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PVS > Parasitology 3 > Flashcards

Parasitology 3 Flashcards

1
Q

What is the definitive host of Toxoplasma gondii?

A

Any member of Felidae

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2
Q

What are the intermediate hosts of Toxoplasma gondii?

A

Any warm-blooded animal

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3
Q

Describe the life cycle of Toxoplasma gondii

A
  • Unsporulated oocyss passed in cat faeces
  • Oocysts sporulate
  • Contaminate food, ingested by intermediate host
  • Asexual reproduction in muscles of intermediate hosts, can infect each other through tissue cysts
  • Cat infected by ingestion of cysts in tissues of infected IH
  • Sexual reproduction in gut epithelium of cat
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4
Q

What are tachyzoites?

A

Proliferative form of Toxoplasma gondii in blood or CSF, can be acute or recurrent

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5
Q

What is the prepatent period of tachyzoites?

A

> 13 days

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6
Q

What are bradyzoites?

A

Life long “tissue cysts” of Toxoplasma gondii

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7
Q

What is the prepatent period of bradyzoites?

A

3-10 days

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8
Q

When do Toxoplasma gondii oocysts become infective?

A

After 48 hours or more environmental incubation

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9
Q

Describe the survival of Toxoplasma gondii oocysts in the environment

A
  • Survive months to years despite extreme conditions (freezing, heat, dehydration)
  • Prepatent period >18 days
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10
Q

Describe Toxoplasma oocyst shedding from the cat

A
  • Thousands to millions shed per cat
  • But only shed for 1-2 weeks
  • Only ~1% of cats are shedding oocysts at a given time
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11
Q

What factors trigger tachyzoite to bradyzoite switching?

A
  • High pH
  • Presence of nitric oxide
  • Nitric oxide donor Sodium Nitroprusside
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12
Q

What factors trigger bradyzoite to tachyzoite switching?

A
  • Th2 cytokine bias
  • Lack of IL-12
  • Lack of IFN-y
  • Lack of TNFalpha
  • Lack of nitric oxide
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13
Q

What is the purpose of bradyzoite switching?

A
  • Protection and therefore persistence in the host
  • May occur in response to treatment or immune response of host
  • When immune weakness is indicated, switch back to tachyzoite
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14
Q

List the most common signs of feline toxoplasmosis

A
  • Anorexia
  • Weight loss
  • Lethargy
  • Dyspnoea
  • ocular signs
  • Myositis
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15
Q

List the less common signs of feline toxoplasmosis

A
  • GI signs
  • Neurological signs
  • Jaundice
  • Abortion
  • Pneumonia
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16
Q

How can toxoplasmosis be diagnosed?

A
  • Detection of oocysts in felines difficult

- Serology better: IgG and IgM

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17
Q

What treatment is used for toxoplasmosis in cats?

A

Clindamycin and pyrimethamine combination

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18
Q

Why is oocyst detection in cat faeces difficult?

A
  • Shedding occurs before clinical signs
  • Only 10% of cats shed
  • Intermittent shedding
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19
Q

Outline the prevention of Toxoplasma infection in cats

A
  • Do not allow cats to hunt rodents and birds
  • Feed only cooked meat or processed food from commercial sources
  • No vaccine available
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20
Q

Outline toxoplasmosis in food production animals

A
  • Pork greatest risk to humans and animals
  • Can survive in pigs for over a year after infection
  • Lamb second most common source of infection, then beef and chicken
  • Wild game also high risk food source
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21
Q

Outline the zoonotic potential of Toxoplasma

A
  • Cats main reservoir for infection of other mammals

- Can spread to humans via contaminated food/water and soil

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22
Q

Describe human toxoplasmosis in humans

A
  • 40% chance of mother passing disease to foetus
  • 10% have severe neurological and ocular disease
  • 30-40% of people have antibodies suggesting exposure
  • Linked to schizophrenia in humans
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23
Q

How can toxoplasmosis in humans be prevented?

A

Ensure food is properly processed - freezing and boiling kills tissue cysts

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24
Q

Describe human toxoplasmosis in immuno-competent individuals

A
  • Typically no symptoms

- May be in-apparent or mild flu-like illness (lymphadenopathy, fever, malaise, psychiatric disease)

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25
Q

Describe human toxoplasmosis in immuno-compromised individuals

A
  • Severe encephalitis

- Recrudescent infection

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26
Q

Describe human toxoplasmosis in pregnant women

A
  • Mainly affects foetus
  • Foetal death
  • Hydrocephalis
  • Chroidoretinitis
  • Mental retardation
  • Blindness
  • Epilepsy
  • May not manifest in offspring for years
  • May also be asymptomatic
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27
Q

Outline the diagnosis of congenital toxoplasmosis

A
  • Serological tests to diagnose acute infection in pregnant women (frequent false positives)
  • Sero-diagnosis confirmed at reference lab before treatment started
  • PCR of amniotic fluid for test confirmation/exclusion
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28
Q

Describe the treatment of congenital toxoplasmosis

A
  • Pyrimethamine and sulphonamide where PCR of amniotic fluid is positive
  • Spiramycin where PCR of amniotic fluid is negative
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29
Q

Describe the treatment of acute toxoplasmosis in humans

A
  • Generally not indicated for most people
  • Pregnant or immunocompromised
  • Diagnosis by IgM, IgG Ab titres
  • Pyrimethamine +sulphadiazine or clindamycin
  • Folinic acid to overcome thrombocytopaenia nad leukopaenia caused by damage to bone marrow from toxoplasmosis
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30
Q

Outline the treatment of toxoplasmosis in AIDs patietns

A
  • In seropositive patietns with CD4+ lymphocyte count of <100/ul: prophylaxis against toxo ence[halitis, trimethoprim-sulphamethoxazole or Dapsone
  • For toxo-encephalitis patients: pyrimethamine plus sulphadiazine or pyrimethamine + clindamycin
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31
Q

What are the consequences of infection with Neospora caninum in cattle?

A
  • Abortion

- Infertility

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32
Q

What are the consequences of infection with Neospora caninum in dogs?

A

Neuromuscular disorder

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33
Q

What is Neospora caninum?

A

Protozoan parasite

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34
Q

What is the key difference between Neospora caninum and Toxoplasma gondii?

A
  • Neospora is disease of dogs (DH) and cattle (IH), with uncertain zoonotic risk to humans
  • Toxoplasmosis mainly disease of humans, sheep and goats and cats are the only definitive hosts
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35
Q

Describe the life cycle of Neospora caninum

A
  • Dog ingests tissue cysts
  • Unsporulated oocysts shed in dog faeces
  • Oocysts sporulate
  • Contaminated food/water ingested by intermediate hosts or pregnant animal
  • Form tissue cysts in intermediate hosts
  • Tachyzoites transmitted through placenta to infect foetus in pregnant animal
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36
Q

What factors are related to infection risk with Neospora caninum?

A
  • Age
  • Presence of farm or wild canids
  • Absence of cats
  • Climate and season
  • Farm-raised replacement heifers
  • Proximity to town or village
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37
Q

How does age increase the risk of infection with Neospora caninum?

A

Increased potential for horizontal and vertical transmission and recrudescence

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38
Q

How does presence of farm dogs and absence of wild canids increase risk of infection with Neospora caninum?

A
  • Farm dogs increase risk as are definitive host
  • Wild canids decrease risk of infection as there is negative interaction between the presence of farm dogs which pose infection risk, and wild canids
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39
Q

How does the absence of cats suggest increased infection risk with Neospora caninum?

A
  • Absence of cats related to presence of dogs which increase risk
  • Cats would decrease the rat population which are intermediate hosts
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40
Q

How do farm-raised replacement heifers increase the risk of infection with Neospora caninum?

A

Increase risk as existing prevalence in a herd may persist

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41
Q

How does proximity to a town or village increase the risk of infection with Neospora caninum?

A

Associated with increased dog density

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42
Q

What are the 2 pathways of transplacental transmission of Neospora caninum?

A

Exogenous and endogenous

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43
Q

Explain exogenous transplacental transmission of Neospora caninum in cattle

A
  • First time exposure

- Cow infected while pregnant and infection straight to calf

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44
Q

Explain endogenous transplacental transmission of Neospora caninum in cattle

A
  • Cow infected when not pregnant
  • Becomes chronically infected and latent stage reactivated once pregnant
  • Crosses placenta and infects calf
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45
Q

What factors increase the risk of infection with Neospora caninum associated with reproduction?

A
  • Previous abortions
  • High annual rate of cows returning to oestrus post-pregnancy
  • Retained afterbirths
  • USing calving pens to hospitalise sick animals
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46
Q

What factors decrease the risk of infection with Neospora caninum associated with reproduction?

A
  • Use of beef-bull semen to inseminate dairy cattle
  • Cross-breed pregnancies
  • Attendance at cattle shows
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47
Q

What are the methods for controlling Neospora in cattle herds?

A
  • Selective culling
  • Farm biosecurity
  • Reproductive management
  • Chemotherapy
  • Vaccination
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48
Q

Why is there no general strategy for the control of neosporosis?

A
  • Regional differences in epidemiology of bovine neosporosis

- Important to study regional epidemiology before starting control programme

49
Q

Outline farm biosecruity measures used in the control of neosporosis in cattle

A
  • Quarantine and testing of replacement and purchased cattle
  • Prevention of transmission from dogs and other potential definitive hosts (test to ensure free from disease)
  • Prevent waterborne transmission
  • Rodent cotnrol
  • Prevent putative factors for disease that may lead to recrudescence in congenitally infected cattle e.g. reduce stress (may lead to transformation from brady to tachyzoite)
50
Q

Outline reproductive management measures in the control of neosporosis

A
  • Embryo transfer

- Artificial insemination of sero-positive dams with semen from beef bulls

51
Q

Outline testing and culling in the control of neosporosis in cattle

A
  • Expensive
  • But minimises losses through infection or abortion
  • Reduces level of infection in herd minimising losses
52
Q

Outline chemotherapy in the control of neosporosis in cattle

A
  • Hypothetical

- Expensive

53
Q

Outline vaccination in the control of neosporosis in cattle

A
  • Can be effective but N. caninum is intracellular
  • Immune response to N. caninum in dam may be incompatible with survival of the foetus
  • There are diverse strain differences and 2 clinical forms of the disease
54
Q

What drugs can be used to treat toxoplasmosis in sheep?

A
  • Rumensin (monensin)

- Decox (decoquinate)

55
Q

Outline the control of toxoplasmosis in sheep

A
  • Rumensin or decox to lessen effects of Toxoplasma
  • Live vaccine Toxovac in use
  • Isolate infected individuals and aborted foetuses
  • Prevent dogs from eating foetal membranes and unprocessed meat
56
Q

What are some limitations of using faecal egg counts for diagnosis of parasitic infection?

A
  • Not all parasites can be found in faeces as eggs
  • Intermittent shedding of eggs
  • Single sex infections may mean no eggs are shed
57
Q

Outline the agar larval development test

A
  • Culture eggs until reach infective larval stage in different drug concentrations
  • Development suggests resistant to the drug
  • Theoretically can be used for benzimidazoles, levamisole, ivermectin
  • Higher sensitivive cf faecal egg count reduction test
  • Expensive and time consuming
  • Interpretation is complex
58
Q

What tests can be used to assess parasitic drug resistance?

A
  • Faecal egg count reduction test
  • Agar larval development test
  • Molecular assay analysis
59
Q

Describe molecular assay analysis to assess parasitic drug resistance

A
  • PCR assays (also Strain fingerprinting assays)
  • Expensive, time consuming, require expertise
  • Cannot be done in house
  • Allows comparison of identified parasite with database of known resistances in those parasites
60
Q

Outline the process of genotyping worms

A
  • Collect specimens of worms from affected animals
  • Genotype worms from each attack in a reference lab
  • Look for similarities/differences between worm populations
61
Q

Compare the genotypes of worms found in a recurrent infection and a new infection

A
  • Recurrent: same genotype

- New: different genotypes

62
Q

What is the significance of finding a recurrent parasitic infection?

A
  • If treatment used previously then this suggests resistance
  • Overstocking
  • Bringing in of new stock
  • Poor environmental management
  • Inappropriate choice of anthelmintic
63
Q

What is MAR?

A

Multiple anthelmintic resistance

64
Q

Outline the action points regarding MAR

A
  • Prompt isolation and treatment of symptomatic animals
  • No treatment of asymptomatic animals that may act as a reservoir (undesirable and ineffective)
  • Prevention by development of vaccine and immunisation
  • Research into development of a “super-anthelmintic” against GI nematodes
  • Better techniques and effective surveillance
65
Q

What animals does the EU Pet Travel Scheme apply to?

A
  • Cats
  • Dogs
  • Ferrets
66
Q

What is the maximum number of all types of pet animals each person may bring into the EU from most non-EU listed countries?

A
  • 5
  • More than 5 if for competition/exhibition/sporting events/training for sporting events (require written evidence/registration, all animals over 6mo)
67
Q

What are the requirements for pets travelling directly between UK and RoI?

A

Pet must have EU passport

68
Q

What are the 5 main steps necessary for animals entering the UK from EU and listed non-EU countries (in chronological order)

A
  • Microchipped
  • Vaccination against rabies (after MC, min 12 weeks old)
  • Rabies antibody test (non-EU only) (at least 30 days after date of vaccination, no less than 3 months before date of movement)
  • Treatment against Echinococcus multilocularis (not more than 120 hrs and not less than 24 hours before the time of scheduled entry)
  • Accompanied by a passport and declaration
69
Q

List some exotic disease of concern in veterinary species

A
  • Rabies
  • Dirofiliaria immitis (heartworm)
  • Leishmaniosis
  • Babesiosis
  • Ehrlichiosis
70
Q

What is the likely effect of climate change on the prevalence of exotic diseases in the UK?

A
  • Likely to increased
  • Improved environment for the vectors with increasing temperatures
  • increased range of movement of vectors
71
Q

Outline the role of the vet in minimising the incidence of exotic diseases

A
  • Vigilant for emerging diseases, consider as differential diagnoses
  • Awareness of disease manifestations
  • Confidence in confirmation of diagnosis
  • report confirmed cases
  • Advise clients regarding travel risks
72
Q

What are the vectors of transmission for babesiosi?

A
  • Ticks (Dermacentor reticulatus)

- Contaminated instruments or needles

73
Q

What is the vector for the transmission of leishmaniasis?

A

Phlebotomine sandflies

74
Q

Describe the clinical signs of leishmaniasis

A
  • Can be subclinical
  • Lethargy, inappetance, weight loss, lymphadenomegally, splenomegaly, polyuria, polydipsia, V+D, non-pruritic exfoliative dermatitis +/- alopecia,erosive ulcerative dermatitis
  • Nodular/papular dermatitis, pustular dermatiis, onnychogryphosis, keratoconjuncitivitis, blepharitis, anterior uveitis
  • lameness, epistaxis, mucosal lesions, myositis, cutaneous and systemic vasculitis
75
Q

What is the vector of transmission for ehrlichiosis?

A

Rhipicephalus sanguineus tick

76
Q

What is the vector of transmission for dirofilariasis?

A

Mosquitoes

77
Q

What are the clinical signs of acute phase ehrlichiosis?

A
  • Weight loss
  • Oculonasal discharge
  • Lymphadenopathy
  • Thrombocytopaenia
  • Leukopaenia
  • Low anaemia and hypergammaglobulinaemia
78
Q

What are the clinical signs of chronic phase ehrlichiosis?

A
  • Varying degrees of depression
  • Fever, weight loss
  • Combination of bleeding tendencies
  • Pallor due to anaemia
  • Abdominal tenderness
  • Anterior uveitis
  • Retinal haemorrhages
  • Neurological signs
  • bone marrow destruction
79
Q

What is the main species of Leishmania that infect dogs?

A

Leishmania infantum

80
Q

Outline the zoonotic potential of Leishmania infantum

A
  • Can infect humans, particularly immunocompromised adults and children
  • However dog to human transmission not reported
  • Must be transmitted by Phlebotomine sandfly
81
Q

What measures can be taken to prevent leishmaniasis in dogs?

A
  • Vaccination
  • Fly repellents
  • Keep dogs indoors when flies are most active (7pm to 7am)
82
Q

What measures can be taken to prevent heartworm?

A
  • Mosquito repellent
  • Monthly preventative treatment using Ivermectins
  • In collies use milbemycin
83
Q

What are the key clinical signs of heartworm?

A

Coughing, exercise intolerance, cachexia, anorexia, heart murmur, ascites

84
Q

Outline the ideal features of an antiparasitic

A
  • Selective
  • Effective at removing adults and immature forms of parasites from the body
  • Wide therapeutic index
  • Easy to administer
  • Inexpensive/economically justifiable
  • No residue problems
  • Specific advantages in terms of pharmacokinetics and/or metabolism
85
Q

What are endoparasiticides?

A

Antiparasitics that kill parasites living inside the animal

- includes anthelmintics and antiprotozoals

86
Q

What are ectoparasiticides?

A

Antiparasitics that kill parasites living on the outside of the animal
- Including fleas, ticks, mites, lice

87
Q

What are endectocide?

A

Parasiticides that act on ecto and endoparasites

88
Q

What are the group 1 parasitices?

A
  • Benzimidazoles

- White drenches

89
Q

What are the group 2 parasiticides?

A
  • Levamisole

- Yellow drench

90
Q

What are the group 3 parasiticides?

A
  • Macrocyclic lactones (avermectins and milbemycins)

- Clear drenches

91
Q

What are the group 4 parasiticides?

A
  • Monepental

- Orange drench

92
Q

Why are parasiticides better than parasitistatics?

A
  • Parasitisides remove pathogen entirely

- With parasitistatics, infection can recur

93
Q

What are the broad mechanisms of action of antiparasitics?

A
  • Paralysis of parasites via mimicking the action of neurotransmitters
  • Alteration of metabolic processes
  • Alteration of parasite reproduction
94
Q

Outline the paralysis of parasites via mimics of neurotransmitters

A
  • Ach, GABA, glutamate, octpamine, serotonin can all be targets
  • Can be present in more than one parasite category (nematode, cestode, trematode, arthropods)
  • Affect homeostasis of depolarisation of NMJ
  • Broad spectrum
95
Q

Give examples of ways in which metabolic processes that can be altered by antiparasitics

A
  • Inhibition of microtubule synthesis
  • Uncoupling of oxidative phosphorylation
  • Inhibition of folic acid synthesis/metabolism
  • Inhibition of thiamine utilisation
  • Inhibition of chitin formation (arthropods)
  • Stimulation of insect juvenile hormones
  • Ion gradients/membrane potential
  • Inhibition of protein synthesis
  • Inhibition of DNA synthesis
96
Q

Give examples of ways in which antiparasitics can alter parasite reproduction

A
  • Inhibition of egg production in nematodes
  • Inhibition of multiplication of protozoa
  • Note: this is not an anthelmintic action, but a consequence of an anthelmintic action
97
Q

Explain the mode of action of benzimidazole

A
  • Bind to beta-tubulin in molecules
  • Leads to inhibition of polymerisation and disorders of intracellular homeostasis
  • Tubulin structure altered, all body functions affected
98
Q

Explain the mode of action of levamisole

A
  • Affect nicotinic Ach receptors
  • Mimic Ach action, change permeability of post-synaptic membrane
  • Lead to depolarisation and spastic paralysis of worms
99
Q

What “mode of action” group of anthelmintics does levamisole belong to and give examples of others in this group

A
  • Cholinergic anthelmintics
  • Pyrantel
  • Morantel
100
Q

What parasites are macrocyclic lactones effective against?

A
  • Are endectocides
  • Arthropods and nematodes
  • Cestodes, tramtodes and adult heart worms are insensitive
101
Q

What are the signs of macrocyclic lactone toxicity in dogs?

A
  • Mydriasis
  • tremor
  • Ataxia
  • Emesis
  • Salivation
  • Coma
102
Q

Explain the mode of action of macrocyclic lactones

A
  • Acts on membrane channels causing permanent depolarisation of membranes
  • Leads to paralysis
  • Affects pharynx, somatic muscle and uterus of nematode
103
Q

What is the mechanism through which vertebrates (other than collies) are protected against the effects of macrocyclic lactones?

A

P-glycoprotein transmembrane transport pump (prevents entry of MLs in brain and CNS)

104
Q

Explain the mechanism of action of monepantel

A
  • Binds to, and irreversibly opens, MPTL-1 receptor in nervous system
  • Prevents coordination of movement
105
Q

Explain the mechanism of action of emodepside

A
  • Acts on specific class of transmembrane G-protein coupled receotirs (depsiphilins)
  • Latrophilin receptor class
  • Ultimately leads to flaccid paralysis of pharynx
106
Q

Explain the mechanism of action of praziquantel

A
  • Binds to beta-subunit of voltage gated calcium channels
  • Leads to spastic and tetanic muscle contractions
  • May also have vacuolation/degradation of tegument
107
Q

Against what parasites if praziquantel active?

A
  • Cestodes (in particular used for Echinococcus)

- Some helminths are not susceptible e.g. Fasciola spp.

108
Q

Explain the mechanism of resistance against benzimidazoles

A
  • Genetic changes in drug target
  • Several single-nucleotide polymorphisms (SNPs) in drug’s target molecule beta-tubulin isotype 1
  • Can lead to amino acid substitution in drug target protein and so changes affinity of drug for target
109
Q

What is the most common SNP in benzimidazole resistance?

A

Phenylalanine to tyrosine substitution at postion 200 in the gene (Phe200piyr)

110
Q

What are the potential mechanisms of antiparasitic resistance?

A
  • Point mutations (target alterations)

- Increased efflux

111
Q

Explain the mechanism of resistance against macrocyclic lactones

A
  • Increased drug efflux into GI lumen

- Reduces concentration in the cell leading to reduced effect

112
Q

Outline the potential reasons for therapeutic failure

A
  • Interactions with other drugs or health condition diminishing drug efficacy
  • Failure to diagnose and treat present of miced infections
  • Patient immunodeficiency
  • Quick re-infection due to cotnaminated environment
  • Failure to deliver or receive correct dosage (compliance, out of date drugs etc)
113
Q

Outline the advice you would give to an owner in the case of Felicola infestation

A
  • Treat with: fipronil + S-methoprene OR imidacloprid OR selamectin OR surolaner
  • Wash cat
  • Clean environment (basic hygiene should be sufficient)
  • Treat any in contact animals
  • Is not zoonotic
114
Q

Outline the advice you would give to an owner in the case of finding a Rhipicephalus sanguineus tick

A
  • Remove tick correctly and look for others
  • Close monitoring, in particular for signs of Ehrlicha
  • Rhipicephalus can carry babesia, ehrlicha, rickettsia, Anaplasma
  • Recommend tick teatment if go abroad again e.g. pyrethroids, deltamethrin collars
  • Treat with fipronil to kill ticks, and deltamethrin in order to repel
115
Q

Outline the advice you would give to a farmer in the case of bovicola infestation

A
  • Chewing louse
  • Pour on synthetic pyrethroid e.g. deltamethrin
  • 3-macrocyclic lactons clear 98% of chewing lice
  • Treat in contact animals
  • But treatment is generally rare
116
Q

Outline the advice you would give to an owner in the case of Sarcoptic mange

A
  • Treat using: advocate (imidaclorpid and moxidectin) OR amitraz OR selamectin OR sarolaner
  • Advise owner of zoonotic risk
  • Environmental cleaning required as can live in environment for several weeks
  • Use household flea spray as this will be effective on mites
117
Q

What drugs are effective againse mites?

A
  • Pyrethroids
  • Avermectins
  • Amitraz
  • Deltamethrin
118
Q

What drugs can be used to prevent tick infestation?

A
  • Isoxazolines e.g. flurolaner
  • Pyrethroids e.g. deltamethrin collar
  • Phenylpyrnazoles e.g. fipronil

PVS (23 decks)

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