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Fall 22: Parasites > 02 + 03. nematodes > Flashcards

02 + 03. nematodes Flashcards

1
Q

—- are round worms

A

nematodes

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2
Q

nematodes have a coating of —

A

cuticle
acellular, protective coating

nematodes= round worm

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3
Q

alae are —

A

cuticular evaginations

wings

on nematodes (round worms)

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4
Q

bursate nematodes have —

A

male tail has a copulatory bursa to clasp onto the female during mating

round worms- nematodes

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5
Q

non-bursate nematodes have —

A

pre-cloacal sucker used to hold female during sex

nematodes= roundworm

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6
Q

nematodes go through a — from L1-L2

A

moult
get bigger

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7
Q
A

exsheathment

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8
Q

direct lifecycle of nematode

A

parasite to host, no intermediate

can either ingest egg(hatched or unhatched) or free-living larvae

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9
Q

indirect nematode life cycle

A

Intermediate host required for development of pre-
parasitic larvae

Definitive host ingests intermediate host(paratenic)

Intermediate host serves as a vector

passive transmission

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10
Q

Definitive host

A

Sexual reproduction in the definitive host

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11
Q

intermediate host

A

Provide physiological requirements for development of larvae

Provide advantages for transmission of parasitic nematodes

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12
Q

Paratenic

A

No development of larval stages

transport

Predator/prey relationship with definitive host

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13
Q

— in ascaris suum life cycle acts as a paratenic host

A

earthworm

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14
Q

another name for arrested development

A

hypobiosis

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15
Q

— is the inhibition of larval development

A

arrested development
hypobiosis

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16
Q

why does parasite go into hypobiosis

A

survival mechanism against adverse environment (winter)

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17
Q

True or false

drugs work better when a parasite is in hypobiosis

A

false

parasite is not metabolically active, most drugs will not work

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18
Q

Larvae arrest at the L4 in the fall; emerge the following spring in —

A

spring rise
periparturient rise

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19
Q

strongylida are — parasites

A

GI

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20
Q

what stage of strongylida are found in the environment?

A

L1-L3

nematodes (roundworm)

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21
Q

strongylida are — copulators

A

bursa

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22
Q

— are hookworms

A

Superfamily Ancylostomatoidea

bent head, oral cutting plate or teeth

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23
Q

— have cutting plates or teeth

A

Ancylostomatoidea: hookworms

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24
Q

strongylida have a large — and are — feeders

A

buccal

plug or blood feeders

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25
Q

Primary pathogenic mechanism in hookworm disease

A

ingestion of blood by adult worms in the small intestine

Ancylostomatoidea: hookworms
order: strongylida
nematodes- round worms

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26
Q

Bunostomum phlebotomum
L3 will go through —

A

exsheathment inside the host

can invade by mouth or skin

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27
Q

PPP

A

prepatent period

time animal is infected without clinical signs or diagnosis

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28
Q

seasonality of parasite activity

A

hypobiosis

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29
Q

hookworms cause edema by —

A

hookworms eat blood

loss of proteins cause fluids to leak out of vessels and cause edema

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30
Q
A

strongyle egg

order strongylida
ancylostomatoidea (hookworms)
Strongyloidea( excluding syngamus trachea)
Trichostrongyles

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31
Q

hookworms have what kind of eggs

A

oval shape
thin shell
contain embryo (many cells) or larva

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32
Q

Bunostomum phlebotomum effect —-

A

hookworms of cattle

enter through skin or mouth

cause edema

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33
Q

hookworm of dogs and cats

A

Ancylostoma caninum

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34
Q

Ancylostoma caninum effect what animal

A

hookworm of dogs

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35
Q

what type of hookworm has a transmammary route?

A

ancylostoma caninum

effect dogs and cats

can cause larval migrans in humans

strongylida- hookworm- oval shape, thin shell

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36
Q

life cycle of ancylostoma caninum

A

skin penetration by L3

systemic circulation in blood- can lead to reservoir of arrested L3 in skeletal muscle and gut wall-> can transfer by milk (lactogenic) or placenta to pup

or

tracheal migration (coughed up and swallowed- move to intestine and grow into adults that bred and lay eggs

hookworm, strongylida, bursate nematodes

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37
Q

ancylostoma caninum can transfer to pups by

A

milk and placental transmission

will penetrate skin, into blood and arrest as L3 in skeletal muscle or gut wall, activated when host becomes pregnant, directly into puppies GI tract (does not need somatic migration)

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38
Q

— causes cutaneous larva migrans in human

A

ancylostoma caninum
hookworm, strongylida, bursate nematodes

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39
Q

transmammary route of hookworms will cause — in puppies

A

patency 7 days earlier

does not need to migrate, goes directly to the GI tract

ancylostoma caninum
hookworm, strongylida, bursate nematodes

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40
Q

ancylostoma caninum will come out of hypobiosis when —

A

hormones- host pregnant- leads to increased parasite and transmammary and transplacental route of transmission to puppies

ancylostoma caninum
hookworm, strongylida, bursate nematodes

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41
Q

oral route or transmammary route will have a faster prepatent period

A

transmammary- 12-14 days

ancylostoma caninum
hookworm, strongylida, bursate nematodes

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42
Q

what is the only hookworm with prenatal infection that infect dogs and cats

A

ancylostoma caninum
hookworm, strongylida, bursate nematodes

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43
Q

which hookworm can eat blood as a L4

A

ancylostoma caninum

dog and cat hookworm, strongylida, bursate nematodes

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44
Q

significant blood loss prior to patency is caused by —

A

L4 able to eat blood before it is an adult

ancylostoma caninum
dog and cat hookworm, strongylida, bursate nematodes

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45
Q

what type of dog and cat hookworm has the most per day blood loss

A

ancylostoma caninum
L4 can also eat blood

dog and cat hookworm, strongylida, bursate nematodes

46
Q

why are older animals less susceptible to hookworms

A

bigger animals can lose more blood- anemia does not effect them as much

acquired immunity

ancylostoma caninum

hookworms= strongylida, bursate nematodes

47
Q
A

strongyle egg

hookworm, strongylida, bursate nematodes

48
Q
A

Repopulation of gut by arrested larvae in tissues (relatively resistant to anthelmintic treatment).

hypobiosis

49
Q

A litter of puppies showing failure to thrive, pale membranes and low hematocrit. Some puppies are critically ill. Many, but not all, of these puppies show distinctive objects in the proceeds of a fecal floatation.

What kind of parasite causes this disease?

A

ancylostoma caninum

hookworms= strongylida, bursate nematodes

50
Q

A litter of puppies showing failure to thrive, pale membranes and low hematocrit.

How may this parasite gain entry into its host?
What is the most likely way it got into these puppies?

A

skin or oral

transmammary or transplacental

ancylostoma caninum

hookworms= strongylida, bursate nematodes

51
Q

A litter of puppies showing failure to thrive, pale membranes and low hematocrit.

Why don’t all the puppies show those objects in the feces?
How does this parasite cause the anemia you see?

A

puppies get different amounts of parasite from mother, patency might not have occurred yet

adult hookworm will drink blood inside the intestine

ancylostoma caninum
hookworms= strongylida, bursate nematodes

52
Q

A litter of puppies showing failure to thrive, pale membranes and low hematocrit.

Can this parasite cause any other lesions?
Are there drugs available to control this infection?
Can this parasite infect people?

A

yes. skin penetration by L3 can lead to arrested L3 in skeletal muscle or gut cell wall

yes

yes can cause cutaneous larva migrans

ancylostoma caninum
hookworms= strongylida, bursate nematodes

53
Q

strongyloidea are — worms with —- and a — life cycle

A

large
copulatory bursa, buccal capsules
direct - can infect through skin

54
Q

what strongyloidea does not have a strongyle-type egg

A

syngamus (bioperculated)

55
Q

strongyloidea like to live —

A

in the large intestine

except for stephanurus (kidney- pigs)
syngamus (trachea- chicken)

56
Q

— is a tracheal worm of fowl and game birds

A

syngamus

strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

57
Q

life cycle of syngamus trachae

A

egg in environment

bird ingest L3, paratenic host or egg with L3 inside

L3 penetrates intestine and migrates to the lungs

adults will grow in the trachea, bi-operculate eggs will be coughed up and swallowed and passed in feces

gapeworm - strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

58
Q
A

syngamus trachea
gapeworm

strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

59
Q

how do syngamus trachea eggs get into environment

A

adult gapeworms live in the trachea, will produce eggs that are coughed up and swallowed and passed in feces

bi-operculate egg will mature into L3 and be ingested as hatched L3, egg with L3, or L3 in paratenic host

L3 into the intestine then migrate to lungs where it matures into adult

strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

PPP- 18 days

60
Q

— is the only parasite in the trachea of domestic birds

A

Syngamus trachea
gapeworm

strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

61
Q

gapeworms have what kind of eggs

A

bi-operculate eggs

strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

62
Q

symptoms of syngamus trachae

A

gapeworms

Hemorrhagic tracheitis with mucus production (immune response)
“Gaping ”
Shaking, gasping, asphyxia, suffocation
young birds coughing, severe pneumonia, death

strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

63
Q

diagnosis of Syngamus trachae

A

gapeworm in chickens

bioperculate eggs in feces
post mortem ID

strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

64
Q
A

bi-operculate egg

syngamus trachae- gapeworm

strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

65
Q

— are football shaped with two openings

A

syngamus trachea- gapeworms

bioperculate egg

66
Q

— is found in the per-renal fat and walls of the kidney

A

Stephanurus dentatus
kidney worm in swine

strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

67
Q

life cycle of Stephanurus dentatus

A

ingest L3, skin penetration of L3s, or ingestion of paratenic host with L3

immediate moult into L4 and move through blood to liver

L4-L5 moult in liver

migrate through peritoneum to kidney

adults form kidney cysts

strongyle type eggs passed in urine

Stephanurus dentatus- kidney worm in pigs- strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

PPP: 6-19 months. survive 3 years

68
Q

how does stephanurus dentatus get into host

A

ingest L3, skin penetration of L3s, or ingestion of paratenic host with L3

kidney worm in swine

69
Q

how do eggs get out of host in Stephanurus dentatus

A

in urine
strongyle type eggs

adults move from liver to kidney and form cysts

kidney worm in pigs

70
Q

prepatent period for kidney worm in swine

A

6-19 months take a while to move from liver to kidney

Stephanurus dentatus

71
Q

pathogenesis of Stephanurus dentatus

A

cause cirrhosis and liver failure
L4-L5 final molt in the liver, then travel to the kidney and cause inflammation and thickening of the kidney and ureter

green pus around kidney

failure to gain weight

kidney worm in pigs

72
Q
A

Stephanurus dentatus
kidney worm in swine

strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle

73
Q

what kind of eggs does Stepganurus dentatus have

A

strongyle type

74
Q

clinical signs of stephanurus dentatus

A

failure to gain weight
liver cirrhosis on necropsy/meat inspection

75
Q

Oesophagostomum dentatum infect —

A

pigs and large intestine

family chabertidae, strongyloidea,, large, bursa, buccal capsule, direct life cycle

76
Q

Oesophagostomum infect —

A

cattle, sheep and goat

large intestine

77
Q

— have radial alae

A

Oesophagostomum

family chabertidae, strongyloidea,, large, bursa, buccal capsule, direct life cycle

78
Q

life cycle of Oesophagostomum spp.

A

adults live in colon

strongyle-type eggs in feces

development into L3 in 3-7 days (in good weather)

ingestion of L3

exsheathed in the small intestine

penetrate the mucosa of SI and LI, molt into L4

hypobiosis if needed

pass to colon and become adults

prepatent period 28-42 days

cause enteritis in ruminants and pigs

79
Q

where do adults of Oesophagostomum spp. live?

A

colon

80
Q

what kind of eggs do Oesophagostomum spp. have?

A

strongyle-type eggs

81
Q

— are exsheathed in the small intestine

A

L3

Oesophagostomum spp.- nodular worms

82
Q

pathogenesis of Oesophagostomum spp.

A

L3 in nodules with greenish pus in mucosa of small and large intestine

severe enteritis, anemia, protein loss, weight loss, diarrhea,

chronic: ulcerative colitis and inappetence and emaciation

83
Q

— are called nodular worms

A

Oesophagostomum spp.

84
Q
A

Oesophagostomum spp.

short pre-patent period- 28-42 days

85
Q

diagnosis of Oesophagostomum spp.

A

diarrhea occurs before patency- no eggs in stool yet

clinical signs- not eating, losing weight, diarrhea, decreased milk production

necropsy show nodules in cecum and colon

86
Q

two family of strongylidae

A

subfamily strongylinae (large strongyles)

subfamily cyathostominae (small strongyles)

87
Q

— strongylus effect horses and donkeys and cecum and colon

A

large strongyles

Strongylus vulgaris Strongylus equinus Strongylus edentatus

88
Q

— are the most destructive parasite in horses

A

strongylus

89
Q

lifecyle of strongylus vulgaris

A

adults in cecum and eggs passed in feces

grow into L3 in 2 weeks in environment

ingestion of L3

penetration into intestinal mucosa

L4 migrate to cranial mesenteric artery

molt to L5(young adult in 2-3 months

return to intestine via arterial lumina

nodules form in mucosa and burst to release adults into the gut

90
Q
A

Strongylys vulgaris

effect horses

L4- molt into L5 in cranial mesenteric artery then return to intestine

91
Q

what is special about the lifecycle of Stronylus vulgaris

A

L4 migrate to endothelium in cranial mesenteric artery

molt to L5 (young adult in 2-3 months

return to intestine via arterial lumina

92
Q

lifecycle of Strongylus equinus

A

ingestion of L3
exsheath in mucosa
molt to L4 (nodules
migrate to liver for 6-7 weeks
migrate to pancreas
molt to L5 (16-17 weeks post infection)
return to large intestine- adults

PPP=8-9 months

93
Q

where does L5 molt occur in strongylus equinus

A

pancreas (16-17 weeks post infection)

94
Q

what organs are infected by strongylus equinus

A

intestine
liver
pancreas
large intestine

95
Q

lifecycle of strongylus edentatus

A

ingestion of L3

exsheath in small intestine
migrate to liver by portal vein

molt to L4 in 2 weeks PI

migrate to flanks

molt to L5 in peritoneum

return to large intestine

nodule formation

rupture of nodules (adults)

PPP= 10-12 months

96
Q

where does the L4 molt for strongylus edentatus

A

liver

migrate from small intestine in portal vein, L4 in liver, migrate to flanks and molt into L5, then back to large intestine for adult formation

97
Q

where does the L5 molt for strongylus edentatus

A

peritoneum

L4 in liver, migrate to flanks and molt into L5, then back to large intestine for adult formation

98
Q

which strongylus has

L4 in liver, migrate to flanks and molt into L5, then back to large intestine for adult formation

A

strongylus edentatus

99
Q

which strongylus has migration from intestine, to liver, to pancreas to large intestine

A

Strongylus equinus

100
Q

which strongylus has migration from intestine to cranial mesenteric artery to intestine

A

Strongylus vulgaris

101
Q

— cause inflammation in cranial mesenteric arterial walls

A

larvae

Strongylus vulgaris

102
Q

symptoms of strongylus vulgaris

A

inflammation of arterial walls

rare aneurysms and thinning of walls
fever, decreased appetite and colic
intestinal ulcers, bleeding and scarring

103
Q

what type of eggs do strongylus vulgaris have?

A

strongyle-type eggs

104
Q

— are small and cause disease due to shear number of worms

A

small strongyles
Subfamily cyathostomes

105
Q

lifecycle of cyathostomes

A

small strongyles

egg-L3 in environment (can arrest if needed)

ingest L3
burrow into mucosa of large intestine
into adults and egg production

PPP 6-12 weeks
NO MIGRATION

106
Q

big difference between large and small strongyles

A

large- migrate to other organs

small- intestine only- NO migration

107
Q

pathogenesis of cyathostomosis

A

hemorrhagic enteritis (shear number)
rapid weight loss
colic
L4 in feces
peripheral edema
sudden onset diarrhea from larvae emerging into lumen of intestine
seasonal occurrence

small strongyles

108
Q

what causes symptoms in small strongyles

A

emergence of larvea into the large intestine from nodules

can arrest and all emerge at once with favorable conditions

109
Q

Chickens are gasping for breath; piglets are failing to thrive and hogs have blasting watery diarrhea. Horses also have acute diarrhea and colitis, and some of them are critically ill with colic.

What kind of parasites cause these diseases?
How does each of these parasites gain entry into its host?

A

gapeworms - Syngamus trachae - chickens- ingest L3, ingest egg with L3, ingest paratenic host with L3

Stephanurus dentatus- kidney worm in pigs- ingest L3, L3 through skin, eat paratenic host with L3

Strongyles- ingest L3

110
Q

Chickens are gasping for breath; piglets are failing to thrive and hogs have blasting watery diarrhea. Horses also have acute diarrhea and colitis, and some of them are critically ill with colic.

Why don’t all the failing piglets show those ovoid eggs in the feces?

How do the various parasites cause gasping in chickens, failure to thrive in pigs and colic in horses

A

patency takes 6-19 months

gapeworms - Syngamus trachae - chickens- ingest L3, ingest egg with L3, ingest paratenic host with L3, from intestine to lungs, grow in trachea produce bi-operculate eggs

Stephanurus dentatus- kidney worm in pigs- ingest L3, L3 through skin, eat paratenic host with L3,
molt to L4, move to liver, L5 in liver, move to kidney, adult cysts in kidney, strongyle-type eggs passed in urine

small Strongyles- ingest L3, grow in intestine, produce strongyle-like eggs

large strongyles, ingest L3, travel to different systems and then back to intestine, produce strongyle-like eggs

111
Q

Why do many of the horses have acute onset of their disease in the spring

A

worms will go through arrested development until more favorable conditions

112
Q

— have a ringed alae

A

oesophagostomum spp.

cause enteritis in ruminants and pigs

Fall 22: Parasites (32 decks)

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