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Clinical Veterinary Science and One Health 23/24 > Sustainable Control of Parasites > Flashcards

Sustainable Control of Parasites Flashcards

1
Q

List the neglected zoonoses.

A

Anthrax
Brucellosis
Bovine tuberculosis
Cystic echinococcosis
Leishmaniasis
Cysticercosis
Rabies
Trypanosomiasis

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2
Q

What is the disease and hosts of echinococcus granulosus?

A

Cystic echinococcosis (Hydatid disease)

DH: canines
IH: ruminants, horses, humans

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3
Q

What is the disease and hosts of echinococcus multiocularis?

A

Alveolar echinococcosis (alveolar hydatid)

DH: canines, cats
IH: rodents, humans

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4
Q

What is the disease and hosts of taenia solium?

A

Taeniasis cysticercosis/neurocysticercosis (pork tapeworm)

DH: humans
IH: pigs, humans

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5
Q

What is the disease and hosts of taenia saginata?

A

Taeniasis (beef tapeworm)

DH: humans
IH: cattle

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6
Q

What is the disease and hosts of taenia asiatica?

A

Taeniasis/cysticercosis (asian tapeworm)

DH: humans
IH: cattle, pigs, humans

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7
Q

What is the disease and hosts of diphyllobothrium latum?

A

Diphyllobothriosis (fish tapeworm)

DH: humans
IH: crustaceans, fish

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8
Q

Briefly summarise the lifecycle of echinococcus granulosus.

A

PPP in dog = 40-50 days. Humans exposed to contaminated dog faeces. Infection of dog by consumption of offal from fallen stock.

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9
Q

How is cystic echinococcus controlled?

A
  • Prevent dogs from scavenging carcasses
  • Avoid feeding uncooked offal to dogs
  • Praziquantel for dogs every 28-42 days in endemic areas
  • Hygiene – hand washing after touching dogs helps prevent human infection
  • Public information campaigns
  • Vaccination trials
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10
Q

How is canine definitive host vaccinated against echinococcus?

A

Oral recombinant E.granulosus vaccine

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11
Q

How is ruminant intermediate host vaccinated against echinococcus?

A

EG95 is a cloned recombinant antigen from the parasite oncosphere

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12
Q

Summarise the lifecycle of echinococcus multiocularis.

A

Cysts produced in intermediate hosts contain lost of cysts and they spread like a neoplastic manner, slowly around the body. Is almost impossible to cure. PPP = 30 days. Hard to eliminate if both IH and DHs are wild animals – IH is vole, DH is canids.

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13
Q

How is echinococcus multiocularis controlled?

A
  • Prevent access of dogs and cats to rodents
  • Hygiene
  • Praziquantel for cats and dogs every 28 days in endemic areas, anthelmintic baits for wild and stray definitive hosts
  • Pet travel: treatment more than 24h and less than 120h before travel
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14
Q

What is the effect of praziquantel in echinococcus multiocularis?

A

Praziquantel does not kill eggs

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15
Q

What is the structure of the taenia saginata tapeworm?

A

Larval tapeworm at a stage in which the scolex at the anterior end is inverted in a sac, typically found encysted in the muscle tissue of the intermediate host

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16
Q

What is cysticercus bovus?

A

Cysticercus bovus = Taenia saginata metacestode

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17
Q

Summarise the lifecycle of taenia saginata.

A

Proglottids with thousands of eggs in faeces into environment, ingested by grazing animals, encyst in muscle and this can be ingested in infected meat in humans. If gets into sewage system can infect lots of land.

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18
Q

Distinguish taenia saginata from other taenia species.

A

Large tapeworm at 5-15m long. No hooks or rostellum on scolex – unarmed, distinguishes from T.solium and other taenia

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19
Q

What does taenia saginata infection cause in humans?

A
  • Relatively minor zoonosis
  • Usually asymptomatic
  • Occasionally diarrhoea or hunger
  • Rarely more serious complications
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20
Q

How are cattle infected with cysticercosis?

A

Contamination of pastures or feed by improperly treated waste water, sludge or human faeces

Usually asymptomatic

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21
Q

How is transmission of bovine cysticercoids prevented?

A
  • Thorough cooking of beef
  • Compliance with regulations on treatment and use of wastewater and sludge
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22
Q

Name and describe the main control intervention of bovine cysticercoids.

A

Meat inspection, followed by condemnation or freezing treatment when necessary as prescribed by legislation:

  • Visual inspection of specific muscles
  • Incisions in internal and external masseter muscles – cattle under 6 weeks of age
  • Lengthwise incision of heart – all ages
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23
Q

What are the hosts of taenia solium?

A

Humans are sufficiently like pigs that we can get infected and have the same disease caused as pigs. Human DH and pig IH – metacestode is cystercercus cellulosae, measly pork. Human also accidental/dead-end host to taenia solium metacestodes.

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24
Q

Describe the taenia solium tapeworm anatomy.

A

Hooks = armed. Large adult tapeworm in small intestine – 3-5m long, over 50,000 eggs released per day

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25
Q

What is the consequence of taenia solium going to the brain?

A

Causes CNS infection and epilepsy is common

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26
Q

Why does WHO think that taenia solium could be eradicated?

A
  • Humans are the only DH
  • Pigs are the only IH
  • Human tapeworm infections sole course of infection for intermediate host pigs
  • Domestic pigs can be managed
  • No wildlife reservoirs exist
  • Safe and effective chemotherapy available
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27
Q

How is taenia solium taeniosis detected in humans?

A
  • Observation of proglottids in stool - low sensitivity
  • Routine coprology - low sensitivity 10%
  • Coproantigen detection - more sensitive
  • Serology EITB - specific for T.solium infection-related antibody
  • Biopsy of subcutaneous nodules
  • Neuroimaging
  • Immunodiagnostics
  • Autopsy
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28
Q

How is taenia solium detected in pigs?

A
  • Lingual exam - sensitivity less than 50%
  • Antigen detection
  • Antibody detection - may not have active exposure, maternal antibodies in young pigs
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29
Q

How is human taenia solium taeniosis treated?

A

Praziquantel
Niclosamide

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30
Q

How is human taenia solium cysticercosis treated?

A

Praziquantel
Albendazole

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31
Q

How is porcine cysticercosis treated?

A

Oxfendazole

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32
Q

What are the strategies for intervention of taenia solium?

A
  • Cook meat
  • Control slaughter
  • Meat inspection
  • Mass taeniacidal treatment
  • Improve sanitation
  • Restrain/confine pigs – need to find alternative food source
  • Treat pigs
  • Vaccinate pigs
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33
Q

How can taenia solium be controlled?

A

Mass treatments may give a good impact in the short term and the long-term impact is limited.

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34
Q

What are the hosts of taenia multiceps?

A

DH = domestic dog, fox, coyote, jackal

IH = sheep, cattle, deer, pig, horse

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35
Q

Describe the disease caused by taenia multiceps.

A
  • Very rare and minor zoonosis
  • Although severe in those affected
  • Control like echinococcosis
  • Common in sheep and causes circulating behaviour in disease called gid
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36
Q

What are the hosts of diphyllobothriosis latum?

A

DH = humans

IH = procercoid larvae in crustaceans, plerocercoid larvae in fish

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37
Q

Briefly give the lifecycle of diphyllobothriosis latum.

A

Humans are DH, adults in small intestines, embryonate in water and infect invertebrates, infect fish and is called a plerocercoid in fish, works way up food chain.

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38
Q

What are the symptoms of disease caused in humans by diphyllobothriosis latum?

A

Most are asymptomatic:
- Abdominal discomfort
- Diarrhoea and vomiting
- Weight loss
- Vitamin B12 deficiency leading to megaloblastic anaemia

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39
Q

What are complications of diphyllobothriosis latum infection in humans due to?

A

Intestinal obstruction and gall bladder disease caused by migration of proglottids

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40
Q

How can diphyllobothriosis latum controlled and treated?

A

Cooking or freezing fish prevents transmission to humans

Praziquantel or niclosamide

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41
Q

What is trichinella spiralis?

A

Nematode parasite with a wide host range. Transmission by carnivory

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42
Q

Describe the disease caused by trichinella spiralis.

A

Zoonosis. Diagnosis in slaughtered pig meat by microscopic examination of HCl/pepsin digest for larvae

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43
Q

What are the hosts of fasciola hepatica?

A

DH = cattle, sheep, (horses, rabbits, other grazing animals and humans)

IH = galba truncatula

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44
Q

Which diseases does fasciola hepatica increase the susceptibility of?

A

Black disease
Salmonella Dublin
Bovine TB

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45
Q

Briefly describe the fasciola hepatica lifecycle.

A
  1. Eggs in faeces
  2. Miracidium enters snail (stays for 5 weeks to a few months)
  3. Sporocyst
  4. Redia
  5. Cercaria leaves the snail
  6. Encysts on herbage and ingested
  7. Juvenile and adult in sheep/cattle. PPP is 10-12 weeks
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46
Q

Describe the development of fasciola hepatica cercariae.

A
  1. Cercariae within redia
  2. Motile cercaria with tail
  3. Cercaria loses its tail and forms a cyst
  4. Metacercaria cyst persists on vegetation (is how ruminants are infected)
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47
Q

What are the epidemiological features of galba truncatula?

A
  • Development is optimal at 15-22˚C and stops under 5˚C
  • Aestivation – prolonged torpor or dormancy over winter
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48
Q

Explain summer and winter infections of galba truncatula.

A

Summer infection of snails: metacercariae on pasture that can overwinter. Number on pasture go down gradually but get ingested by sheep. By the time infection matures in sheep, it is ready to infect snails and then fresh metacercariae on pasture in autumn.

Winter infection of snails if infection of sheep earlier on in the year.

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49
Q

What are the clinical signs of bovine fasciolosis?

A
  • Chronic condition
  • Weight loss
  • Anaemia
  • Sub-mandibular oedema – severe cases = “bottle jaw” from hypoalbuminaemia
  • Poor growth
  • Reduced milk yield
  • Young cattle after first autumn at grass
  • Immunity in older cattle
  • Late autumn, winter disease in cattle
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50
Q

What are the subacute clinical signs of ovine fasciolosis?

A
  • Animals found dead
  • Anaemia
  • Dyspnoea
  • Swollen livers
  • Abdominal pain
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51
Q

What are the subacute clinical signs of ovine fasciolosis?

A
  • Rapid weight loss over 1-2 weeks
  • Anaemia
  • Enlarged liver
  • Abdominal pain – resent palpation
  • Some deaths
  • Autumn – early winter
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52
Q

What are the chronic clinical signs of ovine fasciolosis?

A
  • Progressive loss of condition
  • Severe anaemia
  • Submandibular oedema
  • In severe cases – emaciation, ascites and death
  • Late winter, early spring
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53
Q

How is faecal examination for fasciola hepatica eggs done?

A
  • Only for patent infections, such as adult fluke/chronic infections
  • Conventional McMaster nematode egg count method using saturated saline is not effective
  • Specifically request fluke egg count, specific sedimentation methods and flotation using zinc sulphate
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54
Q

How can biochemical tests detected fasciola hepatica?

A

Non-specific liver damage - GGT, GLDH levels increase from 2-3 weeks after infection

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55
Q

What are the immunological tests to detect fasciola hepatica?

A

Bulk tank milk ELISA
Serum ELISA
Coproantigen ELISA

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56
Q

How can galba truncatula be controlled?

A
  • Fencing off risky areas which is unpopular with farmers
  • Drainage to discouraged to protect biodiversity
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57
Q

What must fasciola hepatica preventative treatments target?

A
  • Targets larvae migrating through liver parenchyma
  • Agent used must be effective against immature fluke
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58
Q

What are 3 agents to target immature flukes?

A

Triclabendazole – all ages of Fasciola. Concerns about resistance

Closantel – reasonable activity against immature fluke. From 3-4 weeks, more so > 5 weeks

Nitroxynil – effective from 6-7 weeks

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59
Q

Name 3 agents effective against adult fasciola hepatica flukes.

A

Clorsulon – only suitable for cattle
Oxyclosanide
Albendazole

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60
Q

Which agent is used to treat dairy cattle fasciola hepatica?

A

Triclabendazole permitted in dry period, 50-day milk withdrawal. None licensed for lactation.

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61
Q

How is tricabendazole resistance managed?

A
  • Avoid use unless essential
  • Quarantine treatment of newly introduced stock
  • Cannot stop spread completely – deer and rabbits hosts
  • Try to reduce reliance on fasciolicides – snail control also problematic
  • Vaccination
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62
Q

Describe the epidemiology of bovine lungworm/dictyocaulus viviparus.

A
  • Temperate regions with high rainfall
  • Acquired immunity strong following infection or vaccination
  • Typical of young cattle in first grazing season
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63
Q

When are the seasons of infection of bovine lungworm?

A
  • Disease outbreaks June – November
  • Most common July – September
  • Disease is usually not apparent until calves at grass for 2-5 months following spring turnout
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64
Q

Name the 4 possible stages of parasitic bronchitis caused by dictyocaulus viviparus.

A

Acute
Subacute
Postpatent phase
Re-infection syndrome

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65
Q

Describe acute phase of parasitic bronchitis.

A

Prepatent phase, days 8-25. Exudate in airways = alveolitis, bronchiolitis and bronchitis. No larvae in faeces

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66
Q

Describe subacute phase of parasitic bronchitis.

A

Patent phase, days 26-60. 100s-1000s of adults in in bronchi. Parasitic pneumonia – aspiration of eggs and L1. Larvae in faeces

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67
Q

Describe the post-patent phase of parasitic bronchitis.

A

Days 61-90. Lung fibrosis and epithelialisation. Secondary bacterial infection. No larvae in faeces

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68
Q

Describe re-infection phase of parasitic bronchitis.

A

Previous exposed animals with lapsed immunity. Hypersensitivity reaction

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69
Q

Explain how acquired immunity is very effective to dictyocaulus viviparus?

A

Phase 1: resistance to colonisation of lungs by larvae. Weakens rapidly (3-6 months) if no further exposure occurs. Similar to GI mucosal immune responses (short lived)

Phase 2: destruction and elimination of larvae/adults from lungs – lasts longer (over 2 years), systemic responses tend to be longer lasting

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70
Q

What are the challenges of the acquired immune response to dictyocaulus viviparus?

A
  • Immunity is not lifelong, requires boosting, especially phase 1
  • Heavy challenge can lead to re-infection syndrome - no phase 1 immune response, so larvae get to lungs and are killed by phase 2 response (8-10 days after pasture change), can result in hypersensitivity
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71
Q

How is bovine lungworm diagnosed?

A
  • Grazing at pasture, time of year and coughing
  • Larvae in faeces – Baermann apparatus (after d23, only few larvae needed to cause disease)
  • Antibody-ELISA by APHA (after d23, only few larvae needed to cause disease)
  • Post-mortem examination
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72
Q

What are the clinical signs of parasitic bronchitis?

A

Anorexia
Cough
Tachypnoea
Hyperpnoea
Adventitious lung sounds
Typical posture
Reluctance to move
Movement elicits cough
Severe drop in milk yield in dairy cows

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73
Q

What is causing increasing incidence of bovine lungworm in dairy cattle?

A
  • Vaccination not used, or used inappropriately
  • Heavy use of anthelmintics in first and second year grazing so no natural immunity developed
  • Movement of animals
  • Changing grazing patterns
  • Climate change
  • Epidemiology not predictable
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74
Q

Which anthelmintic agents can be used to treat bovine lungworm?

A

Benzimidazoles, levamisole, macrocyclic lactones all effective. Choice depends on criteria such as duration of action and ease of administration

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74
Q

How are mild and severe cases of bovine lungworm treated?

A

Mild cases: dose and move to clean pasture

Severe cases: house and give supportive care

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75
Q

What about bovine lungworm treatment must you warn the farmer about?

A
  • Treatment can sometimes produce fatal reaction – warn the farmer
  • Some animals may never recover fully
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76
Q

When and how is lungworm vaccination administered?

A

Use where lungworm known to be present on the farm. Live irradiated 3rd stage larvae given orally: 2 x 25 ml doses, 4 weeks apart to calves over 8 weeks. Do not mix vaccinated and unvaccinated animals

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77
Q

Why are anthelmintic boluses used to block larval challenge of bovine lungworm?

A

If larval challenge is low, unvaccinated animals not likely to develop immunity and vaccinated animals may have immunity that weans

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78
Q

Name 3 main cattle GI nematodes.

A

Ostertagia ostertagi
Cooperia oncophora
Nematodirus battus - a sheep nematode that can infect cattle

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79
Q

Why can co-grazing cattle and sheep be inappropriate?

A

Co-grazing inappropriate for fasciola hepatica as these infect both cattle and sheep and avoiding co-grazing with sheep helps to control Johnes disease transmission.

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80
Q

What are the characteristics of cattle GI nematodes?

A
  • No migratory phase in the host
  • 2 sexes and mating is required to produce fertile eggs
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81
Q

What are the characteristics of infective L3 larvae of cattle GI nematodes?

A
  • Protected by an outer sheath, which is the retained ‘skin’ of second stage larvae. Makes them relatively resilient and they can survive on pasture for many months-1 year.
  • Sensitive to desiccation, so larval survival is reduced during hot, dry spells of weather.
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82
Q

Summarise the lifecycle of ostertagia ostertagi in cattle.

A

Eggs in faeces > hatch to L3 > ingestion > abomasum > adults in 3 weeks > females lay eggs

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83
Q

Summarise the lifecycle of cooperia oncophora.

A

Eggs in faeces > hatch to L3 > ingestion > proximal small intestine > adults in 3 weeks > females lay eggs

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84
Q

When does acquired immunity develop against cattle GI nematodes?

A

1 full grazing season for C. oncophora and up to 2 grazing seasons for O. ostertagi.

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85
Q

What is the risk of over-protecting calves in their first grazing season?

A

Calves that are over-protected in their first season at grass by excessive anthelmintic treatment are also at risk of slow development of immunity.

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86
Q

What is the rule of thumb for immunity development in calves?

A

Cattle must be at grass for at least eight months on pasture that has been used for cattle in the previous year, to get enough exposure for immunity to develop

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87
Q

What are the other factors affecting development of immunity in calves?

A

Climate on development and survival of infective larvae
Age
Sex
Nutrition
Potentially genetics.

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88
Q

What is the consequence of poor immunity development in dairy cattle?

A
  • Greater susceptibility
  • Production losses
  • Herds in which this occurs tend to have high levels of detectable anti-nematode antibodies in the bulk milk
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89
Q

What is the epidemiology of cattle GI nematodes?

A

Winter-spring = larvae survive well over winter and drop off in spring as temperatures rise

Spring-summer = worm eggs are shed after turnout and new larvae develop

Autumn-winter = egg counts drop off with immunity but larval levels continue to rise until autumn

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90
Q

What are the control strategies of cattle GI nematodes?

A
  • Grazing strategies
  • Strategic seasonal anthelmintic use to minimise pasture contamination
    -Targeted anthemintic treatments of the whole group based on diagnostic information - FEC, weight monitoring
  • Targeted strategic treatment of individual animals, based on monitoring stock health and growth rates
  • Housing treatments
  • Quarantine
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90
Q

How can grazing strategies control cattle GI nematodes?

A

If using clean pastures, 1st season grazing calves will have no opportunity to build up immunity.

If there are sheep on the farm, they can participate in mixed or sequential grazing, which can potentially benefit both types of stock through worm control and improved pasture utilisation. Care with liver fluke.

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91
Q

How does strategic seasonal anthelmintic use control cattle GI nematodes?

A
  • Kill worms before they reach maturity and prevent large numbers of worm eggs contaminating the pasture.
  • Autumn/winter born calves in 1st grazing, spring born calves in 2nd grazing
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92
Q

How does housing treatments control cattle GI nematodes?

A

Cattle go out to pasture the following year, they will not immediately contaminate pasture with worm eggs. Opportune time to treat for lungworm and liver fluke and to prevent lice and mange infestations later in winter.

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93
Q

Roughly how long should cattle be at pasture in order for them to be considered to have enough exposure for immunity to roundworms?

A

8 months

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94
Q

When are ‘strategic’ anthelmintic treatments most effective in cattle?

A

Within 1-3 weeks after turnout

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95
Q

Which of the following cattle GI parasites are of most concern in terms of Anthelmintic Resistance in Europe?

A

Cooperia oncophora

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96
Q

Name a benefit of FECs.

A

FECs measure the effectiveness of an anthelmintic in reducing egg excretion

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97
Q

When are larval numbers of cattle GI nematodes at their peak on pasture?

A

Late summer

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98
Q

What is strategic anthelmintic use?

A

Treating groups to limit pasture contamination

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99
Q

What does FEC not tell you?

A

Accurate total worm burden

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100
Q

What is the approximate pre-patent period of bovine nematodes?

A

21 days

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101
Q

Which class of anthelmintic is preferably used to minimise Ostertagiosis type II disease?

A

Macrolytic lactones

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102
Q

Plasma pepsinogen concentrations indicate the level of damage to what organ?

A

Abomasum

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103
Q

How can you test for level of exposure to ostertagia during the first grazing season?

A

Plasma pepsinogen testing at housing

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104
Q

What is it important to take into account when making any changes to control measures aimed at gastrointestinal worms?

A

Risk of lungworm infection

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105
Q

What is the effect of GI nematodes on young cattle?

A

Can reduce growth rate up to 30%

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106
Q

Before performing an anthelmintic efficacy check, you’d carry out a FEC. At what levels would the FEC be to proceed with treatment?

A

> 200epg

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107
Q

In which weather conditions will slow down the build-up of nematode larvae on pasture the most?

A

Hot, dry

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108
Q

What is the main disease mechanism caused by cattle GI nematodes?

A

Decreased protein absorption

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109
Q

When should repeat faecal samples be collected when completing an anthelmintic efficacy assessment?

A

14-17 days

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110
Q

Where can roundworm ‘overwinter’ and reinfect cattle which have been housed and turned back out in spring?

A

Larvae on pasture and worms which have hyperbiosed in the intestines of older cattle

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111
Q

When performing an anthelmintic efficacy check, what is the recommended minimum percentage efficacy?

A

95%

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112
Q

What is the cause of Type II Ostertagiosis?

A

Mass emergence of arrested/hyperbiosed larvae

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113
Q

What is the hosts and site of telodorsagia circumcinta?

A

Sheep, goat, deer, camel, llama
Abomasum

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114
Q

What is the hosts and site of haemonchus contortus?

A

Sheep, goat, cattle, deer, camel, llama Abomasum

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115
Q

What is the hosts and site of nematodirus battus?

A

Sheep, goat, (cattle)
Small intestine

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116
Q

How is telodorsagia circumcinta transmitted?

A
  • Direct life cycle
  • Periparturient rise in ewe egg counts is main route of transmission to lambs
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117
Q

What are the clinical signs of telodorsagia circumcinta?

A

Weight loss
Diarrhoea

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118
Q

What is the epidemiology of telodorsagia circumcinta?

A

Disease mainly in first season lambs in later summer/autumn, can get type 2 disease the following spring

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119
Q

How is nematodirus battus transmitted?

A
  • Direct life cycle
  • Lamb-lamb transmission
120
Q

What are the clinical signs of nematodirus battus?

A

Scouring, dehydration, death, disease in pre-patent period

121
Q

What is the epidemiology of nematodirus battus?

A
  • Specific batching conditions is a cold snap followed by temperatures of over 10˚C
  • Spring disease
  • Climatic conditions and pasture contamination level can help to mitigate risk
  • PPP = 14 days
122
Q

How is haemonchus contortus transmitted?

A
  • Direct life cycle
  • Hypobiosis and re-emergence in ewes main mode of transmission
123
Q

What are the clinical signs of haemonchus contortus?

A

Anaemia
Oedema
Weight loss
(no diarrhoea)

124
Q

What is the epidemiology of haemonchus contortus?

A

Disease any time from mid-spring to autumn, needs warm humid conditions

125
Q

How are sheep nematodes controlled?

A

Strategic anthelmintic control is a balancing act to prevent economically significant levels of infection, while allowing the build-up of immunity, and leaving at least some of the parasite population unexposed to anthelmintics, called in refugia.

126
Q

How is strategic anthelmintic control achieved?

A
  • Prevention by use of anthelmintic
  • Evasion of infective larvae by strategic grazing
  • Decrease contamination by decreasing the effective density of susceptible animals
127
Q

What are alternative methods of controlling ovine nematodes?

A
  • Vaccines – lungworm, slow to materialise for PGE
  • Nutrition – protein supplementation, but is expensive
  • Nematophagous fungi predate on nematodes, but need daily intake
  • Bioactive forages (high in condensed tannins) but have practical and nutritional problems
  • Breeding for parasite resistance or resilience
128
Q

What does development of resistance of ovine nematodes depend on?

A

Numbers of worms in refugia. Larvae on pasture and worms in untreated animals.

129
Q

What are candidate indices for targeted selective treatment in sheep?

A
  • Faecal egg count
  • Diarrhoea/dag score
  • Body condition
  • Weight gain
  • ‘Farmer’s eye’
130
Q

How is resistance in ovine nematodes prevented?

A
  • Use quarantine dosing
  • Treat adult sheep only when necessary
  • Do not under-dose
  • Check for resistance using FECRT
  • Reduce dosing frequency by using FEC
  • Tailor control to the main problem parasite species
  • Avoid dose-and-move to clean pasture
  • Breed from worm-resistant rams
131
Q

What are the 3 steps of quarantine treatments?

A
  1. Treatment – 2 broad spectrum groups with the lowest frequency of resistant worms
  2. Keep in for 24-48 hours to allow eggs produced before treatment to pass out
  3. Turn out to ‘dirty’ high risk pasture to minimise impact of any residual resistant parasites
132
Q

How are parasites controlled in January born lambing systems?

A
  • If housed intensively or turned out onto clean forage, crops will not come into contact with worms
  • If turned out, main risk is from early hatch of Nematodirus
  • Worming often unnecessary but replacement ewes from these flocks will have no/poor immunity
133
Q

How are parasites controlled in February/March born lambing systems?

A
  • Most at risk from Nematodirus and concurrent coccidiosis
  • Usually finished before main risk period for Teladorsagia
  • Use a benzimidazole if high risk, FEC monitoring to keep check on Teledorsagia and Haemonchus
134
Q

How are parasites controlled in March/May lambing systems?

A
  • At risk from Nematodirus on high risk pastures
  • Treatment with BZ if Nematodirus risk high, FEC pre-and post-weaning at 3-4 week intervals
135
Q

How are parasites controlled in September+ born lambing systems?

A
  • Frequently challenged by high worm burdens on grass in autumn and often of unknown history
  • Quarantine bought in stock
  • FEC monitoring essential at regular intervals
136
Q

How can resistance to flukicides be prevented?

A
  • Rotational use of TCBZ, closantel and nitroxinil
  • Avoid us of combination products
  • Reduce infection risk by identification and exclusion of snail habitats (drainage), keep flocks off wettest fields at peak season
137
Q

What are the clinical signs of acute ovine fasciolosis and how is this treated?

A

Sudden death, anaemia ascites (July-October)

FEC 0. Use Triclabenazole to treat all sheep and move, or re-treat 3 weeks later

138
Q

What are the clinical signs of subacute ovine fasciolosis and how is this treated?

A

Rapid weight loss and anaemia (October-January)

FEC 0. Use Triclabenazole to treat all sheep and move, or re-treat 3 weeks later

139
Q

What are the clinical signs of chronic ovine fasciolosis and how is this treated?

A

Progressive weight loss anaemia (January-April).

FEC 100+. All flukicides are active against the mature fluke. Treat and move to lower risk pasture

140
Q

How do cyathostomins cause disease in equine?

A

Mass emergence causes colitis with severe diarrhoea and endotoxaemia.

141
Q

What is the epidemiology of cyathostomins?

A
  • Larvae can encyst over 3 years
  • Immunity is slow/incomplete to emerge
142
Q

How do strongyles cause disease in equine?

A

Arteritis causes vascular compromise and ischaemic bowel requiring surgical resection

143
Q

How is strongyles eliminated?

A

Long prepatent period of over 4 months so mostly eliminated by serial dosing

144
Q

How does anoplocephala perfoliata?

A

Implicated in intussusception colic. In heavy burdens, cause damage to the caecal mucosa where they latch on and feed

145
Q

What is the epidemiology of anoplocephala perfoliata?

A
  • Rarely identified on conventional faecal worm egg counts
  • Not truly seasonal
146
Q

What is the epidemiology of parascaris equorum in equine?

A
  • Most significant foal parasite
  • Good immunity develops so rarely a problem in adults
147
Q

How are equine parasites diagnosed?

A
  • Post mortem – gold standard but invasive
  • Faecal egg counts – can’t differentiate cyathostomins from large strongules unless eggs cultured to L3 stages
  • Cyathostomin (redworm) ELISA
  • Seroloy tapeworm ELISA, saliva tapeworm ELISA, sedimentation/flotation method best
148
Q

Describe faecal egg counts as a diagnostic measure for equine parasites.

A
  • Only demonstrates presence of reproducing adult females, not necessarily reflect adult worm burdens
  • Notoriously poor for assessing tapeworm
  • Variability in daily shedding level
149
Q

What does clumping on FEC indicate?

A

False positives

150
Q

How are cyathostomin FECs interpreted?

A

Take care particularly in late autumn as lower positive counts may be significant with encysted cyathostomins

151
Q

How are ascarid FECs interpreted?

A

Ascarids are highly prevalent layers and counts to not accurately represent burden, treat when positive

152
Q

What are the uses of small redworm bloods tests?

A
  • Indication of antibody levels to the larvae
  • Tells you if animal is exposed to high or low level of this parasite recently
  • Used along side risk of animal and FEC
153
Q

What are the limitations of small redworm blood tests?

A
  • Does not tell you exactly whether larvae are encysted
  • Not appropriate to use in high risk animals with high FEC and you know pasture management is not good.
154
Q

What are the anthelmintic pharmaceutical options in equine?

A

Benzimidazoles – Fenbendazole, Mebendazole

Tetrahydropyrimidines – Pyrantel

Acylated quinoline pyrazines – Praziquantel

Macrocyclic lactones - Avermectins (Ivermectin), Milbemycins (Moxidectin

155
Q

What must be done before a faecal egg count reduction test in equine?

A
  • FEC before – d0
  • Dose at 110% estimated bodyweight
  • Then WEC 14 days after worming
  • = (FWEC days 0 – FWEC day 14) / FWEC day 0
156
Q

Describe a faecal egg count reduction test in equine.

A
  • Pick a FECRT test with low detection limits
  • Need to test over 6 horses in herd to be accurate, ideally all
  • If inconsistent results consider mis-dosing or underdosing
157
Q

What is the 80:20 rule of high shedders in equine?

A
  • 80% of the worms in a population were shed by 11% of TB horses and 15% of leisure horses
  • But can horses change group – individual horses in yard based system tend to stay in the same group and environmental conservation system horses changed group
158
Q

What is the gold standard approach to worm control options in equine?

A
  • Target dosing in response to a positive worm egg count – not all horses on a yard simultaneously. Leave some inrefugia and need good records to manage all horses effectively
  • Strategic dosing for tapeworm and encysted cyathostomins
  • Remember to treat foals for ascarids
159
Q

Describe pasture management for equine worm control.

A

Poo picking – removes contamination, twice weekly prevents transmission effectively

Rotation – move then dose. Contaminates new environment with susceptible worms before worming

Harrowing – only helpful if dry and hot

Cross grazing – care with cohorts carrying triodontophorus axei and dictycaulus viviparus

160
Q

How can you monitor equine for worming control?

A
  • Use shorter acting formulations where possible
  • Long acting formulations increase chronic low dose exposure and increase selection pressure for resistance
  • Minimise pasture contamination by maximising pasture management
161
Q

What are the control measures for echinococcus granulosus in dogs?

A
  • Praziquantel every 6 weeks in high risk areas to 3 months – highly effective, more frequent for higher risk groups, such as working dogs
  • Hygiene – carcass removal, pick up faeces, break sheep-to-dog cycle
162
Q

What are some key features of dipylidium caninum?

A
  • Flea is key in transmission
  • Pass gravid proglottids in faeces
  • Release tough egg packets that can survive for some time
163
Q

Briefly outline the lifecycle of toxocara species.

A
  • Large, intestinal nematode of dogs and foxes
  • Hepato-tracheal migration
  • Reactivation – transplacental and transmammary infection
  • Paratenic hosts – larval migration, ingestion by definitive host
  • Embryonated eggs – animal fur, environment, food, undercooked meat
  • People are accidental hosts
164
Q

What are the clinical signs of toxocara species?

A
  • Ascites
  • Hypoalbuminaemia
  • Cachexia – anorexia and weight loss
  • Constipation or diarrhoea in pups
165
Q

How can toxocara species be controlled?

A
  • Routine worming of dogs
  • Early worming of pups, as they shed the most eggs when under 13 weeks of age
  • Special care and worming during pregnancy and nursing as can pass from mother to pups
  • Remove faces
  • Prevent access to raw meat/hunting rodents
166
Q

Name the 5 anthelmintics used for routine worming in dogs.

A

Benzimidazoles
Macrocyclic lactones
Piperazine citrate
Praziquantel (tapeworm)
Combination products

167
Q

How should you worm a dog that lives indoors only, no direct contact with other dogs, sandpits, parks, snails, slugs or raw meat and prey aniamsl?

A

Treat 1-2 times a year against roundworms or carry out faecal examination

168
Q

How would you treat a dog that goes outdoors, has direct contact with other dogs, but no contact with prey animals, raw meat, slugs or snails?

A

Treat 4 times a year against roundworms or carry out faecal examination

169
Q

How would you treat a dog that goes outdoors, has direct contact with other dogs, contact with prey animals, raw meat, slugs and snails?

A

Treat 4-12 times a year against roundworms and tapeworms depending on risk analysis

170
Q

How would you treat a dog that lives in a fox tapeworm endemic area, eats prey animals, goes outside to hunt without supervision?

A

Treat monthly against tapeworms, 4-12 times a year against roundworms depending on risk analysis

171
Q

Describe transmission of toxocara cati.

A

No transplacental transmission. Transmammary transmission – treat kittens from 3-4 weeks old

172
Q

How should you worm a cat that lives indoors with low infection pressure from worms and eating rodents is unlikley?

A

1-2 times a year faecal examination and treatment if necessary, or treat 1-2 times a year against roundworms

173
Q

How should you worm a cat that is free to roam with high infection pressure from worms and will likely eat rodents?

A

Carry out faecal examination and treatment is necessary at least 4 times a year or treat against roundworms and tapeworms at least 4 times a year

174
Q

What is the basic control measures for fleas?

A

Insecticides applied to all living quarters, vacuum everywhere possible – even under furniture. Treat all susceptible animals in the home

175
Q

Name 7 insecticides.

A

Pyrethrin and pyrethroids
Neonicotinoids
Phenyl-pyrazoles
Spinosad
Oxadiazines
Macrocyclic lactone
Isoxazolines

176
Q

How are adult flea burdens eliminated?

A
  • Hair coat length
  • Bathing, swimming and shampooing (imidacloprid, fipronil)
  • Ease of administration
177
Q

How do insect growth inhibitors decrease the environmental reservoir of fleas?

A

Mimic juvenile growth hormone thus preventing the fall of the natural hormone in flea larvae. The flea life cycle is broken at the larval stage. Decrease egg viability to varying degrees

178
Q

Why may there be re-infection with insect growth inhibitors?

A
  • Pupae and pre-emerged adults remain unaffected and viable for long periods
  • Potential for re-infestation of treated animals will remain until all pre-existing pupae have hatched
  • Re-infestation with adult fleas may occur at any time that the animal visits a contaminated indoor or outdoor environment
179
Q

Why is chitin as essential component of the insect exoskeleton?

A

Gives rigidity to the egg tooth (essential for hatching larvae)

180
Q

What is the effect of chitin synthesis inhibitors?

A
  • Eggs to have decreased viability/poor hatchability
  • Subsequent larval moults may be abnormal if affected eggs do manage to hatch
181
Q

Why may tick abundance increase?

A
  • Increasing deer populations?
  • Changes in sheep populations and distribution?
  • Many other species are hosts
  • Climate warming? Prolonged tick ‘season’?
  • Forestry plantations
182
Q

Name 2 vector borne diseases and their vectors.

A

Dirofilariasis immitis with mosquito vector

Leishmania with sandflies

183
Q

What are the clinical signs of angiostrongylosis?

A

Early infection can be asymptomatic
Coughing
Dyspnoea
Anaemia
Depression
Anorexia
Signs of coagulopathy

Chronic verminous pneumonia leads to anorexia, weight loss, emaciation and pulmonary hypertension

184
Q

How is angiostrongylosis diagnosed?

A

Faecal examination (Baermann)
Bronchial lavage
Blood test (worm antigen)

185
Q

How is angiostrongylosis treated?

A

Anthelmintics and supportive care

186
Q

How is angiostrongylosis controlled?

A

MCL based products monthly as prophylaxis

187
Q

What are the risks of ectoparasite treatment?

A

Risk of resistance – already developed in farm animals and horses

Risk to non-target invertebrates – environmental contamination

188
Q

What is the BVA’s 5 point plan?

A
  1. Work with clients to prevent and check for parasites
  2. Understand the potential risks to animals, humans and the environment
  3. Take a risk-based approach to prescribing
  4. Ensure appropriate use
  5. Record and monitor use
189
Q

What are the disease that could be contracted when travelling abroad with pets?

A

Rabies
Echinococcus multilocularis (tapeworm)
Exotic ticks
Tick-borne diseases – Rickettsia, Babesiosis
Leishmaniosis
Dirofilaria species

190
Q

What are the measures to protect against echinococcus when travelling aborad?

A
  • Be approved for use in the country it’s being given in
  • Contain praziquantel or an equivalent proven to be effective against the Echinococcus multilocularis tapeworm
  • Be recorded in pet passport or animal health certificate
  • Be given at least 24 hours and no more than 120 hours before entering the UK
191
Q

What ectoparasites affect alpacas?

A
  • Chorioptes, scabies, psorptes (rarely demodex or trombiculids) mange mites
  • Lice – biting and sucking
  • Flies – horse, stable, face, horn, blowflies, horse, deer
  • Culicoides species – an allergic skin disease of camelids
192
Q

Where are choroptes bovis mites found on alpacas?

A
  • Surface dwellers
  • Mild pruritis, alopecia and scaling of the feet and tail base
  • Extension to ventral abdomen, medial limbs and the ears
  • Superficial skin scrapes at the margin of the lesional areas
193
Q

How must llamas be treated for mites and why?

A

Llamas do not absorb ivermectin as well as ruminants, oral or injectable. Successful treatment of alpacas with lice, sarcoptic and psoroptic mange with 2 injections of moxidectin 7-10 days apart

194
Q

Why are topical applications of insecticidal/acardicidal products less effective in camelids?

A

Llama hair/fibre does not contain lanolin – topical applications used in other ruminants may not be as effective in camelids

195
Q

How are chorioptes infections treated?

A
  • Macrocyclic lactone-based products may not be very effective
  • Topical therapy - fipronil spray, selenium sulphide shampoos, lime sulphur dips, pour on preparations
  • Bathing with keratolytic agents such as dog shampoos
  • Environmental management of bedding
  • Ivermectin
196
Q

What dose of ivermectin is used for camelids for chorioptes infections?

A

400 ug/kg by subcutaneous injection on a weekly basis. Weigh and treat all animals. Treat for two life cycles – 6 weeks

197
Q

What are the ectoparasites of goats?

A

Mites - chorioptes, sarcoptes, psoroptes, demodex, deotrombiculids, forage mites

Ticks

Lice - bovicola caprae, bovicola crassipes, bovicola limbatus, linognathus stenopsis, linognathus africanus

Fleas

Culicoides

198
Q

How are chorioptic infections of goats treated?

A
  • Environment/housing
  • Topical – selenium sulphide, fipronil, amitraz, lime sulphur dip
  • Treat the whole group
  • Milk and meat withdrawal
  • Systemic – macrocyclic lactones
  • Severely affected individuals – isolate and treat separately, hypersensitive individuals, cull
199
Q

How are macrolytic lactones administered to goats?

A

Topical, subcutaneous or oral

Topical - trapped in skin layers
Metabolic state and subcutaneous fat
Double dose for goats

200
Q

What is bot fly in sheep?

A

Oestrus ovis squirts larvae into nostrils. Can cause sneezing, nasal discharge, head rubbing/shaking

201
Q

How is bot fly infection treated with macrolytic lactones in sheep?

A
  • Do we need to treat if fly/larvae numbers low?
  • Risk of resistance for endoparasites – avoid prophylactic treatment
  • Treat based on clinical signs/individual risk
  • Twice a year flock treatment if risk high
202
Q

What is blowfly strike increased by?

A

Warm weather
High humidity
Undocked tails
Faecal soiling
Lowland flocks
High blowfly numbers
Foot rot
Head wounds in rams
Thick fleeced breeds
Lack of preventative insecticide use

203
Q

What is blowfly strike decreased by?

A

Good parasitic worm control
Tail docking
Dagging and crutching
Foot rot control
Shearing
Frequent flock inspection, especially at high risk times
Appropriate insecticide use

204
Q

How can blowfly strike be treated prophylactically?

A

Insect growth regulators (IGRs), not a treatment so still need to monitor flock, as eggs hatch within 12 hours to L1

205
Q

Name 3 tickborne diseases in sheep.

A

Louping ill virus - CNS signs, vaccination

Tickborne fever - suppress immune system, abortion

Tick pyaemia - no treatment

206
Q

What are organophosphate dips?

A
  • Treats a range of other ectoparasites
  • Need certificate of competence to use
  • Environmental risk
  • Must be a dip and not shower/jet
207
Q

Which ectoparasites affect cattle?

A

Mites - chorioptes, psoroptes, rarely Scabies/Demodex

Lice – Warble

Flies - head fly/hydrotea irritans, horn fly/haematobia irritans, face fly/musca autumnalis

Ticks – Besnoitiosis

208
Q

What are the diagnostic methods for ectoparasites?

A
  • Clinical presentation
  • Hair plucks and scale for mites, lice and eggs
  • Superficial skin scrapes for surface and epidermal dwelling mites
  • Microscopic examination
  • Serology
  • Hair plucks/deep skin scrapings/skin biopsy
209
Q

What are the lice that affect cattle?

A
  • Bovicola bovis
  • Haematopinus eurysternus (short-nosed sucking louse)
  • Linognathus vituli (long-nosed sucking louse)
  • Solenopotes capillatus (little blue cattle louse)
210
Q

What are the clinical signs of a lice infestation/pediculosis?

A

Pruritus
Alopecia
Excoriation
Self-wounding
Anaemia

211
Q

How are lice infestations treated?

A
  • Synthetic pyrethroids spot-on/pour-on
  • Macrocyclic Lactones pour-on/injectable
  • Therapeutic options for chorioptic mange are similar to those for lice
212
Q

What is used to treat bovine psoroptic mange?

A
  • Use glucocorticoids not meloxicam for skin disease
  • 4 % permethrin pour-on product – under cascade at increased frequency (three treatments at two weekly intervals)
  • Possible failure to respond to macrocyclic lactones
213
Q

What management strategies can be used to treat bovine psoroptes mange?

A
  • Removal and destruction of crusts and bedding
  • All animals in the group and any in-contacts
  • Move out of infected housing
214
Q

Which ectoparasites affect equids?

A

Mites – chorioptes

Lice

Flies +insect bite hypersensitivity
- Culicoides
- Musca (house and face)
- Stomoxys (stable)
- Haematobia (horn)
- Tabanus (horse)
- Culicidae (mosquitoes)
- Simulium (black)

215
Q

What are the seasonal and viral factors of quine culicoides?

A

Seasonal – cutaneous hypersensitivity

Viral agents – bluetongue virus, Schmallenberg virus, African Horse Sickness

216
Q

What chemical controls can be used for equine culicoides?

A
  • Topical repellents
  • Insecticide treated mesh/protective housing/treated nets – some degree of control with cypermethrin/pyrethrins
  • Host systemic treatments - MLs
  • In door sprays/CO2/insect traps
  • Kairomones
  • Synthetic pyrethroids
217
Q

Why do coccidiosis cause economic losses?

A
  • Inadequate productivity of animals
  • Morbidity and mortality
  • Costs of prophylaxis and therapy
  • Predisposition to other conditions, such as necrotic enteritis, intussusception, ruptured tendons
218
Q

What do coccidial oocysts require for sporulation?

A

Warmth, moisture and oxygen

219
Q

How can environmental management be used to control coccidiosis?

A
  • Avoid overstocking
  • Keep litter dry
  • Building ventilation and drainage to control humidity
  • Avoid contamination
  • Disinfect buildings between batches of animals to kill oocysts.
  • If litter is not replaced between batches, it can be heaped, which results in it heating up (50ºC kills oocysts), then forked over and the process repeated to ensure all oocysts are destroyed.
  • Biosecurity
220
Q

Which coccidial agents are used in poultry?

A

Amprolium
Toltrazuril
Diclazuril
Lasalocid
Monensin

221
Q

Which coccidial agents are used in cattle and sheep?

A

Decoquinate
Toltrazuril
Diclazuril

222
Q

Which coccidial agent is used in pigs?

A

Toltrazuril

223
Q

Which coccidial agents are used in rabbits?

A

Sulfamethoxazole
Trimethoprim

224
Q

Why is prevention of coccidiosis better than cure?

A

The same agents can be used but by the time clinical signs appear the intestine has already been damage and it is better to try to prevent further cases

225
Q

How are coccidial agents administered to broiler chickens?

A
  • Lifelong in-feed medication
  • Withdrawal period 5-7 days
  • Switching drugs between batches recommended – avoid development of resistance
226
Q

How are coccidial agents administered to layer chickens?

A
  • On wire floors – may not require medication
  • On litter – regimen to protect from clinical disease while allowing the development of immunity
  • Stepwise decreasing level administered over first 16-18 weeks
227
Q

How can poultry be vaccinated against coccidiosis?

A
  • Virulent or attenuated strains
  • Attenuated vaccines - ‘precocious’ strains, undergo rapid development in the intestine with minimal damage
  • 8 species of Eimeria incorporated in vaccines
228
Q

Why is natural infection important to coccidiosis vaccination in poultry?

A

Vaccination requires that immunity is boosted by natural infection – litter must be sufficiently moist to allow sporulation. As there is no cross-protection between species

229
Q

What does cryptosporidium cause in neonatal calves and lambs?

A

Diarrhoea in neonatal calves and lambs: batch rearing, hygiene. On-farm zoonosis

230
Q

What is given to calves to prevent cryptosporidium?

A

Halofuginone – prophylaxis in calves

231
Q

Which parasite can earthworms be a paratenic host for?

A

Histomonas meleagridis

232
Q

What is the importance of toxoplasma gondii to pregnant sheep and goats?

A

Abortion
Mummification
Stillbirth
Weakly lambs

233
Q

What is the importance to pregnant and immunocompromised people?

A

Pregnant - abortion, stillbirth and foetal abnormalities, such as hydrocephalus

Immunocompromised - leading to acute generalised disease

234
Q

How is toxoplama gondii diagnosed?

A

Fluorescent Antibody Test (FAT)
Immunohistochemistry
PCR
Indirect Fluorescent Antibody Test (IFAT)
ELISA
Latex agglutination test

235
Q

What are the differential diagnoses of ovine abortion?

A

Enzootic abortion (Chlamydophila abortus)
Toxoplasmosis
Schmallenberg virus
Campylobacter
Salmonella
Listeria
Q-fever
Brucella melitensis (not in UK)

236
Q

How is toxoplasma gondii transmitted to the definitive host?

A
  • Carnivory of infected intermediate hosts
  • Ingestion of sporulated oocysts (secondary importance)
237
Q

How is toxoplasma gondii transmitted to intermediate hosts?

A
  • Ingestion of sporulated oocysts (excreted by definitive host)
  • Carnivory of infected intermediate hosts
  • Vertical transmission (sheep, human, rodents)
238
Q

What can decrease the effectiveness of toxoplasmosis vaccination in sheep?

A

Vaccination would be less effective if endogenous TPI common

239
Q

How is toxoplasmosis controlled in sheep?

A
  • Prevent contamination by oocysts from cats
  • Cats are difficult to eliminate from farms
  • Beneficial in controlling vermin
  • Vaccination of ewes
  • Anticoccidial agents
240
Q

Describe toxoplasmosis tachyzoites.

A
  • Rapidly multiplying crescent-shaped stage
  • Lytic cycle – endodyogeny
  • During the acute tissue phase
241
Q

Describe toxoplasmosis bradyzoites.

A
  • Slow-growing, comma-shaped forms
  • Found in clusters in the tissues
  • Enclosed by cyst (part host, part parasite)
  • Chiefly muscles and the brain, in chronic (latent) toxoplasmosis
  • Protected from host immune response by cyst wall
242
Q

What type of vaccine is the toxoplasma gondii vaccine and when is this administered?

A
  • Live vaccine (so cold chain needed)
  • Single dose at least 3 weeks prior to tupping (mating)
  • Re-vaccination after 2 years
243
Q

What is Decoquinate?

A

Anticoccidial agent for sheep. 6% premix for medicated feed to prevent abortions and perinatal losses due to toxoplasmosis. Feed continuously for the last two-thirds of pregnancy/final 14 weeks prior to lambing.

244
Q

What are the hosts of neospora caninum?

A

Cattle act as intermediate hosts – tachyzoites and bradyzoites

Dogs act as the definitive host – oocysts, tachyzoites and bradyzoites

245
Q

What does neospora caninum cause?

A
  • Severe encephalomyelitis
  • Abortion and neonatal death in cattle
246
Q

How is neospora caninum vertically and horizontally transmitted?

A

Horizontal transmission in cattle – cattle infected by the ingestion of oocysts shed by infected dogs

Vertical transmission – foetus infected by parasite migration from persistently infected dams, very efficiency over several generations, infected animals mya pass to offspring of successive pregnancies.

247
Q

How is neospora caninum transmitted exogenously and endogenously?

A

Exogenous transplacental transmission: dog > cow > foetus

Endogenous transplacental transmission: cow > foetus > cow > foetus

248
Q

How is neospora caninum diagnosed?

A

PCR on foetal brain tissue
Immunohistochemistry
ELISA

APHA routinely tests for N.caninum antibodies in bovine sera, together with Leptospira hardjo, IBR and BVD

249
Q

What are the differential diagnoses for bovine abortion?

A

Neospora
Campylobacter
Salmonella
Leptospirosis
Listeriosis
Schmallenberg virus
BVD
Q-fever
Brucellosis – not UK

250
Q

How is neospora caninum prevented in cattle?

A
  • Reduce risk of infection of/from dogs
  • Feed, hay, bedding, water: keep free of dog faeces
  • Grazing, especially footpaths
  • Prompt disposal of placentas, foetuses and stillborn calves
251
Q

What is the vaccination for neospora caninum in cattle?

A
  • Arguably the only feasible solution
  • Killed N. caninum tachyzoite vaccine
  • Immunisation of cattle with live tachyzoites before pregnancy confers some protection against a fetopathic challenge given during pregnancy
252
Q

Distinguish biological and mechanical vectors.

A

Biological – where the parasite must go through some stage of their lifecycle within the host

Mechanical – less efficient, transmit via mouthparts from host to host

253
Q

What factors affect a vector’s ability to be infectious?

A

Vector survival rate
PPP
Period of infectiousness
Biting rate/meal size
Vector-host density
Distribution of infection

254
Q

What are the characteristics of mechanical vectors?

A
  • Interrupted feeds
  • Short re-feeding interval
  • High fly mobility
  • High survival of pathogens on insect
255
Q

How long is the tick lifecycle?

256
Q

How can you distinguish female and male ticks?

A

Only female ticks engorge fully with blood. Has dorsal scutum plate, of which females have a small scutum so that they can engorge fully with blood.

257
Q

What are the conditions needed for tick questing bhevaiour?

A

Optimal is 17-20˚C
Relative humidity above 80%

258
Q

What are the direct effects of tick feeding?

A
  • Blood loss, anaemia
  • Inflammation
  • Bacterial infection
  • Restlessness, poor feeding
  • Reduced body condition and lower productivity
  • Tick paralysis
259
Q

How do ticks transmit pathogens?

A
  1. Attach securely to host
  2. Relatively non-host specific
  3. Large blood meals
  4. Trans-stadial transmission
  5. Trans-ovarial transmission
  6. Transmission at co-feeding (SAT)
  7. Saliva production during feeding
260
Q

What about tick saliva production makes them good at spreading pathogens in the skin?

A

Produce a lot of water that needs to be removed so often extract water and defecate at the same time. Because they produce a lot of saliva, there are lots of pathogens in the saliva back into the host.

261
Q

What is the bacterium that causes anaplasmosis/tick borne fever?

A

Anaplasma phagocytophilum

262
Q

What are the clinical signs of anaplasmosis?

A
  • Sustained high temperature, anorexia and depression
  • Tickborne fever suppresses the animals immune system predisposing it to further diseases
  • More severe manifestation of louping ill, tick pyaemia and respiratory disease
  • Abortion
  • Severe metritis
  • Infertile for a month
263
Q

What are the clinical signs of babesiosis/redwater fever?

A
  • Increased temperature
  • Diarrhoea which ceases after around 36 hours and then becomes constipation
  • Red urine (due to haemoglobin produced by the rupture of the red blood cells)
  • Increased pulse rate
  • Abortion
264
Q

What are the clinical signs of tick pyaemia?

A

Debility
Crippling lameness
Paralysis.
Pyemic abscesses

265
Q

What are the clinical signs of louping ill?

A

Initial fever
Depression
Anorexia

Acute phase – muscular trembling, unsteady or high stepping

Seizures and paralysis might develop with a typical posture being the head thrown back over the shoulder

Coma and death occurs in a proportion of animals

266
Q

How is louping ill diagnosed?

A

Confirmed by blood test, detecting the presence of virus in the brains from dead animals and/or typical microscopic lesions.

267
Q

Why are tick and deer abundance linked?

A

Because adults reproduce after feeding on deer, deer abundance and tick abundance are strongly correlated. Deer may be described as reproductive hosts.

268
Q

Why are deer dead end hosts for Lyme borrelia?

A

Deer do not transmit infection - so deer are described as dead-end hosts. They are also dilution hosts because they divert ticks away from competent hosts and effectively remove circulating pathogens from the system

269
Q

What causes increased incidence of tick borne disease?

A
  • Warmer climate
  • Increasing UK deer population
  • Urban wildlife encroachment
  • Travelling pets on holiday
    *- Refugees – transhumance
270
Q

Why are ticks difficult to control?

A
  • Only 2% of lifecycle spent on the host
  • The timing of peak activity is weather dependent and can be hard to predict
271
Q

What are the advantages of plunge dips as tick control in livestock?

A
  • Immediate and effective
  • Protects against sheep scab, blwofly strike, lice and keds
272
Q

What are the disadvantages of plunge dips as tick control in livestock?

A

Operator safety
Environmental toxicity
Legal controls on use and disposal

273
Q

What are the advantages of pour-on treatments for tick control in livestock?

A

Longer protection and easier to administer

274
Q

What is the disadvantage of pour-on treatments for tick control in livestock?

A

No immediate tick kill

275
Q

What is cysticercus cellulosae?

A

Larval stage is just the head of tapeworm in a cyst. Adult is a long ribbon.

276
Q

What do taenia solium eggs contain?

A

An oncosphere or hexacanth larva which when ingested by pigs, excysts in the intestines

277
Q

Briefly outline the lifecycle of taenia solium.

A
  1. Eggs capsules from human stools contaminate vegetation which pigs may eat. Eggs viable for up to 9 months.
  2. Passes through the mucous membranes entering the bloodstream and develops into a cysticercus/bladderworm in the pig’s muscles.
  3. If pork is eaten poorly cooked, the cysticercus evaginates its scolex in the duodenum and grows into an adult up to ten meters in length.
278
Q

How is taenia solium controlled?

A
  • Can treat humans but hard to tell when you have it
  • Can improve sanitation which would have a large effect
  • Can inspect carcasses and reject anything with cysticercosis
  • Cook or freeze meat before eating
279
Q

What are the common tissues in humans for taenia solium cysticercosis?

A

Skeletal muscles
Extraocular muscles
Eye - detachment of the retina and blindness
Brain - intraventricular, subarachnoid, parenchymal cysts
Tongue/cheek - easier to treat via surgery

280
Q

How is intraventricular neurocysticercosis treated?

A

Traditionally treated by surgical removal, but studies have shown that high levels of Albendazole (roughly double a normal dose) and steroids are also effective.

281
Q

How is subarachnoid neurocysticercosis treated?

A

With high doses of Albendazole and steroids

282
Q

How is parenchymal neurocysticercosis treated?

A

Albendazole treatment length depends largely on the number of lesions present in the brain. If the number of cysts is very high, albendazole may not be administered, because it would cause massive swelling as it destroys the cysts.

283
Q

Briefly outline the life cycle of taenia saginata.

A
  1. Eggs passed through faeces of infected DH and ingested by the cow
  2. The digestive enzymes will break the thick shell of the egg and allow the zygote to form
  3. The zygote then penetrate the mucous layer and enter the circulation of the bovid
  4. Young larval stages of taenia saginata form a pea sized fluid filled cyst/cysticercus in skeletal and cardiac fibres, and very rarely in liver and lungs.
284
Q

How is beef inspection for taenia saginata done?

A
  • 1 cut in internal pterygoid muscles
  • 2 cuts in external masseter muscles parallel to the plane of the mandible
  • 1 cut through the intraventricular septum
  • 2nd most likely site for lesions is the shoulder but no cute made in shoulder
285
Q

What is cold treatment of meat?

A

Not exceeding -7˚C not less than 3 weeks, not exceeding -10˚C not less than 2 weeks

286
Q

How is meat affected with canine tapeworms disposed of?

A

Rejected as category 2 – aesthetic for humans but pathogenic to dogs. Category 2 as can’t go into pet food

287
Q

What is the metacestode of echinococcus granulosus?

A

Hydatid cysts

288
Q

What is the metacestode of taenia hydatidgena?

A

Cysticerus tenuicollis

289
Q

What is the metacestode of taenia ovis?

A

Cysticercus ovis

290
Q

What is the metacestode of taenia multiceps?

A

Coenurus cerebralis

291
Q

What is the metacestode of taenia pisformis?

A

Cysticercus pisformis

292
Q

What is the metacestode of taenia serialis?

A

Coenurus serialis

293
Q

How are metacestodes classified by heads?

A

Single head = cysticercus
Multiple heads attached to the wall = coenurus
Hydatid = many heads, detached scolices ‘sand’

294
Q

Where does taenia ovis metacestode form?

A

Skeletal and cardiac muscle in sheep

295
Q

Which canine tapeworms are rejected as category 2?

A

Echinococcus granulosus
Taenia ovis
Taenia multiceps
Taenia hydatidgena
Taenia serialis

296
Q

Where do taenia multiceps metacestodes form?

A

CNS, especially brain

297
Q

Where do taenia hydatidgena metacestodes form?

A

On surface of abdominal organs

298
Q

Where do taenia pisformis metacestodes form?

A

Abdominal cavity of lagomorphs

299
Q

Where do taenia serialis metacestodes form?

A

Subcutaneously attached tissue and connective tissue

Clinical Veterinary Science and One Health 23/24 (36 decks)

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