parasitology 2

Question 1

helminth life cycle-route of infection

Answer 1

ingestion of infective stage
ingestion of paratenic/intermediate host
maternal (transplacental, transmammary)
skin penetration
arthropod-borne

Question 2

generalities about helminths

Answer 2

macroparaites-do not multiple inside of definitive host: number of parasites the host is infected with is what they have
complex multicellular organs
often highly host specific in definitive host but not always
direct life cycle
fecal oral transmission
environmental oral

Question 3

nematoda

Answer 3

thread
non-segmented, cylindrical, generally tapered at both ends
most successful of all worms
free living soil nematodes
major plant and animal parasite
range in size from micrometer to meter

Question 4

general characterisitic

Answer 4

cuticle: body surface
cuticle is flexible not metabolically active
like arthropod exoskeleton
may form spines, ridges, secondary sexual structures
fluid filled body cavity
intestine and reproductive system are suspended in cavity
body wall has a muscle layer provides movement
lost of structures for sensing the environment

Question 5

neurotransmitter in nematoda

Answer 5

acetylcholine
gamma-aminobutyric acid (GABA)

Question 6

nematoda digestive system

Answer 6

food depends on species and location in host
oral opening: buccal capsule (Cavity)
esophagus (pharynx) intestine

Question 7

reproductive system

Answer 7

general separate sexes
females usually bigger than males
males have secondary structures: spinules
females produce eggs or larvae

Question 8

nematoda development

Answer 8

cuticle restricts growth
all nematodes go through 4 molts
stages between molts are L1, L2, L3, L4, and adult

Question 9

L3 rule

Answer 9

nematode stage infective for definitive host is almost always L3

Question 10

strongylida porphology

Answer 10

bursate nematodes: bursa used in reproduction holds female
macroscopic to 10cm
slender
most of the important species in the GI tract
depending on species, larva or adult may be most pathogenic stage

Question 11

strongylida pathogenic mechanisms

Answer 11

varies with species
damage from tissue-phase of development
blood or tissue feeding
inflammation/immune response-affected GI function
anorexia-multifactorial

Question 12

strongylid eggs

Answer 12

direct life cycle
oval, thin shelled contain a morula (blastomeres) cant be differentiated
diagnosis: fecal flotation

Question 13

strongylida life cycle (Except metastrongyloidea)

Answer 13

egg voided in feces
L1 hatch and develop to L3 ( 2 molts)
L3 retains cuticle of L2 as protective sheath (ensheathed L3)
L3 ingested by host (infective stage)
larvae travel to predilection site and develop to adults

Question 14

eggs and larvae dont like

Answer 14

temperature extremes
freezing and thawing cycles
desiccation

Question 15

tropisms

Answer 15

hydro +
thermo +
geo -
photo +

Question 16

hypobiosis

Answer 16

arrested or inhibited development until conditions are ideal

Question 17

L3 hypobiosis

Answer 17

trichostrongylus, ancylostoma, cyanostominae

Question 18

L4 hypobiosis

Answer 18

osteragia, teladorsagia, haemonchus

Question 19

stimulus for arrested develelopment

Answer 19

environmental
host immnunity

Question 20

superfamily trichostrongyloidea

Answer 20

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 period: usually 3-4 weeks depending on species
hypobiosis common-affect epidemiology and control
adult life span-month
all grazing ruminants have trychostrongyle parasites

Question 21

trichostrongyloidea

Answer 21

in Gi tract
parasitic gastoenteritis (PGE)
diarrhea
weight-loss

Question 22

in cattle

Answer 22

ostertagia ostertagi (brown stomach worm)

Question 23

small ruminants

Answer 23

haemonchus contortus (barber pole worm)

Question 24

ostertagia ostertagia

Answer 24

after ingestion at L3, larvae enter gastic gland for at least several days, then emerge into lumen and become adults
most pathogenic change-L4 emerging of the abomasal mucosa (L4 is hypobiotic), may remain as hypobiotic larvae for several months
adults not very pathogenic

Question 25

impact of larvae on gastic glands

Answer 25

cell differentiation
hyperplasia
formation of nodules
changes to stomach function
reduction of acidity of abomasal fluid-pH increased from 2-7
failure to activate pepsinogen to pepsin
loss of bacteriostatic effect
increase permeability of abomasal epithelium
leakage of pepsinogen into circulation
loss of plasma protein

Question 26

adults and immune cattle, little to no effect

Answer 26

light to moderate infection
subclinical, most common in US
no impact or decreased weight gain/growth from anorexia and gastric disturbance

Question 27

heavy infection in young or immunocompromised animals

Answer 27

diarrhea
weight loss
hypoproteinemia: bottle jaw
death in weeks

Question 28

heamonchus contortus

Answer 28

abomasal parasite of small ruminants
female up to 3cm
most important helminth in small ruminants
more pathogenic than most other trichostrongyles because blood feeding
pathogenic stage: adults

Question 29

in heavier infection: haemonchus contortus

Answer 29

anemia-not diarrhea
anorexia
bottle jaw
weight loss
death

Question 30

type 1 diease

Answer 30

caused by larvae that have developed without interruption
represent accumulation of adult worms during grazing season
usually occurs in late-summer or autumn in pasture young animals
any sheep or goat with anemia in the grazing season has heamonchosis until proven otherwise