva nourished by fluids from milk glands
- Female feeds repeatedly to support larva
- Full grown larva deposited on soil just prior to pupation
Transmits T congolense and other trypanosomes
Nagana in cattle
African sleeping sickness in humans
Control:
- deltamethrin acaricide for cattle
- ground and aerial spraying of insecticides
- sterile insect technique
Trypanosoma: What does it cause in cattle?
Major constraint of livestock in Africa Lymphoid enlargement/splemomegaly Anaemia is a major feature Depends on development of parasitaemia: haemalytic, low and intermittent Lethargy, fever Chronic and fatal if unteated
Tabanidae: Which species affect cattle? Significance?
Haematopota and Tabanus
Tranmit Trypanosoma theileri to cattle - non pathogenic so not a worry (found in WBCs)
Which biting and non biting muscidae affect cattle?
Non biting: - Hydrotaea irritans 'head fly' - Musca autumnal 'face fly' - Musca domestica 'house fly' Biting: - Stomoxys calcitrans 'stable fly' - Lyperosia irritans 'horn fly'
Hydrotaea irritans: Appearance? How common? Life cycle? Typical habitat? What does it spread?
Orange wing base and greenish abdomen Most notorious pest species of livestock Life cycle: - deposits eggs on pasture soil and only one generation of flies the following summer Typical habitat = wooded pasture Spreads summer mastitis
Musca autumnalis: What does it spread? Where found? Appearance?
Spreads infectious bovine keratoconjunctivitis
Found on eyes, muzzle and face
Southern parts of England
Brown-grey, house fly like, no proboscis
Fly control in cattle?
Synthetic pyrethroids: sprays, pour-ons or incorporated into ear tags (for Hydrotaea irritans and other pasture flies)
Treat at turn out
May need 2 tags; history, incidence of SM
Treat surfaces - such as walls and fences (mainly S. calcitrans)
Barrier:
- Tape on teats
- Stockholm tar on teats (summer mastitis)
Good husbandry, dung removal delays/reduces build up of Stomoxys and other inside-breeding species: remove at least every 4 days
But populations disperse in Summer between farms
Cattle lice: when a problem? Types? Appearance? Life cycle? Which ones affect cattle? Signs?
Winter problem when housed cattle have thick coats
Mallophaga = biting/chewing lice (feed on skin, skin scale, feathers), head same width as body
Anoplura = sucking lice (suck blood, not found on birds), thinner heads than body
Small, wingless, flattened, stout legs, claws
Life cycle:
- entire egg-adult life cycle can be completed in 3-4 weeks
Sucking:
- Haematopinus eurysternus: poll, horn base, eyes, nostrils
- Linognathus vituli: head, heck, dewlap
- Solenopotes: head, neck, dewlap
Chewing:
- Bovicola/Damalinia: forehead, shoulders, back and rump (= most common species in UK)
Signs:
- heavy infestations result in intensive irritation, rubbing, hair loss, hide damage, anaemia (sucking), weakness
Severe pediculosis may mask underlying chronic condition
Which tick is the main vector for bovine babesiosis in UK? Which species of babesia? Life cycle of the tick? Appearance?
Ixodes ricinus
Babesia divergens
(Also Babesia major, transmitted by Haemophysalis punctuate in SE England but uncommon)
Life cycle:
- 3 year life cycle
- lives in damp low lying lamb and rough hill scrub
- needs high humidity
Appearance: long palps, hypos tome, groove in front of anus, spurs on legs
Babesia: Which phylum does it belong to? Where does it live in the body? What does it look like on a blood smear? Life cycle?
Phylum: Apicomplexa
Intra-erythrocytic
Sits on periphery of RBCs - divergent paired merozoites at margin of cell, apical complex, nucleus
Life cycle:
- merozoites divide by asexual binary fission
- tick ingests infected RBCs
- multiplication and sexual reproduction in tick
- dissemination of Babesia throughout tissues of tick, move to ovaries
- trans-ovarian transmission
- infection passes onto new host by the next generation of ticks
- as tick attaches and starts to feed, sporogony occurs in salivary glands
- sporozoites injected into host with saliva of tick
- sporozoites invade RBCs, start to divide (merogony)
Pathogenesis of Babesia divergens? Signs?
= Red water fever Signs: - fever - listlessness - dehydration - diarrhoea - haemolytic anaemia - haemoglobinuria - acute onset - high mortality Progresses to severe haemolytic anaemia without treatment During terminal stage -> hypoxia/anaemia and toxaemic shock Jaundice can be severe
Which species of Babesia are highly pathogenic in Africa, Australia and America? Signs? Transmitted by which tick? Life cycle?
Babesia bovis (highly pathogenic):
- acute disease 1-2 weeks after tick commences to feed
- fever, low parasitaemia
- neurological signs e.g. convulsions (sudging of RBCs in brain capillaries)
- haemoglobinuria (‘Red water’)
- death within days: PCV falls to 20 %
Babesia bigemina
Transmitted by Rhipicephalus spp (exclusively ticks of cattle)
One host tick:
- 3 weeks on same animal from unfed larva to fed adult
Diagnosis of Babesia? Treatment?
Clinical signs
History of exposure
Giemsa staining of blood smears to identify merozoites
Treatment - imidocarb, blood transfusions
Endemic stability of Babesia?
In endemic areas, prevalence in cattle and transmission rates are relatively high
Most animals are exposed when young and are hence protected by inverse age resistance (resistant to disease but susceptible to infection up to 9mo)
Premunity = asymptomatic carriers that are immune to disease
So disease is uncommon
= ‘endemic stability’.
Outbreaks of disease occur if endemic stability is disturbed e.g. changes in tick control measures, buying in naive animals
Control of cattle ticks in the tropics/subtropics?
OPs Pyrethroids Amitraz Treatment every 4-6 weeks Pos vaccines
What are the 2 types of mange mites of cattle and sheep? Morphology?
Chorioptes bovis:
- less severe than Psoroptes but more common
- morphology: rounded head, unjointed pedicels with bell shaped end
- affects head, neck, udder, base of tail
- hair loss, pruritus, scaling
- treat with ivermectin
- often seen towards end of housing
Psoroptes ovis:
- pierce skin and feed on lymph
- sheep scab: extremely debilitating, highly contagious
- severe irritation, scratching, skin damage, weight loss
- difficult to treat (failure of moxidectin and ivermectin), 4% permethrin successful sometimes
- morphology: suckers have 3 jointed pedicels
Osteragia ostertagi: Where found? What does it cause? Morphology?
Cattle abomasum Parasitic gastritis Morphology of adults: - 1cm in length - slender pinky-brown - fine cervical papillae - males have bursa and spicules Life cycle: - Typical trichostrongyle life cycle - Direct (no intermediate host) - Typical trichostrongyle eggs in faeces: 90 x 45μm, barrel shaped, undifferentiated - L1-L3 on pasture, L3 infective stage - L3 is ensheathed - Cattle eat L3 as they graze - L3 swallowed and reaches abomasum - Burrows into gastric glands - Develops to L4 and L5 L5 (immature adults) emerge, into lumen of abomasum - Matures to adult, mates and females lay eggs - PPP = ~ 3 weeks Pathogenesis: - Disease associated with large numbers of developing larvae - Damage caused by developing larvae in gastric glands and emerging L5
What are the 2 types of bovine ostertagiosis?
Type I: - Dairy replacement calves - End of the first grazing season - Disease occurs in late summer - July to September, typically August - Calves ingest large numbers of L3 in July - Green watery diarrhoea - Majority of calves within a group are affected Type II: - Less common these days - Yearling calves - Disease in late winter, early spring - Acute disease - Intermittent diarrhoea - Anaemia - Thirst - High levels of mortality - L4 go into a state of hypobiosis in gastric glands in the autumn, due to drop in temperatures - Remain there over the winter - Extends the PPP - At the end of winter their development resumes - Trigger for re-activation not known - Simultaneous emergence of L5 - Severe clinical disease
When is bovine ostertagiosis seen?
May:
- first season dairy calves turned out
- overwintered L3 from previous year
- too few L3 for disease
June:
- overwintered L3 die by beginning of June
- L3 mature
- eggs produced onto pasture
- ambient temperatures start to increase so eggs start to develop
July:
- eggs developing on pasture
- peak of L3 on pasture in mid July
- ingested by calves
Ausuat:
- larvae numbers of L3 develop in abomasum of calves
- type I disease 3 weeks later in Aug-Sept
Autumn:
- L3 on pasture exposed to drop in temp
- after a dry summer L3 may be released from faecal pats by rainfall
- calves may be moved back onto contaminated pasture used to graze calves earlier in summer
- any L3 on pasture exposed to decreasing termperatures
- triggers L4 to go into hypobiosis
- accumulation of hypobiosed L4 in gastric glands
Late winter-early Spring:
- larval development resumes
- simultaneous emergence of L5
- type II ostertagiosis
- severe clinical disease, high mortality
Ostertagiosis in beef herds?
Clinical disease less common:
- calves graze with immune mothers
- autumn born calves may be at risk when turned out in spring - graze and ingest overwintered L3
Definitive diagnosis of Ostertagiosis in cattle?
Raised plasma pepsinogen levels
Define metaphylaxis
Timely mass medication of a group of animals to prevent or minimise an expected outbreak of disease
Plan for control of PGE on farm with 24 heifer holstein-fresians, being turned out in May and then housed from October
Delay turnout until Jun = safe pasture – should then be fine for rest of season
But expensive to keep in so farmer may not be keen and also don’t build up immunity
So if do turn out in May, treat just before 3 weeks after turn out so kill larvae and stop eggs from being shed - need to kill larvae stages so use Benzimidazole or macrocyclic lactone, not Levamisole (only kills adults)
Treat whole group as more practical and don’t have faecal samples yet
Calves can still be infected after this from overwintered larvae – if used Ivermectin this has 2 week residual activity so protects until beginning of June, if used benzimidazole then treat again 3 weeks later
Usually give another ivermectin treatment 5 weeks after the first treatment - 3, 8, 13 week regime recommended by manufacturer (2 week residual activity + 3 week PPP between treatments) - pasture contamination so low after last treatment that controls type II as well
Housing dose to kill hypobiosed larvae – benzimidazole or macrocyclic lactone
Which lungworm affect sheep? Features?
Dictyocaulus filaria - pathogenic - anterior cuticular knob on L1 Muellerius capillaris: - metastrongyle - not pathogenic in sheep - highly pathogenic in goats - commonly seen at abattoir - hair-like adults in grey/green eosinophilic nodules in lung parenchyma - L1 in faeces (kink and spike on tail) - intermediate hosts = slugs/snails -
Life cycle of Dictyocaulus viviparous?
Direct Female worms are ovo-viviparous: lay larvated eggs, hatch immediately -> L1 in lungs -> Coughed up, swallowed, passed in faeces -> L1 in faeces (short and stumpy, refractive food granules) -> L1-L2-L3 (all ensheathed, larvae don't feed) -> L3 in 5-7d in optimum conditions, L3 is infective stage 1. Penetration phase: - 0-7d after infection - L3 ingested - Lympho-tracheal migration - Moults to L4 in lymph nodes - L4 reaches lungs 2. Pre-patent phase: - 8-25 days - L4-L5 in lungs - L5 migrate up bronchial tree - Adults in bronchi and trachea 3. Patent phase: - 26-55d after infecion - Adult worms in URT - Eggs and L1s 4. Post-patent phase: - 55d+ - Immune expulsion of adults - Protective immunity
Which phases of lungworm in cows are the most pathogenic?
Pre-patent and patent phases
Pathology and clinical signs seen in the pre-patent, patent and post-patent phases of Lungworm in cattle?
Pre-patent phase: - Intense inflammatory response - Alveolitis, bronchiolitis, bronchitis - Interstitial emphysema - Pulmonary oedema - Coughing, respiratory distress, tachypnoea, weight loss Patent phase: - Mature adults in bronchi/trachea - Eggs and L1 swept into alveoli - Intense inflammatory response - Frothy, white mucus - Emphysema, hypoxia - Gasping, coughing, death Post-patent: - Resolution of clinical signs - In some animals, epithelialisation of lung tissue, never completely recover
What impacts does liver fluke have on animal production?
Growth rates
Milk yield
Wool and fibre
Liver condemnation
What are the acute, sub-acute and chronic forms of liver fluke? Differences between the two, including cause, timing, clinical signs and pathology?
Determined by the number of metacercariae ingested and the time period over which they are ingested
Acute fasciolosis:
- juvenile flukes
- large numbers
- usually only in sheep in UK
- Disease in Oct-Dec
- juvenile flukes migrate through liver parenchyma -> haemorrhagic tracts, inflammation, hepatomegaly, fibrosis
- sudden death, weakness, abdominal pain, anaemia
Chronic fasciolosis:
- sheep and cattle
- low numbers of metacercariae ingested over longer period of time
- disease in Jan-March
- adult flukes in bile ducts feed on blood -> spines on tegument irritate bile duct walls -> hyperplasia, fibrosis, calcification, cholangitis
- progressive weight loss, anaemia, sub-mandibular oedema, ascites
Sub-acute:
- sheep ingest metacercariae over longer period of time
- insufficient to cause acute disease
- disease caused by both juvenile and adult flukes
- rapid weight loss, anaemia
Life cycle of liver fluke?
Undifferentiated eggs shed in faeces of definitive host (e.g. cow, sheep)
- > eggs develop
- > miracidia hatch and swim through plane of water to find mud snail as intermediate host
- > sporocyst, rediae and cercariae develop in the snail (clonal amplification)
- > after about 6 weeks, flukes break out of snail and cercariae encyst on pasture to form metacercariae
- cysts on herbage eaten by grazing herbivores
- adult fluke develop in liver
A year in the life of a liver fluke?
Spring:
- low snail population
- eggs on pasture
- increasing temperature: snail population increases, eggs develop, miracidia infect snails
June-Aug:
- ‘summer infection of snails’
- sporocyst-rediae-cercariae
- if warm, wet summer: large numbers of cercariae released simultaneously -> acute disease 2-6w later
- if cool, dry summer: fewer metacercariae produced as released gradually from snails -> chronic disease in winter-early spring
Dicrocoelium dendriticum: What is it? Life cycle? What does in cause?
Lancet fluke (1cm)
Life cycle involves land snails and brown ants
Causes liver cirrhosis and cholangitis
Schistosoma spp: What is it? Features?
Blood flukes ‘Dioecious’ i.e. separate sexes Very important human disease Important cause of production losses in ruminants in the tropics Snail intermediate host
Tapeworm life cycle?
Adults in small intestine Proglottids break off Eggs/proglottids shed in faeces Eggs immediately infective Eggs eaten by intermediate host Metacestode develops in intermediate host Metacestode eaten by definitive host Adult tapeworm develops in small intestine
Which tapeworms sheep the intermediate host for? Where found? Definitive host?
Taenia ovis: cysticercus in muscles
Taenia hydatigena: cysticercus in peritoneum
Taenia multiceps: coenurus in brain
Echinococcus granulassi: hydatid cyst
Definitive host is dogs
Taenia ovis: Definitive host? Intermediate host? Significance? Control?
Definitive host: dogs
Intermediate host: cysticercus in muscles
Affects value of the carcase
Highly effective vaccine but no commercial uptake as infection doesn’t cause disease
Taenia hydatigena: Definitive host? Intermediate host? Significance?
Definitive host: dogs
Intermediate host: cysticercus migrates through liver of sheep to form mature cysticercus in peritoneum
Liver condemnation
Taenia multiceps: Definitive host? Intermediate host? Significance?
Definitive host: dogs
Intermediate host: gid cyst in brain of sheep (coenurus)
Space occupying lesion: neurological complications
Echinococcus granulosus: Definitive host? Intermediate host? Significance? Control?
Definitive host: dogs
Intermediate host: hydatid cyst in liver and lungs of sheep and cattle
No pathogenic significance for sheep/cattle
Serious human pathogen - from eggs in dogs’ faeces (not from hydatid cysts in meat)
Control:
- praziquantel for dogs every 6 weeks to remove adult tapeworm
- break life cycle by controlling access to metacestodes: don’t feed dogs raw meat and don’t allow to scavenge
Taenia saginata: Definitive host? Intermediate host? How common? Significance? Control?
Definitive host: humans (in SI) Intermediate host: cysticercus in muscle of cattle Rare in UK No disease in cattle Mild disease in humans - hunger pains, aesthetically unpleasant Control: - meat inspection (heart, masseters) - cooking or freezing meat - sewage disposal
Monezia spp: What is it? Where found? Appearance? Life cycle?
Common tapeworm
SI of sheep, cattle and goats
Long: 2m+
Metacestode stage (cysticercus) develops in orbited mite (intermediate host)
What are the 5 Rs for anthelmintic use?
Choose the right product for the type of worm Treat the right group of animals Treat at the right time of year Treat using the right dose rate Administer the product in the right way
Avian coccidiosis: Which species? Life cycle? Pathogenesis? Control?
7 in chickens: Eimeria tenella main one
2 in turkeys: Eimeria melaegrimitis main one
Life cycle:
- unsporulated oocyst in environment
- sporogony to form sporulated oocyst
- sporulated oocyst ingested
- schizogony (asexual division)
- gametogony (sexual division to form macrogametes and microgametes)
- macrogametes and microgametes form a zygote = unsporulated oocyst
- unsporulated oocyst excreted
Pathogenesis:
- severity of disease related to parasite density
- damage to epithelial cells
- haemorrhage with heavy infections
- impaired absorptive capacity of gut with lighter infections
Control:
- ionophores
- aim to eliminate disease in broilers
- aim to allow immunity to develop in layers (strong immunity)
- vaccination
- hygiene
What affects the epidemiology of avian coccidiosis? Why and when does disease occur?
Factors:
- Parasite (survival of oocysts in environment, low numbers persist in housing as impractical to completely remove)
- Host (naïve, susceptible young day old chicks)
- Immunity (good immunity follows natural infection)
- Environmental conditions (intensive husbandry, can provide ideal conditions for sporulation and oocyst survival)
Disease occurs due to:
- Rapid rise in oocysts
- Population of susceptible birds
- Disease at 3-6 weeks of age
- Most disease is due to incorrect dosage/concentration of ionophores
What anticoccidials are available for poultry?
Ionophores: - monensin - narasin - lasalocid - salinomycin - maduramicin Quinolones: - decoquinate Guanidines: - robenidine Carbanilides: - nicarbazin (synergistic with narasin) Febrifugins: - halofuginone Benzeneacetonitrile derivatives: - diclazuril - toltrazuril
How are Isospora oocysts different to other coccidia?
Isospora oocysts have 2 sporocysts, each with 4 sporozoites
Rather than 4 sporocysts, each with 3 sporozoites
Sheep Coccidiosis: Which species? When is disease seen? Where found? Signs?
>10 species 2 are most pathogenic: Eimeria crandalis and Eimeria ovinoidalis Disease in young lambs (2-3mo) Caecum and colon infected Clinical signs: - diarrhoea - dehydration - abdominal pain - anorexia
Cattle Coccidiosis: Which species? When is disease seen? Where found? Signs? Treatment?
20 species Most pathogenic are Eimeria zuernii and Eimeria bovis Housed, older animals (>1yo usually) Caecum and colon affected Clinical signs: - diarrhoea - dehydration Treatment: - sulphonamides - monensin - decoquinate
What ectoparasites are important in chickens?
Burrowing mites:
- Knemidocoptes mutans (scaly leg mite)
- Knemidocoptes gallinae (depluming itch)
Non burrowing mites:
- Dermanyssus gallinae (red mite)
- Ornithonyssus silviarum (Northern Fowl Mite)
Lice:
- Menacanthus stramineus (chicken body louse)
- Lipeurus capons
- Menopan gallinae (shaft louse)
Dermanyssus gallinae: What is it? Where found? Appearance? Clinical signs?
= Poultry red mite Blood feeding Lives in environment, feeds on host at night Appearance: - 1mm in size - long legs - D shaped anal plate - black then red when fully blood engorged May survive months in environment Populations rapidly build up Clinical signs: - may be pruritus, papules, crusts - debilitation, stop feeding - anaemia
Knemidocoptes mutans and Knemidocoptes gallinae: What are they? Appearance? What do they cause?
Knemidocoptes mutans = scaly leg mite
Knemidocoptes gallinae
= depluming itch
Both cause extensive crusting and lesions
Similar in appearance and life cycle to Sarcoptes scabiei
Ornithonyssus silviarum: What is it? What do they cause? Appearance?
= Northern Fowl Mite
Morphology similar to D gallinae but pear shaped anal plate
Permanent blood sucking mite
Causes discolouration of feathers, anaemia, death
Poultry lice: Species? Clinical signs? When seen? Which birds affected?
3 major genera/species:
- Lipeurus caponis (underside of wings, tail feathers)
- Menacanthus stramineus (the chicken body louse)
- Menopon gallinae (the shaft louse)
Affects all domestic fowl
Feed on feathers and down.
Clinical signs:
- unable to rest
- irritated
- body weight decreases
- egg production drops
- feather damage
Mainly occurs in the autumn and winter
Lice not highly pathogenic to mature birds but may be fatal to chicks
Damage to the skin may lead secondary bacterial infections.
Birds which have been beak trimmed and are unable to groom properly or that are in poor condition are particularly susceptible
Nematodes of poultry?
Syngamus trachea (poultry gape worm) Capillaria spp. Trichostrongylus tenuis Ascaridia galli Heterakis gallinarum
Syngamus trachea: What is it? Which animals affected? Reservoir? Where are adults found? Signs? Life cycle? PPP?
= Poultry gape worm
Hookworm
Affects chickens, game birds, turkeys etc
Wild bird reservoir
Adult worms in trachea, permanently paired
Disease - mechanical blockage of trachea, asphyxia, coughing, gasping
Life cycle:
- characteristically shaped egg passed in faeces
- L3 develops in egg
- ingest L3 in egg, hatched L3, or L3 in paratenic host (earthworm)
- L3 migrates to lungs via bloodstream
- adults develop in lungs
PPP: 18-20d
Capillary spp: What are they? Appearance? Where found? Life cycle? Life cycle? PPP? Disease and signs?
Three species Direct and indirect life cycles Appearance: - very thin (capillary-like) worms - 1-5cm long Found in the upper digestive tract (crop, oesophagus) or small intestine Characteristic eggs (barrel shaped with two mucoid plugs) Life cycle: - L1 develops in egg - intermediate host = earthworm - birds infected by ingesting earthworm PPP 3-4 weeks Disease and signs: - can be highly pathogenic - head of worm buried deep in mucosa -> diphtheritic inflammation - inappetence, weight loss, drop in egg production
Poultry ascarids: Species? Where found? Appearance? Life cycle? Significance?
Ascaridia galli: - small intestine - large (12cm) Heterakis gallinarum: - caeca - small (1.5cm) Eggs indistinguishable Life cycle: - infective stage is L2 in egg - no migration Low pathogenicity but Heterakis gallinarum is vector for highly pathogenic protozoan: Histomonas melaegridis
Control of poultry nematodes? Difference between housed and outdoor birds?
Housed birds:
- Only parasites with direct lifecycles important
- Most have resistant eggs (Ascaridia, Heterakis and Capillaria)
- Biosecurity: prevent introduction of nematodes with new batches of birds
- Use of in feed BZs (flubendazole)
Outdoor birds:
- Parasites with direct AND indirect lifecycles important
- Resistant eggs and intermediate/transport hosts means parasite stages persist in environment
- Wild birds important source of infection
- Biosecurity: prevent introduction of nematodes with new batches of birds
- Use of in feed BZs (flubendazole)
- Rotate pens between batches of birds
Histomonas melaegridis: What is it? Significance? Pathogenesis? Clinical signs? Transmission? Control?
Amoeboid protozoan with single flagellum
Highly pathogenic for turkey poults
‘Blackhead’: severe entero-hepatitis
High levels of mortality
Transmission:
- transmitted in eggs of Heterakis gallinarum
- only transmitted in the lariated egg
Pathogenesis:
- Trophozoites in caecum erode caecal epithelium
- Invade liver causing necrosis and typical (pathognomic) saucer-like lesions
Clinical signs:
- depression
- ruffled feathers
- sulphur yellow faeces
- cyanosis of the wattle and comb (hence blackhead)
Control:
- good biosecurity
- control of Heterakis
- avoid rearing turkeys on ground previously used for chickens as chickens are asymptomatic carriers
Hexamita melaegridis: What is it? Which animals affected? Clinical signs? Transmission? Treatment? Control?
Protozoa Young game birds Watery bright yellow diarrhoea. Direct transmission Treatment Prevent by all in/all out, mix age groups, rotate pens
Trichomonas gallinae: Which animals affected? What does it cause? Clinical signs? Transmission?
Finches, pigeons, birds of prey
Oral canker: cheesy yellow material around beak
Direct transmission
