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441 Cards in this Set

  • Front
  • Back
endoparasites
helminths (nematodes, cestodes, trematodes)
protozoa (mastigophora, apicomplexa)
nematodes
roundworms
nematodes (direct lifecycle - generalized)
L1 - L3 in environment (eg. soil)
L3 ingested
"L5" = immature adult
moults between ea. stage
nematodes (indirect lifecycle - generalized)
L1 ingested by IMH(eg. mosquito)
L3 transmitted to DH
nematode larval migration
hepato-tracheal:
from gut to liver (portal)
to heart via hepatic vein and PVC
to lung via pulmonary artery
to gut (coughed and swallowed)
arrested larval development (ALD)
if in immune adult, goes into tissues and arrests to avoid death by immune system; passed to offspring and comes out of arrest;
pre-patent period (PPP)
time from infection (eggs/larvae) to mature egg laying adults
Nematode superfamilies
Ascaridoidea (Toxocara, Ascaris)
Strongyloidea (Strongylus, Ancylostoma)
Trichostrongyles (Trichostrongylus, Ostertagia, Haemonchus)
Trichuroidea (Trichuris, Capilleria, Trichinella)
Filariodea (Dirofilaria, Onchocerca, Parfilaria)
Ascarids (species)
Toxocara (canis, cati)
Ascaris (suum, lumbricoides)
Ascarids (general characteristics)
large white worms
direct life cycle
L2/L3 is infective (oral)
small intestine (SI)
Trichostrongyle species (nematode)
Trichostrongylus
Ostertagia
Dictyocaulus
Haemonchus
Strongyloidea specia (nematode)
Strongylus
Ancylostoma
Syngamus
Trichuroidea species (nematode)
Trichuris
Capillaria
Trichinella
Filariodea species (nematode)
Dirofilaria
Onchocerca
Parafilaria
nematode head (morphological features)
large or small buccal capsule
leaf crowns present or absent
teeth present or absent
nematode tail (male - features vary between species)
spicules
bursa
rays
caudal papillae
caudal alae
precloacal sucker
nematode tail (female - features vary between species)
vulval (cloacal) flap
nematode eggs (morphology)
-Trichostrongyle - thin, oval shell
-Ascarid - thick, pitted shell
-Trichuris - barrel shaped, smooth shell; plug-like operculum (both poles)
-Oxyuris - ovoid, slightly flattend; mucoid plug (1 end)
parasitic gastroenteritis (PGE)
generic term for disease caused by parasitic nematodes in gastro-intestinal tract; usually young, grazing stock
nematode genera (bovine abomasum)
Ostertagia (Trichostrongyloidea)
Trichostrongylus (Trichostrongyloidea)
Haemonchus (Trichostrongyloidea)
nematode genera (bovine SI)
Cooperia (Trichostrongyloidea)
Nematodirus (Trichostrongyloidea)
Trichostrongylus (Trichostrongyloidea)
Bunostomum
Toxicara (Ascarid)
nematode genera (bovine LI)
Oesophagostomum
Trichuris (Trichuroidea)
Trichostrongyloidea (general)
-most important in grazing ruminants
-direct life cycle
-L3 is infective
-PPP ~21 days
-mainly GI nematodes
Ostertagia spp.
Trichostrongyloidea:
***Ostertagia ostertagi
Ostertagia leptospicularis
Ostertagia ostertagi (life cycle)
direct life cycle
PPP = 21 days
adult in abomasum
eggs hatch in faeces
L3 ingested
L3 penetrate abomasal gland
L4 can arrest
ostertagiosis (pathogenesis)
1. hypoproteinaemia - rupture of intracellular jxns and leakage of plasma proteins into lumen
2. elevated plasma pepsinogen - parietal cell distruction (decreased HCl and increased pH so pepsinogen not converted to pepsin)
3. bacterial overgrowth - parietal cell distruction cause pH increase
ostertagiosis (pathology)
hyperplasia of gastric mucosa
'Morrocco leather' appearance
putrid smell of abomasal contents (bacterial overgrowth)
nodules on abomasum
large # of asult worms (1cm, reddigh)
ostertagiosis (clinical forms)
Type I - grazing calves (July - October); larvae acquired from pasture 2-3 weeks earlier

Type II - housed yearlings (March - May); due to maturation of inhibited larvae from pasture during previous autumn
ostertagiosis (Type I clinical signs)
profuse watery diarrhea (bright green)
weight loss
occasional submandibular oedema (hypoalbuminaemia)
morbidity high / mortality low
ostertagiosis (Type II clinical signs)
intermittent diarrhea (not always)
submandibular oedema (hypoalbuminaemia)
weight loss
+/- moderate anaemia
anorexia and increased thirst
morbidity low / mortality high
ostertagiosis (diagnosis)
clinical picture & grazing history
diagnosis on herd (not individual)
faecal egg counts (FECs)
serum pepsinogen
(plama gastrin)
(serum antibody)
fecal egg counts (FECs)
-Cannot discriminate between trichostrongyle eggs (xcept Nematodirus)
-There is NOT a linear relationship between FEC and parasite burden
-Low FEC from individual (or small group) does NOT rule out diagnosis of PGE
serum pepsinogen (diagnostic)
-specific for abomasal parasatism (ie. ostertagia)
-useful in calves (less reliable for older animals)
-useful indicator of parasite burden at end of grazing season
serum antibodies (diagnostic)
-ELISAs for parasite antibody (research)
-good measure of exposure
-not commercially available
Ostertagia (immunity)
-slow to develop
-takes at least 1 grazing season
-2nd season calves and adults generally immune
-immune animals still carry burdens (arrested L4)
ostertagiosis (Type I epidemiology)
-development of egg to L3 is temperature dependent
-development in June is slower than July
ostertagiosis (Type I epidemiology)
April/May - calves ingest overwintered L3 (patent infection established but no clinical disease)
May/July - 1st gen of adult parasites produce eggs (contaminate pasture)
July/Aug - large # of L3 on pasture ingested by calves
ostertagiosis (Type II predisposing factors)
Ingestion of many L3 delayed to autum caused by:
1. grazing mgmt - moving animals to contaminated pasture late in season
2. climate - dry summer delay emergence of larvae from fecal pats
ostertagiosis (beef herds)
-uncommon in spring calving herds b/c not weaned until autumn; little pasture contamination during early season
-more common in autumn calving herds b/c weaned in spring (epidemiology similar to dairy calves)
Trichostrongylus axei (cattle)
-abomasum
-very small (<1cm)
-cattle, sheep, goat, horse
-rarely primary pathogen (UK)
-part of PGE mixed infection
-L3 very resistant
Haemonchus
-abomasum
-blood feeding
-'barber's pole' worm
-causes anemia
-not important in cattle (H. placei)
-important in sheep (H. contortus)
Cooperia spp. (cattle)
C. oncophora - temperate (UK), mild pathogen, PGE
C. punctata - tropical (more pathogenic)
C. pectinata - tropical (more pathogenic)
Cooperia oncophora
-common in UK (temperate)
-contributes to PGE (mixed)
-parasitic stages develop on SI mucosa
-mild pathogen (inappetence and reduced weight gain)
-epidemiology similar to O. osteragi
Cooperia oncophora (anthelmintics)
cattle parasite most commonly implicated in anthelmintic resistance (Ivermectin in UK)
Trichostrongylus colubriformis (cattle)
small intestine
<1cm
can also infect sheep/goats
rarely primary pathogen (PGE in UK)
life cycle & epidemiolgy same as T. axei
Nematodirus spp. (cattle)
N. helvetianus (part of mixed PGE)
N. battus - more important in sheep
N. spathiger - more important in sheep
Bunostomum phlebotomum (cattle)
Srongyloidea
small intestine
cattle hookworm (sucks blood)
adult 1-3cm with hooked anterior
Bunostomum phlebotomum (life cycle)
-typical for hookworm - percutaneous route with pulmonary migration (oral route no pulmonary migration)
-PPP = 6 weeks (percutaneous)
-needs warm/wet conditions
-mainly problem in tropics
Bunostomum (identification)
Gross - 1-3cm stout worm
Micro - large buccal capsule (cutting plat3es along top)
Trichosrongylus (identification)
Gross - 1cm thin, straight
Micro - head (excretory notch), male tail (stepped spicules), female tail (colubriformis thin & tapered)
Cooperia (identification)
Gross - 1cm (kink in female)
Micro - head (small cephalic vesicle), male tail (spicule expanded in middle), female tail (oncophora thin & tapered)
Nematodirus (identification)
Gross - 1.5-3cm cotton wool appearance
Micro - head (prominent cephalic vescicle), male tail (long, thin fused spicules), femle tail (battus tapered; others truncate with small spine)
Haemonchus (identification)
Gross - 2-3cm easily visible
Micro - head (tapered), male tail (barbed spicules), female tail (large vulvar flap w/ 100 eggs in uterus)
Ostertagia (identification)
Gross - 0.8-1cm visible
Micro - head (tapered), male tail (long spicules; ostertagi thin picules branched at bottom), female tail (medium vulvar flap w/ 50 eggs in uterus)
Trichostrongylus axei (identification)
Gross - 0.5-0.7cm barely visible
Micro - head (excretory notch), male tail (spicules unequal length), female tail (no vulvar flap w/ 5-7 eggs pole to pole in uterus)
GI nematodes of sheep
Ostertagia - abomasum(PGE)
Trichostrongylus - SI(PGE)
Nematodirus battus - SI
Haemochus - abomasum
ostertagiosis (ovine)
Type I - common
Type II - reemergence of inhibited larvae (not as common but more severe)
ostertagiosis (ovine clinical signs)
-weight loss / failure to gain weight
-intermittent diarrhea (less than bovine)
-appetite loss
ostertagiosis (ovine diagnosis)
-clinical signs
-mainly disease of lambs
-end of grazing season
-fecal egg counts
ostertagiosis (ovine immunity)
-slow to develop
-worm burden & fecal egg output low in adult except during periparturient period (Type II); biggest diff. from cattle
ostertagiosis (ovine periparturient rise)
periparturient rise in fecal egg output (2-6 weeks after lambing) due to:
1. increased overwintered larvae from pasture
2. inhibited L4 reactivating and developing
3. female worms have increased fecundity
NB: occurs in cattle but really phenomena of sheep
ostertagiosis (ovine Type I epedemiology)
build up of L3s on pasture from July-Oct (like cattle):
-eggs passed by ewes during periparturient rise (major diff from cattle - must treat ewes)
-eggs passed by lambs from 1st gen parasites established from overwintered larvae (also impt)
Haemonchus spp. (sheep)
H. contortus (main)
H. similis (more in tropics)
H. placei (more in tropics)
Haemonchus contortus (ovine)
-largest parasite in omasum
-sucks blood (pathology due to this)
-'barber's pole' worm (GI tract wraps around)
-causes haemorrhagic anaemia (5000 adult worms can cause 250ml blood loss per day)
Haemonchus contortus (life cycle)
-typical trichostrongylid
-best adapted to tropical climates (warm & moist)
-development of L1-L3 rapid (in ideal conditions)
Haemonchus contortus (ovine immunity)
ewes remain susceptible
haemonchosis (ovine pathogenesis)
hyperacute (up to 30k adults):
-sudden death due to severe hemorrhagic gastritis

Acute (2k - 20k adults):
-clinical signs ~2wks post infection
-regenerative anaemia followed several weeks later by non-generative anaemia

chronic (several hundred adults):
-weight loss, weakness, inappetence (+/- anaemia)
haemonchosis (ovine clinical signs)
-hyperacute: sudden death
-acute: anaemia, submandibular oedema, ascites, dark faeces, dropping wool, inappetence
-chronic: weight loss, weakness, inappetence
-NB: diarrhea not usually a feature (unlike most other parasites)
haemonchosis (ovine epidemiology - w/o dry season)
-East Africa
-hypbiosis unimportant
-high burden year round
-high worm fecundity
-often year round anthelmintic
-# of L3 on pasture dependent on rainfall
haemonchosis (ovine epidemiology - w/ dry season)
-parts of Australia/Brazil
-dry season: L3 don't survive on pasture
-high levels of inhibited larval development (dry)
-parasite survives predominantly in host
-outbreaks at start of wet season (reactivation of inhibited L3 & rapid increase in pasture L3s)
aelurostrongylus abstrusus life cycle (cat)
ID
ancylostoma caninum life cycle
ID
ancylostoma head
ID
ancylostoma head
ID
anoplocephala perfoliata (head)
ID
anoplocephala perfoliata egg
ID
anoplocephala perfoliata life cycle
ID
bunostomum phlebotomum
ID
bunostomum trigonocephalum
ID
cestode
ID
chabertia ovina life cycle
ID
cooperia
ID
cooperia head
ID
dictyocaulus viviparus (adult worms)
ID
dictyocaulus viviparus (L1 larvae)
ID
dictyocaulus viviparus (L1 larvae)
ID
dipylidium caninum (adult worm)
ID
dipylidium caninum (egg packet)
ID
dipylidium caninum (head)
ID
dipylidium caninum (segments double genital pore)
ID
dipylidium caninum life cycle
ID
dirofilaria immitis (in dog heart)
ID
dirofilaria immitis life cycle
ID
echinococcus (adult SI dog)
ID
echinococcus eggs
ID
dirofilaria immitis life cycle
ID
echinococcus multilocularis
ID
echinococcus multilocularis life cycle
ID
haemonchus
ID
haemonchus contortus (color)
ID
haemonchus female tail
ID
haemonchus head
ID
haemonchus male bursa
ID
haemonchus male tail
ID
haemonchus vulval flap
ID
Hetarakis male tail
ID
hydatid cyst (IMH)
ID
hydatid sand
ID
metastrongylus egg
ID
metastrongylus spp life cycle (pigs)
ID
muellerius capillaris (L1 larva)
ID
nematode anatomy
ID
nematode anatomy
ID
nematode anatomy
ID
nematode morphology (head) 1
ID
nematode morphology (head) 2
ID
nematode morphology (male tail) 1
ID
nematodirus battus egg
ID
nematodirus battus epidemiology
ID
nematodirus battus life cycle
ID
nematodirus egg
ID
nematodirus egg (typical)
ID
nematodirus male tail
ID
nematodirus species egg
ID
number of adult parasites and FECs
ID
oesophagostomum radiatum
ID
oesophagostomum venulosum
ID
oslerus osleri larvae (L1 in sputum)
ID
oslerus osleri larvae (L1 in sputum)
ID
oslerus osleri larvae (L1 in sputum)
ID
ostertagia circumcincta life cycle
ID
ostertagiosis epidemiology (ovine)
ID
ostertagiosis nodules 1
ID
ostertagiosis nodules 2
ID
ostertagiosis nodules 2
ID
ostertagiosis nodules 2
ID
ostertagiosis nodules 2
ID
ostertagiosis type II epidemiology
ID
parafilaria (adult in tissue)
ID
PGE in UK
ID
pilobolus (fungus aids dispersal)
ID
srongylus vulgaris head
ID
strongylus equinus head
ID
strongylus equinus head
ID
taenia (gravid segment)
ID
taenia saginata life cycle
ID
taenia vs dipylidium (genital pore)
ID
tapeworm segment (gravid segment)
ID
tapeworm segment (mature segment)
ID
toxascaris leonina egg (dog&cat)
ID
toxascaris leonina head (dog&cat)
ID
toxascaris leonina larvae (sheathed infective)
ID
toxicara
ID
toxicara canis egg
ID
toxicara canis egg 1
ID
toxicara canis egg 2
ID
toxicara canis fecundity
ID
toxicara canis head
ID
toxicara canis larvae (infective)
ID
toxicara canis life cycle (pups to 3mo)
ID
toxicara cati (b&w)
ID
toxicara cati egg
ID
toxicara vitulorum adults (30cm)
ID
toxicara vitulorum egg (cattle)
ID
toxocara vitulorum larvae (sheathed infective)
ID
Trichostongylus axei
ID
trichostrongyle egg
ID
trichostrongyle egg (typical)
ID
trichostrongylid egg
ID
trichostrongylus colubriformis
ID
trichostrongylus head
ID
trichuris (whipworm)
ID
trichuris globulosa (whipworm)
ID
trichuris globulosa egg
ID
trichuris life cycle (vulpis & suis)
ID
trichuris vulpis egg
ID
uncinaria head
ID
uncinaria stenocephala egg
ID
uncinaria stenocephala life cycle
ID
haemonchosis (ovine epidemiology - temperate)
-larvae do NOT surve over winter
-survives winter inside host
-reacivate in spring
-lambs ingest L3 in summer
nematodes of sheep small intestine
Nematodirus (Trichostrongyloidea)
Trichostrongylus (Trichostrongyloidea)
Cooperia (Trichostrongyloidea)
Bunostomum (Strongyloidea)
Strongyloides (Rhabditoidea)
nematodirus battus (epidemiology)
-May to July peak
-very young lambs
-earlier than others
nematodirus battus (life cycle)
-PPP = 14 days
-develops to L3 inside egg
-only free living L3 infective (ingested)
-hatching requirements: prolonged period of chill followed by day/night temp of 10 degrees
-eggs hatch in mass the following spring
nematodirus battus (host age resistance)
-lambs susceptible from 3wks to 3mo
-ewes very resistent
-physiological immunity (not acquired)
nematodirus battus (epidemiology)
-lamb to lamb disease
-L3s hatch in spring from eggs passed onto pasture from last years lambs
-hatching (L3) must coincide with presence of susceptible lambs (2wk - 3mo)
-depends on climate and lambing period
-mild spring / late lambing or late spring / early lambing = low risk
nematodirus battus (pre-patent period)
14 days (short)
nematodirus battus (pathogenesis)
-due to larval stages
-severe disruption of SI mucosa
-most damage 10-12d post infection (L4-L5 moult)
-eneritis and villus atrophy
nematodirus battus (clinical signs)
-rapid onset (10-12d PI)
-profuse diarrhea
-dehydration (increased thirst)
-lambs affected (ewes normal)
nematodirus battus (diagnosis)
-FECs not reliable (CS due to larvae)
-grazing history
-clinical signs
Nematodirus (others)
-eggs develop to L3 in egg but no special hatching requirements
-part of mixed infection
-contribute to PGE (late summer)
trichostrongylus species in sheep small intestine
*Trichostrongylus vitrinus
Trichostrongylus capricola

NB: T. colubriformis (ruminants)
trichostrongylus (temperate - UK)
-primary pathogen or mixed
-acute PGE in lambs (autumn/early winter)
-very dark faeces
-chronic wasting disease of hoggs & ewes in early winter
-poor skeletal growth & wool quality
trichostrongylus (pathology)
-larvae and adults burrow beneath surface epithelium
-enteritis
-mucus and mucosal hypertrophy
-lamina propria infiltrated with inflammatory cells
-villi shortened & atrophy
-resistance brings localalized 'fingerprint' lesions
cooperia curticei
-small intestine of sheep
-not very pathogenic
-adults 1cm with large bursa
-'watch spring' appearance
-type triconstrongyloidea life cycle
bunostomum trigonocephalum
-superfamily strongyloidea
-sheep and goat hookworm (sucks blood)
-small intestine
-adult 1-3cm with hooked anterior
bunostomum trigonocephalum (life cycle)
-typical hookworm
-PPP = 1-2mo
-infective L3
-percutaneous route with pulomanary migration
-oral route (no pulmonary migration)
nematodes of sheep large intestine
Chabertina ovina (Strongyloidea)
Oesphagostomum spp. (Strongyloidea)
Trichuris ovis (Trichuroidea)
chabertia ovina
-large intestine
-adult 1.5-2cm with large buccal capsule
-plug feeders (mucosa not blood)
-very common
-low level of infection
-contributes to PGE
chabertia ovina (life cycle)
-PPP = 42 days
-hatch L1
-L3 ingested and into SI or LI mucosa
-moults to L4 (1 week) and to caecum
-L4 can arrest
-L5 migrates to colon
chabertia ovina (pathogenesis)
-200 to 300 worms for disease
-mucosal damage
-haemorrhage
-protein losing enteropathy
-diarrhea (mucoid) +/- anaemia
oesophagostomum species in sheep
-oesophagostomum columbianum (nodules)
-oesophagostomum venulosum (no nodules)
-adults 1-2cm
GI nemeatodes of goats
-generally same as sheep
-goats more susceptible (browsing animals)
-acquired immunity less effective
-treat all age groups (higher dose than sheep b/c metab)
-faster drug resistance
fecal egg count (FEC) limitations
-FEC and worm burden not linear relationship
-heavy burden may have low FEC
-individual does not represent status of herd
-does not differentiate between trichostrongyle species (xcept nematodirus)
fecundity between species (daily egg production)
haemonchus 5k-15k
ostertagia 100-200
trichostrongylus 100-200
cooperia 1k-3k
nematodirus 50-100
oesophagotomum 5k-10k
chabertia 5k-10k
nematodes with -ve FEC during acute outbreak
-ostertagiosis type II (cattle)
-nematodirus battus (sheep)
FECs sufficient for clinical disease
Ostertagia:
200 epg (none)
200 to 1000 epg (mild)
>1000 epg (heavy)
Haemonchus: 1k to 20k
Nematodirus: often low or -ve with significant worm burdens
gut nematodes of small animals
-toxocara canis (dog)
-toxocara cati (cat)
-toxocara vitulorum (cattle)
-toxocaris leonina (dog/cat)
toxicara canis
-egg thick and pitted (resistant)
-adult 10-18cm
-3 lips
toxicara cati
-egg thick and pitted (resistant)
-alar flap
-arrowhead appearance
toxocara vitulorum
-cattle
-egg pitted but thinner
-infective larvae sheathed
-large adults (30cm)
toxocaris leonina
-dog/cat
-egg smooth
-infective larvae small & sheathed
-pointed head (adult)
toxocara canis (routes of infection)
-oral (direct): infective larvae in egg
-transplacental
-transmammary
-paratenic host
toxocara canis (outcome of infection)
<3mo - adult develops in SI
>3mo - larvae arrest in tissues
toxocara canis (life cycle < 3mo)
-PPP = 4-5 wks
-adults in SI
-eggs with L2 ingested
-L2 hatches in SI
-via liver to lungs (L2-L3)
-L3 coughed and swallowed (to SI)
toxicara canis (life cycle > 3mo)
-PPP = 16d-3wk
-adult in SI
-L2 ingesteed and hatches in SI
-L2 arrests in tissues
-L2 reactivates ~3 week pre-partum
-L2 migrates to foetal lung (to L3)
-L3 in pup coughed and swallowed
toxicara canis (transplacental transmission)
-infective larvae reactivated 3 week pre-partum
-migrates to fetal lung (moults to L3)
-L3 to SI via trachea
-ensures 100% infection
toxicara canis (transmammary transmission)
-L3 in milk up to 5wk post-parturition
-no migratory phase
toxicara canis (arrested larval development)
-arrested L2 hypobiotic: resistant to anthelmintics
-survive for life of bitch
-reactivate when immunity lowered at pregnancy
toxicara canis (paratenic hosts)
-L2 arrest in bird/rodent/invertebrate
-more important in T. cati
-PPP ~3wk
toxicara canis (egg)
-thick and pitted
-sticky and resistant
-unembryonated egg (freshly shed) not infective
-females very fecund
toxicara canis (clinical signs)
1. migratory phase - coughing, increased resp, pneumonia (heavy)
2. eneral phase - pot bellied pups, failure to thrive
toxicara canis (treatment)
-goal to prevent environmental contaminatin
-min PPP ~16d: treat before eggs
-high dose Fenbendazole (3wk pre-partum, 2wk post) kills reactivated L2
toxicara canis (pre-patent periods)
-transplacental: 16d-3wk pups
-transmammary: ~4wk from birth
-paratenic host: 3wk hunting & scavenging dogs
-direct: 4-5wk all dogs
toxicara cati
-no transplacental infection
-transmammary most important
-no migratory phase
-PPP ~8wk
-diarrhea, pot-belly, poor coat
toxicara vitulorum
-exotic cattle (not UK)
-PPP ~3-4wk
-transmammary route most important (up to 30d)
-no tissue migration in calf
toxascaris leonina
-cats/dogs very common
-direct: egg containing L2
-no migratory phase
-PPP ~11wk
-smooth shell
-paratenic host (eg. L2 in tissue of mice)
ancylostoma caninum (head) - what feature differentiates it from uncinaria species?
teeth (cutting plates in uncinaria)
uncinaria stenocephala (head) - what feature permits identification?
cutting plates
trichuris vulpus egg - features
mucus plugs (bipolar)
trichuris species - where in the host?
large intestine
ancylostoma species - where in the host?
small intestine
skeletal tissue
lungs
superfamily strongyloidea species (hookworms)
uncinaria stenocephala (dog, cat, fox)
ancylostoma caninum (dog)
ancylostoma braziliense (dog/cat)
ancylostoma tubaeforme (cat)
hookworm features (strongyloidea)
-1 to 3 cm, stout, hooked head
-small intestine
-direct lifecycle
-L3 infective (sheathed - L3 with L2 cuticle)
-important in tropics
uncinaria stenocephala (general)
-northern (fox) hookworm
-dog, cat & fox
-oral infection (L3)
-no percutaneous route
-no transmammary infection
-PPP = 14-21d
uncinaria stenocephala (pathology)
-not voracious blood sucker
-grazes on SI mucosa
-protein losing enteropathy
-hypersensitivity response
-pedal dermatitis (tries to get through skin of foot pad but can't and dies)
ancylostoma caninum (transmammary infection)
-very important in pups
-bitch can infect 3 consecutive litters
-reactivating L3 can produce patent infection in bitch
-control difficult
ancylostoma caninum (pathogenesis)
-simple haemorrhage (hookworm)
-immature and adult worms feed
-anaemia (secretes anticoagulant)
-worms change feeding site up to 6x per day (bleeds)
ancylostoma caninum (epidemiology)
-younger animals (immunity in older)
-warmer climates
-2 sources of infection (transmammary and percutaneous)
ancylostoma caninum (control)
-benzimidazoles
-ivermectin/moxidectin
-fenbendazole (high dose in pregnant bitch)
-clean dry bedding (earth or grass runs support L3 survival)
ancylostoma caninum (eggs)
-typical strongyle egg
-pathogenic in prepatent phase
-can have anaemia but no eggs in faeces
ancylostoma braziliense
-cats and dogs
-not blood sucking
-protein losing enteropathy
-cutaneous larva migrans (man) - creep under skin
trichuris species (trichuroidea)
-trichuris vulpis (dogs)
-trichuris suis (pigs)
trichuris (general)
-whipworms
-thin anterier and thicker poster (repro organs)
-direct life cycle
-PPP = 6-12wk
-L1 infective (penetrates LI mucosal glands)
trichuris vulpis (pathology)
-usually asymptomatic
-watery diarrhea +/- blood
trichuris (egg)
bipolar mucoid plugs
metastrongyles (metastrongyloidea)
-indirect life cycle
-IMH = molluscs
-clinically mild / asymptomatic (usually)
oslerus osleri
-host: dog & wild canid
-NO IMH
-site: nodules at tracheal bifurcation
-thin (1-1.5cm)
oslerus osleri (life cycle)
-direct (PPP = 10-18wk)
-adults in tracheal nodules
-hatched L1 coughed up and swallowed
-L1 to pup in sputum or environ
-L2 in SI
-L3 to L5 in alveoli and bronchi before migrating to trachea
oslerus osleri (clinical signs)
-usually asymptomatic
-dry cough +/- (as nodules grow)
-exercise intolerance
-dogs 6-12mo (esp. working dogs)
oslerus osleri
-chronic dry cough and exercise intolerance
-L1 in sputum (or faeces)
-bronchoscopy (nodules & L1)
-L1 has distinctive 'S' shaped tail
oslerus osleri (epidemiology)
-nursing bitch often focus of infection
-L1 immediately infective
aelurstrongylus abstrusus
-host: cat
-IMH: molluscs
-site: lung parenchyma and small brionchioles (lungworm)
aelurstrongylus abstrusus (life cycle)
-PPP = 4-6wk
-adult in lungs
-eggs hatch almost immediately
-L1 in faeces
-L1 to L3 in IMH
-L3 in IMH infective (IMH ingested and to lungs by lymph of blood)
aelurstrongylus abstrusus (pathologenesis)
-not very pathogenic
-small granulomas in lung
-rarely, larger lesions
-muscular hypertrophy/plasia
-granulomas soon resolve
-widespread (ubiquitous IMH)
aelurstrongylus abstrusus (clinical signs)
-mild
-chronic moist cough (esp. after handling)
-mild dysnopea
-dignosis: L1 in faeces
angiostrongylus vasorum
-host: dog
-IMH: molluscs
-site: right ventricle, pulmonary artery
-small brown worms (~2.5cm)
-aka 'French' heartworm
angiostrongylus vasorum (life cycle)
-PPP = 7 weeks
-adults in heart
-eggs hatch in pulmonary capillaries
-L1 to alveoli and up lungs
-L1 in faeces (L1-L3 in IMH)
-IMH ingested (L3) and L4-L5 in mesenteric lymph nodes before right heart
angiostrongylus vasorum (pathogenesis)
-chronic congestive cardiac failure
-fibrosis in arteries ('pipe stem' feel)
-lung mottled (penetrating L1)
angiostrongylus vasorum (clinical signs)
-early: asymptomatic
-later: increased resp / cough on exercise
-fainting
-s.c. haematoma
-diagnosis: L1 in faeces (characteristic tail)
-warm damp winters (increase in slugs)
filariodea species (filarial worms)
-dirofilaria immitis
-inchocerca species
-parafilaria species
filarial worms
-tissue dwelling
-insect vectors
-never in gut
-primitive forms lay eggs (parafilaria)
-more evolved forms release L1 or microfilaria (dirofilaria)
microfilariae
-L1
-sheathed or unsheathed
-blood or skin
-periodicity: numbers peak in blood to cooincinde with biting habits of vectors
dirofilaria immitis
-host: dog, cat, ferret, sea lion
-IMH: mosquito
-site: cv system (rt ventricle, posterior vena cava, pulmonary artery)
-USA, warm temperate zones (Europe), tropics
dirofilaria immitis (life cycle)
-PPP = 6mo
-adults in heart
-release unsheathed microfilariae in blood
-mf ingested by mosquito (L1-L3 in 10-14d)
-L3 transmitted when mosquito feeds
-L3 L5 in s.c., L5 to heart
dirofilaria immitis (pathogenesis)
-chronic congested rt heart failure
-endocarditis in valves, pulmonary endarteritis
-pulmonary embolism
-vena cava syndrome
-glomerulonephritis
dirofilaria immitis (clinical signs)
-cardiovascular dysfunction
-listless/gradular loss of condition
-exercise intolerance
-chronic soft cough
dirofilaria immitis (diagnosis)
-microfiliae in blood
-circulating antigen (currently infected cf antibody)
-clinical signs
dirofilaria immitis (cats)
-very pathogenic (better adapted to dog)
-adult worms live shorter time
-mf are transient
-less prevalent than in dogs
dirofilaria immitis (dog vs cat)
DOG: v. susceptible, worms live 5-7yr, 30+ worms, heart and lungs, persistent microfilaemia
CAT: less susceptible, worms live 2-3yr, <6 worms, lungs only, transient microfilaraemia
dirofilaria immitis (prophylaxis)
-macrocyclic lactones monthly(Ivermectin, milbermycin, selamectin) - kills L3/L4 up to 6wk pi
-DEC (diethylcarbamazine) daily
-prophylactic drugs do not kill adult worms (maybe steralize females)
dirofilaria immitis (mf status and prophylaxis)
-Ivermectin and particularly DEC are microfilaricidal at prophylactic doses
-if mf +ve dog treated, can induce anaphylctic shock
-dogs must be mf -ve before treatment!
dirofilaria immitis (prevention)
-keep animals inside at peak mosquito biting times (dusk)
-insecticide collars or spot-on
-reduce mosquito population (dfficult)
onchocerca species
-onchocerca cervicalis (horse)
-onchocerca gutturosa (cattle)
-onchocerca lienalis (cattle)
-onchocerca volvulus (humans)
onchocerca cervicalis
-host: horse
-IMH: culiicoides (midges)
-microfilaria in skin
onchocerca gutturosa and onchocerca lienalis
-host: cattle
-IMH: simulium (black flies)
-microfilariae in skin
parafilaria species
-host: cattle, buffalo, horse
-IMH: muscid flies
-site: sc and im connective tissue
-distribution: s. europe, sweden, africa, asia
-stick tail through skin to lay eggs (skin lesions)
habronema microstoma (spiroidea)
-host: horses/donkeys
-IMH: muscid flies
-site: adults in stomach
-related to filarial worms
habronema microstoma (summer sores)
-horse/donkey
-cutaneous infestation by L3
-L3 deposited on skin (often around eyes)
-warm weather (often on dark coated horses)
-no further development
aleurostrongylus abstrusus (prediliction site)
lung (mildly pathogenic)
dirofilaria immitis (dog) - sheathed?
no
lungwomrs (large animal)
-trichostrongyloidea (direct)
-metastrongyloidea (indirect)
trichostrongyloidea species
lungworms:
-dictyocaulus viviparus (cattle)
-dictyocaulus arnfieldi (horse & donkey)
-dictyocaulus filaria (sheep & goats)
-dictyocaulus eckerti (deer)
dictyocaulus viviparus (life cycle)
-PPP = 26d
-adults in bronchi/trachea
-hatched L1 up trachea and swallowed
-L1 in faeces
-L3 infective (ingested)
-L4 in lymph nodes to lungs
dictyocaulus viviparus
-adults up to 8cm (slender)
-L1 larvae in faeces (NOT eggs)
-bigger than haemonchus but slender & thread-like
-dark brown granules in worm intestine
dictyocaulus viviparus (immunity)
-strong & rapid acquired immunity following infection
-requires boosting by natural challenge (otherwise will become susceptible again)
dictyocaulus viviparus (parasitic bronchitis)
-penetration phase (0-7d): larvae migrate to lungs
-prepatent phase (8-25d): larvae migrate up through lungs
-patent phase (26-60d): adults producing eggs
-postpatent phase (61-90d): adults expelled from airways by immune system
dictyocaulus viviparus (prepatent phase)
-L4/L5 migrating up respiratory tree
-acute inflammatory response (monocytes & eosinophils)
-heavily infected calves can die from 15d on
-clinical signs 1st seen
dictyocaulus viviparus (patent phase)
-lesions in airways (adults): inflammatory response, hyperplasia of bronchial epithelium and, interstitial emphysema
-lesions (aspirated eggs/larvae): granulomatous response
dictyocaulus viviparus (postpatent phase)
-most animals recover gradually (strong acquired immunity)
-some (up to 25%) clinical signs increase due to:
1. alveolar epithelialization - squamous changes to cuboidal around alveoli (less gas exchange)
2. bacterial infection (acute interstitial pneumonia)
dictyocaulus viviparus (clinical signs)
MILD (100 worms): intermittent cough
MODERATE: cough at rest, tachypnoea, hyperpnoea
SEVERE (1000 worms): harsh cough, tachypnoea, dyspnoea, mouth breathing, pyrexia (secondary bacterial infection), sc emphysema
dictyocaulus viviparus (reinfection syndrome)
-immune animals exposed to massive larval challenge (no adults)
-lots of larvae killed in lungs by immune sys
-no L1s in faeces (no patent infection)
-coughing and slight tachypnoea (mild syndrome)
-small lymphoid nodules surrounding dead larvae
dictyocaulus viviparus (diagnosis)
-clinical signs
-time of year
-grazing / vaccination / anthelmintic history (usually grazing animals)
-eosinophilia
-bronchial lavage
-ELISA (adult & L3 antigens)
dictyocaulus viviparus (epidemiology)
-temperate regions (high rainfall)
-acquired immunity strong (requires boosting)
-all age groups (unlike ostertagia and GIT parasites)
-carrier animals (survival of latent L4)
-outbreak unpredictable
dictyocaulus arnfieldi
-host: *donkeys & horses
-life cycle similar to D. viviparus (xcept eggs in faeces)
-PPP = 2-4mo
-reaches patentcy in donkeys and horse foals/yearling (not adult)
dictyocaulus arnfieldi (clinical signs)
-donkeys: usually none (true definitive host)
-horse: chronic cough and tachypnoea (larval stages)
dictyocaulus arnfieldi (diagnosis)
-donkey: eggs or L1s in faeces
-horse: usually no eggs or L1s, grazing / anthelmintic history, co-grazing with donkeys
dictyocaulus filaria
-sheep and goats
-PPP = 5wk
-sporadic disease: lambs/yearlings in autumn
-clinical signs milder than D. viviparus (chronic cough, unthriftness, nasal discharge)
dictyocaulus filaria (diagnosis)
-L1 in faeces (Baerman technique)
-cuticular knob on anterior
metastrongyloidea species
-metastrongylus apri (pig)
-metastrongylus salmi (pig)
-metastrongylus pudendotectus (pig)
-muellerius capillaris (sheep & goats)
-protostrongylus rufescens (sheep & goats)
metastrongylus spp. (life cycle)
-PPP = 4wk
-adult in small bronchi and bronchioles
-eggs in faeces
-IMH earthworms (L1-L3)
-L3 penetrates intestinal mucosa
-L4 in lymph nodes to lungs
metastrongylus apri and spp.
-adults 6cm (slender)
-most infections light and asymptomatic
-heavy infections: coughing, dyspnoea, nasal discharge
-pigs 6-8mo (access to earthworm)
-eggs in faeces
tachypnoea
increased respiratory rate
hyperpnoea
increased respiratory depth
dyspnoea
difficulty breathing
muellerius capillaris
-sheep & goats
-widespread & common
-brown hair-like worms in alveoli (1-3cm)
-IMH: snails and slugs
-not pathogenic
-'lead shot' lesions
muellerius capillaris (L1 larvae)
L1s in faeces differentiated from D. filaria by:
-smaller size
-absence of anterior cuticular knob
-dorsal spine on tail
horse nematodes
-small strongyles (cyathostomins)
-large strongyles
cyathostomins
-small strongyles (small red worms)
-primary parasitic pathogen of horses
-many species
-common
-not migratory
-may be very pathogenic
cyathostomins (life cycle)
-PPP = 2-3mo+
-adults in caecum and colon
-L1 to L3 on pasture
-L3 penetrates LI wall (may arrest)
-L4 emergence
cyathostomins (pathogenesis)
-larval stagees (in LI): goblet cell hypertrophy
-L4 emergence: eosinophil infiltration ++, catarrhal / haemorrhagic enteritis
-adults feeding: protein losing enteropathy
cyathostomins (clinical signs)
-weight loss
-anaemia
-poor performance
-colic
larval cyathostomosis
-associated with arrest larvae (can be millions)
-larvae reactivated all at once
-very pathogenic (diarrhea, dehydration, 50% fatality)
horse strongyles (epidemiology)
-no strong immunity
-horses of all ages can pass eggs
-pasture contaminated by:
1. re-emergence & development of cyathostomins (spring)
2. over-wintered L3 (sheathed - resistant)
cyathostomins (risk factors)
-high stocking densities
-over grazing
-use of pasture by multiple horses
-presence of young animals
-warm damp weather
-horses with high FEC
cyathostomins (wormers)
-pyrantel
-ivermectin + praziquantiel (not for autumn/winter or risk reactivating larvae)
-moxidectin
-fenbendazole (claims to kills arrested larvae)
large strongyles (horse)
-*strongylus spp (migratory)
-triodontophorus spp (non-migratory)
large strongyles (life cycle)
-adults in LI
-L1 to L3 on pasture
-L3 ingested (sheathed)
-L4 to prediliction site
-L5 remigration
large strongyles (larval prediliction sites & PPP)
-strongylus vulgaris (most pathogenic): cranial mesenteric artery (6-7mo)
-strongylus edentatus: liver, hepatic lig, flank (10-12mo)
-strongylus equinus: liver, pancreas (8-9mo)
strongylus vulgaris (pathogenesis of larval stages)
-arteritis
-thrombosis +/- aneurism
-infarction & necrosis of associated intestine
-very pathogenic (L5 migrates to intestine - forms nodules)
strongylus edentatus(pathogenesis of larval stages)
-pathological changes in liver and subperitoneal tissues
-not as pathogenic as s. vulgaris
large strongyles (adult pathogenesis)
-plug feeders (large buccal capsules)
-ulceration
-haemorrhage
-protein losing enteropathy
large strongyles (clinical signs)
-unthriftness
-anaemia
-colic (S. vulgaris)
triodontophorus species
-triodontophorus serratus
-triodontophorus tenuicollis
-triodontophorus brevicauda
-triodontophorus minor
triodontophorus (features)
-adults in large intestine
-contribute to mixed strongyle infection (not on own)
-shallow buccal capsule
-3 sets of teeth
horse nematodes
-small strongyles (cyathostomins)
-large strongylus (strongylus spp)
-parascaris equorum
-oxyuris equi
-strongyloides westeri
parascaris equorum
-foals and yearlings
-large white worm (~40cm)
-SI (duodenum & proximal jejunem)
-age resistance (>6mo)
-unthriftness
parascaris equorum (life cycle)
-PPP = 10-15wk
-adults in small intestine
-L2 (inside egg - 2wk) infective
-hatches after ingestion (L2 to liver via portal sys)
-L3 to lungs (coughed and swallowed - L4 in SI)
parascaris equorum (pathogenesis)
-migrating larvae damage:
1. liver: focal haemorrhage and fibrosis
2. lungs: focal haemorrhage, lymphocyte infiltration, nodules
-adult worms in intestine: little pathology (unless very large burden - impaction, peritonitis)
parascaris equorum (clinical signs)
1. ill thrift:
-adults in SI
-foals and yearlings
-immunity in older horses
2. respiratory signs
-due migrating larvae
-foals: coughing +/- greyish nasal discharge
parascaris equorum (epidemiology)
-foal/yearling to foal/yearling
-females very fecund (FEC high)
-eggs very resistant and sticky (can survive several years on pasture)
-eggs build up on pasture towards end of season
parascaris equorum (treatment/control)
-adults susceptible to all major classes of anthelmintics
-migratory stages only partly susceptible
-small strongyle control will also control
-may control in animal but pasture still contaminated
strongyloides westeri
-worldwide
-adults small (<1cm)
-only females are parasitic
-common in foals <6mo
strongyloides spp (life cycle)
-complex: free living stage and parasitic stage
-adult females in SI
-eggs to L3 free living
-L3 (unsheathed) to parasitic stage: skin penetration or ingestion
-to lungs (L3-L5)
-also transmammary route (L3 initially dormant in muscle - no migration)
strongyloides westeri (clinical signs)
-only in very young animals (few weeks)
-requires heavy burden
-signs non-specific: diarrhea, anorexia, dullness, reduces weight gain
strongyloides westeri (diagnosis)
-clinical signs
-larvated eggs in faeces (smaller than strongyle egg)
-high FEC may be seen in healthy animals
strongyloides westeri (epidemiology)
-free living L3 not very resistant (unsheathed)
-warm and wet conditions, poor hygiene helps L3 survival
-transmammary route important
-not really a strongyloid
oxyuroidea species
oxyuris equi (horse)
enterobius vermicularis (human)
-pinworms
-large intestine
oxyuris equi
-pinworm
-large intestine
common
-adult female to 10cm (male 1cm)
-long pointed tail
oxyuris equi (life cycle)
-PPP = 5mo
-adults in colon
-eggs laid at anus
-L1 to L3 inside egg (L3 egg shed)
-hatched L3 ingested and penetrates colonic mucosa
oxyuris equi (clinical signs)
-adults in LI usually asymptomatic
-egg laying activity can cause intense prineal irritation (rubbing)
-alopecia/inflammation over rump and tail head
oxyuris equi (epidemiology)
-infective stage (L3) may be reached on perianal skin
-usually flakes of skin with eggs rubbed off
-little immunity
-heavy burdens may build in infected stables
-susceptible to many anthelmintics (small strongyle control will work for this too)
oxyuris equi (diagnosis)
-eggs around the perianal region (usually not in faeces)
-scraping + micro exam of eggs
-adults in faeces
-clinical signs
nematodes of birds
-syngamus trachea (strongyloidea)
-ascaridia galli (ascaridoidea)
-heterakis gallinarum (ascaridoidea)
-capillaria sp. (trichuroidea): related to trichuris
syngamus trachea (strongyloidea)
-domestic fowl & game birds
-adults in trachea
-adults permanantly in copula
-adults Y shaped (male & female)
-aka 'gapeworm'
syngamus trachea (routes of transmission)
1. ingestion of L3 (IN the egg)
2. ingestion of hatch L3
3. ingestion of paratenic host (earthworm) containing L3
*L3 penetrates SI and migrates in blood to lungs
syngamus trachea (pathogenesis)
-migration of many larvae: acute pneumonia and death
-adults: haemorrhagic tracheitis
-partial airway occlusion: "gapes" (gasps)
syngamus trachea (clinical signs)
-depressed
-dyspneoic (pre-patent)
-gasps, shakes head, cough (patent)
syngamus trachea (diagnosis)
-barrel shaped egg with bipolar operculum
-clinical signs
syngamus trachea (epidemiology)
-young birds (adults are carriers)
-turkeys of all ages
-esp. outdoors
-eggs very resistant
-infections can come from wild birds
ascaridia galli (ascaroidea)
-chickens & turkeys
-small intestine
-large white worm (~12cm)
-oval egg (smooth shell)
-L2 (in egg) infective
-not migratory
-not very pathogenic
ascaridia galli (diagnosis)
-eggs difficult to distinguish from heterakis gallinarium
-eggs thick shelled and resistant
-does not look like toxicara egg
heterakis gallinarum
-domestic and wild birds
-ascarid but in LI
-small white worm (~1.5cm)
-not migratory
-not pathogenic
-eggs similar to ascaridia
heterakis gallinarum (pathology)
-not pathogenic in itself
-importance as vector of histomonas meleagridis
-histomonas transmitted from bird to bird in heterakis egg
-causes 'blackhead' in turkeys
capillaria (birds)
-prediliction site depends on species (crop and oesophagous or SI)
-similar to trichurs spp (hookworm)
-eggs parallel sides with bipolar plugs
phylum platyhelminthes
flatworms:
-cestodes: tapeworms
-trematodes: flukes
cestodes (structure)
-segmented body (tapeworm)
-hermaphrodite
-no alimentary canal
-scolex (head): suckers, rostellum and hooks (armed)
-strobila (chain of segments or proglottids)
scolex
head of an adult cestode (tapeworm) - suckers, rostellum and hooks (armed)
strobila
in adult cestode (tapeworm): chain of segments or proglottids
cestode (tapeworm) segments
-mature: organs of repro
-gravid: eggs only (in uterus)
taenia egg (cestode)
-radially striated shell or embryophore
-hexacanth (6-hooked) embryo or oncosphere
cestode (larval stages)
-cyst contains head(s) of future tapeworm
-ingested by final host (cyst digested & head latches onto SI wall)
-starts to bud segments
taeniidae
host: man, cat, dog (SI)
IMH: mammal (larval stages encysted)
-scolex armed (xcept T. saginata)
-adults relatively non-pathogenic
taenia (gravid segment)
organs of sexual repro in mature segment disappear as proglottid matures (uterus filled with eggs)
taeniidae species
-taenia saginata (man SI)
-taenia solium (man SI)
-taenia multiceps (dog SI)
-taenia hydatigena (dog SI)
-taenia ovis (dog SI)
-taenia taeniaeformis (cat)
-dipylidium caninum (dog, cat, man SI)
taenia saginata
-cestode (tapeworm)
-host: man SI
-IMH: cow
-adult 5-15m!
-unarmed
-cysticercus bovis
taenia saginata (life cycle)
-PPP = 2-3mo
-adults in man SI
-millions of eggs per day (gravid segments)
-bovine ingests (oncospherese released in abomasum and penetrate SI wall)
-to skeletal muscle (encysts - cysticercus bovis)
-meat ingested by man (undercooked)
taenia solium
-cestode (tapeworm)
-host: man
-IMH: pig or man (v. pathogenic)
-if man is IMH: auto-infection by reverse peristalsis
-cysticercus cellulosae
taenia solium (pathology)
-adult tapewrom: no pathology
-cysticerci: v. pathogenic if encysts in man (IMH)
-cysts in CNS or eye
taenia solium (epidemiology)
-close association of man & pig
-unrestricted access of pigs to human waste
-poor meat inspection
-latin america
taenia hydatigena
-cestode (tapeworm)
-host: dog (SI)
-IMH: sheep (cysticercus tenuicolis)
-adult: ~500cm
-common in abattoir (UK): condemnation of lamb livers (burrows before encysts)
taenia ovis
-cestode (tapeworm)
-host: dog (SI)
-IMH: sheep (cysticercus ovis)
-adult: ~200cm
-relatively common
taenia multiceps
-cestode (tapeworm)
-host: dog (SI)
-IMH: sheep (coenorus cerebralis)
-causes 'gid' (unbalanced): cysts in CNS
-multiple heads: single cyst results in multiple worms
taenia taeniaeformis
-cestode (tapeworm)
-host: cat (SI)
-IMH: mouse/rat (cysticercus fasciolaris)
-adult: ~60cm
dipylidium caninum
-cestode (tapeworm)
-host: SI of dog, cat, man
-IMH: fleas (larvae only) & lice (all stages)
-adult: ~50cm
-PPP = 3wk
dipylidium caninum (life cycle)
-adults in SI of dog, cat, man
-gravid segments shed (3wk pi)
-ingested by flea/louse
-cysticercoid in haemocoel (body cavity) of flea/louse
-flea/louse ingested
dipylidium caninum (head)
-rostellum with hooks
-suckers
dipylidium caninum (diagnosis)
-egg packets
-double genital pore
-active, motile segments
-elongated shape (rice grain)
-tx: treat parasite like others but also must treat for flea/louse
taenia vs dipylidium
-taenia: single genital pore
-dipylidium: double genital pore
echinococcus species
-echinococcus granulosus granulosus
-echinococcus granulosus equinus
-echinococcus multilocularis
echinococcus granulosus granulosus
-cestode (tapeworm): scolex + 3-4 segments
-host: dog & wild canids (SI)
-IMH: ruminant, pig, man
-zoonotic
echinococcus granulosus equinus
-cestode (tapeworm): scolex + 3-4 segments
-host: dog/red fox (SI)
-IMH: horse/donkey
-NOT zoonotic
echinococcus
-cestode (tapeworm)
-dog (SI)
-scolex + 3-4 segments
-eggs similar to taenia (6-hooks radially striated)
-eggs passed in faeces
echinococcus granulosus granulosus (life cycle)
-PPP = 40-50d
-adults in dog SI
-gravid segments shed 1 per week (per worm)
-resistant onchosphere ingested (penetrates SI)
-hydatid cyst in liver/lungs (6+mo pi)
-cyst ingested by host
protoscoleces
-in cyst of echinococcus granulosus granulosus
-contain hydatid sand
-immature scolexes (head without segments)
echinococcus granulosus granulosus (IMH)
-depends on local animal husbandry (adaptable)
-sheep is natural IMH
-can be camels or deer (or pig/man)
echinococcus granulosus granulosus (zoonosis)
-man is accidental IMH
-sheep farming areas
-close man/dog contact
-man infected by ingestion of oncoshpheres from water, foodstuffs or coat of dog
echinococcus multilocularis
-cestode (tapeworm)
-host: dog, cat, wild canid (fox)
-IMH: rodent, man
-life cycle like echinococcus granulosus granulosus
-important zoonos
-prevalent in Europe
cestodes of the horse
-site: SI & LI
-IMH: mites
-anoplocephala perfoliata*
-anoplocephala magna
-paranolocephala mamillana
anoplocephala perfoliata
-cestode (tapeworm)
-host: horse
-IMH: mite
-SI & LI (ileo-ceocal colic)
-ulcerations at attachment site
-v. prevalent (temperate)
anoplocephal perfoliata (morphology)
-head: suckers & lappets
-egg: pyriform apparatus (supports embryo)
-adult: short & fat (segments wider than long)
anoplocephal perfoliata (life cycle)
-PPP = 6-10wk
-adults @ ileo-caecal jxn (horse)
-eggs (in faeces) ingested by mite (forms cysticercoid)
-horse ingests mite (attaches to gut wall)
largest nematode in horse
-parascaris equorum
-SI
strongylus vulgaris
-horse LI
-large strongyle
-well developed buccal capsule
-2 rounded teeth at base of buccal capsule
strongylus edentatus
-horse LI
-large strongyle
-absence of teeth distinguishes from others
strongylus equinus
-horse LI
-large strongyle
-teeth larger & more pointed than S. vulgaris
tridontophorus
-horse LI
-large strongyle
-shallow buccal capsule
-3 sets of teeth at base of buccal capsule
cyathostomin
-horse
-small strongyles
-shallow buccal capsule
-not migratory
-+/- teeth (hard to distinguish)
-do not need to distinguish species
oxyuris equi (egg)
-slightly flattene on 1 side
-mucoid plug on 1 end
syngamus trachea (morphology)
-adults in permanent copulation (form Y shape)
-egg has operculum on both ends
heterakis (morphology)
-male: large precloacal sucker
-prominent caudal alae & papillae
pig nematodes
1. stomach
-hyostrongylus rubidus
-trichostrongylus axei
2. small intestine
-ascaris suum***
-trichinella spralis**
-strongyloides ransomi
3. large intestine
-oesophagostomum
-trichuris suis
4. lungs
-metastrongylus spp.
nematodes of pigs (species)
-hyostrongylus: outdoor only
-ascaris: outdoor & indoor (extensive & intensive)
-oesophagosomum: outdoor, indoor (extensive & intensive)
-trichuris: outdoor & indoor (extensive only)
hyostrongylus rubidus
-ostertagia of pigs (predominantly lactating sows)
-stomach
-chronic gastritis
-outdoor pigs only
-life cycle (typical trichostrongyloid): direct, PPP = 3wk, L4 can undergo hypobiosis
-clinical signs: inappetence, anaemia, loss of condition, reduce fertility
-pathology: similar to ostertagia (nodule formation)
-diagnosis: eggs in faeces
acaris suum
-pig small intestine
-typical ascarid (large ~40cm)
-direct life cycle
-L2 in egg is infective
-migratory
-1 to 5 adults per host
ascaris suum (life cycle)
-PPP = 6-8wk
-adults in pig SI
-L2 inside egg is infective (hatches after ingestion)
-L2 to liver via portal sys (L3 in liver)
-to lungs (coughed & swallowed)
-L4 in SI
-typical ascarid (like toxicara canis)
relationship between ascaris suum & ascaris lumbricoides
-closely related but separate species (look identical)
-in areas where human infection with A. lumbricoides is endemic, pigs not an important resevoir
-in areas where A. lumbricoides is NOT endemic (USA), sporadic cases of human infection with A. suum (organic veg with pig faeces)
ascaris suum (clinical signs)
-overt clinical signs rarely seen
-reduced productivity (up to 10%): food conversion efficiency, reduced weight gain, increased fattening time
-occasionally transient pneumonia in young pigs (migrating larvae)
-milk spot fever: cloudy white spots (up to 1cm), fibrous repair of inflammatory reaction to migrating L2/L3, liver condemnation (economically important)
-diagnosis: clinical signs & history, FEC, incidence of liver contamination
ascaris suum (epidemiology)
-can complete life cycle indoors
-very fecund (>200k worms per day per worm): eggs resistant
-difficult (impossible?) to eradicate from indoor systems
-primarily young pigs (strong acquired immunity in older pigs)
-minimum 4 weeks maturation for egg maturation
-milk spot fever in end of summer
trichinella spiralis (life cycle)
-L1 in muscle (ingested)
-L1 infects SI mucosal epithelium & grows to adult (L1-L4)
-adult lays eggs & L1 larvae penetrate SI mucosa
-L1 to muscle (via lymph & blood) & encysts
trichinella spiralis (pathogenesis)
-invades single muscle cells & encysts
-destroys actin/myosin
-becomes "nurse cell" (encapsulated)
-domestic cycle (pigs: infected swill, tail biting, rats) & sylvatic cycle (wild animals)
trichinella spiralis (diagnosis)
-pigs: examination of muscle for larvae (artificial digestions with pepsin/HCl; trichinoscopy of thin muscle section)
-prediliction sites: diaghragm, intercostal muscles, tongue, masseters
-serology: ELISA
trichinella spiralis (clinical signs: man)
-transient enteritis (L1-adult)
-1 to 2 weeks later, L1 in muscle: acute myositis, pyrexia, myocarditis, periorbital oedema, ascities, eosinophilia
-can be fatal
-diagnosis: muscle biopsy, ELISA
trichuris suis (life cycle)
-PPP = 6-12wk
-L1 inside egg is infective (1-2mo maturation in faeces - minimum)
-on ingestion, L1 hatches & penetrates glands in caecal mucosa (4 moults occur)
-adults emerge: anterior ends (narrower end of whipworm) embedded in mucosa of LI & caecum
trichuris suis
-whipworm
-mild/moderate infections asymptomatic
-can occur indoors but limited to "traditional systems" (solid floors/straw)
-more common in outdoor systems (organic)
-typically poor hygiene
-common in uK but in low numbers
trichuris suis (clinical signs)
-growers/finishers
-reduced growth rate
-loose faeces to overt scouring
-mucus in faeces
-occasionally blood in faeces (severe)
-facilitates invasion of pathogenic spirochetes
trichuris suis (diagnosis)
-FEC: heavy infections up to 10k eggs
-egg: barrel shaped with mucus plug on both ends
-PPP = 6-10wk: eggs only in faeces of pigs 10wk or older
-FEC -ve does not rule out diagnosis
oesophagostomum
-"nodular worm"
-oesophagostomum dentatum
-oesophagostomum quadrispinulatum
-cephalic vescicles on anterior (head) end
-more important in pigs than cattle/sheep
-usually subclinical
-adults 1-2cm
-more common in outdoor systems (but can be indoors: sows & boars)
-infection accumulates over life of animal
oesophagostomum (life cycle)
-PPP = 18-21d
-adults in LI
-eggs in faeces: L3 ingested & enters SI or LI mucosa
-may induce nodules
-L4 emerges (can arrest in nodules)
-L5 in LI lumen
oesophagostomum (epidemiology)
-life cycle can be completed indoors
-L3 can survive or develop in faeces, contaminated concrete, & skin
-infection accumulates with ages (higher in sows than fatteners)
-with increased immunity: arrest in nodules
-periparturient rise in FEC in sows (2nd half of pregnancy to weaning: treat sows 1wk before farrowing)
-piglets can be born into highly infected environment
-outdoor: L3s overwinter poorly in temperate regions
oesophagostomum (pathology)
-diffuse enteritis in colon & caecum
-oesophagostomum quadrispinulatum: distinct nodules
-oesophagostomum dentatum: indistinct nodules
-acute infections: haemorrhage and secondary infection (form small abscesses)
-chronic infections: fibrous nodules
oesophagostomum (clinical signs)
-burdens < 5k worms: probably asymptomatic
-growing pigs: reduced weight gain
-sows: poor milk yields (contributes to "thin sow syndrome"), reduced fertility
-older breeding stock carry heaviest infections
-diarrhea in very heavy infections (10k+ worms)
-egg: similar to hyostrongylus
fasciola hepatica
-final host: most mammals
-significance: sheep & cattle
-disease: fasciolosis
-distribution: temperate
-IMH: lymnaea truncatula (amphibious small brown snail)
fasciola hepatica (life cycle)
-adults (hermaphrodite) in larger bile ducts of liver (v. fecund)
-eggs (quninone tanned/yellowish): in faeces develop into egg containing MIRACIDIUM
-miracidium hatches under stimulus of light (3hr to find the snail by random)
-develops into 2nd laraval stage in snail: SPOROCYST
-asexual repro forms multiple REDIAE w/in sporocyst (ruptures to release rediae)
-2nd gen rediae formed within 1st gen: 3rd larval stage (CERCARIAE) formed w/in 2nd gen rediae
-cercariae emerge from snail (rainwater stimulus) & migrate to herbage
-encyst to form METACERCARIA (ingested)
-excystation in SI (induces by CO2 & bile): juvenile fluke emerges (to liver for 6-8wk before bile ducts)
-PPP = 10-12wk
fascioloa hepatica (life cycle simplified)
1. EGG
2. MIRACIDIUM (light stimulus to hatch)
3. to snail
4. SPOROCYST (asexual repro)
5. REDIAE (multiple release)
6. REDIAE (2nd gen w/in 1st)
7. CERCARIAE(emerge from snail w/ rainwater stimulus)
8. attach to herbage & encyst: form METACERCARIA (ingested)
9. to LIVER (6-8wk) before BILE DUCT (adult in 4wk)
10: PPP = 10-12wk
fasciolosis (acute)
-detected: autumn/early winter
-occurs: 2-6wk post ingestion of > 2k metacercariae
-caused by: migration of juvenile flukes
-results: liver damage & haemorrhage
-clinical signs: sudden death, weakness, pale mucus membranes, dyspnoea, palpable liver, ascites, abdominal pain
-liver PM: enlarged, rupture of subscapular haemorrhages, necrotic migration tracts, fibrinous exude (ventral lobe)
fasciolosis (subacute)
-detected: late autumn/winter
occurs: 6-10wk post ingestion of 500-1500 metacercaria
cause: juvenile migration & adult fluke in bile ducts
-adults: feed on blood & damage biliary mucosa (inflammation)
-results: liver damage/haemorrhage, cholangitis & anaemia
-signs: rapid/severe haemorrhagic anaemia w/ hypoalbuminaemia, pale mucus membranes, enlarged liver, +/- SM oedema/ascites
-liver PM: rupture of subcapsular haemorrhages is rare; similar to acute
-death w/in 1-2wk if not treated
fasciolosis (chronic)
-detected: late winter/early spring
-occurs: 4/5mo post ingestion of 200-500 metacercariae
-cause: adults feeding in bile ducts
-results: anaemia, hypoalbumenaemia, cholangitis
-signs: loss of condition, emaciation, pale mucus membranes, submandibular oedema (hypoalbumenaemia), ascites
-liver PM: irregular, pale, firm, smaller ventral lobe with fibrosis, scarring of tracts, thickened distended bile ducts
-subclinical: productivity losses (fewer multiple births, reduced weight growth in lambs)
fasciolosis (bovine)
-chronic: productivity loss (milk yield), calcification of bile ducts (extensive), gall bladder enlargement, liver fibrosis
-immune response: limits primary infection (<1yr), inhibits secondary infection
-no acute form
fasciolosis (epidemiology)
1. availability of snail habitat: muddy areas/slow moving shallow water, edges of ponds, banks of streams & ditches
2. moisture: rainfal makes motility easier
3. temperature: >10deg
4. season: snails breed May to October (increased metacercaria on pasture August to October - summer infection of snails)
NB: snails infected in autumn(cold) arrest development & resume in spring (metacercaria produced May to June - winter infection of snails)
fasciolosis (treatment)
-acute: triclabendazole (juveniles & adults) & move to clean pasture
-subacute: closantel, nitroxynil (not v. effective for juveniles)
-chronic: several
fasciolosis (control)
-drainage
-fence off saturated pasture
-move sheep to drier pasture
-anthelmintics: reduce fluke burden (October for acute & January for chronic), reduce pasture contamination (April/May)
-bought in: treat & put on clean pasture
fasciola gigantica
-larger
-tropical areas, SE Europe & SE USA
-IMH: lymnaea auricularia (aquatic snail - not amphibious)
fasciola gigantica (epidemiology)
-MIRACIDA: hatch at beginning of wet season, infect snails & develop by end of wet season
-CERCARIA: shed from snail at beginning & during dry season
-METACERCARIA: encyst on aquatic plants or water
-disease: end of dry/beginning of next wet season
dicrocoelium dendriticum
-Europe, UK, USA
-host: sheep, cattle, horses, rabbits
-site: bile ducts & gall bladder
-IMH: land snails/ants
-fluke
dicrocoelium dendriticum (life cycle)
-adults in bile ducts & gall bladder eggs to faeces (dark brown w/ MIRACIDIUM already developed when passed)
-snail ingests eggs w/ miracidium: released & forms SPOROCYST
-asexual repro through 2 rounds of sporocyst (no rediae stage): form CERCARIAE from 2nd gen
-cercariae released & form slime balls in respiratory chamber of snail
-slime balls extruded via respiratory pore & eaten by brown ant (2nd IMH)
-cercariae encyst to form METACERCARIAE in body of ant (in brain: induces ant to climb to top of grass and clamp on - enslaver parasite)
-final host eats ant: excystation in SI & juveniles directly up main bile duct (do not penetrate SI: less damage)
dicrocoelium dendriticum (pathogenesis)
-heavy infection in older sheep
-fibrosis & distention of bile ducts, progressive cirrhosis, weakness, anaemia, emaciation
-productivity losses: wool production, premature aging, repro
paramphistomum
-conical maggot shaped fluke of ruminants
-adults in rumen & reticulum (forestomach)
-tropics, southern USA
-P. cervi & P. microbothrium
-IMH: aquatic snails (lifecycle similar to F. gigantica)
paramphistomum (pathogenesis)
-due to: juvenile intestinal phase (excyst in duodenum & attach to wall to feed for 6wk)
-result: necrosis & haemorrhage: erosion of duodenal mucosa
-signs: acute gastroenteritis, marked oedema, haemorrhage, ulceration, profuse diahrrea, anaemia, hypoalbumaemia, intense thirst, anorexia
-adult not associated with disease (so FEC not relavent)
schistosoma
-cattle & sheep (tropics & S. Europe)
-IMH: aquatic snails
-S. bovis (cattle/sheep), S. japonicum (man), S. matthei (ruminants)
-male & female paired (female in groove of male)
schistosoma bovis (life cycle)
-pairs of adults in mesenteric veins: deposit eggs in walls of veins
-MIRICIDIUM develops in egg (6-7d) & produces enzymes that weaken vein: rupture
-crossed to gut & passed in faeces: eggs hatch almost immediately (release MIRACIDIUM to snail)
-2 rounds of asexual repro via SPOROCYSTS (no redial stage)
-CERCARIAE from 2nd gen sporocyst (forked tail): emerge from snail & sit on water (phototrophic & thermotrophic)
-cercariae infect final host (not metacercaria!) percutaneously or by ingestion: tails lost & young flukes (schistosomulae) travel to blood via small BVs & lymphatics
-circulate via heart & lungs to portal veins: copulate, become sexually mature adults & migrate to mesenteric veins
-PPP = 6-7wk
schistosoma (pathogeneis)
-inflammatory response to eggs in veins, mucosa & liver
-granuloma formation (intestinal mucosa & liver)
-acute: mucosal haemorrhage, anaemia, hypoalbumaemia, hepatosplenomegaly
signs: anaemia, diahrrea (mucous & blood tinged), thirst, anorexia, emaciation
-chronic (cattle): marked granuloma of intestine & cirrhosis/periportal fibrosis of liver, reduced productivity