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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
Primary pathogenic mechanism in hookworm disease
ingestion of blood by adult worms in the small intestine Ancylostomatoidea: hookworms order: strongylida nematodes- round worms
26
Bunostomum phlebotomum L3 will go through ---
exsheathment inside the host can invade by mouth or skin
27
PPP
prepatent period time animal is infected without clinical signs or diagnosis
28
seasonality of parasite activity
hypobiosis
29
hookworms cause edema by ---
hookworms eat blood loss of proteins cause fluids to leak out of vessels and cause edema
30
strongyle egg order strongylida ancylostomatoidea (hookworms) Strongyloidea( excluding syngamus trachea) Trichostrongyles
31
hookworms have what kind of eggs
oval shape thin shell contain embryo (many cells) or larva
32
Bunostomum phlebotomum effect ----
hookworms of cattle enter through skin or mouth cause edema
33
hookworm of dogs and cats
Ancylostoma caninum
34
Ancylostoma caninum effect what animal
hookworm of dogs
35
what type of hookworm has a transmammary route?
ancylostoma caninum effect dogs and cats can cause larval migrans in humans strongylida- hookworm- oval shape, thin shell
36
life cycle of ancylostoma caninum
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
37
ancylostoma caninum can transfer to pups by
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)
38
--- causes cutaneous larva migrans in human
ancylostoma caninum hookworm, strongylida, bursate nematodes
39
transmammary route of hookworms will cause --- in puppies
patency 7 days earlier does not need to migrate, goes directly to the GI tract ancylostoma caninum hookworm, strongylida, bursate nematodes
40
ancylostoma caninum will come out of hypobiosis when ---
hormones- host pregnant- leads to increased parasite and transmammary and transplacental route of transmission to puppies ancylostoma caninum hookworm, strongylida, bursate nematodes
41
oral route or transmammary route will have a faster prepatent period
transmammary- 12-14 days ancylostoma caninum hookworm, strongylida, bursate nematodes
42
what is the only hookworm with prenatal infection that infect dogs and cats
ancylostoma caninum hookworm, strongylida, bursate nematodes
43
which hookworm can eat blood as a L4
ancylostoma caninum dog and cat hookworm, strongylida, bursate nematodes
44
significant blood loss prior to patency is caused by ---
L4 able to eat blood before it is an adult ancylostoma caninum dog and cat hookworm, strongylida, bursate nematodes
45
what type of dog and cat hookworm has the most per day blood loss
ancylostoma caninum L4 can also eat blood dog and cat hookworm, strongylida, bursate nematodes
46
why are older animals less susceptible to hookworms
bigger animals can lose more blood- anemia does not effect them as much acquired immunity ancylostoma caninum hookworms= strongylida, bursate nematodes
47
strongyle egg hookworm, strongylida, bursate nematodes
48
Repopulation of gut by arrested larvae in tissues (relatively resistant to anthelmintic treatment). hypobiosis
49
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?
ancylostoma caninum hookworms= strongylida, bursate nematodes
50
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?
skin or oral transmammary or transplacental ancylostoma caninum hookworms= strongylida, bursate nematodes
51
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?
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
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?
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
strongyloidea are --- worms with ---- and a --- life cycle
large copulatory bursa, buccal capsules direct - can infect through skin
54
what strongyloidea does not have a strongyle-type egg
syngamus (bioperculated)
55
strongyloidea like to live ---
in the large intestine except for stephanurus (kidney- pigs) syngamus (trachea- chicken)
56
--- is a tracheal worm of fowl and game birds
syngamus strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle
57
life cycle of syngamus trachae
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
syngamus trachea gapeworm strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle
59
how do syngamus trachea eggs get into environment
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
--- is the only parasite in the trachea of domestic birds
Syngamus trachea gapeworm strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle
61
gapeworms have what kind of eggs
bi-operculate eggs strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle
62
symptoms of syngamus trachae
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
diagnosis of Syngamus trachae
gapeworm in chickens bioperculate eggs in feces post mortem ID strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle
64
bi-operculate egg syngamus trachae- gapeworm strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle
65
--- are football shaped with two openings
syngamus trachea- gapeworms bioperculate egg
66
--- is found in the per-renal fat and walls of the kidney
Stephanurus dentatus kidney worm in swine strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle
67
life cycle of Stephanurus dentatus
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
how does stephanurus dentatus get into host
ingest L3, skin penetration of L3s, or ingestion of paratenic host with L3 kidney worm in swine
69
how do eggs get out of host in Stephanurus dentatus
in urine strongyle type eggs adults move from liver to kidney and form cysts kidney worm in pigs
70
prepatent period for kidney worm in swine
6-19 months take a while to move from liver to kidney Stephanurus dentatus
71
pathogenesis of Stephanurus dentatus
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
Stephanurus dentatus kidney worm in swine strongyloidea, family syngamidae, large, bursa, buccal capsule, direct life cycle
73
what kind of eggs does Stepganurus dentatus have
strongyle type
74
clinical signs of stephanurus dentatus
failure to gain weight liver cirrhosis on necropsy/meat inspection
75
Oesophagostomum dentatum infect ---
pigs and large intestine family chabertidae, strongyloidea,, large, bursa, buccal capsule, direct life cycle
76
Oesophagostomum infect ---
cattle, sheep and goat large intestine
77
--- have radial alae
Oesophagostomum family chabertidae, strongyloidea,, large, bursa, buccal capsule, direct life cycle
78
life cycle of Oesophagostomum spp.
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
where do adults of Oesophagostomum spp. live?
colon
80
what kind of eggs do Oesophagostomum spp. have?
strongyle-type eggs
81
--- are exsheathed in the small intestine
L3 Oesophagostomum spp.- nodular worms
82
pathogenesis of Oesophagostomum spp.
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
--- are called nodular worms
Oesophagostomum spp.
84
Oesophagostomum spp. short pre-patent period- 28-42 days
85
diagnosis of Oesophagostomum spp.
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
two family of strongylidae
subfamily strongylinae (large strongyles) subfamily cyathostominae (small strongyles)
87
--- strongylus effect horses and donkeys and cecum and colon
large strongyles Strongylus vulgaris Strongylus equinus Strongylus edentatus
88
--- are the most destructive parasite in horses
strongylus
89
lifecyle of strongylus vulgaris
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
Strongylys vulgaris effect horses L4- molt into L5 in cranial mesenteric artery then return to intestine
91
what is special about the lifecycle of Stronylus vulgaris
L4 migrate to endothelium in cranial mesenteric artery molt to L5 (young adult in 2-3 months return to intestine via arterial lumina
92
lifecycle of Strongylus equinus
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
where does L5 molt occur in strongylus equinus
pancreas (16-17 weeks post infection)
94
what organs are infected by strongylus equinus
intestine liver pancreas large intestine
95
lifecycle of strongylus edentatus
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
where does the L4 molt for strongylus edentatus
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
where does the L5 molt for strongylus edentatus
peritoneum L4 in liver, migrate to flanks and molt into L5, then back to large intestine for adult formation
98
which strongylus has L4 in liver, migrate to flanks and molt into L5, then back to large intestine for adult formation
strongylus edentatus
99
which strongylus has migration from intestine, to liver, to pancreas to large intestine
Strongylus equinus
100
which strongylus has migration from intestine to cranial mesenteric artery to intestine
Strongylus vulgaris
101
--- cause inflammation in cranial mesenteric arterial walls
larvae Strongylus vulgaris
102
symptoms of strongylus vulgaris
inflammation of arterial walls rare aneurysms and thinning of walls fever, decreased appetite and colic intestinal ulcers, bleeding and scarring
103
what type of eggs do strongylus vulgaris have?
strongyle-type eggs
104
--- are small and cause disease due to shear number of worms
small strongyles Subfamily cyathostomes
105
lifecycle of cyathostomes
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
big difference between large and small strongyles
large- migrate to other organs small- intestine only- NO migration
107
pathogenesis of cyathostomosis
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
what causes symptoms in small strongyles
emergence of larvea into the large intestine from nodules can arrest and all emerge at once with favorable conditions
109
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?
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
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
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
Why do many of the horses have acute onset of their disease in the spring
worms will go through arrested development until more favorable conditions
112
--- have a ringed alae
oesophagostomum spp. cause enteritis in ruminants and pigs

Fall 22: Parasites (32 decks)

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