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DWT Exam 2 > Parasitology 4: Nematodes 3 > Flashcards

Parasitology 4: Nematodes 3 Flashcards

1
Q

PGE in ruminants is produced by what?

A

All GIN together, except haemnonchus

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2
Q

What is the MOST pathogenic stage in Ostertagia is?

A

L4

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3
Q

The stimulus that has major influence on the proportion of strongylid worms that become hypobiotic is?

A

Weather conditions
and
Host immunity

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4
Q

Strogyloidea (strongyles) key characteristics are?

A

size up to 15cm
mostly in GI tract
large buccal capsule
plug feeder

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5
Q

What species does Strogyloidea (strongyles) affect?

A

HORSES

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6
Q

What is the small and LARGE Strogyloidea (strongyles)?

A

subfamilys

small= 2cm
Cyathostominae
-cyathostominosis
-cyathostomosis

LARGE= 5cm
Strongylinae
-strongylinosis

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7
Q

Where do Stongyloidea (strongyles) affect?

A

Adults in cecum and colon

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8
Q

Strongyles disease name is?

A

Strongylosis

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9
Q

small stongyles some facts?
species amount?
eggs?
group name?

A

about 50 species

cannot tells eggs or immature stages apart

this group is known as Cyathostomins

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10
Q

Cyathostomins following infection, larvae go to LI and?

A

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

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11
Q

Where do larvae go to mature for Cyathostomins?

A

Lumen

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12
Q

What is the prepatent period for Cyathostomins last?

A

2-3 months

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13
Q

The damage occurs to horses by Cyathostomins when and how?

A

The larvae when they are penetrating the
intestinal wall

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14
Q

Cyathostomins
pathogenesis?
species prevalence

A

Not highly pathogenic parasites

low to moderate #s in healthy horse

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15
Q

Clinical importance of Cyathostomins?

A

MOST pathogenic stage LARVAE, emerging from intestinal wall cause inflammation

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16
Q

Cyathostomins

Type 1: chronic Cyathostominosis

A

Gradual inflammation and thickening of gut wall
possible protein losing enteropathy

clinical signs:
intermittent diarrhea
mild to moderate colic
poor condition
hyporproteinmia

17
Q

Type 2: acute larval Cyathostominosis

A

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

18
Q

Cyathostomins diagnosis

A

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)

19
Q

Large strongyles Stongylus vulgaris Life cycle is?

A

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

20
Q

Stongylus vulgaris Pathogenesis

A

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

21
Q

Clinical signs of Stongylus vulgaris?

A

Colic: thromboembolic colic

abd pain

death
diagnosis difficult

*Larvividal drugs aid in not seeing this disease

22
Q

Anylostomatoidea (hookworms) main concept?

A

Causes ANEMIA

23
Q

Anylostomatoidea (hookworms) canine

A

Ancylostoma canium- most important in this region

Ancylostoma braziliense- south costal US and South america

Uncinaria stenocephala -cold climate hookworm

24
Q

Ancylostoma canium life cycle?

A

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)

25
Q

Larvae motion in heart and lungs ?

A

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)

26
Q

Ancylostoma canium Life cycle?

A

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

27
Q

Ancylostoma canium pathogenesis?

A

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

28
Q

Ancylostoma canium Diagnosis?

A

Fecal exam
-only common strongylid eggs: we can call them hookwork eggs
-Prpatents periods

prevalence
-33%
southeast 53%
lower in dogs recieving monthly products

29
Q

FEline hookworms

A

Lower prevalence than dog hookworms

Not as pathogenic as dog hookworms

little is an mammary transmission

30
Q

Ancylostoma Braziliense

A

Dogs and cats in costal southern US, CARRIBEAN, Latin America

NOT very pathogenic hookworm in definitive host

VIGOROUS skin penetrators
(called CUTANEOUS LARVA MIGRANS)

31
Q

MESTRONGYLOIDEA

A

NOT direct lifecycle

invertabrae-NOT GIT

Long,slender adults in lungs and other tissue sites
usually intermediate host
-invertebrate
add**

DWT Exam 2 (21 decks)

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