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PVS > Parasitology > Flashcards

Parasitology Flashcards

1
Q

Outline the importance of parasites

A
  • Significant production loss
  • Welfare
  • Death of animal
  • Zoonoses
  • Force change in management
  • Substantial cost (treatment, pasture management, manure management, quarantine, diagnostic testing, biosecurity)
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2
Q

What does the method of treatment of endoparasites depend on?

A

The life cycle

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3
Q

What is the significance of finding worm eggs or larvae in faeces?

A
  • Life cycle completed
  • Adult present in animal and able to cause clinical signs
  • Damage has occurred, dealing with an ill animal
  • Parasite has reached patency stage
  • Environmental contamination has occurred
  • If animal has been treated, parasite must be resistant to the treatment
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4
Q

Describe the clinical signs associated with liver flukes

A
  • Jaundice in some cases
  • Loss of appetite, diarrhoea, emaciation
  • Bottleneck may occur in some cases
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5
Q

Describe the clinical signs associated with lungworms

A
  • Persistent cough
  • Lowering of head and stretching of neck
  • Mouth breathing
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6
Q

Describe the clinical signs associated with GI worms

A
  • Weight loss, reduced appetite, diarrhoea, anaemia

- Bottleneck

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7
Q

Outline the laboratory findings associated with liver flukes

A
  • y-glutamyl transpeptidase or transferase
  • Function of liver affected
  • Serological assays
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8
Q

Outline laboratory findings associated with lungworms

A
  • Eosinophilia in blood and tracheal washes

- Serological assays

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9
Q

Outline laboratory findings associated with GI worms

A

Plasma pepsinogen or gastrin (less common) increased

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10
Q

Why is plasma pepsinogen increased with GI worms?

A

Pepsinogen cannot be converted to pepsin due to alteration in abomasal pH

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11
Q

Outline some risk factors that may increase chance of liver fluke infection

A
  • Heavy rains
  • Floods
  • High number of snails present
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12
Q

Outline the typical epidemiology of lungworms

A
  • Unpredictable
  • Dependent on climate
  • Fast development (5 days from first larval stage to infection)
  • Typical signs within 1 week of ingestion of larval stage
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13
Q

Outline the typical epidemiology of GI worms

A
  • Spring rise

- Acute death of lambs 2-3 weeks after turnout onto pasture

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14
Q

Give examples of changing patterns of sheep parasitism

A
  • Haemonchosis: previously only SE England, now more widespread (Wales and Scotland)
  • Nematodirosis: spring problem but now also in Autumn
  • Trichostrongylosis: traditionally in autumn in store lambs, now earlier in summer, loss of younger lambs, or in mild winters so problems later than described
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15
Q

What is the purpose of NADIS regarding anthelmintic use?

A
  • Allows prediction and therefore preventative action

- This minimises the use of anthelmintics and so reduces potential for resistance development

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16
Q

What is meant by parasitic load?

A

The amount of parasite infecting the host

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17
Q

How can parasitic load be assessed?

A
  • Faecal egg count

- Number of parasites in tissue

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18
Q

Why might a parasitic infection be undetectable via faecal egg count?

A
  • Parasite is in pre-patent stage and not yet shedding eggs/larvae
  • Single sex infection (except cestodes and trematodes)
  • Strong immune response from host preventing reproduction of parasites
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19
Q

What are the goals of helminth control?

A
  • Prevention of clinical disease
  • Immunisation
  • Economic (increase/minimise loss of productivity)
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20
Q

What are the options for helminth control?

A
  • Biological
  • Vaccines
  • Anthelmintics
  • Pasture management
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21
Q

Outline an example of biological control of helminths

A
  • Duddingtonia flagrans
  • Aerobic fungus that reduces number of infective larvae on pastures to an economically acceptable level
  • Broad spectrum, no residues, no withdrawal period, active against drug resistant worms
  • Novel mode of action and failed to be commercialised as is impractical to administer to pastures daily
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22
Q

Outline the use of vaccines in helminth control

A
  • Only 1-2 available
  • Antigenes, native or recombinant/synthetic
  • Targets include: intestinal protein, transporters, enzymes
  • Can achieve high protection rate
  • Problems in commercial large scale production
  • Failure to commercialise
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23
Q

Outline the use of chemotherapy in helminth control

A
  • Very high development costs
  • Mainstay of parasite control
  • Fears of anthelmintic resistance
  • e.g. benzimidazoles, imidazothiazoles, macrocyclic lactones
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24
Q

How is anthelmintic resistance diagnosed?

A
  • Faecal egg count comparison before and after treatment of the same animal
  • Larval hatch test (in vitro culture of larvae in presence of anthelmintic compounds)
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25
Q

What is the mechanism for anthelmintic resistance?

A
  • Point mutation leading to altered protein sequence and so anthelmintic is ineffective
  • Established by selective pressure
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26
Q

Outline some treatment strategies to combat anthelmintic resistance

A
  • Treatment frequency as low as possible to reduce selection pressure
  • Grazing management
  • New anthelmintic classes introduced
  • Strict compliance with prescribed treatment regimes
  • Change anthelmintic class annually
  • Ensure are not underdosing
  • no “dose and move”
  • Quarantine infected animals
  • Combination therapy
  • Use plants with anthelmintic activity
  • Avoid overstocking of animals
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27
Q

What is refugia?

A

Parasite finding refuge in tissue and so not exposed to anthelmintic

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28
Q

List the common abomasal helminth parasites of small ruminants

A
  • Ostertagia ostertagi
  • Haemonchus contortus
  • Teladorsagia circumcincta
  • Trichostrongylus axei
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29
Q

What is FAMACHA and how is it used?

A
  • A scale to objectively assess the degree of anaemia due to abomasal worms
  • Aids decision of whether to administer anthelmintic dose
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30
Q

Describe the classical post mortem signs of Haemochus contortus

A
  • Severe gastroenteritis characterised by extensive submucosal hyperaemia and haemorrhage in the abomasum
  • erosions adn ulcers as well as gross thickening of the abomasal wall
  • Some degree of haemorrhages in parts of the small intestine
  • Visible presence of worms
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31
Q

Why is faecal examination a good primary diagnostic tool for endoparasites?

A
  • Eggs in faeces indicates GI worm
  • Larvae in faeces indicates lungworm
  • Non-invasive
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32
Q

How does an animal become infected with lungworm?

A

L3 larvae, either in intermediate host or free on pasture

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33
Q

What causes abdominal bleeding in an Angiostrongylus vasorum infection?

A
  • Migration of larvae from stomach/intestine to lungs
  • Secrete anticoagulants
  • Parasite immune-mediated thrombocytopaenia, disseminated intravascular coagulation (DIC)
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34
Q

Describe the appearance of the heart and lungs of a dog infected with Angiostrongylus vasorum

A
  • Alveolar infiltrates seen
  • Interstitial patterning of lung
  • Heart axis shifted to the left suggesting right ventricular enlargement
  • Cardiac hypertrophy and pathological damages
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35
Q

How do sheep become infected with Haemonchus contortus?

A

Ingestion of L3 larval stage on damp grass

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36
Q

How is sudden death of lambs caused by Haemonchus contortus?

A
  • Anaemia as a consequence of worms feeding

- Loss of appetite

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37
Q

List the parasitic worms that can be found in the intestine of pigs

A
  • Hyostrongylus rubidus
  • Trichuris suis
  • Strongyloides ransomi
  • Oesophagostamum spp
  • Ascaris suum
  • Isospora suis
  • Trichinella spiralis (adult)
  • Macracanthorhynchus hirudinaceus
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38
Q

How do pigs become infected with Trichuris suis?

A

Ingestion of eggs containing L1 larvae

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39
Q

What can be used to treat Trichuris ovis infection?

A

Common anthelmintics e.g. fenbendazole, benzimidazoles, levamisole

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40
Q

What is a proglottid?

A

A segment of cestode worms, containing an ovary and genital pore. It matures as it moves towards to last segment of the cestode, and is shed as the infective agent

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41
Q

What does tapeworm infection in dogs and cats indicate?

A

Presence of fleas

42
Q

Describe the clinical signs of heartworm infection in dogs

A
  • Exercise intolerance
  • Hydrothorax
  • Hydroperitoneum
  • Chronic cough
  • Dyspnoea
  • Haemoptysis
  • Eosinophillian lung
  • Oedema in lung parenchyma
43
Q

Outline the treatment for Dirofilaria immitis

A
  • Kill adult parasite first with adulticide
  • Then all circulating microfilariae with microfilaricide
  • May require surgery if vena cava syndrome occurs
44
Q

Outline control of Dirofilaria immitis

A
  • Entirely preventable using medication
  • Screening and prophylaxis
  • Ensure patient if microfilaria and adult free, can start prophylaxis
45
Q

Which 2 species of Taenia can cause human disease?

A

Taenia saginata, Taenia solium

46
Q

Compare Taenia saginata and solium

A
  • Solium has greater public health implications as it has the capacity to use humans as an intermediate host, develops multiple cysticerci in vital organs often with fatal consequences
  • saginata does not do this
47
Q

How is infection with Eimeria spp acquired?

A

Consumption of food/water contaminated with mature (sporulated) oocysts

48
Q

What dog parasite forms hydatid cysts?

A

Echinococcus granulosus

49
Q

What is the significance of Fasciola hepatic infections?

A
  • Condemnation of livers
  • Emaciation and reduced growth rate
  • High mortality in sheep
50
Q

Outline the control of liver flukes in ruminants

A
  • Treat infected animals with flukicides
  • Eliminate snails in environment
  • Implement sound husbandry measures
51
Q

What is a Baermannn apparatus used for?

A

Used to isolate and concentrate larvae of lungworms from faeces

52
Q

Compare the appearance of sporulated oocysts of Eimeria, Isospora, Cryptosporidium

A
  • Eimeria: 4 sporocysts, each with 2 sporozoites
  • Isospora: 2 sporocysts, each with 4 sporozoites
  • Cryptosporidium: no sporocysts, 4 sporozoites
53
Q

Describe the generic life cycle of GI nematodes

A
  • Eggs in faeces
  • Hatch
  • Moult to L1 to L2 and then L3
  • L3 are infective, ingested on damp pasture by host
  • free-livingn stages 2-12 weeks to complete
  • Host stage 16-21 days to complete (unless L3 arrest in host over winter)
54
Q

Describe the life cycle of Nematodirus

A
  • L1-L3 development occurs in eggs
  • L3 hatch
  • L3-5 moults occur in the host
55
Q

Describe the life cycle of liver flukes

A
  • Eggs shed in faeces
  • Miracidium
  • Ingested by snail
  • Develop to sporocyst
  • Develop to redia
  • Develop to cercaria
  • Metacercaria shed by snail, ingested by sheep
  • Hatch to adult in sheep
56
Q

Describe the clinical signs and seasonality of Haemonchus contortus

A
  • Spring, after rain
  • Weight loss, anaemia
  • Hypoproteinaemia
  • Bottle jaw
  • Does not usually cause diarrhoea
57
Q

Describe the clinical signs and seasonality of Trichostrongylus spp

A
  • Traditionally autumn, now also in late summer months

- Inappetance, diarrhoea, weigh loss, death, black scour

58
Q

Describe the clinical signs and seasonality of Nematodirus battus

A
  • Historically spring, now varying times of year

- Diarrhoea most prominent sign, dehydration

59
Q

Describe the clinical signs and seasonality of acute Fasciola hepatic infection

A
  • July to December

- Sudden death, anaemia, dullness, dyspnoea, ascites, abdominal pain

60
Q

Describe the clinical signs and seasonality of sub-acute Fasciola hepatica infection

A
  • October to January

- Rapid weight loss, anaemia, submandibular oedema, ascites in some cases

61
Q

Describe the clinical signs and seasonality of chronic Fasciola hepatica infection

A
  • January to April

- Progressive weight loss, anaemia, submandibular oedema, diarrhoea, ascites

62
Q

What is the importance of ectoparasites?

A
  • Animal welfare issue
  • Economic impact (large animals)
  • Zoonotic potential
63
Q

List the direct effects of ectoparasites

A
  • Pruritus and cutaneous lesions (secondary infection)
  • Blood loss
  • Myiasis
  • Loss of production
  • Downgrading of hide
  • Allergy
  • Zoonosis
64
Q

List the indirect effects of ectoparasites

A
  • Transmission of pathogens
  • Transmission of zoonotic pathogens
  • Accidental injury (cattle/horses bolting)
  • Reduction in feeding due to discomfort
65
Q

What is meant by eradication?

A

Elimination of a disease or pest without its return

66
Q

Give an example of an ectoparasite that has been eradicated in the UK

A

Anopheles mosquito

- but reappeared in some countries such as India

67
Q

Give reasons why eradication programmes may fail

A
  • Insecticide resistance
  • Socio-economic factors
  • Poor surveillance
68
Q

What is meant by ectoparasite control?

A

Reduction of population leading to reduced transmission, reduce to acceptable level

69
Q

Give examples of ectoparasite control methods

A
  • Chemical
  • Physical
  • Biological
  • trapping
  • Modelling and forecasting
70
Q

What are some considerations when choosing chemical control methods?

A
  • Mode of action of drug
  • Spectrum of activity
  • Mode of application
  • Speed of action required
  • Efficacy/duration/frequency of reapplication
  • Resistance
  • Species to be treated
  • Withdrawal periods
  • Age restrictions
  • Contraindications/drug interactions
  • Cost
  • Environmental contamination/toxicity to non-target species
71
Q

How might the life cycle of a parasite affect its control?

A
  • Indirect life cycle more difficult to control as have to consider intermediate host
  • Not all stages will be susceptible to the same chemical control methods for example
  • Some stages may be persistent in the environment
72
Q

List the groups of chemical control methods for ectoparasites

A
  • Neurotoxins
  • Insect growth regulators
  • Repellants
  • Dessicants
  • Synergists
  • Lime sulphur
73
Q

List the mechanisms of action of neurotoxins for ectoparasite control

A
  • Cholinesterase inhibitors
  • Octopamine receptor stimulant
  • GABA inhibitor
  • Insect nicotininc Ach receptor stimulant (+/- GABA agonist)
  • Na channel activator
  • Na channel blocker
  • Cl channel activators
  • Cl and GABA channel inhibitors
74
Q

List the groups of ectoparasite neurotoxins

A
  • Organophosphates
  • Carbamates
  • Triazepentadienes
  • Phenylpyrrazoles
  • neonicatinoids
  • Pyrethrins
  • Pyrethroids
  • Semicarbazones
  • Macrocyclic lactones
  • Isoxalines
  • Spinosyns
75
Q

What is the mechanism of action of organophosphates?

A

Cholinesterase inhibitors

76
Q

Outline the use of organophosphates and give examples

A
  • Used on animal/in environment
  • Use reduced due to neurotoxicity concerns
  • Fnethion, diazinon, dichlovos, malathion, proprtamphos, dimpylate
77
Q

What is the mechanism of action of carbamates?

A

Cholinesterase inhibitors

78
Q

Outline the use of carbamates and give examples

A
  • Less toxic than organophosphates

- Propoxur, carbaryl, methiocarb, butocarb, fenoxycarb

79
Q

What is the mechanism of action of triazepentadienes?

A

Octopamine receptor stimulant

80
Q

Outline the use of triazepentadienes and give examples

A
  • Broad action vs mites, ticks
  • No effect on SA insects, but used for lice in cattle/pigs
  • Dip/rinse, spot on
  • Contraindicated in horses and cats
  • e.g. Amitraz
81
Q

What is the mechanism of action of phenylpyrrazoles?

A

GABA inhibitor

82
Q

Outline the use of phenylpyrrazoles and give examples

A
  • Action vs felas and ticks
  • e.g. Fipronil and pyriprole
  • Fipronil active vs Trichodectes canis but toxic to rabbits
83
Q

What is the mechanism of action of neonicatinoids?

A

Insect nicotinic Ach receptor stimulant

84
Q

Outline the use of neonicatinoids and give examples

A
  • Action vs fleas
  • e.g. Imidacloprid, Nitenpyram, dinotefuran
  • Imidacloprid active against Trichodectes canis
  • Nitenpyram fast acting but short lived effect
85
Q

What is the mechanism of action of pyrethrins?

A

Na channel activator

86
Q

Outline the use of pyrethrins and give examples

A
  • Rapid knockdown vs insects/fleas
  • Poor persistence
  • Toxic to cats
  • e.g. Dichlorvos, fenitrothion
87
Q

What is the mechanism of action of pyrethroids?

A

Na channel activator

88
Q

Outline the use of pyrethroids and give examples

A
  • Active vs fleas, flies, keds, lice, ticks
  • Repellant +/- knockdown
  • Toxic to cats and fish
  • e.g. permethrin, cypermethrin, deltamethrin, flumethrin
89
Q

What is the mechanism of action of semicarbazones?

A

Na channel blocker

90
Q

Outline the use of semicarbazones and give examples

A
  • Active vs fleas
  • e.g. Indoxacarb
  • Indoxacarb is a pro-druc, activated by insect only and so has low mammalian toxicity
91
Q

What is the mechanism of action of macrocyclic lactones?

A

Cl channel activators

92
Q

Outline the use of macrocyclic lactones and give examples

A
  • Action vs selected ecto and endoparasites
  • Absorbed systemically so ectoparasite effect not affected by bathing
  • Especially good for parasites with tissue stages e.g. warbles
  • Care re neurotoxicity if MDR1 gene mutation (collies/herding breeds)
  • Avermectins and milbemycins
93
Q

Name the avermectins

A
  • Ivermectin
  • Selamectin
  • Doramectin
94
Q

Name the milbemycins

A
  • Milbemycin oxime

- Moxidectin

95
Q

What is the mechanism of action of isoxazolines?

A

GABA and Cl channel inhibitor

96
Q

Outline the use of isoxazolines and give examples

A
  • All licensed for fleas/ticks
  • Unaffected by bathing
  • Rapid onset - kill fleas before eggs laid
  • e.g. Afoxolaner, flurolaner, sarolaner, lotilaner
  • Serolaner also licensed for Sarcoptes, demodex, otodectes in dogs
97
Q

What is the mechanism of action of spinosyns?

A

Nicotinic Ach receptor stimulant and GABA agonist

98
Q

Outline the use of spinosyns and give an example

A
  • Oral tablet for dogs/cats
  • Unaffected by bathing, rapid effect
  • May vomit after administration although effect usually short-lived
  • e.g. Spinosad
99
Q

What is the side effect of neonicatinoids of greatest concern?

A

May be causing the declining bee population

100
Q

What are the 3 groups of Insect Growth Regulators?

A
  • Juvenile growth hormone analogues
  • Chitin synthesis inhibitors
  • Triazine derivatives

PVS (23 decks)

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