parasitology: helminths (trichostrongyles) Flashcards
helminth routes of infection
Multiple routes of infection
* Ingestion of infective stage
* Ingestion of paratenic/intermediate host
* Maternal (transplacental, transmammary)
* Skin penetration
* Arthropod-borne
general helminth info
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)
oviparous
produce eggs
ovoviviparous
produce larvae
nematodes
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
nematode cuticle
Possess cuticle: body surface
flexible, but not metabolically active
Sort of like arthropod exoskeleton
Cuticle may form spines, ridges, secondary sexual structures
nematode general body structure
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)
nematode digestive system
Food depends on species and location in host
Oral opening: buccal capsule (cavity)
Esophagus (pharynx)
Intestine
nematode reproduction system
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)
nematode development
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
strongylida in general
nematodes
<5 cm
Slender
Most live in GI tract
Males have copulatory bursa (bursa used in reproduction, holds female)
strongylida families
strongylida order
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
pathogenic mechanisms of strongylida
Damage from tissue - phase of development
Blood or tissue feeding
Inflammation/immune response - affected GI function
Anorexia - multifactorial
strongylida eggs
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
diagnosis of strongylida
fecal flotation
strongylida life cycle
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
- L3 ingested by host: infective stage
- Larvae travel to predilection site and develop to adults.
Strongylida in the host
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”
“arrested” or “inhibited” development, or “hypobiosis
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
immunity against strongylida
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
premunition
Active infection required to keep immunity fully stimulated
Periparturient egg-rise
immunological compromise near partuition
parasite produces more eggs
Trichostrongyle family
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
Trichostrongyle life cycle
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
Ostertagia ostertagi (Brown stomach worm)
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
What stage of Ostertagia ostertagi goes into hypobiosis?
L4
impact of Ostertagia ostertagi on gastric glands
Cell differentiation
Hyperplasia
Formation of nodules
Changes to stomach function
Ostertagia ostertagi clinical signs
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
Haemonchus contortus (Barber’s pole worm)
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
Haemonchus contortus - Clinical importance
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
Parasitic gastroenteritis in ruminants is produced by:
* Cooperia
* Haemonchus
* ostertagia
* all except haemonchus
all except haemonchus
What is the most pathologic stage of ostertagia?
* L2
* L3
* L4
* adult
L4
