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Parasitology Flashcards

1
Q

What anatomical features can be used to determine taxonomic groups of nematodes?

A
  • Structure of buccal capsule (teeth plates vs plates)
  • Bursa
  • Spicules
  • Intestinal cells
  • Features of eggs
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2
Q

Describe the common features of nematodes in the superfamily Trichuroidea

A
  • Male posterior coiled
  • Females longer
  • Bioperculated eggs
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3
Q

What are the important genera found in the family Trichostrongylidae?

A
  • Trichostrongylus
  • Haemonchus
  • Ostertagia
  • Nematodirus
  • Cooperia
  • Hyostrongylus
  • Teladorsagia
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4
Q

Describe the appearance of Nematodirus eggs

A
  • Very large (175-75um)

- Obvious 2-8 cells (morula)

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5
Q

Describe the appearance of Strongyle eggs

A
  • Similar to Nematodirus
  • Thin shelled, conspicuous morula
  • Know it isnt nematodirus as are only found in the horse
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6
Q

List the important families of the superfamily Strongyloidea

A
  • Strongylidae (horses)
  • Chabertiidae (sheep, pigs)
  • Syngamidae (birds, pigs in tropics)
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7
Q

List the important genera of the family Strongylidae

A
  • Strongylus
  • Triodontophorus
  • Cyathostomum
  • Cylicocyclus
  • Cylicodontophorus
  • Cylicostephanus
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8
Q

What are the important genera of Charbertiidae?

A
  • Charbertia

- Oesophagostomum

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9
Q

List the important families of the superfamily Ascaridoidea

A
  • Ascaridiae
  • Ascaridiidae
  • Toxocaridae
  • Hetrakidae
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10
Q

List the important genera of the family Ascarididae

A
  • Ascaris
  • Parascaris
  • Toxascaris
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11
Q

Describe ascarid eggs

A
  • Round
  • Thick shelled
  • Proteinaceous outer coating
  • Very resistant
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12
Q

List the important abomasal worms of cattle

A
  • Haemonchus placei
  • Trichostrongylus axei
  • OStertagia ostertagi
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13
Q

List the important small intestinal worms of cattle

A
  • Cooperia oncophora
  • Trichostrongylus colubriformis
  • Nematodirus spathiger
  • Chabertia
  • Oesophagostomum
  • Trichuris
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14
Q

Describe the general nematode life cycle

A
  • Adult worms in GI tract (males and females)
  • Strongyle-type egg in faeces
  • Free-living L1 larval stage
  • Free-living L2 larval stage
  • Infective L3 in L2 sheath ingested with water droplets on herbage
  • L4 migrating larvae wihin GI causing pathology
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15
Q

Describe the life cycle of Nematodirus

A
  • Eggs in faeces
  • Develop to L3 in egg
  • L3 hatches
  • Ingested with herbage
  • Moult from L3 to L5 in host
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16
Q

Describe the life cycle of Ascarids

A
  • Eggs in faeces
  • L1 to L2 in eggs
  • Eggs containing L2 ingested from contaminated pasture
  • Hatch in intestine
  • Migrate to HP vein and liver, L3 develops
  • Migrate to heart and lungs (L4 develops)
  • Coughed up and swallowed
  • Adults develop in intestine
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17
Q

Describe the life cycle of Trichuris

A
  • Eggs in faeces
  • L1 in eggs
  • Ingest eggs containg L1 from contaminated pasture
  • Hatch in small intestine
  • Migrate to LI
  • Moult from L1 to L5 in host
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18
Q

Name the types of oesophagus present in nematodes

A
  • Rhabditiform
  • Filariform
  • Bulb
  • Double bulb
  • Musculargalndular
  • Trichuroid
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19
Q

Describe strongyle type eggs

A
  • Elongated
  • 75-95um x 40-50um
  • Similar to hookworms, but larger
  • Ends more pointed
  • Lots of cells visible inside
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20
Q

Describe nematode respiration

A
  • Gaseoues exchange across cuticle
  • Aerobic and anaerobic phases
  • TCA, glycolysis and alternative pathway
  • Dependence on pathway varies with location and life cycle stage
  • O2 in GIT low, free livign O2 high
  • Glycolysis genetically wasteful, only 2 molecules of ATP vs 36-37 in TCA
  • Glucose in abundance in intestine, wastefulness unimportant
  • Glycogen is major energy reserve
  • Some can use CO2 to benefit (few)
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21
Q

Describe the role of lipids in nematodes

A
  • Important energy reserve in eggs adn free living larvae
  • Used as energy source in aerobic conditions
  • Cholesterol important sterol in cell membranes
  • Sterols needed as hormon precursors
  • Can also excrete/secrete lipids that influence host biology
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22
Q

Describe the role of tubulin and microtubules in the metazoan animals

A
  • Similar to other eukaryotic organissm microtbules importat to the functioning of nematode cells
  • alpha and beta-tubulin subunits form heterodimers
  • Polymerised to form microtubules
  • Meiosis, mitosis, cytokinesis and molecular transport utilise network of miccrotubules in nematodes
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23
Q

What are the muscle types found in nematodes?

A
  • Longitudinal and radial

- NO circular!

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24
Q

Describe the muscles of nematodes

A
  • Obliquely striated
  • somatic muscles below cuticle used in locomotion
  • Dense bodies rather than Z discs
  • Each dense body and sarcomere attached directly to muscle cell membrane
  • M line attaches filaments to each other and to the plasmalemma within each sarcomere
  • Attached directly to motor neurones
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25
Q

Describe the locomotion of parasites

A
  • Hydrostatic skeleton
  • Force applied on off
  • Forces opposed by hydrostatic pressure of coelom
  • Dorso-ventral bending
  • ACh = contraction = bends up, facilitated by GABA on top part = relaxation allowing bending
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26
Q

Describe the structure of the pharynx of nematodes

A
  • Buccal capsule
  • Procorpus
  • Metacorpus
  • Isthmus
  • Terminal bulb
  • Pharyngeal glands present
  • pharyngeal muscles throughout pharynx
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27
Q

Describe the role of the pharynx

A
  • Feeding
  • Connects buccal capsule to intestine
  • Secrete substances which may influence host biology
  • Pumping action but also peristalsis
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28
Q

Describe the nematode nervous system

A
  • Circumpharyngeal commissure (aka nerve brain)
  • Around isthmus of pharynx
  • System has a few hundred neurones (+ and -)
  • Ventral dorsal nerve cords go back from nerve ring
  • Connected by more commissures
  • Pharyngeal nerves extend anterior from nerve ring
  • Complex array of neurotransmitters and receptors
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29
Q

What are the important nematode neurotransmitters?

A
  • ACh, GABA, glutamate, serotonin

- Dopamine, adrenaline, noradrenaline

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30
Q

What neurotransmitters of nematodes are teh best targets for therapeutics?

A
  • ACh
  • GABA
  • Glutamate
  • Serotonin
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31
Q

Describe the inhibitory neurotransmitters of nematode pharyngeal neurones

A
  • Glutamate and GABA
  • Bind to receptors in post-synaptic neuronal membranes
  • Opens receptor, allows passage of Cl- but not cations
  • Hyperpolarisation
  • Inhibits muscle contraction
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32
Q

Describe the excitatory neurotransmitters of the pharyngeal nerves

A
  • Serotonin induces rhythmic contractin of pharyngeal muscles (pumping)
  • ACh controls rate of pharyngeal pumping
  • Some FaRPS (not important)
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33
Q

Describe the action of ACh and GABA in locomotion

A
  • ACh excitatory to contraction
  • GABA inhibitory to contraction
  • Antagonistic pair
  • To generate upward flexion of body, ACh active on ventral side to generate contraction, GABA active on dorsal side to generate relaxation allowing flexion
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34
Q

Describe the role of GABA in nematode defaecation

A
  • Excitatory for defaecation

- Need to defeacate when feeding otherwise will explode

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35
Q

What is the importance of nematode excretory/secretory produces?

A
  • Make host environment beneficial to parasite
  • Major source of nematode antigen
  • Can inhibit contractino of host intestine preventing removal of parasite
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36
Q

What are some of the excreteory/secretory proteins produced by nematodes?

A
  • AChE - function unknown

- Vasoactive intestinal peptide may secreted, may inhibit intestinal contraction

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37
Q

Describe some nematode lipids which influence host biology

A
  • Polyunsaturated fats (arachidonic acid) react with cyclo-oxygenase to produce prostagalndins and leukotrienes
  • Arachidonic acid can be used to produce unstable PG precursors, synthases produce series of PGs from these
  • PGs inhibit immune response
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38
Q

Explain how benzimidazoles exert their action

A
  • Inhibit beta-tubulin polymerisation
  • No productino of microtubules
  • Basic life processes not possible, no reproduction, eventually die
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39
Q

Explain how proton ionophores can be used as anthelmintics

A
  • Alter H+ gradients
  • No more synthesis of ATP
  • Basic life processes cannot take place, unable to reproduce, die
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40
Q

Explain how diethylcarbamazine can be used in anthelmintics

A
  • Blocks arachidonic acid synthesis
  • No more production and secretion of PGs
  • Unable to generate favourable host environment
  • Immune system can tackle infection
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41
Q

Explain how GABA inhibitors can be used in anthelmintics

A
  • GABA excitatoryto defaecation
  • Need to defaecate when feeding or will explode
  • Inhibitors e.g. ivermectin prevent this so wil die
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42
Q

What is meant by pseudocoelomate?

A

An invertebrate that has a fluid filled body cavity not lined with mesoderm tissue

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43
Q

What is meant by dioecious

A

Having male and female reproductive organs in separate organs

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44
Q

What is meant by cephalisation?

A

The concentration of sense organs, nervous control etc at the anterior end of the body forming head and brain both during evolution and during the course of the embryo’s development

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45
Q

What are nematodes, cestodes and trematodes?

A
  • Nematodes: nemathelminths, roundworms
  • Cestodes: platyhelminths, segmented flatworms
  • Trematodes: platyhelminths, non-segmented flatworms
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46
Q

Describe gerenal features of nematodes

A
  • Pseudocoelomate
  • Bisymmetrical, non-segmented
  • Dioecious
  • Females larger than males
  • 4 larval moults before becoming adults
  • Usually L3 that are infectious
  • Cephalisation
  • Buccal capsule
  • Oesophagus and digestive tract present
  • Reproductive tract
  • Complex nervous system with many different NTs
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47
Q

Give the main features of Monezia expansa

A
  • SI of ruminant adults, cysticercoids in mites
  • Long tape worms - 2m or more
  • Suckers
  • 2 sets of genital organs visible along lateral margin of each section
  • Cestode
48
Q

Describe factors that shows that parasitic infection is a dynamic balance between host and parasite

A
  • More parasites during periods of reduced immune competency (spring rise)
  • Parasite has effect on host immune system, reducing its effect
49
Q

What is the succession of important GI nematodes on pasture?

A
  • June: Nematodirus
  • July: Teladorsagia
  • Sept: Trichostrongylus
50
Q

What is meant by succession of nematode species on pasture?

A

Genera peak at different times of year depending on favourable conditions

51
Q

What is the importance of succession of nematode species on pasture?

A
  • Animals constantly exposed to parasitic threat
  • Over summer on pasture, will be infected with different nematodes at different times
  • In some cases immuntiy will occur quickly while in other cases will take long time
52
Q

Describe immunity to N battus in young lambs

A
  • Immune response to this faster than to other nemaodes (occurs at less than 3 months, 6-7months for others)
  • N. battus hatches early, very young lambs exposed
  • With immature response will die so need to have an early response
53
Q

How can immunity be measured?

A
  • Reduced worm burden
  • Increased larval arrest
  • Low faecal egg count
54
Q

Outline some of the innate host response mechanisms to parasitic infection

A
  • N. battus coils around villi so villi are shed - clears infection
  • Mast cells and eosinophils
  • Serum IgM converts IgG as infection progresses - attract eosinophils
  • IL-5 and IL-13 stimulate chemotaxis and degranulation
55
Q

Outline some of the acquired immune response mechanisms to parasitic infection

A
  • Th2 cells

- IL-4, B cell activator - promotes differentiation into plasma cell to produce different antibodies

56
Q

Why does sterile immunity never occur in cattle infected by O. ostertagi?

A
  • L4 and adults suppress T cell division
  • DCs and macrophages presenting Ostertagia antigens may induce regulatory (suppressor) T cells
  • Production of important cytokines reduced with Ostertagia
57
Q

What are some mechanisms of immune evasion employed by parasites?

A
  • Hypobiosis
  • Evading host immune response
  • Neonatal immunological unresponsiveness
  • Concomitant immunity
  • Polyclonal stimulation of immunoglobulin
58
Q

Describe how some parasites are able to evade the host immune response

A
  • Produce cuticular proteins not recognised by immune system

- e.g. Pinworms - little pathology or immune responsiveness

59
Q

Describe how neonatal immunological unresponsiveness can aid parasitic infection

A
  • Sometimes do not have vigorous enough immune response until exposed to reinfection
  • Reduce immune response of foetus in situ
  • When first born has to be exposed to pathogen
  • Immune response working, but not seen disease before so gets disease before immuntiy built up
60
Q

Describe concomitant immunity

A
  • Immunity which protects from subsequent infections but unable to clear existing
  • Parasites coated with host antigen, not recognised by immune response
  • Immune response for other parasite and remove these
61
Q

Describe polyclonal stimulation of immunglobulin

A
  • Some nematode species stimulate polyclonal IgE
  • Mast cell may be coated with IgE that does not recognise parasite antigen
  • Mix of different antigens and Ig produced, not very effective
62
Q

Explain how Ostertagia can suppress the immune response

A
  • Produces GH-beta
  • This suppresses Th1 and Th2 systems
  • Activates suppressor T cells
  • Reduces immune attack
63
Q

Explain the importance of hypobiosis in clinical disease

A
  • Arrested development/arrested larval development
  • Some larvae of nematode stop developing in host
  • Biological switching to ALD when unfavourable conditions
  • Switch back on to growth when favourable conditions e.g. through stress such as pregnancy/birth or environmental conditions like weather
  • Important in timing of treatment and pasture management
64
Q

List GI nematodes in which hypobiosis is important

A
  • Ostertagia ostertagi
  • Cooperia spp.
  • Haemoonchus contortus
  • Teladorsagia circumcincta
65
Q

Briegly outline the consequences of hypobiosis in O. ostertagi

A
  • Arrested in gastric gland of host

- All develop at same time, destroys large numbers of gastric glands when reactivate

66
Q

List important factors on hypobiosis

A
  • Phenotype
  • Temperature
  • Moisture
  • Stress
  • State of host immune system
67
Q

Describe how spring rise occurs

A
  • Eggs and larvae overwintered on pasture
  • Low immune competency just before lambing and after
  • Arrested L4 develop into adults and produce eggs
  • Eggs excreted by sheep from 2 weeks before and 4-6 weeks after birth
  • L3 acquired from pasture
  • Increased number of eggs and L3 on pasture at same time as new borns and susceptible ewes
  • Increase of disease incidence in spring
68
Q

Explain the disease management where peri-parturient rise is likely to occur

A
  • Some anthelmintics kill arrested larvae, other do not
  • Use anthelmintics just prior to lambing
  • Rotation of pasture to avoid putting lambs and ewes on pasture with overwintered eggs and larve
  • Need to know how long they can be viable in the environment in order for rotation to be effective
69
Q

Describe the life cycle of Toxocara canis in pups

A
  • Eggs containing L2 ingested
  • L2 hatches
  • Tracheal migration (L2 to L3)
  • Swallowed
  • L3 to L4 in stomach
  • Adults in SI
70
Q

Describe the life cycle of Toxocara canis with transmission to pup from dam

A
  • Eggs containing L2 ingested
  • L2 hatches and migrates to liver
  • Somatic migration of L2
  • Encyst in tissue
  • In pregnant bitch can have transplancental migration of L2 to foetal liver then neonatal lung
  • Can also go via mammary gland (L2-L3) and L3 ingested by suckling pups
71
Q

Describe the life cycle of Toxocara canis via a paratenic host

A
  • Dog ingests paratenic host (mouse)

- L2-adult in dog intestine

72
Q

Outline the difference between Toxocara cati and Toxocara canis life cycle

A
  • Similar
  • cat infected by ingesting eggs or paratenic host
  • Kittens infected transmammary
  • No in utero infection in cats
73
Q

Describe the life cycle of Oxyuris equi

A
  • Horse ingests eggs containing L3
  • L3 to L5 in intestine
  • Adult inhabits caecum, colon, rectum
  • Female migrates to anus to lay eggs
  • Develop to L3 in egg
74
Q

What are the pathological effects of Nematodirus battus?

A
  • Many burrowing larvae ingested at once
  • Can cause acute diarrhoea and death in lambs
  • Larvae are cause of pathology
75
Q

What are the pathological effects of Cooperia punctata?

A
  • Adults burrow into SI and cause little pathology except in heavy infections
76
Q

What are the pathological effects of Trichostrongylus axei?

A
  • Adults penetrte lining of abomasum and sometimes SI
  • Reduce appetite
  • Cause diarrhoea
77
Q

What are the pathological effects of Trichostrongylus colubriformis?

A
  • Larvae and adults cause pathology
  • Chronic diarrhoea in adults
  • Acute diarrhoea in younger animals
  • may cause bottle jaw
78
Q

Describe the life cycle of Ancylostomatidea

A
  • L3 ingested or penetrate the skin
  • Eggs in faeces
  • L1 hatch and develop to L3
79
Q

Describe Ostertagia ostertagi

A
  • Abomasal worm
  • Cattle
  • Trichostrongyle
  • Nematode
  • Brown stomach worm
  • Bursate
  • Square head
  • 16 intestinal cells
  • Generic nematode life cycle
80
Q

Describe the effect of Ostertagia ostertagi on gastric glands

A
  • L4 emerge from gastric glands causing pathology
  • HCl not produced
  • pH increases
  • High pH prevents conversion pepsinogen to pepsin
  • Reduced protein digestion
  • Pepsinogen and gastrin increase in blood
  • Blood proteins increase in abomasum abomasum (hypoalbuminaemia)
81
Q

What are teh clinical signs of Ostertagiasis?

A
  • Severe diarrhoea
  • Rapid weight loss
  • Cobblestone lesions as gastric glands are destroyed
  • Sub-mandibular oedema (bottle jaw)
82
Q

Describe immunity to O. ostertagia

A
  • First immune response does not protect agains reinfection with L3
  • Delays larval development, increases number of inhibited worms - immune induved hypobiosis
  • Second immune response may take up to 2 years
  • No sterile immunity
  • Eosinophils and mast cells increase in intestine
  • Th1 and Th2 cytokines present
83
Q

What are the control measures for O. ostertagi?

A
  • Ivermectin (kill hypobiotic L4)
  • Frequent drenching around calving (prevent type II)
  • Frequent drenching in first grazing season (prevent type I)
  • Lower stocking density
  • Rotate calves and adults
  • Rotate onto fresh pasture
84
Q

How can O. ostertagi be diagnosed?

A
  • McMaster slides to count eggs
  • Adults on necropsy
  • Condition of abomasum (cobblestone)
85
Q

Describe Haemonchus contortus

A
  • Abomasal
  • Sheep
  • Trichostrongyle
  • Barber’s pole worm
  • Normal nematode life cycle
86
Q

What happens in Haemonchus contortus infections?

A
  • Anaemia due to feeding of worms
  • May cause death
  • Diarrhoea
  • Loss of body condition
  • Loss of wool quality
  • May cauase bottle jaw
87
Q

How is infection with Haemonchus contortus be diagnosed?

A
  • Famacha scale (anaemia)
  • McMaster technique
  • Adults on necropsy (final diagnosis)
  • Red haemorrhagic surface of abomasum
88
Q

Describe type I Ostertagiasis

A
  • Younger animals when enough L3 have been ingested
  • Hypobiotic larvae activated in mother, more eggs released, increased risk of calf infection
  • April/May
  • Pasture grazed in previous years
  • L3 overwinter so large numbers already present
  • Peak is Aug/Sept
89
Q

Describe type II Ostertagiasis

A
  • Animals old enough to have arrested larvae from previous grazing seasons
  • Already in animal
  • Reactivated larvae, infect host
  • In early autumn to late winter
  • Or calves 9-12 months
90
Q

What is the global significance of Haemonchus contortus in sheep and goat farming?

A
  • Anthelmintic resistant

- Makes sheep farming non-sustainable in some areas

91
Q

How can anthelmintic resistance be tested?

A
  • Faecal egg coutn reduction
  • Compare number of eggs before and after treatment
  • Less than 60% reduction in number of eggs = resistance
92
Q

Describe the McMaster technique

A
  • Known mass of faeces
  • Known vol of saline
  • Add 10ml to faeces, shake to break
  • Homogenous solution
  • Strain, continue adding saline
  • Use pipette o put final solution on McMaster slide
  • View under LM
  • Methodically count
  • Calculate number of eggs per g of faeces
  • (ml solution used x no. of eggs)/(vol of both sides of McMaster combined (usually 0.3)xmass of faeces used)
93
Q

Describe the epidemiology of Nematodirus

A
  • Trichostrongyle
  • Common in temperate zones
  • Scottish border, Northern England
  • Small intestine of ruminants
94
Q

List the common species of Nematodirus and their host species

A
  • N. battus: Sheep (occasionally calves)
  • N. fillicolis: sheep
  • N. spathiger: sheep and cows
  • N. helveticus: cattle
95
Q

What stimulates N. battus hatching?

A
  • Cold period followed by mean day/night temperature of around 10degreesC
  • Is L3 that hatches
96
Q

What is the importance of the N. battus egg?

A
  • Extremely tough
  • Resistant to freezing and drought
  • Viable up to 2 years on pasture
  • Hatching does not only occur in spring from eggs excreted in previous year
  • Some eggs deposited in spring can hatch in autumn of same year
97
Q

What are the clinical signs of infection with N. battus?

A
  • Acute onset in young recently weaned lambs (6 weeks -4 months)
  • Rapid weight loss
  • Watery diarrhoea
  • Dehydration
  • Sudden death
98
Q

What is the pathology of N. battus caused by?

A
  • Developing larval stages and their migration

- Leads to damaged villi and erosions of mucosa

99
Q

Describe the L3 larval appearance of N. battus

A
  • 8 gut cells
  • Head braod, rounded sheat
  • Tail filamentous and exsheathed
  • Tail notched or lobed
100
Q

Compare N. battus eggs with other Nematodirus eggs

A
  • N. battus brown
  • Larger
  • Straight sides
  • Morula visible in both
101
Q

Describe the climatic factors involved with nematodirus

A
  • Warm March = early hatch
  • Cool wet April/May increases larval survival on pasture
  • Can forcast problems using weather
102
Q

Describe the control/treatment of Nematodirus

A
  • 3 treatments during May-June in years with predicted severe diseases, 2 in other years
  • Ewes dosed prior to lambing
  • Rotational grazing (swapping between sheep and cattle does not work for N. battus as cows can also be infeted by this)
103
Q

Describe the immunity to N. battus

A
  • Strong age related (after 3 months of age)
  • Increased eosinophils and mast cells
  • Nematode specific serum IgA and IgG
  • Villus shedding (rejection mechanisms, organisms wrap around villi of SI)
104
Q

Describe the epidemiology of Trichostrongylus species

A
  • Alimentary tract of animals and birds
  • Direct, non-migratory life cycle
  • Typical life cycle
  • Destroys villi
  • Subclinical infection possible
105
Q

Describe the general appearance of Trichostrongylus spp.

A
  • Small
  • Hair like worms
  • Up to 0.7mm long
  • Bursated
  • Small buccal capsule
106
Q

List some of the common Trichostrongylus spp. and their host species

A
  • T. colubriformis: sheep, goats cattle
  • T. capricola
  • T. citrinus
  • T. axei: sheep, goats cattle
  • T. tenius: birds
107
Q

Where is Trichostrongylus colubriformis found?

A

Small intestine of sheep, goats and cattle

108
Q

Where is Trichostrongylus axei found?

A

Abomasum of sheep, goats and cattle

109
Q

Describe the appearance of T. colubriformis

A
  • 16 gut cells
  • Head tapered
  • Sheath forms short cone
  • 560-796um lenght
  • Male bursa with 2 spicules
  • Lots of eggs visible in females
110
Q

Describe the clinical signs of infection with Trichostrongylus spp.

A
  • acute diarrhoea in young
  • Chronic diarrhoea in older animals
  • Intestine inflamed with hyperplasia
  • May be blood spots
  • Mesenteric lymph nodes enlarged
  • May cause bottle jaw
111
Q

Describe immune exclusion to trichostrongylus

A
  • Exlusion of/barrier against L3
  • Mucus from immune sheep prevents establishment of T. colubriformisn in naiive sheep intestine
  • sIgA and mucus IgG recognises 3 different classes of L3 cuticular antigens
112
Q

Describe the self cure fo Trichostrongylosis

A
  • Expulsion of adults in intestine
  • Mast cells, IgE, eosinophils (Th2 induced hypersensitivity response)
  • IL-5 activates eosinophils, IL-13 stimulates eotaxin and eosinophil migration and class switching to IgE
  • Self cure is T-cell induced
  • Can be induced when naiive animals have T-cells from immune animals adoptively transferred to them
113
Q

Describe subclinical infections of T. colubriformis

A
  • Reduce weight gains by 35%
  • Decrease wool growth by 10%
  • Decrease milk production by 20%
114
Q

Describe the epidemiology of T. tenius

A
  • Hypobiosis and warm wet summers increase larval survival
  • Chicks very susceptible if ingest enough L3
  • When enough L3 on pasture, sudden death
  • Fluctuation in grouse number due to T tenius
  • In early spring food quality poor, high worm burden, adults more likely to die
  • Normal nematode life cycle
115
Q

Describe the control of T. tenius

A
  • No self cure reported

- Fenbendazole used to cure infection

116
Q

Discuss the veterinary importance of T. tenius in game birds

A
  • Infects chickens, guinea fowl, pheasants, quail, many others
  • Most notable impact on red grouse populations in North East and West england and Scotland
  • Grouse shooting industry worth a lot of money

GI (31 decks)

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