Parasitology 4: Nematodes 3 Flashcards
PGE in ruminants is produced by what?
All GIN together, except haemnonchus
What is the MOST pathogenic stage in Ostertagia is?
L4
The stimulus that has major influence on the proportion of strongylid worms that become hypobiotic is?
Weather conditions
and
Host immunity
Strogyloidea (strongyles) key characteristics are?
size up to 15cm
mostly in GI tract
large buccal capsule
plug feeder
What species does Strogyloidea (strongyles) affect?
HORSES
What is the small and LARGE Strogyloidea (strongyles)?
subfamilys
small= 2cm
Cyathostominae
-cyathostominosis
-cyathostomosis
LARGE= 5cm
Strongylinae
-strongylinosis
Where do Stongyloidea (strongyles) affect?
Adults in cecum and colon
Strongyles disease name is?
Strongylosis
small stongyles some facts?
species amount?
eggs?
group name?
about 50 species
cannot tells eggs or immature stages apart
this group is known as Cyathostomins
Cyathostomins following infection, larvae go to LI and?
Enter crypts of Lieberkuhh, penetrates mucosa for period of larval development
return to lumen to mature
minimum prepatent period 2-3 months
larvae in wall may become hypobiotic
dynamic relationship-as adults lost from lumen, new larvae move in–maintain population of adults
seasonal effects on arrest also seen
Where do larvae go to mature for Cyathostomins?
Lumen
What is the prepatent period for Cyathostomins last?
2-3 months
The damage occurs to horses by Cyathostomins when and how?
The larvae when they are penetrating the
intestinal wall
Cyathostomins
pathogenesis?
species prevalence
Not highly pathogenic parasites
low to moderate #s in healthy horse
Clinical importance of Cyathostomins?
MOST pathogenic stage LARVAE, emerging from intestinal wall cause inflammation
Cyathostomins
Type 1: chronic Cyathostominosis
Gradual inflammation and thickening of gut wall
possible protein losing enteropathy
clinical signs:
intermittent diarrhea
mild to moderate colic
poor condition
hyporproteinmia
Type 2: acute larval Cyathostominosis
Rapid onset
occurs when large number of arrested larvae synch emerge
fever
diarrhea- dehydration
edema, hypoproteinemia
drug treatment of horses with high worm burden
seasonal:late wint or early spring
Cyathostomins diagnosis
Chronic Cyathostominosis
-large number of strongyle eggs in feces is supportive
Actue Cyathostominosis
-may not be many eggs in manure
Typical strongylid nematodes, most normal adults can control worm population immunity
Immunity
<3-4 years most susceptible (adult horse age)
Large strongyles Stongylus vulgaris Life cycle is?
adults in LI: 3-5cm
complex larval migration
-following infection, molt, L4 migrates through arteries
reaches jt of cranial mesenteric artery and aorta
return to LI about 4 months after infection
occasionally larvae migrate to other locations
Prepatent period: 6 months
Stongylus vulgaris Pathogenesis
causes verminous arteries/aneurysm
larvae damage arterial vessels leading to thrombus formation
thrombus can reduce blood flow
Portion of thrombus may break off, block blood flow distally, ischemia
severe cases necrosis of portions of bowel occur
Lesion regresses after worm leave or treatment
Clinical signs of Stongylus vulgaris?
Colic: thromboembolic colic
abd pain
death
diagnosis difficult
*Larvividal drugs aid in not seeing this disease
Anylostomatoidea (hookworms) main concept?
Causes ANEMIA
Anylostomatoidea (hookworms) canine
Ancylostoma canium- most important in this region
Ancylostoma braziliense- south costal US and South america
Uncinaria stenocephala -cold climate hookworm
Ancylostoma canium life cycle?
External: same development from egg to L3
Best moist, shaded, slightly sandy soil
Dogs infected from environment by:
-ingestion of L3
-skin penetration by L3: MORE important
–migrate to heart/lungs and then either coughed up, swallowed and develop in SI
–OR travel to tissues and become dormant ( called somatic reservoir larvae)
Larvae motion in heart and lungs ?
They start in heart then lung:
-They either go up to trachea to be swallowed to SI (prepatent 3-4 weeks)
-They can go to tissue to become dormant (larval leak 3-4 weeks)
–become active in PREGNANCY OF HOST and go migrate to mammary gland to infect offspring (they stay in L3) (prepatent period in puppies 2 weeks)
Ancylostoma canium Life cycle?
Single infection of female dog can result in infection of more than once little
after treatment of adult population, arrested larvae can move into the intestine and replace adults larval leakage
Egg laying worms in the intestine can come from:
- skin penetration
- transmammary infection
- ingestion of L3
- Paratenic hosts
Ancylostoma canium pathogenesis?
Low worm numbers asymptomic
**young animals very susceptible; also heavy exposure or immunocompromised
-switch sucking sites at a few hours interval
-diarrhea, melena
-anemia, hypoproteinemia
-skin lesions
Immunity
-like large animal strongylids
develops following exposure
Ancylostoma canium Diagnosis?
Fecal exam
-only common strongylid eggs: we can call them hookwork eggs
-Prpatents periods
prevalence
-33%
southeast 53%
lower in dogs recieving monthly products
FEline hookworms
Lower prevalence than dog hookworms
Not as pathogenic as dog hookworms
little is an mammary transmission
Ancylostoma Braziliense
Dogs and cats in costal southern US, CARRIBEAN, Latin America
NOT very pathogenic hookworm in definitive host
VIGOROUS skin penetrators
(called CUTANEOUS LARVA MIGRANS)
MESTRONGYLOIDEA
NOT direct lifecycle
invertabrae-NOT GIT
Long,slender adults in lungs and other tissue sites
usually intermediate host
-invertebrate
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