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Year 3 > Parasitology > Flashcards

Parasitology Flashcards

1
Q

The intermediate hosts of lungworms are usually what?

A

Molluscs

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2
Q

Give some features common to bursate nematodes (trichostrongyles)

A

Direct life cycle
Adult male worms have a ‘bursa’
Small buccal capsule behind mouth
Pharynx
Cuticular decorations aid identification
Posterior end of male worm has an inflation of the cuticle and spicules which aid in reproduction
Eggs are undifferentiated

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3
Q

Which is the infective stage of trichostrongyles?

A

L3 (ensheathed)

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4
Q

What is meant by pre-patent period?

A

Time taken from the time of infection (ingesting L3) to the detection of infection (eggs in faeces)

A patent infection is one which can be detected (ie eggs in faeces)

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5
Q

Give some features common to strongyloidea

A

Well-developed buccal capsule, leaf crowns around mouth, teeth usually present
Direct life cycle
L3=infective stage

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6
Q

Give some features of hookworms

What family do they belong to?

A

Strongyloidea
Typical strongyle eggs
Life cycle similar to other strongyles except route of infection is via direct ingestion of L3 followed by systemic migration of L3
Adult worms have a large buccal cavity, cutting plates and a hooked morphology

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7
Q

What are metastrongyles?

A

Lungworms

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8
Q

Give some features of metastrongyles (lungworms)

A

Adults found in lungs or adjacent blood vessels
Usually indirect life cycle (intermediate host=mollusc)
L1 in faeces, characteristic ‘kinky’ tail
L3= infective stage
Lympho-tracheal migration

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9
Q

What are ascarids?

Give some general features

A

Large white roundworms (nematodes)
No bursa in male worms
Females lay huge numbers of highly resistant eggs
L2 larvae develop inside egg (infective stage)
Direct life cycle
Paratenic and transport hosts (not necessary for the development of the worm)
Adults in SI (cause blockage but don’t damage mucosa)

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10
Q

Give some features of filarial nematodes

A

Large (20+cm)
Adult worms found in blood vessels, ligaments, tendons or skin
L1 is laid by female and found in bloodstream or skin of host
Indirect life cycle usually involving flies eg mosquitoes

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11
Q

Regarding ostertagia, what is the stage that infects the host?

A

Overwintered L3

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12
Q

How do L3 of Dictyocaulus viviparus become dispersed from faecal pats?

A

L3 escape from faecal pat using fruiting bodies from Pilobolus fungi. Fruiting bodies explode and catapult L3 away from faecal pat further afield on the pasture. Could blow onto neighbouring field via wind.

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13
Q

What species does Dictyocaulus viviparus affect?

Where is it found?

A

Cattle, dairy replacement heifer calves

Trachea and bronchi

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14
Q

What are the only lungworm found in cattle?

A

Dictyocaulus

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15
Q

Trichostrongyle eggs are usually how big?

What is the exception?

A

150 um

Ostertagia= 90um

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16
Q

Give a diagnostic feature of Ostertagia

A

Fine cervical papillae on head end

Males have a bursa and spicules

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17
Q

Describe ostertagia’s development within the host

A

Cattle ingest L3 -> abomasum -> gastric glands -> L4 and L5 develop -> L5 (immature adult) emerges into lumen -> adult -> mates -> female lays eggs
Adults sit on abomasal surface, don’t cause damage

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18
Q

What is the PPP of ostertagia?

A

3 weeks

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19
Q

How many parasites are required to cause disease with ostertagia?

A

40,000+ L4 and L5

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20
Q

Regarding ostertagia, which part of the life cycle causes damage to the host?

A

Developing larvae in gastric glands

Emerging L5

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21
Q

What are the clinical signs of Ostertagia infection?

A

Profuse watery diarrhoea
Weight loss
Loss of appetite

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22
Q

Describe how gastric glands are affected by Ostertagia

A

Gastric glands contain parietal cells -> produce HCl -> bacteriostatic effect, maintains acid pH 2.0, converts pepsinogen to pepsin
L4 and L5 develop in glands -> damage -> parietal cells replaced by undifferentiated epithelial cells -> loss of acid production -> pH increases to 7.0 -> loss of bacteriostatic effect -> no conversion of pepsinogen to pepsin -> increased permeability of mucosa (loss of cell-cell junctions -> leakage of pepsinogen into plasma -> loss of plasma proteins from circulation into gut)
When L5 emerges, nodules form over gland caused by hyperplasia of epithelial cells

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23
Q

Of the 2 types of bovine ostertagiosis, which is more common?

A

Type 1

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24
Q

Describe bovine ostertagiosis type 1

A

Dairy replacement calves (born in Autumn/Winter)
End of first grazing season
Disease occurs in late summer (July-Sept)
Calves ingest large numbers of L3 in July, disease 2-3 weeks later
Green watery diarrhoea
Majority of calves within group affected

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25
Q

Describe bovine ostertagiosis type 2

A 
Less common
Yearling calves
Disease in late winter, early spring 
Acute disease
Intermittent diarrhoea
Anaemia
Thirst
High levels of mortality '
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26
Q

What triggers free living L3 Ostertagia to hypobiose?

A

Decreased ambient temperature (in Autumn)

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27
Q

Which species of worm are found in the abomasum of sheep and cattle?

A 
Haemonchus contortus  (3cm)
Ostertagia ostertagi (1cm)
Trichostrongylus axei (0.5cm)
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28
Q

Which species of worm are found in the small intestine of sheep and cattle?

A 
Nematodirus spp (cephalic vesicle)
Trichostrongylus spp
Cooperia spp ('watch-spring')

Nairobi Travel Centre

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29
Q

Which species of worm are found in the large intestine of sheep and cattle?

A

Chabertia spp
Oesophagostomum spp
Trichuris spp

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30
Q

Babesia is transmitted by what?

A

Ixodes ricinus (tick)

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31
Q

What is the name of the babesia condition present in the UK?
How big is it?

A

Babesia divergens

1-2um (small species)

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32
Q

What are the clinical signs of Babsiosis?

A 
Haemolytic anaemia (direct cell lysis by parasite, oxidative damage, increased RBC phagocytosis)
Diarrhoea
Thrombocytopenia
Tissue hypoxia 
Haemoglobinuria
Fever 
Splenomegaly
Disease: red water fever

Acute onset
High levels of mortality

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33
Q

What is the treatment for Babesiosis?

A

Blood transfusions

Imidocarb

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34
Q

Briefly describe the life cycle of Babesia

A

Merozoites divide by asexual binary fission
Tick ingests infected RBCs -> multiplication and sexual reproduction
Dissemination of Babesia throughout tick, moves to ovaries -> trans-ovarian transmission
Infection passes onto new host by next generation of ticks
As tick feeds, sporogony occurs in salivary glands (asexual process of spore formation; spores contain sporozoites)
Sporozoitess injected into host with tick saliva
Sporozoites invade RBCs, start to divide (merogony)

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35
Q

Why can’t you do FEC to identify Dictyocaulus viviparus?

A

L1 found in faeces, not eggs

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36
Q

What is the only lungworm of cattle?

A

Dictyocaulus viviparus

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37
Q

What is unique about female Dictyocaulus viviparus?

A

They are ovo-viviparous; lay larvated eggs which hatch immediately

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38
Q

What is the infective stage of Dictyocaulus viviparus?

A

L3

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39
Q

What are the 4 phases of infection of Dictyocaulus viviparus?

A

Penetration phase (L3 ingested, lympho-tracheal migration -> L4 -> reaches lungs)
Pre-patent phase (L4 -> L5 in lungs, L5 migrate up bronchial tree, adults in trachea and bronchi; alveolitis, bronchiolitis, coughing, resp. distress)
Patent phase (Adult worms in URT -> eggs and L1s; frothy white mucous, gasping, coughing, death)
Post-patent phase (immune expulsion of adults, resolution of clinical signs)

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40
Q

How can you diagnose Dictyocaulus viviparus?

A

ELISA
Clinical signs (only lungworm in cattle)
L1 in faeces

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41
Q

How many Dictyocaulus are required to cause disease?

A

Very few

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42
Q

Describe the immunity from Dictyocaulus viviparus

A

Short-lived, needs continual boosting

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43
Q

What are the most pathogenic stages of Dictyocaulus infection?

A

Pre-patent phase and patent phase

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44
Q

In which parts of the lungs are adult Dictyocaulus viviparus commonly found?

A

Trachea and bronchi

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45
Q

How are Dictyocaulus viviparus expelled from the faecal pat?

A

Pilobolus fungi

Fruiting bodies explode and catapult L3 from faecal pat

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46
Q

Can you use field rotation as a means for control of ostertagia and fluke?

A

Yes for ostertagia as it only affects cattle, doesn’t affect sheep
No for fluke as it affects both sheep and cattle

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47
Q

What is the meaning of ‘clean pasture’?

A

Not grazed by cattle for the previous 12 months

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48
Q

What is the meaning of ‘safe pasture’?

A

Used the previous year but safe by beginning of June

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49
Q

Describe benzimidazoles

A

No residual activity, white drenches, kills worms, larvae and eggs

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50
Q

Describe imidazothiazoles

A

Yellow drenches eg levamisole: narrower spectrum of activity, less effective against developing larvae, no residual activity, used for parasitic roundworms

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51
Q

Describe macrocyclic lactones

A

Clear drenches, pour ons, injectables

eg ivermectin: 2-week residual activity, not ovicidal

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52
Q

Neospora affects which species?

A 
Dogs= definitive hosts
Cattle= intermediate hosts
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53
Q

What are the main clinical signs of Neosporosis?

A

Neurological disease, ascending hind limb paresis -> paralysis in young pups
Abortion in cattle

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54
Q

What are the different stages of neospora?

A 
Tachyzoites= rapidly divide asexually 
Bradyzoites= found in cysts in neural tissue and muscle
Oocysts= sexual reproduction, found in dogs faeces
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55
Q

How long do neospora oocysts take to sporulate and become infective?

A

12 hours

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56
Q

Recrudescence of neospora within a pregnant PI (persistently infected) cow leads to what?

A

Early gestation: foetal death

Late gestation: PI calf

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57
Q

Which testing can you do to diagnose neospora?

A 
Maternal ELISA (test in 2nd half of pregnancy as antibody levels are low in first half, may get false negatives)
Foetus: antibody detection in foetal fluids, histology (brain, heart, non-suppurative encephalitis), immunohistology
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58
Q

How can you diagnose cryptosporidium infection?

A

Oocysts in faeces
Stain with Ziehl-Neelson or Safronin
Age
Clinical signs

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59
Q

How does cryptosporidium affect cattle intestines?

A 
Villus atrophy
Enteritis
Crypt hyperplasia 
Loss of mature epithelial cells 
Common cause of diarrhoea in young calves
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60
Q

Nematodirus battus affects which animals?

A

Lambs aged 4-12 weeks old (typically 6 weeks old)

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61
Q

Describe the morphology of Nematodirus battus

A 
2cm long 
Often found in groups like cotton wool
Cephalic vesicle
Males have long thin spicules
Females have large eggs within uterus
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62
Q

What is the pre-patent period of N. battus?

A

15 days

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63
Q

Describe the life cycle of N. battus

A 
Unembryonated egg shed in faeces 
L3 develops in egg -> hatches -> infective stage -> ingested 
L3-L4 in lumen of SI
L4 burrows into mucosa
L4-L5
L5 emerges, adults mature 
PPP= 15 days
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64
Q

What value of WEC represents a heavy infestation of N. battus?

A

> 500epg

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65
Q

What must happen for disease to occur with N. battus?

A

Hatching must coincide with presence of susceptible lambs (old enough to graze, but before age immunity develops)

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66
Q

When does Nematodirus battus disease occur?

A

May-June

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67
Q

What are the hatching requirements for N. battus?

A

Cold period then period of increasing warmth (spring)

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68
Q

Describe the pathology of N. battus

A 
Developing L5 destroy mucosa in SI
Catarrhal enteritis 
Villous atrophy 
Fluid and nutrient absorption disrupted 
2000 worms can cause clinical disease 
Morbidity up to 100%, mortality up to 20%
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69
Q

Which parasite causes black scour?

A

Trichostrongylus spp

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70
Q

Describe the morphology of trichostrongylus spp

A

Small (0.5cm)

Excretory notch

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71
Q

Describe the pathogenesis of trichostrongylus spp

A

Contributes to PGE
SI: larvae (L4, L5) develop deep in mucosa -> sub-epithelial tunnels -> villous atrophy -> haemorrhage -> oedema -> diarrhoea

Black scour
Weight loss/ poor weight gain
Poor skeletal growth

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72
Q

Describe the morphology of Cooperia

A

‘Watch-spring’ worm- always coiled
Cephalic vesicle
Male has short, stumpy spicules

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73
Q

Describe the life cycle of Teladorsagia

A

Direct
Sheep
Adult females in abomasum -> lay eggs -> passed in faeces
L1 hatches, feeds on bacteria in faecal pat -> L2 -> ensheathed L3
Ingested by sheep -> abomasum -> burrows into gastric glands -> L4 and L5 -> L5 emerge into lumen of abomasum, mate, lay eggs etc

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74
Q

Pathogenesis of Teladorsagia depends on what 3 things?

A

Nutritional status of sheep
Concurrent infection
Development of immune response

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75
Q

Which species are involved in PGE?

A

Primary species: Teladorsagia circumcincta

Secondary species: Trichostrongylus spp, Cooperia spp, Nematodirus spp

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76
Q

What is meant by PPR (peri-parturient rise)?

A

Reduced immunocompetence of ewe around parturition

Seasonal reactivation of hypobiosed larvae

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77
Q

What is the main source of pasture contamination with Teladorsagia?
When are eggs usually shed?
When is there a flush of L3 on pasture?
When does disease occur?

A

Ewe
Spring
Flush of L3 on pasture in July
Disease Aug- Sept

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78
Q

Describe the morphology of adult Teladorsagia

A

1cm length
Slender, pinky brown
Fine cervical papillae
Males have a bursa and spicules

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79
Q

Describe the morphology of adult Haemonchus contortus

A

Large 3cm
Cervical papillae
White ovaries wrapped around gut - ‘Barbers pole worm’
Asymmetrical dorsal lobe

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80
Q

Briefly describe the life cycle of Haemonchus contortus

A 
Typical Trichostrongyle life cycle
PPP= 3 weeks 
Larvae develop in mucosa 
Adults are voracious blood feeders 
Hypobiosis
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81
Q

Describe the pathogenesis of Haemonchus contortus

A

Adults feed on blood -> acute anaemia and death
Erosion of abomasal wall
Severe haemorrhagic gastritis

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82
Q

What are the clinical signs of Haemonchus contortus

A

Severe anaemia
Weight loss
Oedema (neck)

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83
Q

What would you find in a post mortem of a sheep infected with Haemonchus contortus?

A

Abomasal haemorrhages, emaciation, anaemia, extension of red marrow in long bones

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84
Q

Describe the FAMACHA method of diagnosing Haemonchus contortus

A

Method by which only certain sheep in a flock are treated against Haemonchus based on the degree of anaemia they show in their mucous membranes
1= pink-red mucous membranes, not requiring treatment
5= white and requiring immediate treatment

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85
Q

What is the definitive host of tapeworms?

A

Dogs

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86
Q

What is a cysticercus?

A

Larval tapeworm, typically found encysted in muscle tissue

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87
Q

Describe the typical tapeworm life cycle

A

Adults in SI of definitive host (dog)
Proglottids break off
Eggs/proglottids shed in faeces
Eggs immediately infective -> eaten by intermediate host
Metacestode develops in intermediate host (sheep) -> eaten by definitive host
Adult tapeworm develops in SI

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88
Q

Which protozoan parasite species affect sheep?

A

Toxoplasma gondii
Cryptosporidium spp
Eimeria spp
Sarcocystis spp (not a problem in UK)

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89
Q

Describe the life cycle of Toxoplasma gondii

A

Cats= definitive host. Infected by ingesting Bradyzoite cysts in prey tissues
Sexual cycle in SI, oocysts shed in faeces
Oocysts sporulate and contaminate environment. Eaten by any war,-blooded animal
In intermediate host (rodents, birds), sporozoites are released -> cross gut wall -> Tachyzoites -> bradyzoites -> cysts

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90
Q

What are the clinically manifestations of Toxoplasma gondii

A

Still births, abortions, ,mummifications, whose discrete lesions on cotyledons (‘strawberry cotyledons’)

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91
Q 
Describe what would happen if a pregnant ewe was infected with Toxoplasma gondii:
Before pregnancy
Before day 40 of pregnancy 
Between day 40 and 110
Between day 110 and 145/ parturition
A

Before pregnancy: immune ewe
Before day 40 of pregnancy: infertile/ barren ewe/ resorption of foetus
Between day 40 and 110: abortion
Between day 110 and 145/ parturition: congenital infection

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92
Q

How do you diagnose toxoplasma gondii infection?

A

Serology- antibody detection in serum or foetal fluids (Dye test= gold standard in humans)
Histology- cotyledons, foetal brain tissue, typical non-suppurative inflammation

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93
Q

Describe the pathogenesis of Cryptosporidium spp

A

Parasitises mucosa (intracellular, extra cytoplasmic, found at microvillus border of Enterocytes)
Sporulation inside host
Life cycle identical to neospora
Cause villous atrophy, crypt hyperplasia, enteritis, loss of mature epithelial cells

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94
Q

How can you control toxoplasma?

A

Management: introduce new stock well before tupping. Infection induces strong immunity
Vaccination: Toxovax- vaccinate before mating, yearly booster, cell-mediated immunity

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95
Q

Cryptosporidium infection is common in which animals?

A

Common cause of diarrhoea in young calves and lambs (0-6 weeks old)
Faeco-oral transmission

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96
Q

Describe eimeria spp with regards to sheep

A

Pathogenic and non-pathogenic species
Faeco-oral contamination
Ewe= main source of infection
Lambs, 1-6 months old
Diarrhoea, dehydration, inappetence, weight loss
Damaged intestinal mucosa, oedematous, inflamed +/- mucosal haemorrhage
Treatment with toltrazuril or diclazuril

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97
Q

Which nematode species affect:
Indoor and outdoor pigs
Outdoor pigs

A

Indoor and outdoor pigs:

  • Ascaris suum (SI)
  • Strongyloides ransomi (SI)
  • Trichuris suis (LI)
  • Oesophagostomum spp

Outdoor pigs:

  • Hyostrongylus rubidus (stomach)
  • Metastrongylus apri (lungs)
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98
Q

How big are ascaris suum worms?

Describe their eggs

A

Large: 15-25cm

Thick-walled, 70um diameter

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99
Q

Describe the typical ascarid life cycle

A

Eggs passed in faeces
Develop on the ground; temp-dependent (approx 4 weeks, L2 in egg)
Paratenic host= earthworm, L2 hatches
Egg or earthworm eaten by pig
L2 migrate to liver, lung, L2-L3
Coughed up, swallowed, L4-L5m (adult) in SI
PPP= 8 weeks

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100
Q

Describe the pathogenesis of ascaris suum (pig nematode)

A

Hypersensitivity response to migrating larvae:
- Liver= fibrous reaction (‘milk spot’)
- Lungs= transient pneumonia
Adults in SI (poor weight gain, mechanical blockage)
Major economic costs (reduced weight gain, liver condemnation)

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101
Q

How do you diagnose ascaris suum?

A

Abattoir results
Transient respiratory disease
Reduced weight gain
Eggs in faeces (MgSO4 flotation)

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102
Q

Describe the morphology of Strongyloides ransomi in pigs

A 
Small (6mm)
Hair-like 
No ovijectors 
Very long oesophagus (1/3 of body)
Small eggs (40-50um)
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103
Q

What is unique about the life cycle of Strongyloidea ransomi?
Describe.

A

Free-living AND parasitic cycle

Free-living:

  • Male and female adults
  • Soil, bedding
  • Feed in bacteria

Parasitic:

  • Females only in SI (pointed tails)
  • Reproduce by asexual parthenogenesis (offspring are clones of female)
  • Larvated eggs or L1 in faeces
  • L3 are infective, migration via lungs to SI, PPP= 15 days
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104
Q

Describe the disease caused by Strongyloides ransomi

A

Piglets- transmammary infection
Diarrhoea, weight loss
Treat with BZs, MLs

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105
Q

Describe Trichuris spp

A

‘Whip worm’ (eggs in thicker end, head in thinner end)
Worldwide
LI
Eggs look like lemons, highly resistant (thick capsule)
Egg containing L1= infective stage

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106
Q

What is the intermediate host of Metastrongylus apri?

A

Earthworm

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107
Q

Describe the life cycle of Metastrongylus apri

A

Larvated, thick-shelled eggs in faeces -> hatch -> L1 infects earthworms
L1-L2-L3 in earthworm (L3 survives as long as earthworm)
Earthworm infested by pig
L3 released in gut, L3-L4 in Mesenteric lymph node
L4 reaches lung via lymphatics and bloodstream
Matures to adult in lungs
PPP= 3-4 weeks

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108
Q

What disease is associated with Metastrongylus apri?

A

Typical in 4-7 month old pigs
Catarrhal and eosinophilic bronchiolitis
Coughing, dyspnoea, nasal discharge
Reduced weight gain, inappetence
Exacerbates other respiratory disease eg Staph infections

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109
Q

What is the incubation period for Leishmania?

A

3 months to 7 years

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110
Q

What effect do leishmania, babesia and ehrlichia have on the spleen?

A

Splenomegaly

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111
Q

What is onychogryphosis?

A

Hypertrophy and increased curvature of the claws

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112
Q

Whic dog breeds are more prone to Leishmaniasis?

A

Boxer, German shepherd, cocker spaniel, Rottweiler, foxhound

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112
Q

Which dog breed is resistant to Leishmania?

A

Ibizan hound
When it comes into contact with Leishmanina, produces Th1 cell-mediated response, whereas other breeds produce a humoral response

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113
Q

Is leishmania zoonotic?

A

Yes

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114
Q

What are the target organs of Leishmania?

A

Renal glomeruli
Anterior uvea
Synovial membrane of joints
Vascular wall

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115
Q

What would you find in a fine needle aspirate of a lymph node of a dog infected with leishmania?

A

Macrophages with amastigotes inside

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116
Q

Which are the most effective therapeutic combinations for canine leishmania?

A

Allopurinol (leishmanistatic) and meglumine antimonate or miltefosine (both Leishmanicidal)

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117
Q

What is the vector of Leishmania?

A

Female sandflies of the genus Phlebotomus/Lutzomia

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118
Q

Is there a vaccine against leishmania in humans?

A

No

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119
Q

Is there a vaccine against leishmania in dogs?

A

Yes- 70% efficacy
3 injections, 3 weeks apart + annual boosters
Very expensive
Induces strong cellular immune response
Some dogs develop necrosis at injection site

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120
Q

What are the host species of Leishmania?

A

Rodents, marsupials, dogs, cats

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121
Q

Which is the effective immune response that is able to control leishmania infection?

A

Cell-mediated immune response (Th1)

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122
Q

What is the difference between a susceptible and resistant dog with regards to leishmania?

A

Susceptible: increased Th2 humoral immune response (antibody production; clinical signs)
Resistant: increased Th1 cell-mediated immune response (killing of macrophages; carrier but no clinical signs)

Resistant dogs who are carriers, if become immunocompromised (parasites, infection, neoplasm, drugs), can develop clinical signs

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123
Q

What is the main cause of death in dogs affected with Leishmania?

A

Chronic proteinuric glomerulonephritis

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124
Q

How would you diagnose CanL?

A

Clinical signs, travel history, diagnostic tests:
DIRECT: FNA of lymph nodes, cytology (BM, lymph nodes, spleen, buffy coat of blood), histology (amastigotes in macrophages), real-time PCR (BM/lymph node)
INDIRECT: ELISA, IFAT (titre test), immunologic (CD4+/CD8+ levels)

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125
Q

Which are the best tissue samples for diagnostic PCR and cytology (for leishmania)?

A 
(In descending order)
Bone marrow
Lymph nodes
Spleen
Conjunctiva 
Blood
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126
Q

What is the difference between real time and conventional PCR?

A

Real time: gives positive or negative result, plus quantity (eg of DNA copies of Leishmania)
Conventional: Only gives positive or negative

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127
Q

What are the main aims of therapy of Leishmania?

A

Reduce parasite loads as much as possible (can’t eradicate it)
Improve dog health

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128
Q

What is the mechanism of action for domperidone for the prevention of Leishmania?

A

Increases prolactin secretion -> stimulates cell-mediated Th1 immune response -> activation of macrophages and NK cells
Dopamine D2 receptor antagonist
80% efficacy

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129
Q

In which EU countries is leishmania endemic?

A

Cyprus, Greece, Portugal, Spain, France, Italy, Croatia, Albania

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130
Q

What are the reported methods of transmission of CanL?

A

Blood transfusions, sexual transmission

Vertical (in-utero)

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131
Q

What are the suspected methods of transmission of CanL?

A

Dog bites, fleas and ticks

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132
Q

List factors that can lead to further spread of CanL

A

Increased pet travel (infected animals moving to non-endemic areas and vice versa)
Global warming
Use of untested and infected dogs as donors for blood transfusions
Drug resistance

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133
Q

List potential causes of human infection of leishmania

A

Non-immune person moving to an endemic area

Immunosuppression

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134
Q

How can the risk of CanL infection be reduced?

A 
Keep dogs inside when sandflies are most active (dawn and dusk), and away from stagnant water 
Prophylactic medication (eg domperidone; skews immune response towards Th1-like response)
Insecticides 
Products containing synthetic pyrethroids, permethrin or deltamethrin which repel sandflies (spot-on or collar form)
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135
Q

What are the two forms of the leishmania parasite?

A

Promastigote (infectious stage)

Amastigote (intracellular, found within macrophages)

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136
Q

Describe the life cycle of leishmania

A

May-November:

  • Female sandfly takes blood meal from host which contains amastigotes
  • Amastigote -> Promastigote
  • Sandfly bites mammalian host and injects metacyclic promastigotes which invade macrophages
  • Promastigotes -> amastigotes, multiply by simple division (48 hrs)
  • Amastigotes released when the macrophage dies and are phagocytosed by other macrophages
  • Transferred to sandfly during feeding
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137
Q

What is the target cell of Leishmania?

Where do they invade next?

A

Macrophages

Invade reticuloendothelial system (BM, spleen, liver, lymph nodes)

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138
Q

What is the incubation time for leishmania?

A

Years

Once established, infection persists in tissues

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139
Q

How is epistaxis a clinical sign of Leishmania?

A

Paraglobulinaemia (albuminous protein) -> interfere with fibrin polymeration -> thrombocytopathy -> increased bleeding tendency (+/- nasal ulcers and hypertension -> epistaxis)

140
Q

Give some clinical signs of leishmania

A

Lymphadenopathy, skin crusting and ulceration, weight loss, cachexia (loss of condition), PUPD, hyperthermia, conjunctivitis, splenomegaly, abnormal nails, polyphagia (increased appetite), epistaxis, KCS (keratoconjunctivitis sicca - dry eye)

141
Q

What effects does leishmania have on the body?

A

Glomerulonephritis, vasculitis, polyarthritis, uveitis, meningitis, antibody production against RBCs and platelets

142
Q

What would you see on a biochemistry of a dog infected with leishmania?

A 
Hyperglobulinaemia
Hypoalbuminaemia
Anaemia (non-regenerative)
Proteinuria
Thrombocytopenia
143
Q

What are the 4 clinical classifications of dogs regarding Leishmania?

A

Stage A: exposed dogs

  • Negative direct tests, low titres against CanL
  • No clinical signs

Stage B: infected dogs

  • Positive direct tests, low titres
  • No clinical signs

Stage C: sick dogs
-Positive cytology and/or high titres, more than 1 clinical sign

Stage D: severely sick dogs

  • Sick + protein nephropathy/chronic renal failure
  • Unresponsive to repeated course of anti-Leishmania drugs
144
Q

How does allopurinol work in terms of treating Leishmania?

A

Blocks xanthine-oxidase -> interferes with uric acid synthesis

145
Q

How long should allopurinol be used when treating Leishmania?

A

Until negative PCR (recheck at 6 months)

146
Q

What are Babesia and what are the 2 main kinds?

A 
Intrerythrocytic protozoan parasites of the phylum Apicomplexa
Large species (3-7um)
Small species (1-3um)
147
Q

Give an example of a species of Babesia found in dogs and cats

A

Dogs: Babesia gibsoni, Babesia canis
Cats: Babesia cati, Babesia felis

148
Q

What are the clinical signs of feline babesiosis?

A 
B. felis
Fever
Anorexia
Icterus
Pale mm due to anaemia (generally regenerative)
Often concurrent FIV/FeLV infection
149
Q

Which diagnostic assays are available for babesiosis diagnosis?

A

Cell culture (whole blood), requires several weeks’ incubation
Cytology (whole blood, buffy coat smears, tissue aspirates), poor sensitivity
IFA serology (serum),
PCR (whole blood, spleen), confirms active infection

150
Q

What treatment is available for large babesias?

A 
Imidocarb dipropionate  (6.6mg/kg, IM/SC) (active for 4 weeks after treatment, prevents infection for up to 6 weeks)
Diminazene aceturate

Generally good success

151
Q

What treatment is available for small babesias?

A

No truly effective therapies

Some success with Azithromycin (10mg/kg) and Atovaquone (13.3mg/kg)

152
Q

What treatment is available for feline babesias?

A

Primaquine phosphate (1mg/cat IM)

153
Q

Give some examples of large and small species of Babesia that affect small animals

A

Large canine:

  • Babesia canis
  • Babesia rossi

Small canine:

  • Babesia gibsoni
  • Babesia conradae

Small feline:

  • Babesia felis
  • Babesia cati
154
Q

How can you prevent Babesia in dogs?

A

Tick prevention

Prevention of dogs fighting

155
Q

How is ehrlichia transmitted?

156
Q

What are the names of the Demodex species that affect dogs and cats?

A 
Cats= Demodex gatoi or cati 
Dogs= Demodex canis or injai
157
Q

Describe the life cycle of Taenia multiceps

A

Intermediate host: sheep (also cattle, pigs, horses)
Definitive host: dogs and foxes
Intermediate host is infected via ingestion of the parasite eggs.
Eggs hatch in the small intestine.
Parasite migrates to spinal cord and brain via the blood stream.
The definitive host becomes infected when it eats the spinal cord or brain of the intermediate host.

158
Q

Give some clinical signs of acute phase ehrlichiosis

A

Lethargy, inappetence, weight loss
Splenomegaly, lymphadenomegaly
Uveitis, retinal haemorrhage, retinal detachment, optic neuritis
Cutaneous petechial and ecchymotic haemorrhages
Epistaxis
Polyarthritis
Neurological signs due to meningitis and/or haemorrhage

159
Q

Give some clinical signs of chronic phase ehrlichiosis

A

Develops only in some infected dogs
Pancytopenia due to hypoplasia of all bone marrow cells
Secondary infections due to immunosuppression
Granular lymphocytosis
Immune-complex glomerulonephritis

160
Q

How can you diagnose ehrlichiosis in dogs?

161
Q

How can you treat canine ehrlichiosis?

A

Doxycycline 10mg/kg SID PO

Oxytetracycline 7.5-10mg/kg BID IV

162
Q

How does early removal of ticks prevent canine ehrlichiosis?

A

24-48 hour delay between attachment and feeding

163
Q

What is the leading cause of death from leishmania?

A

Glomerulonephritis

164
Q

Which drug can be used to prevent canine leishmania? How does it work?

A

Domperidone (stimulates prolactin production -> invokes cell-mediated Th1 response)

165
Q

Which drugs can be used to treat canine Leishmania?

A

Allopurinol
Miltefosine
Meglumine antimoniate

166
Q

Harvest mites are potential vectors of what?

A 
Borrelia burgdorferi (lyme disease)
Anaplasma phagocytophylum
167
Q

What are the 2 types of hookworms in dogs?

A 
Uncinaria stenocephala (unpathogenic, UK)
Ancylostoma caninum (abroad)
168
Q

Describe the appearance of Uncinaria stenocephala

A

Northern hookworm, dogs and foxes
1cm long
Typical hooked appearance
Large buccal capsule with 2 cutting plates

169
Q

Describe the life cycle of Uncinaria stenocephala

What are the types of infection?

A 
Adults in SI
L3=infective stage
PPP=15 days
Types of infection: 
-Ingestion of L3, migration
-Ingestion of L3, no migration
-Percutaneous infection (rarely results in mature infection)
170
Q

What are the clinical signs of infection with Uncinaria stenocephala?

A

Anaemia, weight loss, lethargy, diarrhoea

Pedal dermatitis due to hypersensitivity following repeat exposure to L3

171
Q

How can you control Uncinaria stenocephala?

A

Dry conditions, concrete runs (as grass runs increase transmission)

172
Q

Give the routes of transmission of Ancylostoma caninum (hookworm)

A

L3 ingestion +/- migration
Skin penetration
L3 in milk (bitch=reservoir of infection)

173
Q

Describe the migration of hookworms

A

Percutaneous: L3 migrate via bloodstream to lungs (L3-L4). Swallowed -> SI (L4-L5)
Ingestion: Penetrate buccal mucosa, migrate via bloodstream to lungs (L3-L4). L3 swallowed, develop to adults in SI
A proportion of L3 which reach the lungs migrate to skeletal muscles, remain dormant until pregnancy

174
Q

How do you diagnose hookworms?

A

Eggs in faeces, clinical signs

175
Q

How do you treat hookworms?

A

Susceptible to most anthelmintics eg MLs, BZs

176
Q

Give the clinical signs of ancylostoma caninum (hookworm)

A

Disease typical in dogs

177
Q

What are the intermediate hosts of spirurida

A

Invertebrates eg mosquitoes

178
Q

What are the major genera of filarial nematodes?

A

Dirofilaria spp
Onchocerca spp
Brugia spp

179
Q

What is Dirofilaria immitis transmitted by?

A

Mosquitoes

180
Q

Give the life cycle of Dirofilaria immitis

A

Adult worms in pulmonary arteries or right ventricle of heart
Microfilariae (L1) in blood
Dog bitten by mosquito, which sucks up L1
L1-L3 (10-14 days)
Infective L3 inoculated into dog when bitten by mosquito, migrates to subcutaneous/subserosal tissues
Moults to L4 (3-4 days), migrates to abdomen
Moults to L5 (2 months), penetrates jugular
Adults in pulmonary arteries
Microfilariae in circulation 6-9 months later

181
Q

In which parts of the heart are dirofilaria immitis found?

A

Pulmonary arteries and right ventricle

182
Q

What size are male and female heartworms?

A

Males: up to 20cm
Females: up to 30cm

183
Q

What is the difference in disease between cats and dogs regarding Dirofilaria immitis?

A

Cats and ferrets support lower worm burdens than dogs (1-3 adults)
Adult worms are stunted
No/transient microfilaraemia

184
Q

How may Dirofilaria immitis affect humans?

A

Pnuemonitis (‘coin lesion’) on chest radiograph/CT scan: granuloma around dead/dying worm

185
Q

What are the clinical signs of Dirofilaria immitis in dogs?

A

(Disease associated with large numbers of adult worms)
Exercise intolerance, chronic cough, dyspnoea, lipothymia (faintness), right-sided congestive heart failure (ascites, anorexia, death following resp distress)
Small dogs: acute ‘caval syndrome’-intravascular haemolysis and haemoglobinuria-surgery

186
Q

What are the clinical signs of Dirofilaria immitis in cats?

A

Digestive or neurological signs alone or in conjunction with pulmonary symptoms. Sudden death more common than in dogs

187
Q

How can you diagnose Dirofilaria immitis?

A

Knott test to detect microfilariae (although 30% of dogs and most cats are amicrofilaraemic)
Immunoassays for adult worm antigen (doesn’t detect male-only burdens)
Radiograpgs, ECG
Clinical signs of CV dysfunction

188
Q

How would you recognise infection with Dirofilaria repens?

A

Adults are located subcutaneously within nodular swellings, relatively benign

189
Q

How can you differentiate microfilariae of D.immitus from D.repens?

A

Staining with acid phospatase
D.repens are larger
Different morphologies

190
Q

Describe the prophylaxis and treatment for Dirofilaria

A

Monthly prophylaxis with MLs prevents lar

191
Q

What are the 3 classes of anthelmintics?

Give examples from each

A
  1. Benzimidazoles- Fenbendazole (Panacur), triclabendazole
  2. Imidathiazoles/ tetrahydroprimidines- levamisole, Pyrantel (parasitic roundworms)
  3. Macrocyclic lactones- avermectins eg ivermectin, milbemycins eg Moxidectin
192
Q

Name 4 anthelmintics used to treat cyathostomins?

A

Ivermectin
Moxidectin
Benzimidazoles
Pyrantel

193
Q

Give the cyathostomin life cycle

A 
L3 ingested on pasture 
Migrates to large intestine
Mucosa: EL3 -> LL3 -> DL4
Lumen: L4 -> L5 
(takes 6-8 weeks for EL3 to become L5)
Eggs laid on pasture in faeces
L1 -> L3 on pasture
194
Q

Briefly describe the epidemiology of cyathostomins

A

20% of horses carry 80% of the burden

Horses don’t develop strong immunity

195
Q

How do you diagnose cyathostomins in horses?

196
Q

Give the 3 large strongyles that affect horses

A

S.vulgaris
S.edentatus
S.equinus

197
Q

Where does S.vulgaris (horse strongyle) migrate to within the horse?

A

Cranial mesenteric arteries

198
Q

Give the life cycle of S.vulgaris (equine strongyle)

A 
Horse ingests L3 (infective stage)
Enters large intestine
L3 in mucosa migrates to cranial mesenteric arteries 
Returns to lumen as L5
Eggs shed onto pasture
L1-L3 on pasture
199
Q

How does S.vulgaris affect the horse?

A

Severe colic

200
Q

Which is the primary species of tapeworm that affects horses?
Where are adults found?
What is the intermediate host?

A

Anoplocephala perfoliata
Adults found in SI
Intermediate host=free-living oribatid mite

201
Q

Where are adult tapeworms found?

A

Ileo-caecal junction

202
Q

Describe the life cycle of equine tapeworms

A

Adult tapeworm at ileo-caecal junction
Proglottids passed in faeces, disintigrate, eggs released
Eggs ingested by free-living oribatid mites (found in soil, shavings, hay)
Infected mite ingested by horse (takes 2 months to reach ileo-caecal junction)

203
Q

Describe an egg of an equine tapeworm

A

D-shaped

Smaller than normal strongyle eggs (50-80um)

204
Q

Describe the pathogenesis of equine tapeworms

A

Spasmodic colic, intussusception, ileal impaction, rupture

205
Q

Give the clinical signs of equine tapeworm infection

A

Ulceration and pathological changes to intestine
Failure to put on weight
Enteritis
Colic (spasmodic/ileal impaction)

206
Q

How do you diagnose equine tapeworm infection?

A

ELISA
FEC
Saliva test

207
Q

What would you give to treat equine tapeworm infection?

How would you control infection?

A

Double dose of pyrantel

Control with praziquantel

208
Q

What name is given to the equine pinworm?

A

Oxyuris equi

209
Q

Describe the control for Parascaris equorum

A 
Anthelmintics (ivermectin resistance reported)
Pasture rotation (although eggs are resistant and long-lived)
210
Q

Where are ascarid nematodes found in horses?

A

Small intestine

211
Q

Give some general features of ascarid nematodes in horses

A

Females lay huge numbers of highly resistant eggs
L2 develops in egg=infective stage
Direct life cycle
Paratenic and transport hosts
Hepato-tracheal migration
Migrating larvae stimulate profound inflammatory response -> disease and economic losses
Adult worms browse on intestinal contents -> mechanical blockage (no damage to mucosa)
Most are susceptible to all 3 classes of anthelmintics

212
Q

What is the PPP of Parascaris equorum?

213
Q

Describe the clinical signs seen with Parascaris equorum infection

A 
Foals
Transient cough
Poor weight gain
No diarrhoea
Possible obstruction in heavily infected animals
Foal-foal infection
Adults immune
214
Q

What is the difference between interval and strategic dosing of anthelmintics?

A

Interval dosing: treat at regular intervals based on egg reappearance period
Strategic dosing: treat specifically based on epidemiology

215
Q

Where does Oxyuris equi (pinworm) reside in the horse?

A

Larvae develop in mucosal crypts of LI

Adults are found in lumen of LI

216
Q

How big are the eggs of Oxyuris equi?

217
Q

What is the PPP of oxyuris equi (pinworm)?

218
Q

How do you diagnose oxyuris equi (pinworm)?

A

Eggs on peri-anal area

Selotape test

219
Q

A value of what in a FEC would tell you that a horse is a major contributor to pasture contamination?

A

> 200epg (eggs per gram)

220
Q

Which species of ascarids affect dogs?

A 
Toxocara canis (dogs and foxes)
Toxoascaris leonina (cats and dogs)
221
Q

Which species of ascarids affect cats?

A

Toxocara cati

Toxocara leonina

222
Q

Which species of ascarids that affect dogs and cats are zoonotic?

A 
Toxocara canis (foxes and dogs)
Possinly Toxocara cati
223
Q

How big are the eggs of dog/cat ascarids?

224
Q

Give the 4 modes of infection of Toxocara canis
What is the difference with Toxocara cati?
What is the difference with Toxascaris leonina?

A 
Direct transmission (ingestion of eggs containing L2-migration)
Transplacental transmission
Paratenic transmission (via paratenic host-no migration)
Transmammary transmission (no migration)

Toxocara cati: same modes except no transplacental transmission
Toxascaris leonina: same except no transplacental or transmammary

225
Q

How do humans become infected with Toxocara? (ascarid)

A

By ingesting larvated eggs (L2)

226
Q

How can you diagnose Toxocara infection?

A

Age of dog
Clinical signs
Eggs in faeces (salt floatation)
Adult worms may be passed or vomited

227
Q

How can you control Toxocara infection (ascarids)?

A

Intestinal stages are susceptible to BZs and MLs

Fenbendazole given daily from 42 days of gestation can prevent trans-placental transmission

228
Q

Give some clinical signs of Toxocara canis infection

A

Asymptomatic in adults, heavy burdens in puppies:

  • Pot bellies
  • Poor weight gain
  • Intestinal obstruction
  • No diarrhoea (worms just cause mechanical blockage, no damage to mucosa)
229
Q

Describe the life cycle of Toxocara canis

A

Dogs ingest larvated eggs/paratenic invertebrate hosts
Larvae move through body in bloodstream -> lungs
Coughed up, swallowed -> SI
Larvae encyst in gut wall tissues in older dogs
The cysts can reactivate in pregnant females to infect puppies through placenta/milk

230
Q

Give the general characteristics of tapeworms (platyhelminths)

A 
Segmented
No gut
Always parasitic 
Indirect life cycles
Stage in intermediate host=metacestode
Hermaphrodites
231
Q

What is contained within the mature proglottid of a tapeworm?

A 
Uterus
Genital pore
Ovary
Testes
Vitelline gland
232
Q

What is contained with gravid proglottids of adult tapeworms?

233
Q

Give the general life cycle of tapeworms

A 
Adults in SI
Proglottids break off
Proglottids/eggs in faeces
Eggs immediately infective 
Eggs eaten by intermediate host (eg sheep)
Metacestode develops in intermediate host
Metacestode eaten by definitive host
Adult tapeworm develops in SI
234
Q

What are the 4 types of metacestode?

A

Hydatid (cyst)
Coenurus (infects CNS of host)
Cysticercus (encysted in muscle tissue)
Cysticercoid (cyst)

235
Q

How many species of tapeworm are there in dogs?

A

8
5 species of Taenia
2 species of Echinococcus
1 species of Dipylidium

236
Q

What are the 3 major Taenia species of dogs?
Where are the metacestode stages found in each?
What is the intermediate host?

A

T. ovis (cysticercus in muscles)
T. hydatigena (cysticercus in peritoneum)
T. multiceps (coenurus in brain)

Intermediate host=sheep

237
Q

How do you treat an adult tapeworm infection?

A

Praziquantel every 6 weeks (PPP=6 weeks)

238
Q

Which species of Taenia tapeworm affects cats?

What is the intermediate host?

A

Taenia taeniformis

Intermediate host=mouse

239
Q

What are the 2 species of Echinococcus tapeworms that affect dogs?

A

E. granulosus (UK, sheep=definitive host)
E. multilocularis (Europre)
Zoonosis

240
Q

Describe human hyatid disease

A

Infection by ingesting eggs from dogs
Space occupying hydatid cyst in liver, lungs, bone marrow, brain
Slow-growing
Symptoms: jaundice, cholangitis, abdominal pain, pleurisy, anaphylactic reaction after rupture

241
Q

Give the guidelines regarding parasite control from the PET travel scheme

A

All dogs must be treated with Praziquantel 1-5 days before entry in to UK by a vet, and have it recorded in their passport

242
Q

Describe Dipylidium caninum

A 
Tapeworm found in SI of dogs and cats
50cm long
Scolex has 4 suckers and a protrusible rostellum with 4-7 rows of small hooks
Gravid segments are barrel-shaped
2 genital pores on each proglottid
Egg capsules, each containing 10-15 eggs
243
Q

Describe the life cycle of D.caninum

A

Adult tapeworm in SI of cat/dog. PPP=4-6 weeks
Actively motile proglottids are passed in faeces, disintegrate, eggs released
Eggs eaten by flea larvae in environment
Develop to cysticercoid in adult flea
Infected flea eaten as animal grooms

244
Q

Give the life cycle of Neospora caninum

A

Dogs scavenge infected bovine tissues, ingest bradyzoite cysts
Enteric sexual cycle in dog
Oocysts excreted in dog faeces, contaminate food and water, ingested by cattle. Asexual reproduction- tachyzoites, bradyzoites
Tachyzoites cross placenta and infect foetus

245
Q

Give the clinical signs of Neosporosis of younger and older dogs that are intermediate hosts

A

Younger dogs: ataxia, hindlimb paresis, loss of reflexes, ascending paralysis, dysphagia, hyperextension of HLs
Older dogs: CNS disturbances, abnormal behaviour, vision defects, seizures, myocarditis, dermatitis, pancreatitis

246
Q

How do you diagnose neospora in dogs?

A

Clinical signs
Serology
Muscle biopsy (ID parasites by PCR or immunocytochemistry)
Creatine kinase elevation

247
Q

How do you treat neospora in dogs?

A

Clindamycin

248
Q

What are the 2 stages of Giardia?

A

Dividing trophozoite, resistant cyst

249
Q

Describe the morphology of Giardia trophozoites

A

Bi-nucleated
8 flagella
ADhesive disc

250
Q

Describe the morphology of Giardia cysts

A

Oval
8 by 12um
2-4 nuclei

251
Q

How are Giardia species named?

A

By assemblages-relate to infectivity for different hosts

252
Q

Give the life cycle of Giardia

A

Infective cysts ingested by host
Excyst in SI-trophozoites
Trophozoites multiply asexually by longitudinal binary fission
Form multi-nucleated resistant cysts excreted in faeces

253
Q

Describe the disease caused by Giardia

A

Trophozoites erode mucosa and villi
Malabsorptive diarrhoea
Steatorrhea (greasy stools)

254
Q

How would you treat Giardia?

A

Metronidazole

Fenbendazole licensed for puppies

255
Q

What family does Leishmania belong to?

A

Kinetoplastidae

256
Q

What are the 2 forms of Leishmania?

A

Amastigote (in host)

Promastigote (in sandfly)

257
Q

How do you diagnose canine babesiosis?

A

History of recent travel
Clinical signs
Giemsa-stained blood smear to identify merozoites

258
Q

How do you diagnose Ostertagia?

A

Clinical signs (eg calves with diarrhoea in summer)
Season
Grazing history
Definitive diagnosis: raised plasma pepsinogen levels (not FEC)

259
Q

How does L3 ostertagia survive in the environment?

A

Ensheathed (wears old cuticle of L2)
Tolerates cold temperature
Seeks moisture (desiccation is lethal)
Has limited food reserves (can’t feed when has a sheath)

260
Q

Give the morphology of Dictyocaulus viviparus

A

4-8cm long
Slender, white
Male has reduced bursa

261
Q

Describe the vaccine for Dictyocaulus viviparus

A 
'Huskvac'
Live, attenuated
Each dose contains 1000 irradiated L3
2 oral doses, 4 weeks apart, before turnout
Requires natural boosting
262
Q

How can you identify Dictyocaulus viviparus infection using faeces?

A

Baerman apparatus: L1 in faeces (short and stumpy, refractile food granules, ensheathed)

263
Q

Describe endemic stability with regards to Babesia of cattle

How can it break down?

A

Exposing young stock to infection will not cause clinical signs (as they are resistant up to 9 months old). Cycling of Babesia between cattle and ticks without disease.
Can break down when buying in naive stock, or introducing partial tick control

264
Q

Define premunity with regards to Babesia

A

Asymptomatic carriers that are immune to disease

265
Q

Give some examples of flukicides

A

Triclabendazole (kills all stages of fluke from 2 weeks old)
Albendazole (kills adult flukes only)
Closantel (kills late immature flukes and adults)

266
Q

What treatment can you give to prevent ostertagiosis?

A

Ivermectin at 3, 8 and 13 weeks after turnout

267
Q

How is ehrlichiosis caused and transmitted?

A

Caused by intracellular gram -ve bacteria
Ehrlichia canis. Infects monocytes
Transmitted by Rhipicephalus sanguineous (brown dog tick)

267
Q

Where is cryptospordium found?

A

Microvillus border of enterocytes

267
Q

How does transmission of Cryptosporidium occur?

A

Faeco-oral

268
Q

How do you control cyrptosporidium infection?

A

Halofuginone is licensed in calves
Control of environmental contamination
Boil water
Hygiene

269
Q

Describe the 2 kinds of oocyst of Cryptosporidium

A

Thick-walled oocyst sporulates in host -> shed in faeces

Thin-walled oocyst sporulates in host -> sporozoites infect epithelial cells in SI

270
Q

What are the clinical signs of Nematodirus battus

A

Sudden explosive outbreaks of acute watery diarrhoea
Inappetence, dehydration, increased thirst, abdominal pain, weight loss
Disease in lambs 4-12 weeks old

271
Q

How do you control Nematodirus battus infection?

A 
Grazing management: don't use same fields for lambs year after year as transmission occurs via ingestion of overwintered L3
Prophylactic treatment (May-June, every 2 weeks)
Disease forecasting
272
Q

How do you diagnose N.battus infection?

A

Season (May-June)
Grazing history
Age of lambs (4-12 weeks)
Clinical signs (eg watery diarrhoea)

273
Q

What is the main source of pasture contamination of PGE?

274
Q

Give the epidemiology of PGE

A

Eggs shed on pasture by ewes in Spring, development of eggs to L3 is temp-dependent
Flush of L3 on pasture in July
Disease in lambs in Aug-Sept

275
Q

How can you control PGE?

A

Clean pasture
Good husbandry
Accurate dosing- treat lambs as well as ewes (although repeated blanket treatments increase resistance)

276
Q

How do you diagnose haemonchus contortus?

A

Clinical signs (anaemia, weight loss, hypoproteinaemia, bottle jaw)
Season (disease in late summer)
FEC
FAMANCHA test (assesses degree of anaemia)

277
Q

What is the main source of pasture contamination of Haemonchus contortus?

278
Q

How can you prevent Haemonchus contortus?

A

Barbervax vaccine

279
Q

Where do Trichinella spiralis exist within the host?

A

Pig
Adults in SI
L1 encysts in muscles

280
Q

How does transmission of Trichinella spiralis occur?

A

Through ingestion of cysts in muscles

281
Q

Describe the disease caused by Trichinella spiralis

A

No disease in domestic animals, serious disease in humans: fever, oedema, muscle pains, peri-orbital oedema, myocarditis, meningitis, death
People become infected by eating undercooked, contaminated pork

282
Q

Describe the control measures surrounding Trichinella spiralis

A

EU legislation 2014 states that all pigs from non-controlled housing must be tested at slaughter
Cooking and freezing meat will kill trichinae

283
Q

What is taenia solium?

A

Pork tapeworm

284
Q

How can humans act as both intermediate and definitive hosts of Taenia solium?

A

Definitive host: infected by eating cysts in undercooked pork, develop tapeworm in their SI
Intermediate host: infected by ingesting eggs, develop metacestodes in brain and neurological tissues -> neurocysticercosis

285
Q

What is Balantidium coli?
What disease does it cause?
How is it transmitted?

A

Ciliated protozoan parasite in LI of pigs
Apathogenic in pigs, diarrhoea in humans
Faeco-oral transmission via cysts in faeces

286
Q

Describe Isospora suis

A

Protozoa
Causes severe enteritis in young piglets
Presents as diarrhoea that is unresponsive to antibiotics
Often low/negative oocyst counts
Oocysts (20um) produced by the sow contaminate the environment
Tx: sulphonamides eg toltrazuril

287
Q

Briefly describe the life cycle of Isospora suis

A

Infection by ingesting sporulated oocysts
2 rounds of asexual reproduction in epithelial cells of SI
Sexual reproduction -> oocyst
PPP=5 days
Unsporulated oocyst leaves host, sporulates in environment (2 sporocysts, each containing 4 sporozoites)

288
Q

What is the only louse found on pigs?

A

Haematopinus suis

289
Q

Describe haematopinus suis

A 
Only louse on pigs
Sucking louse
Large
Eggs visible on hairs
Pruritus
Common, may be present at low levels
Reduces feeding and growth rates, affects hide value
Tx: MLs
290
Q

Describe sarcoptes in pigs

A

Sarcoptes scabiei var suis
Burrowing mite, spends entire life on pig
Lesions start on ears, spread to back, flanks, abdomen
Severe immune reaction, pruritus, erythema
Intense itching, thickened skin, secondary bacterial infection
Sow -> piglet transmission
Treat/prevent with avermectins

291
Q

A sheep has been found stargazing and circling, which parasite would you suspect?
What is the prognosis?

A

Taenia multiceps -> coenurus in brain. Space-occupying lesion causing neurological signs.
Whole cysts can be removed surgically if valuable animal, otherwise euthanasia

292
Q

Describe echinococcus granulosus metacestodes

Comment on its pathogenicity

A

Hydatid cyst in liver and lungs of cattle and sheep

Non-pathogenic to cattle and sheep, pathogenic to dogs and humans

293
Q

Describe taenia multiceps metacestodes

Comment on its prognosis

A

Coenurus in brain of sheep, space-occupying lesion -> neurological conditions: star-gazing, circling, locomotory problems -> euthanise
Whole cysts can be removed surgically if valuable animal

294
Q

Describe taenia hydatigena metacestodes

Comment on its pathogenicity

A

Immature cysticercus migrate through liver of sheep
Mature cysticercus in peritoneum
Liver condemnation, but not pathogenic to people or dogs

295
Q

Is meat always condemned at the abattoir if it contains tapeworms?

A

Only in the case of large infections

296
Q

Which lungworm of sheep is often seen at the abattoir? How do they appear?
Comment on their pathogenicity

A

Muellaris capillaris
Non-pathogenic in sheep, highly pathogenic in goats
Hair-like adults and eosinophilic grey/green nodules in lung parenchyma

297
Q

Monezia tapeworms: what are the intermediate and definitive hosts?

A 
Intermediate= oribatid mite
Definitive= cattle, sheep (SI)
298
Q

Describe human cysticercosis

A

Ingestion of eggs, poor sanitation/lack of meat inspection

Human disease: epilepsy, headaches, sub-cutaneous lumps, neuro and ocular cysticercosis

299
Q

How can you control Toxoplasma gondii?

A

Toxovac vaccine 4 weeks before tupping

Introduce new stock well before tupping

300
Q

What is unusual about the sporulation of Cryptosporidium?

A

Takes place INSIDE host

301
Q

Which nematode parasites of pigs only affect outdoor pigs?

A 
Hyostrongylus rubidus (stomach)
Metastrongylus apri (lungs)
302
Q

Which 4 nematode parasites of pigs affect both outdoor and indoor pigs?

A

Ascaris suum
Strongyloides ransomi
Trichuris suis
Oesophagostomum spp

303
Q

What is the intermediate host of Ascaris suum and Metastrongylus apri?

304
Q

Describe the pathogenesis of Ascaris suum (pig ascarid)

A

Hypersensitivity response to migrating larvae (milk spots in liver, transient pneumonia in lungs)
Adults in SI (mechanical blockage, poor weight gain)
Major economic losses (liver condemnation, reduced weight gain)

305
Q

How can you diagnose Ascaris suum?

A 
Abattoir reports
Transient resp disease
Decreased weight gain 
Eggs in faeces (MgSO4 floatation) 
Highly resistant eggs
306
Q

Describe the unique life cycle of Strongyloides ransomi

A

Free-living and parasitic stages
Free-living: male and female adults, live in soil and bedding
Parasitic: only females in SI-reproduce by parthenogenesis (offspring are clones of female)
Can switch between the 2 life cycles

307
Q

What disease is caused by Strongyloides ransomi?

How can you treat it?

A

Diarrhoea and weight loss in piglets

Tx: BZs, MLs

308
Q

What is the infective stage of Trichuris spp?

A

Egg containing L1

309
Q

Where is Oesophagostomum spp found in pigs?

310
Q

Where are adult Metastrongylus apri found?

A

Lumen of bronchi and bronchioles of pigs

311
Q

Give the life cycle of Metastrongylus apri

A

Larvated eggs in faeces, L1 hatches -> infects earthworm
L1-L3 in earthworm, L3 survives as long as earthworm (up to 7 years)
Earthworm ingested by pig
L3 released in gut, L3-L4 in mesenteric lymph nodes
L4 reaches lung via lymphatics and bloodstream
Adult in lungs

312
Q

Describe the disease caused by Metastrongylus apri

A 
4-7 month old pigs
Catarrhal and eosinophilic bronchiolitis
Coughing, dyspnoea, nasal discharge 
Decreased weight gain, inappetence
Exacerbates other resp disease
313
Q

How can you control pig nematodes medically?

A

In feed BZs

MLs (injectable ivermectin)

314
Q

Give the 2 species of Knemidocoptes mites that affect poultry

A

Knemidocoptes mutans -> scaly leg mite
Knemidocoptes gallinae -> depluming itch
Cause extensive crusting and lesions

315
Q

What is the proper name of the red poultry mite?
Where does it live?
How would you recognise it?

A

Dermanyssus gallinae
Blood-feeding mite
Lives in environment in day, host at night
D-shaped anal plate
Red when filled with blood, black otherwise

316
Q

How can you distinguish between Dermanyssus gallinae and Ornithonyssus silviarum?

A

Dermanyssus gallinae has a D-shaped anal plate, Ornithonyssus silviarum has a pear-shaped anal plate

317
Q

When do lice infestations usually occur?

A

Autumn and winter

318
Q

Give 3 examples of in-feed anti-coccidials for poultry

A

Halofuginone
Toltrazuril
Diclazuril

319
Q

How is coccidiosis transmitted?

A

Faeco-oral transmission

320
Q

How can you diagnose eimeria in poultry?

A

Clinical signs (diarrhoea +/- blood, listless, death)
PM (parasitic stages eg merozoites)
Drop in feed conversion ratio

321
Q

What is the goal regarding prophylaxis for eimeria in broilers and layers?

A

Broilers: aim to eliminate disease (life-time in-feed prophylaxis eg halofuginone)
Layers: aim to allow immunity to develop (with drugs of low efficacy)

322
Q

Coccidiosis affects sheep of which age?

A

2-3 months

323
Q

Which part of the body is affected by coccidiosis in sheep and cattle?

A

Caecum and colon

324
Q

What are the clinical signs of coccidiosis in sheep?

A

Diarrhoea, dehydration, abdominal pain, anorexia

325
Q

What are the clinical signs of coccidiosis in cattle?

How do you treat it?

A

Diarrhoea, dysentery, dehydration

Sulphonamides

326
Q

What part of the body is affected by Eimeria in rabbits?

What are the clinical signs?

A

Epithelium of bile ducts -> enlarged liver, white nodules

Wasting, diarrhoea, jaundice

327
Q

Which class of drugs can you give in-feed to prevent poultry nematodes?

A

BZs eg flubendazole

328
Q

What causes ‘Blackhead’ in poultry?

A

Histomonas meleagridis (protozoa)

329
Q

What is the name of the poultry gape worm?

A

Syngamus trachea

330
Q

Describe the disease caused by Syngamus trachea (poultry gapeworm)
Where are adults found?

A

Mechanical blockage of trachea, asphyxia, coughing, gasping

Trachea

331
Q

What are the 3 ways a bird can become infected with Syngamus trachea (gapeworm)?

A

Ingestion of hatched L3
Ingested of L3 in egg
Ingestion of L3 in transport/paratenic host (earthworm)

332
Q

Where are adults of Capillaria spp found in birds?

A

Upper digestive tract (crop, oesophagus) and SI

333
Q

Describe the eggs of Capillaria spp (poultry)

A

Barrel-shaped, 2 mucoid plugs

334
Q

What is the intermediate host of Capillaria spp?

335
Q

What are the clinical signs of Capillaria infection in poultry?

A

Inappetence, weight loss, decreased egg production

336
Q

What is the infective stage of all ascarids?

337
Q

What are the 2 species of ascarid found in poultry?

A 
Ascaridia galli (SI)
Heterakis gallinarum (caeca)
338
Q

‘Blackhead’ is highly pathogenic in which bird?

339
Q

Give the pathogenesis and clinical signs of Histomonas meleagridis (‘Blackhead’)

A

Trophozoites in caecum erode caecal epithelium
Invade liver -> necrosis, saucer-like lesions
Clinical signs: depression, ruffled feathers, yellow faeces, cyanosis of wattle and comb (hence name)

340
Q

How is ‘Blackhead’ (Histomonas meleagridis) transmitted?

A

In the larvated eggs of Heterakis gallinarum (poultry ascarid)

341
Q

How can you control ‘Blackhead’ transmission?

A

Good biosecurity
Control Heterakis infection
Chickens are asymptomatic carriers, so avoid rearing turkeys on ground previously used for chickens

342
Q

Which drug would you give dogs to prevent Dirofilaria?

Which drug could you give to kill adult Dirofilaria?

A

Prevent: ivermectin

Kill adults: melarsomine

343
Q

When giving sheep anthelmintics, how do you make sure you leave some of the nematode population in refugia?

A

Leave at least 10% of sheep untreated
Don’t do ‘dose and move’ (ie don’t move the sheep onto a new pasture- put them back in contaminated pasture after treating)

344
Q

Taenia ovis cysts are seen where in sheep?

A

Muscles

Condemned at abattoir

345
Q

Acquired immunity of lambs to nematodes occurs when?

A

5-6 months old

Year 3 (28 decks)

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