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VETMED: Dealing With Threats > Parasitology: Nematodes > Flashcards

Parasitology: Nematodes Flashcards

1
Q

What are some common routes of infection for helminth parasites?

A
  • ingestion of infective parasite
  • ingestion of transport/ intermediate host
  • maternal (transmammary/transplacental)
  • skin penetration
  • blood feeding arthropod vectors
  • non-blood feeding arthropod vectors
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2
Q

T/F: Worm populations in animals are aggregated (overdispersed).

A

true, 70-30 rule

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3
Q

T/F: Infection equals disease

A

false

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4
Q

Which is worm phylum is the most succesful?

A

Nematoda

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5
Q

T/F: There are many free-living nematodes.

A

True

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6
Q

Is it possible to see soil nematodes in fecal samples?

A

yes. We need to be able to distinguish these from intestinal parasites

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7
Q

What is the nematode body made of? What kind of adaptations are present that allow the nematode to remain in the host?

A

cuticle, which is flexible, but not metabolically active.

- the cuticle may be modified to form several structures (spines, ridges, secondary sexual structures, etc.)

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8
Q

Describe the internal morphology of nematodes.

A

“it’s like a tube with two tubes running through it.”

  • the body cavity is filled with hemolymph.
  • the body wall has a layer of longitudinal muscle
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9
Q

What kind of skeleton do nematodes have? How does it work?

A

a hydrostatic skeleton. Flexing the muscles of the body changes the pressure of the hemolymph within the body, allowing the nematodes to move “like snakes”

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10
Q

T/F: Nematodes have several sensory structures that allow them to sense their environment.

A

true

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11
Q

What kinds of neurotransmitters are present in nematodes? which is more common?

A
  • Acetylcholine (most common)

- GABA

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12
Q

T/F: Nematode diet depends on the worm and the location

A

true

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13
Q

Describe the digestive system of a nematode.

A

(From anterior to posterior):

- oral opening -> Buccal capsule -> esophagus (aka pharynx) -> intestine -> anus (females) or cloaca (males)

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14
Q

What is one way to differentiate worm species by their digestive system?

A

look at their esophagus.

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15
Q

Which sex of worm is bigger?

A

females

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16
Q

Which sex of worm has secondary sexual structures? What is their function?

A

males

primarily, these structures are used to stabilize the female during mating

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17
Q

Where may the vulva be on a female worm?

A

anterior, posterior, or in the middle?

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18
Q

Does a female worm strictly lay eggs?

A

no, some eggs may hatch before she lays them

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19
Q

How many molts will a nematode undergo before it reaches the adult form?

A

4

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20
Q

What is the L3 rule?

A

The L3 stage of nematode development is almost ALWAYS the infective stage for a definitive host

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21
Q

Describe the general life cycle of a nematode.

A

Egg -> L1 -> L2 -> L3 -> L4 -> Adult

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22
Q

What are the six orders of Nematodes covered in this course?

A
  • Strongylida
  • Asacardida
  • Spirurida
  • Enoplida
  • Oxyurida
  • Rhabditida
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23
Q

Which order of worm can be characterized as large, stout-bodied, and robust?

A

Order Ascaridida

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24
Q

What are Ascarids generally referred to as?

A

roundworms

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25
Q

Where do Ascarids generally live?

A

in the small intestine

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26
Q

What do ascarids feed on?

A

NOT THE HOST

- they feed on the lumen contents

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27
Q

T/F: Ascarids attach to the host.

A

false; ascarids do not attach, and must swim constantly to stay within the small intestine

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28
Q

How long do adult ascarids generally live?

A

a few months in a host

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29
Q

How is an ascarid infection diagnosed?

A

find eggs in feces

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30
Q

T/F: The ascarid egg is easily susceptible to environmental conditions.

A

false, its very resistant and hardy

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31
Q

How long does it take an ascarid egg to develop to the infective stage?

A

2-4 weeks

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32
Q

What are the two genera of Ascarids we are focusing this course?

A

Parascaris spp.

Toxocara spp.

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33
Q

What is the host of Parascaris spp.?

A

horses

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34
Q

What is the host of Toxocara spp.

A

cats and dogs

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35
Q

How long can Parascaris spp. get?

A

males: up to 30 cm
females: up to 50 cm

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36
Q

Parascaris equorum life cycle

A
  1. Eggs passed in manure. In a few weeks, there’s an infective egg.
  2. Horse comes along and ingests the infective egg, which hatches in the gut.
  3. Larva penetrates gut wall, gets into hepatic portal system, ends up in the liver, and then carried to the heart, and then lungs.
  4. Gets coughed up, and swallowed, then larvae end up in small intestine, where they develop into adults
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37
Q

What is hepatotracheal migration

A

the journey a nematode larvae undertakes when it travels from the GI tract through the liver to the lungs

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38
Q

What is the prepatent period of Ascarids? Why is this important?

A
  • roughly 3 months

- because you won’t see eggs for nearly 3 months, it makes it difficult to diagnose an infection.

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39
Q

Clinical importance of Parascaris.

A
  • common in young horses

- low worm burdens may be subclinical

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40
Q

Clinical signs of Parascaris infection.

A
  • unthriftiness, poor condition
  • pot belly
  • a very heavy infection can lead to perforation or impaction
  • the larvae in the lungs may increase host susceptibility to pathogens (many have permanent effects in severe cases)
  • nasal discharge due to larval lung infection
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41
Q

T/F: as horses mature and their immunity develops, patent infections of Parascaris rarely occur.

A

True

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42
Q

How long do Parascarid eggs require to reach infectivity?

A

2 weeks

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43
Q

Treatmenta and control of Parascarids.

A
  • nematodicidal antihelmintics
  • feces removal and composting (best method)
  • wash udders before foaling
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44
Q

T/F: all nematocidal equine anthelmentics are effective against both adults and larvae

A

false

all are effective against adults, only some against larvae

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45
Q

Why are small animal ascarids (toxocaras spp) called arrowhead worms?

A

they have anterior cervical alae (makes them look like arrowhead)

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46
Q

What is the species name of the ascarid that infects dogs and other canids?

A

Toxocara cani

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47
Q

What is the species name of the ascarid that infects cats and other felids?

A

Toxcara cati

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48
Q

Simplest Toxocara canis infection pattern

A
  1. Dog ingests infective eggs.
  2. Hepatotracheal migration
  3. Adult worms in small intestine.
  4. PPP 5 weeks
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49
Q

1st variation of simple Toxocara canis infection pattern

A
    1. Dog ingests infective eggs.
  2. Hepatotracheal migration
  3. Adult worms in small intestine OR larvae become distributed in blood from lung to tissues, become encysted. (AKA somatic migration)
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50
Q

What is a somatic reservoir of larvae?

A

a variation of T. canis infection in which the larvae become encysted in the host instead of being coughed up and swallowed.

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51
Q

2nd variation of T. canis

A

larvae in somatic reservoir activated in late pregnancy (~45 days), and enter pups transplacentally
- pups born with larvae in liver, which then complete the migration to SI and mature.
PPP: 3 weeks

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52
Q

3rd variation of T. canis infection pattern

A
  • another animal consumes infective larvae, which then lay dormant in tissues. Dog eats intemediate host. becomes infected with parasite (which no longer has to undergo any migration)
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53
Q

What are some possible paratenic hosts of T. canis?

A
  • rabbits
  • birds
  • rodents
  • elephants (wut)
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54
Q

What aspect of the dog helps the Toxocara larvae determine which migration system its going to undergo?

A

the immune status of the dog

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55
Q

When is somatic migration more likely?

A

more likely in immune dogs and older dogs

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56
Q

Clinical signs of Toxocara canis in puppies

A

low burdens: no or few signs

moderate to heavy burdens:

  • diarrhea/constipation
  • colic and pot belly
  • vomiting
  • unthrifty, poor hair coat
  • intestinal obstruction
  • pneumonia
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57
Q

Why is it recommended to treat puppies every 2-3 weeks for up to 12 weeks?

A

the most commonly used drugs affect nematode adults, not the larvae. You need to get the larvae too.

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58
Q

Is there a commercial test available to test for a T. canis somatic reservoir?

A

nope

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59
Q

How can you control Toxocara canis infection rates?

A
  • remove feces (eggs in environment take 2-4 weeks to become infective, and can survive for long periods of time in ideal conditions)
  • wash surfaces w/ 1% bleach solution (doesn’t kill them, but it strips away the sticky outer protein coat on the egg, making them easier to wash away
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60
Q

Why is prevalence lower in the Western US than the Eastern US?

A

drier environment

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61
Q

Compare and contrast T. cati and T. canis.

A

T. cati similar in nearly all regards, except:

  • transmammary transmission is more important than transplacental
  • longer prepatent period
  • higher prevalence because the cats are consuming more paratenic hosts
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62
Q

Can humans be paratenic hosts for Toxocara?

A

yes, but we’re still shitty hosts

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63
Q

Clinical disease syndromes of humans affected by Toxocara migration.

A
  • visceral larva migrans

- ocular larva migrans

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64
Q

Which order of nematode is known as the “bursate nematode?”

A

strongylida

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65
Q

What is a bursa? which sex of strongylids have it and why?

A
  • a bursa is a “skirt” that male nematodes have. It allows them to stabilize females during mating
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66
Q

Morphology of Strongylids

A
  • a Buccal capsule at anterior end which the worm uses to suck in a plug of mucosa to attach to the host.
  • size varies from barely macroscopic to about 15 cm
  • pathogenic stage is dependent on the species
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67
Q

T/F: you can distinguish between strongylid eggs only.

A

false, most members of strongylida produce similar egs

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68
Q

Strongylida egg morphology

A
  • ovular
  • thin shell
  • contain morula
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69
Q

How many layers of cuticle does an L3 Strongylida have?

A

2, it kept the previous cuticle

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70
Q

T/F: infective stages of the order Strongylida develop on the egg

A

false, they develop freely in the environment.

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71
Q

Where do Strongylida larvae develop?

A

in feces

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72
Q

What is the purpose the Strongylida L3 stage retaining the L2’s cuticle?

A

its a protective sheath

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73
Q

is it easier to kill a strongylid larvae in the host or the environment

A

environment

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74
Q

Can strongylid eggs and larvae withstand extreme temperatures or freezing/thawing cycles?

A

nope

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75
Q

Differentiate between the infective stages of Ascarids and Strongylids

A
  • L3 of ascarids are in eggs

- L3 of Strongylids are free-living

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76
Q

In general, the ____ the temperature, the faster the development of strongylids

A

higher

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77
Q

T/F: many GI strongylids have a life cycle period in which they enter the gut wall and undergo further development before becoming an adult in the lumen

A

true.

they will remain in gut wall for a minimum period of time before emerging. Occurs between L3 and L4 stages

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78
Q

What is hypobiosis?

A

a period of dormancy, in which strongylid development undergoes arrest for a variable period of time in definitive host tissue.

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79
Q

What is one observation in regards to why larvae undergo hypobiosis

A

seasonal changes. You generally see number of adults peak in summer time and larvae peak in spring/winter time

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80
Q

What affects competence of the host’s immune response?

A

age and stress

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81
Q

T/F: host immunity develops over time, and is often expressed fully before maturity.

A

false, it is not fully expressed until maturity

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82
Q

What are the three superfamiles of Order Strongylida, and what are their preferred hosts?

A
  • Trichostrongyloidea: ruminants
  • Strongyloidea: horses
  • Ancylostomatoidea: small animals
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83
Q

General characteristics of Trichostrongyloidea

A
  • generally small, threadlike worms
  • ID based on male bursa and spicules
  • small buccal capsule
  • GI parasites + 1 lungworm genus
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84
Q

How do you diagnose Trichostrongyloidea infections?

A

fecals

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85
Q

Prepatent Period of Trichostrongylids

A

3-4 weeks

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86
Q

T/F: if your ruminant is eating ANY grass, it has trichostrongylids.

A

true, there’s really nothing you can do about it

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87
Q

How long can the L3 stage survive in environment?

A

weeks to months, depending on the weather

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88
Q

What do all of the genera of Trichostrongyloidea contribute to?

A

parasitic gastroenteritis

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89
Q

What are the two most important Trichostrongyloids in the US and what are their preferred species of host?

A
  • Ostertagia: cattle

- Haemonchus: small ruminants

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90
Q

Which part of the cattle stomach will you find Ostertagia?

A

the abomasum

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91
Q

What is the scientific name of the brown stomach worm of cattle?

A

Ostertagia ostertagi

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92
Q

Where does the Ostertagia larvae end up after ingestion? How long are they there?

A
  • they enter the gastric glands.

- are in the gastric glands for a minimum of several days

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93
Q
  • What is the minimum PPP of Ostertagia?

- What is the maximum PPP of Ostertagia?

A
  • 21 days

- 4-6 months

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94
Q

What is the biggest impact of Ostertagia as larvae emerge from the gastic glands?

A
  • cell dedifferentiation and hyperplasia; the changes lead to nodule formation.
  • this dedifferentiation causes the stomach pH to go up. This more basic stomach acid diminishes the strength of the acid barrier of the stomach, leading to digestive issues due to failure to cleave pepsinogen into pepsin.
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95
Q

What is the clinical importance of Ostertagia?

A
  • in Adults and young animals with light infection, there is little to no effect
  • in young animals with moderate infection (subclinical), we see anorexia, decreased production (including weight gain)
  • In heavy infections (clinical signs), we see:
  • anorexia
  • diarrhea
  • weight loss
  • unthriftiness
  • hypoproteinemia (bottle jaw)
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96
Q

What is the most important Trichostrongylid in small ruminants of N. America?

A

Haemonchus contortus

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97
Q

Haemonchus placei can be a problem for which species and in which US region?

A
  • bovine

- Southern US

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98
Q

Where would you find Haemonchus in the ruminant host?

A
  • abomasum
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99
Q

what does Haemonchus feed on?

A

abomasal blood

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100
Q

How does Haemonchus access the abomasal blood of its host?

A

it pierces the stomach surface and causes capillary bleeding

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101
Q

T/F: Female Haemonchus are very prolific

A

true

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102
Q

What is the preferred climate of Haemonchus?

A

warm weather with high humidity

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103
Q

T/F: Haemonchus population can build rapidly, thus making it an extremely successful parasite

A

true

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104
Q

What is the PPP of Haemonchus

A

roughly 2-3 weeks

105
Q

What is the clinical importance of Haemonchus in heavier infections?

A
  • anemia (not diarrhea)
  • failure to gain weight or weight loss
  • anorexia
  • bottle jaw
  • death
106
Q

What is the general rule for sheep/goats with anemia?

A

until proven otherwise, it has Haemonchus

107
Q

When will Haemonchus and Ostertagia undergo hypobiosis?

A

during the winter

108
Q

What is type 1 clinical syndrome for Trichostrongylids?

A
  • represents accumulation of worms during the grazing season
  • cattle-> usually low mortality, may see only subclinical effects
  • small ruminants-> may become more seriously affected as season progresses. Severe anemia can develop in some animals

its more a gradual onset compared to type 2

109
Q

What is Type 2 clinical syndrome Trichostrongylids?

A
  • a synchronous emergence of arrested larvae in infected host, usually due to seasonal effects
  • this can produce severe fatal disease due to severe inflammation or anemia
110
Q

What are some general characteristics of the superfamily Strongyloidea?

A
  • mostly parasites of the GI tract
  • generally have a large buccal capsule
  • are plug feeders
111
Q

Where would you find adults Strongyles?

A

in the cecum and colon

112
Q

What are the two types of equine strongyles?

A

small and large strongyles

113
Q

What is another name for small strongyles?

A

Cyathostomins

114
Q

Where do 3rd stage larvae go in hosts?

A

large intestine, where they enter the cryps of Lieberkuhn, and penetrate the mucosa

115
Q

T/F: if a horse grazes, it has Cyathostomins

A

true

116
Q

minimum PPP of Cyathostomins

A

2-3 months

117
Q

length of adult Cyathostomins

A

roughly 2 cm

118
Q

T/F: in the horse mucosa, you can see cyathostomins grossly

A

true, they appear are little red coils

119
Q

How long can Cyathostomins remain under hyopobiosis?

A

up to 2 years

120
Q

when do cyathostomins arrest/resume development?

A
  • seasonal effects (adults in summer, larvae in winter)

- as adults die, new larvae emerge to replace them

121
Q

What is the most pathogenic stage of Cyathostomins?

A

again, the larvae

122
Q

What are some key clinical signs and symptoms of chronic Cyathostomiasis?

A
  • accumulation of large worm numbers due to
    > inflammation and thickening of gut wall
    > possible protein losing enteropathy
  • clinical signs:
    > digestive disturbance (intermittent diarrhea +/- colic)
    >poor condition, unthriftiness
    > hypoproteinemia and anemia
123
Q

What are some key clinical signs and symptoms of acute Cyathostomiasis?
- when does it occur?

A
  • rapid onset
  • Fever
  • Diarrhea
    > dehydration
  • edema, hypoproteinemia

– simultaneous emergence of large numbers of arrested larvae
> drug treatment of horses with high worm burdens
> seasonal

124
Q

how do you diagnose chronic and acute Cyathostomiasis?

A

Chronic: large numbers of Strongyle eggs in feces

Acute: may not be eggs in manure, but there will be larvae (they’re red)

125
Q

T/F: adult horses can develop immunity to control cyathostomin populations.

A

true, just like other parasites

126
Q

What is the only large strongyle of importance for this class?

A

Strongylus vulgaris

127
Q

Where do S. Vulgaris adults reside?

A

large intestine

128
Q

what is the PPP of S. Vulgaris?

A

6 months

129
Q

Where does the infective S. Vulgaris larvae go after infection? When does S. Vulgaris return to large intestine after infection?

A
  • it molts, and the L4 migrates through the arteries to reach the junction of cranial mesenteric artery and aorta, stimulating thrombus development
130
Q

How long after infection does the Larvae return to the large intestine?

A

about 4 months

131
Q

Which stage of the S. vulgaris is the most concerning? Why

A

the larval stage, L4

When it is in the junction of the cranial mesenteric artery and the aorta, it leads to thrombus formation, which can impair or block blood flow,

132
Q

How does thrombus formation occur due to S. vulgaris?

What are the dangers of this thrombus formation?

A

The L4 larvae damage the blood vessels, causing a verminous arteritis.

  • The thrombus can reduce blood flood and interfere with nerve transmission.
  • it could also break off, and block distal bloodflow, leading to necrosis of portions of bowel in severe cases
133
Q

Is it possible to treat verminous arteritis

A

to a degree yes, the lesions regress after the worms leave and with treatment

134
Q

Strongylus vulgaris used to be the primary cause of what disease in horses?

A

colic

135
Q

What is the common name used for the Superfamily Ancylostomatoidea?

A

hookworms

136
Q

What do ancylostomatoids feed on?

A

blood, not tissue

137
Q

General morphology of acylostomatidae

A
  • typically 1-2 cm in length
  • large buccal capsule
  • teeth or cutting plates
138
Q

What are some common canine hookworms?

A
  • Ancylstoma caninum*** (most important in this region)
  • A. braziliense (seen in southeastern coastal US and south)
  • Uncinaria stenocephala (cold climate hookwarm (canada))
139
Q

Differentiate between canine strongylids and cattle/horse strongylids.

A
  • canine hooks like being on the soil, while horse and cow strongylids like grass
  • vector of penetration:
    > canine strongylids: skin penetration
    > cattle and horse strongylids: ingestion
140
Q

Where is development for Canine acylostomatidae best?

A

in moist, shaded, slightly sandy loam (think dog runs)

141
Q

What are the routes of transmission for Ancylostoma caninum?

A
  1. skin penetration
  2. transmammary
  3. ingestion of larvae
  4. (minor) transplacental
  5. (minor) transport hosts
142
Q

Once in the to tissues, where will hookworm larvae be carried to?

A

The lungs

143
Q

What is the primary form of vertical hookworm transmission

A

transmammary

144
Q

Once a hookworm larvae enters the dog, it can _____ or _____

A
  • become an adult in the small intestine

- undergo hypobiosis in the gut or tissues

145
Q

Where will adult hookworms develop?

A
  • without arrest from mom in the milk

- with or without a period of arrest following infection from other routes

146
Q

Is Ancylostoma more or less commonly found as an adult infection than Toxocara

A

more common

147
Q

T/F: Low hookworm numbers generally appear asymptomatic.

A

true

148
Q

What are some clinical signs of hookworm infection?

A
  • diarrhea-> melena
  • anemia, hypoproteinemia
  • unthriftiness
  • skin lesions
149
Q

What are some susceptible hosts that you would predominantly see these symptoms in?

A

puppies, immunocompromised digs, or if the exposure were heavy

150
Q

When does immunity develop against hookworms?

A

as always, after exposure

151
Q

What is melena?

A

oxidized blood in stool, it looks dark and tarry

152
Q

Diagnosis of ancylostoma caninum

A

fecal example (only common strongylid egg in small animal samples)

153
Q

T/F: hookworm PPP is in independent of infection route

A

false, it is entirely dependent on infection route

154
Q

What is the minimum PPP of a transmammary infection?

A

2 weeks

155
Q

Treatment and Control of Ancylostoma caninum

A
  • pick up the Poop!

- most canine anthelmintics are effective against adults, but there’s no good treatment for arrested larvae

156
Q

What is the scientific name of the feline hookworm?

A

Ancylostoma tubaeformae

157
Q

T/F: Ancylostoma tubaeformae has a higher prevalence than Ancylostoma caninum

A

false

158
Q

T/F: A. tubaeformae has a high perinatal transmission rate

A

false

159
Q

T/F: A. tubaeformae is not as pathogenic as A. caninum

A

true

160
Q

T/F: A dog who eats cat feces will develop an A. tubaeformae infection.

A

false, the larvae need time to develop

161
Q

Which species of canine hookworms is a”vigorous skin penetrator?”

A

A. braziliense

162
Q

What are cutaneous larva migrans?

A

serpiginous tracks produced by A. brasiliense larvae migrating in the skin of people

163
Q

T/F: A. braziliense infections are more likely to occur in those who are most frequently in lots of soil

A

true

164
Q

What is the difference in strongylid tolerance between large and small animals?

A

Small animals have a zero tolerance policy regarding parasites. If its peresent we try to get rid of it.

Large animals have threshold that they try to stay under because it is all but impossible to eliminate the parasites because of all the grazing on grass

165
Q

What is the goal of GI worm control in sustainable systems?

A
  • to keep the worms at a level that doesn’t have detrimental health effects
166
Q

What are the three tools to control parasites in grazing animals? What is the acronym?

A

RID

R- reduce parasite exposure on pasture (rotate field portions, etc.)

I- immunity level of host (keep them healthy, and keep young livestock off of recently used pasture)

D- drugs. Use anthelmintics where necessary to prevent infection

167
Q

Which animals are most vulnarable to infection?

A

the young, periparturient, stressed, and high-performance animals

168
Q

How can you reduce exposure to strongylid larvae?

A
  • don’t let them on pasture
  • reduce stocking density
  • pasture rotation and rest
  • alternate/mix grazing (change the grazing species, since the Strongylids are host-species specific)
  • remove manure (works best in horses and camellids)
  • respect host behavior (use their habits to your advantage)
169
Q

What is a “ring of repugnance?”

A

the perimeter that surrounds a fecal mass that animals will not eat near

170
Q

How do you get rid of a ring of repugnance?

A

harrow the ground after animals rotate of that part of pasture

171
Q

What is the benefit of goats being browsers?

A

They spend less time grazing because they’re chompin down on plants above the ground and away from parasites. This prevents them from ingesting infective larvae

172
Q

How does camelids defecating in community piles help reduce parasite transmission?

A

easier to clean up an isolated area of dung

173
Q

T/F: there is a nematode-eating manure fungus.

A

true

174
Q

Which animals should you cull or select for your herd?

A
  • cull highly susceptible animals

- select highly resistant animals

175
Q

How can you determine whether or not to deworm an animal?

A
  • for horses, you can perform an egg count. If it goes over the threshold, deworm.
  • use an anemia assessment tool. Depending on the level of anemia, it may be required/recommended.
176
Q

Which animals will worm problems appear first?

A
  • animals with “temporary” low immunity (young, lactating, or stressed animals)
  • animals with inherited high susceptibility
177
Q

Which order of nematodes has a common characteristic of needing an arthropod intermediate host

A

Order Spirurida

178
Q

What do we generally call members of the superfamily Filaroidea?

A

filarids, filaroids

179
Q

What kind of tissue do filarids parasitize?

A
  • connective tissue
  • blood vessels, lymphatics, etc.
  • adults feed on lymph or plasma
180
Q

Physical description of filarids

A

long slender worms, incredibly small

181
Q

T/F: Females produce microfilariae, a stage between the egg and L1 stages

A

true

182
Q

What is the definitive host of Dirofilaria immitis?

A

dogs and wild canids

- ferrets

183
Q

What are some abnormal hosts of Dirofilaria immitis?

A

cats, humans, and other mammals

184
Q

Where would you primarily find D. immitis in the host?

A

the pulmonary arteries primarily

185
Q

What is the common name of Dinofilaria immitis

A

heartworms

186
Q

What is the intermediate host of D. immitis

A

mosquitoes

187
Q

T/F: heartworms are considered endemic in the US and worldwide

A

true

188
Q

What is the prepatent period of D. immitis

A

6 months

189
Q

How long can adult D. immitis live?

A

nearly 5 years

190
Q

T/F: your dog can get heartworms from a blood transfusion from another dog.

A

false

The microfilariae produced by the adult female

191
Q

Where does the microfilariae mature?

A

in the mosquito

192
Q

How long can microfilariae circulate in peripheral blood?

A

1-2 years

193
Q

How early do microfilariae appear in blood?

A

as early as six months post infection

194
Q

How are infective D. immitis larvae transmitted to the host? Which stage?

A

by mosquito bites

L3!!!!!

195
Q

Where does the L3 stage of D. immitis mature? How long does this take?

A

in the subcutaneous tissue of the host at the bite wound. Takes 1-3 days to mature

196
Q

How long does it take an L4 to mature to an adolescent stage?

A

50-70 days

197
Q

How long does it take a sexually immature worm to migrate to the heart and lungs from date of infection?

A

as early as 70 days

198
Q

What is the biggest issue of disease in regards to heartworms?

A

The host reaction to the parasite

199
Q

Villous lesions are formed from _____

A

endothelial hyperplasia

200
Q

What is the BASIC pathgenesis of heartworm disease?

A
  • to start, there is the physical barrier of the heartworm obstructing blood flow.
  • a complex reaction occurs where the vessel wall comes into contact with the filarid. leads to villous lesions (villous endarteritis) forms due to endothelial hyperplasia. So now in addition to worm presence, the blood vessel wall is also messed up.
  • can lead to progressive fibrosis in the vessel, and also has the potential for producing a thromboemboli
201
Q

T/F: vessel damage is proportion to number of filarids present

A

true

202
Q

T/F: more dogs die of heartworm than with heartworm.

A

false, more dogs die with heartworm than of heartworm

203
Q

What happens as heartworm disease gets more severe?

A
  • the heart now has to work harder to get past the obstruction.
  • reduced cardiac output and compensatory right heart disease
  • right heart enlargement and failure
204
Q

Clinical signs of D. immitis

  • low to mild
  • mild to moderate
  • moderate to severe
A

low to mild: Asymptomatic

mild to moderate:

  • chronic cough
  • dyspnea
  • Decreased exercise tolerance

Moderate to high:

  • syncope (fainting)
  • hemoptysis (coughing blood)
  • congestive heart failure
  • ascites
205
Q

What are some uncommon clinical signs of D. immitis infection?

A
  • vena caval synodrome: occurs with very heavy infection. worms move back into heart, leading to severe passive congestion of the liver. can cause acute collapse
  • abnormal migration leads to unusual problems. ex: a heartworm on a testicle.
206
Q

Prevalence of D. immitis in US.

A

considered endemic in 48 states, but highest prevalence is in Mississippi and Eastern coast

207
Q

T/F: coyotes are great reservoirs for heartworm in southern CA

A

true

208
Q

How can you diagnose a D. immitis infection?

A
  • antigen tests (you test for the antigen of the parasite, not the parasite)
209
Q

Which sex of D. immitis generates the antigen primarily tested for in diagnosis?

A

the females

210
Q

What are some limitations of antigenic D. immitis testing?

A
  • the antigen chosen needs to not be present on other parasites, or it could cause a false positive
211
Q

What tests can check for microfilariae?

A
  • peripheral blood sample checks

- Knott’s test is best (its a concentration technique)

212
Q

How do you treat heartworm disease?

A
  • Prevention is much better than treatment

- may require surgery

213
Q

T/F: by getting rid of the symbiotic bateria Wolbachia, can interfere with heartworm reproduction

A

true

214
Q

Which drug is most commonly used to treat heartworm infections

A

doxycycline

215
Q

T/F: you can treat a cat with heartworms.

A

false, what kills the worm kills the cat

216
Q

Is heartworm disease likely to develop in cats?

A

no, most worms die soon after infection

217
Q

What are some clinical signs of HW infection in cats?

A

(most of these are in response to dying worms or abnormal migration)

  • respiratory signs
  • vomiting
  • exercise tolerance
  • sudden death
  • signs associated with migration to another part of the body
218
Q

T/F: ferrets are immune to HW disease

A

false, they can get typical heartworm disease

219
Q

What should you assume if you “see a long thin worm in necropsy that isn’t in the GI tract?”

A

its probably a filarial worm

220
Q

General physical morphology of other species of Spirurida.

A

Eggs: elliptical, smooth, thick shell wall containing a coiled larva

Adults are small to medium in size, but not threadlike
- these require an intermediate arthropod host

221
Q

Where do Habronema spp. live?

A

nodules of equine stomach

222
Q

What are the intermediate hosts of Habronema spp.?

A

stable and house flies

223
Q
  • Which spirurid causes “summer sore?”
  • what is “summer sore?”
  • Can larvae continue development?
  • what can summer sore be mistaken for?
A
  • habronema spp. when it gets deposited in mucocutaneous junction wounds.
  • A persistent cutaneous granuloma
  • larvae cannot continue development
  • can be mistaken for exuberant granulation tissue, neoplasia
224
Q

What worms are associated with the Order Enoplida?

A

Trichuris, capillarids,

225
Q

What are the characteristic factors of enoplida eggs?

A
  • egg has to polar plugs, slightly elliptical in appearance
226
Q

Which is the scientific name for whipworms in dogs

A

Trichuris vulpis

227
Q

Where are Trichuris worms typically located in the host?

A

in the large intestine

228
Q

physical morphology of Trichuris

A
  • a whip-shaped body, the narrower anterior end is entwined within a layer of epithelial cells.
229
Q
  • What kind of life cycle do Trichuris spp. have?
  • Where are eggs passed?
  • where do infective larvae develop? how long does it take?
A
  • direct life cycle
  • in feces
  • develop in the egg; takes at least 2 weeks
230
Q

T/F: Trichuris eggs are highly resistant to environmental condtions.

A

true

231
Q

What is the PPP of Trichuris vulpis?

A

3 months

232
Q

Clinical symptoms of clinical T. vulpis infection

A
  • smelly diarrhea
  • vomiting
  • anemia
233
Q

T/F: Trichuris infections can occur in dogs of all ages

A

true

234
Q

How wold you treat a T. vuplis infection?

A
  • remove feces to prevent further infection

- treat with meds, then treat again in three weeks

235
Q

What other species can you find Trichuris spp. in?

A
  • pigs
  • ruminants
  • cats (only in Fl. and other countries)
  • people (have their own species)
236
Q

T/F: capillarid eggs look similar to whipworm eggs

A

true

237
Q

Where would you find a Trichinella spp in the host?

what is the geographical distribution of Trichinella?

A

adult worms are in the small intestine of warm blooded animals

worldwide distribution

238
Q

Why should you never eat undercooked pork?

A

you don’t want a Trichinella infection caused by encysted Trichinella larvae

239
Q

How are pigs infected with Trichinella?

A

they eat garbage, rats, and each other

240
Q

Where do you most commonly see Trichinella cases?

A
  • in wildlife that consume pigs (pigs, bears, seals, etc.)
241
Q

What are some symptoms and the causes of Trichinosis?

A
  • enteritis caused by adult Trichinella
  • migrating larvae cause inflammation
  • myalgia, fever
  • Respiratory and cardiac failure in heavy infections
242
Q

What worm is associated with Order Oxyurida?

A

pinworms

243
Q

Where would you see pinworm adults in the host species?

A
  • large intestine
244
Q

What species will you primarily find pinworms in? what other species can be infected?

A

mostly seen in horses.

other species include:
- horses, rodents, ruminants, reptiles, people

245
Q

T/F: Pinworms are very pathogenic

A

false

246
Q

Describe a pinworm egg.

A

one polar plug, often flattened appearance on one side

247
Q

What is the scientific name of the equine pinworm

A

Oxyuris equi

248
Q

Geographical distribution of Oxyuris equi

A

worldwide

249
Q

How are hosts infeted with O. equi?

A
  • ingestion of eggs
250
Q

Where do fertilized females deposit their eggs?

A

The migrate from large intestine and rectum onto skin, then glue eggs to hairs in perianal area

251
Q

How do the O. equi eggs end up in the environment?

A
  • the glue and the worm movement are very irritating, so the horse rubs the itchy area, and the eggs fall off and into the environment
252
Q

How can you diagnose O. equi?

A

“scotch tape test;” apply a piece of scotch tape to rear, then examine it under a microscope to find eggs

253
Q

How do you treat O. equi infections?

A
  • most modern nematocides work; also wash blankets, as eggs might have gotten onto them
254
Q

T/F: Human pinworms are caused by animals

A

False; it is strictly human to human transmission

255
Q

What animal parasite genus is associated with the Order Rhabditida?

A

Strongyloides

256
Q

How are hosts infected with Strongyloides?

A
  • skin penetration, transmammary transmission
257
Q

Eggs are commonly seen in young ____, less often in ____ and ____, and are uncommon in_____.

A
  • ruminants
  • foals
  • pigs
  • dogs
258
Q

What is are Strongylid eggs generally mistaken for?

A

Strongylids

VETMED: Dealing With Threats (11 decks)

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