parasitology: helminths (trichostrongyles)

Question 1

helminth routes of infection

Answer 1

Multiple routes of infection
* Ingestion of infective stage
* Ingestion of paratenic/intermediate host
* Maternal (transplacental, transmammary)
* Skin penetration
* Arthropod-borne

Question 2

general helminth info

Answer 2

macroparasites: do not multiply in host
They are complex, multicellular organisms (like vertebrates!)
Often highly host specific in definitive host, but not always
Reproductive products of adults are eggs (oviparous) or larvae (ovoviviparous)
Many important helminths have direct life cycle
* Often referred to as “fecal-oral” transmission: this means that eggs passed in feces and infection is acquired directly by next host
* Really environmental-oral (most animals avoid eating feces)

Question 3

oviparous

Answer 3

produce eggs

Question 4

ovoviviparous

Answer 4

produce larvae

Question 5

nematodes

Answer 5

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 micrometers to meters
* Placentonema gigantisma: 8 meters

Nematos: thread

Question 6

nematode cuticle

Answer 6

Possess cuticle: body surface
flexible, but not metabolically active
Sort of like arthropod exoskeleton
Cuticle may form spines, ridges, secondary sexual structures

Question 7

nematode general body structure

Answer 7

Fluid filled body cavity
Intestine and reproductive system are suspended in cavity
Body wall has a muscle layer provides movement
Lots of structures for sensing environment
Neurotransmitters
* Acetylcholine (most common)
* Gamma-aminobutyric acid (GABA)

Question 8

nematode digestive system

Answer 8

Food depends on species and location in host
Oral opening: buccal capsule (cavity)
Esophagus (pharynx)
Intestine

Question 9

nematode reproduction system

Answer 9

Generally separate sexes (sexual dimorphism)
Females usually bigger than males
Males have secondary structures: spicules (cuticula rods used in mating)
Females produce eggs or larvae (often diagnostic stages)

Question 10

nematode development

Answer 10

Cuticle restricts growth
All nematodes go through 4 molts
Stages in between molts referred as to L1, L2, L3, L4, and adults
L3 rule: the nematode stage infective for definitive host is (almost always) the L3

Question 11

strongylida in general

Answer 11

nematodes
<5 cm
Slender
Most live in GI tract
Males have copulatory bursa (bursa used in reproduction, holds female)

Question 12

strongylida families

Answer 12

Question 13

strongylida order

Answer 13

Bursate nematodes: bursa used in reproduction, holds female
Size from barely macroscopic to about 10 cm
Generally slender
Most of the important species in GI tract
Depending on species, larva or adult may be most pathogenic stage

Question 14

pathogenic mechanisms of strongylida

Answer 14

Damage from tissue - phase of development
Blood or tissue feeding
Inflammation/immune response - affected GI function
Anorexia - multifactorial

Question 15

strongylida eggs

Answer 15

direct life cycle
Most members produce eggs that look the same: oval, thin shell, contain a morula (bunch of cells or blastomeres): can’t be differentiated
These eggs are called strongylid eggs

Question 16

diagnosis of strongylida

Answer 16

fecal flotation

Question 17

strongylida life cycle

Answer 17

except Metastrongyloidea
1. eggs voided in feces
2. L1 hatch and develop to L3 (2 molts)
3. L3 retains cuticle of L2 as protective sheath (ensheathed L3): climb grass, L3 cannot eat (have nutrient stores)
— L3 need to move into the environment: Want to stay around as long as possible to maximize chances of find a host, Cuticle of the second larval stage retained as sheath: protective, but cannot eat, When metabolic reserves exhausted: they die

4. L3 ingested by host: infective stage
5. Larvae travel to predilection site and develop to adults.

Question 18

Strongylida in the host

Answer 18

Many GI strongylids spend a period of larval development in gut wall before becoming adults in lumen
After infection, the larva enters gut wall for a species-specific amount of time, then returns to lumen and become adult
Under certain conditions, larva become dormant in host tissue site and then resumes development to adult later time
This phenomenon is known variously as “arrested” or “inhibited” development, or “hypobiosis”

Question 19

“arrested” or “inhibited” development, or “hypobiosis

Answer 19

Under certain conditions,larva become dormant in host tissue site and then resumes development to adult later time
can occur in different larval stages
parasites are undetectable and don’t cause disease

most common stimulus is environmental
adaptation mechanism for optimizing chances of survival for the next generation by synchronizing the parasite life cycle with external events – affects control

Question 20

immunity against strongylida

Answer 20

Immunity develops gradually
* Typically not fully developed until host maturity - prolonged exposure
* Young animals vulnerable

Active infection required to keep immunity fully stimulated (premunition)

Immunocomprimise can shift balance in favor of parasite:
* Parturition (“Periparturient egg-rise”)
* Malnutrition
* Concurrent disease

Usually clinical disease develops when large numbers are present, subclinical infections may have no impact or cause reduction in growth/weight gain

Question 21

premunition

Answer 21

Active infection required to keep immunity fully stimulated

Question 22

Periparturient egg-rise

Answer 22

immunological compromise near partuition
parasite produces more eggs

Question 23

Trichostrongyle family

Answer 23

in order strongylida
Most important ruminant helminths
Slender
Less than 10 cm

All together can cause a condition called parasitic gastroenteritis (PGE) - except Haemonchus
* Diarrhea
* Weight-loss

Other species, like Cooperia spp., play supportive roles in PGE
All grazing ruminants have a worm community in the GI tract

Question 24

Trichostrongyle life cycle

Answer 24

Life cycle: typical strongyle
L3 develop and survive in weeks to months depending on weather
Pasture parasites, generally don’t do well in housing or on dirt
Minimum prepatent periods: usually 3-4 weeks, depending on species
Hypobiosis common, affects epidemiology and control
Adult life span: months
All grazing ruminants have trychostrongyle parasites

Question 25

Ostertagia ostertagi (Brown stomach worm)

Answer 25

Trichostrongyle
most important helminth in cattle
After ingestion, larvae enter gastric glands for at least several days
Then, they emerge into lumen and become adults
Most pathogenic changes: L4 emerging of the abomasal mucosa (spring)
May remain as hypobiotic larvae as L4 for several months
Adults are not very pathogenic

Question 26

What stage of Ostertagia ostertagi goes into hypobiosis?

Answer 26

L4

Question 27

impact of Ostertagia ostertagi on gastric glands

Answer 27

Cell differentiation
Hyperplasia
Formation of nodules
Changes to stomach function

Question 28

Ostertagia ostertagi clinical signs

Answer 28

Adults and immune cattle, little or no effects
* Light to moderate infection
* Subclinical, most common in the US
* There is no impact or decreased weight gain/growth from anorexia and gastric disturbance

Heavy infections in young or immunocompromised animals, clinical disease:
* Diarrhea
* Weight loss
* Hypoproteinemia: bottle jaw
* Death in weeks

Question 29

Haemonchus contortus (Barber’s pole worm)

Answer 29

Trichostrongyle
most important helminth in small ruminants
Abomasal parasite of small ruminants
Female up to 3 cm
More pathogenic than most other trichostrongyles because blood feeding = ANEMIA
Pathogenic stage: Adults
NOT in gastric glands

Question 30

Haemonchus contortus - Clinical importance

Answer 30

Subclinical infections:
* amount of parasites is low =host can compensate blood loss and no measurable illness result
* reduced weight gain

heavier infections:
* host is unable to compensate blood loss - the disease is characterized by anemia
* Fatal infections: can remove 1/5 of circulating erythrocyte volume per day, Non-fatal infections: 1/10 in a 2-month period
* NOT diarrhea
* Anorexia (multifactorial)
* Bottle jaw - hypoproteinemia
* Weight loss
* Death
* If hematocrit decrease 15% or more, extreme weakness and shortness of breath can be present, poor prognosis

Question 31

Parasitic gastroenteritis in ruminants is produced by:
* Cooperia
* Haemonchus
* ostertagia
* all except haemonchus

Answer 31

all except haemonchus

Question 32

What is the most pathologic stage of ostertagia?
* L2
* L3
* L4
* adult

Answer 32

L4