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DWT Exam 2 > Parasitology 2/3: Nematodes 1&2 > Flashcards

Parasitology 2/3: Nematodes 1&2 Flashcards

1
Q

Helminths have a few routes or a lot routes?

A

Many routes
-Ingestion of infective stage
-ingestion of paratenic/intermediate host
-maternal
-skin penetration
-arthropod-borne

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2
Q

ALL helminths are what kind of parasites?
hint*-parasites

A

MACROparasite

do NOT multiply in host

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3
Q

Describe Helminths?
cellular?
host?
repro outcomes?
life cycle?
transmission?

A

Complex and multicellular

some are host specific definitive but not always

Repro products of adults are eggs (OVIPAROUS) or larvae (OVOVIVIPAROUS)

Commonly have DIRECT life cycle

environmental-oral ( better way to describe than fecal-oral because many animals don’t eat direct feces)

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4
Q

Helminths breaks into which 2 groups?

A

Nematoda

Platyhelminthes

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5
Q

Nematoda

Word meaning?
Location?
Organisms?
Size?
Shape??

A

Thread

non-segmented, cylindrical, generally tapered at both ends

most successful of all the worms

many free living soil nematodes

major plant and animal parasite species

Range in size from micrometer to meters

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6
Q

Skin/outer surface of Nematodas?

A

Cuticle
-flexible, but NOT metabolically active
-many shapes
— spines, ridges, secondary sexual structures

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7
Q

Nematodes inside body descriptions?

A

Fluid filled body cavity

intestine and repro system are suspended in cavity

body wall has a muscle layer provides movement

lots of structures for sensing the environmnet

neurotransmitters:
-Ach**
-GABA

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8
Q

Nematoda digestive system

A

Food depends on species and location in host

oral opening: buccal capsule (cavity)

Esophagus (pharynx)

Intestine

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9
Q

Nematoda repro system

females and males

A

generally separate sexes

females usually bigger than males

Males have 2nd structures: spicules (* for repro)

females produce eggs or larvae

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10
Q

Development of nematodes occurs by?

A

Cuticle restricts growth

all nematodes go through 4 molts

stages in between molts referred as to L1, L2, L3, L4, and adults

L3 rule: stage is infective for definitive host UNTIL L3

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11
Q

What stage is infective when talking about Nematodes?

A

L3

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12
Q

Strongylida superfamily has how many ?

A

4

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13
Q

What is a difference between a male and female strongylidas?

A

Males have a Bursa (spicules) and smaller

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14
Q

what is the pathogenic mechanism in Strongylida?

A

damage from tissue- phase of development

blood or tissue feeding

inflamm/immune response-affected GI function

anorexia- multifactorial

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15
Q

What kind of life cycle do MOST strongylida have?

A

Direct

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16
Q

Describe strongylida eggs?

A

smooth/thin shell

have morula

can NOT be differentiated

diagnosis: fecal flotation

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17
Q

Describe the general life cycle for MOST of strongylida?

A
  • eggs voided in feces

-L1 hatch and develop L 3 (2 molts)

-L3 retains cuticle of L2 as protective sheath (ensheathed L3): climb grass

-L3 ingested by host: INFECTIVE STAGE

-Larvae travel to predilection site and develop to adults

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18
Q

How do strongylida survive when living outside of host?

A

They use reserves from L1 and L2 for energy

L2 sheath to travel through the environment

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19
Q

How are parasites able to move around after being excreted in feces?

A
  • after being excreted from animals the manure then it must escape manure

-the parasite want to go towards water, warmer surface, and go towards sunlight relative amount of all these tropisms

It uses the sheath from L2 to protect itself & go about in the environment

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20
Q

Hypobiosis means what?

A

arrested or inhibited development

ONLY occurs INSIDE the host

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21
Q

What are the RELATIVE tropisms?

A

Hydro +

Thermo +

Geo -

Photo +

22
Q

Characteristics of L3 ?

A

Sheathed by L2

Energy reserves for L1 and L2

The tropisms

23
Q

Hypobiosis can occur in different larval stage; what are some examples?

A

L3-
Trichostrongylus
Anceylostoma
Cyathostominae

L4-
Ostertagia
Teladorsagia
Haemonchus

24
Q

What is the most common stimuli for arrested development?

A

Environmental

25
Q

What is the other (not most common) stimuli for arrested development?

A

Host immunity

26
Q

Is the immunity development for Strongylida aggressively fast or gradual?

A

Gradual

27
Q

Immunological compromise can shift balance in favor of a parasite and allow numbers to increase. Examples are:

A

Parturition (“ Periparturient egg-rise”)

Malnutrition

Concurrent

28
Q

Why is Parturition and important immunological compromise?

A

Periparturient egg rise

Makes more eggs and plays a big part in parasitic and disease control

29
Q

What does large numbers of parasite mean?

A

Animals have clinical signs

30
Q

Trichostrongyloidea is present in what species?

A

RUMINANTS

31
Q

What life stage are trichostrongylidea infective?

A

L3

they develop and survive in weeks to months depending on weather

32
Q

Is Hypobiosis common or rare in Trichostrongyloidea?

A

Common hypobiosis

33
Q

which ruminants have Trichostrongyle parasites?

A

ALL grazing ruminants

34
Q

Which Trichostrongyloidea are we talking about and what species do they effect?

A

Ostertagia/Teladorsagia: Cattle

Haemonchus contortus: Sheep/Goat

*OCCURS IN ABOMASUM

35
Q

What do the all the Trichostrongyloidea together cause thats important (except Haemonchus)?

A

Parasitic Gastroenteritis (PGE)
-diarrhea
-weight loss

36
Q

What is the best indication you are seeing a Haemonchus parasite?

A

ANEMIA

37
Q

What is the common name of OStertagia?

A

Brown stomach worm

38
Q

What is the common name of the Haemonchus c?

A

Barbers pole worm

39
Q

Ostertagia most pathogenic changes are?

A

L4 emerging of the abomasa mucosa – in GASTRIC GLAND to lumen

NODULES

40
Q

Are Ostertagia adults very pathogenic?

A

False

41
Q

When you have hypobiosis is the infection worse or better?

A

it will be WORSE

because instead of having maybe 3 parasites emerging; you can have 100 emerging all together at the same time (they come out at at ideal ENVIRONMENT)

42
Q

Tell importance of L3 and L4 when talking about Ostertagia?

A

L3: is the infective stage

L4: is when the larvae are emerging

43
Q

Ostertagia impact of larvae on gastric glands cause what?

A

Cell diff

Hyperplasia

formation of NODULES

44
Q

What other impact does Ostertagia larvae have?

A

Theres a failure to activate pepsinogen due to higher pH and then that causes failure to activate pepsin

This low pH causes pepsinogen to build up and spill into blood (leakage)

This then causes loss of plasma proteins

45
Q

What is the clinical importance of Ostertagia?

A

Pathological stage is L4

young and immune comp animals cause

diarrhea
weight loss
hypoproteinemia: bottle jaw
Death in weeks

46
Q

Haemonchus affects which ruminants?

A

Small ruminants

47
Q

Are Haemonchus contortus infectious as larvae or adults?

A

ADULTS

48
Q

Why is Haemonchus more pathogenic than most other trichostrongyles why?

A

blood feeding

49
Q

Why is Haemonchus the most important helminth in small ruminants?

A

They are a global problem

50
Q

What is the clinical importance of Haemonchus?

A

Heavy infections
–anemia, NOT diarrhea, anorexia, bottle jaw, weight loss, death

-fatal infect: can remove 1/5 of circulating blood volume per day
-nonfatal infect: 1/10 in a 2 month period

51
Q

Type 1 disease for Trichostrongyloidea is described as?

A

cause larvae daily and continuously

represent accum. of adult worms during grazing season

usually in late summer or autumn, in you animals in pasture

any sheep/goat with anemia in the grazing season has haemonchosis till proven otherwise

52
Q

Type 2 Trichostrongyloidea disease is described as?

A

Happens AFTER larvae that has been arrest resume their life cycle

synch emergence of arrested larvae

It occurs in late-winter or spring, more common on Ostertagia

Can produce severe fatal disease due to severe abomasal disease or anemia

DWT Exam 2 (21 decks)

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