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Parasitology #2 > GI Nematodes-cattle > Flashcards

GI Nematodes-cattle Flashcards

1
Q

Diagnosis of GI parasitic nematodes of ruminants

A

-relies on quantitative Fecal egg counts

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2
Q

Control of GI parasitic nematodes of ruminants

A

Regular use of broad spectrum antihelmintic
*but antihelmintic resistance is a main challenge

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3
Q

Parasitic gastroenteritis (PGE)

A

-generic term for disease caused by parasitic nematodes in the GI tract

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4
Q

Who does Parasitic gastroenteritis mainly effect?

A

Predominantly a disease of young stock, poorly fed animals, and animals with concurrent disease

*Adult animals can gradually develop acquired immunity

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5
Q

Trichostrongyles

A

Most important nematodes in grazing ruminants
-direct life cycle, infective L3, PPP 21 days,
-commonly occur as mixed infections

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6
Q

Economic burden of Cattle GI nematodes

A

-Very costly 2 billion/yr
-clinical disease presentation is usually small
-subclinical production loss is larger and more important

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7
Q

Burdens and clinical disease of GI nematodes in cattle

A

-increasing worm burdens further south, and towards the coasts

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8
Q

Egg types

A

-mostly Trychostrongyle type eggs
-Nematodirus spp eggs
-Trichuris spp eggs

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9
Q

Trichostrongyle Life cycle

A
  1. Eggs pass in feces
  2. Free living stages of 1st and 2nd stage larvae in manure
  3. (L3 develop in egg?) Infective 3rd stage larvae develop in about 1 week and remain infective for weeks to mths in manure or on vegetation. Larvae migrate following rainfall
  4. Cattle ingest infective 3rd stage larvae while grazing
  5. Immature worms migrate into mucosa
  6. Worms mature in digestive tract where adult worms lay eggs
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10
Q

Trichostrongyles in abomasum of cattle

A
  1. Ostertagia ostertagi
  2. Trichostrongylus axei
  3. Haemonchus placei
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11
Q

Ostertagia ostertagi

A

-most important parasitic nematode species in cattle in Canada and N. USA
-L4 may enter arrested development (hypobiosis) to survive harsh weather conditions

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12
Q

Ostertagia ostertagi appearance, gross and histology

A

-Appearance: ~1cm in length, red in colour
-Gross: Morocco Leather abomasum
-Histology: Dilated gastric gland with larvae

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13
Q

Ostertagiosis impact on gastric gland

A
  1. rupture of intercellular junctions
    2.leakage of plasma proteins = hypoproteinemia

1.Damage to parietal cells, leads to less HCl, and increased in abomasal pH.
2.Results in reduced pepsinogen to pepsin conversion and therefore reduced protein digestion

Overall:
-malabsorptive diarrhea, anorexia
-increased blood pepsinogen
-bacterial overgrowth (putrid smell)

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14
Q

Summer ostertagiosis

A

-grazing calves (usually 1st season)
-onset may be gradual
-larvae acquired on pasture that grazing season
-large number of adult worms, High fecal egg counts
-high morbidity, low mortality

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15
Q

Ostertagiosis syndromes

A

Type 1= summer ostertagiosis (July-Oct)

Type 2= Winter ostertagiosis (March-May)

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16
Q

summer ostertagiosis Pathogenesis

A

-bright green watery diarrhea
-weight loss
-anorexia

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17
Q

Winter ostertagiosis

A

-yearlings (can be off pasture)
-sudden onset
-larvae acquired in past grazing season
-inhibited larvae emerge at once, low fecal egg count because not adults yet
-low morbidity, high mortality

18
Q

Winter ostertagiosis pathogenesis

A

-depression
-weight loss
-anorexia
-hypoalbuminemia
-submandibular edema
-profuse, irresponsive diarrhea

19
Q

Diagnosis of Ostertagia ostertagi

A

Diagnose herd, not individual
-Fecal egg counts/post mortum
-Europe has commercial Ab ELISA for bulk milk tank
-Serum pepsinogen is in research/testing

20
Q

Haemonchus placei

A

-Barber pole worm
-Blood sucker= NO DIARRHEA
-L4 may enter hypobiosis
-Low abundance in Canada; more in warmer regions
-Fecal egg count can be low or very high

21
Q

Clinical signs of Haemonchus placei

A

-Hyperacute- sudden death due to haemorrhaguc anemia
-Acute- anemia, bottle jaw ascites, dark feces, anorexia
-Chronic- weight loss, weakness, anorexia

22
Q

Diagnosis of Haemonchus placei

A

L3 coproantigen, PCR or adults at necropsy

23
Q

Treatment of Haemonchus placei

A

-difficult because of multi drug resistance is emerging

24
Q

Cooperia spp

A

-small intestines
-common and sometimes dominant GI nematode
-adults 1cm long
-contributes to Parasitic gastroenteritis as part of mixed infection
-parasitic stages develop on surface of SI mucosa
-may seen inappetence and reduced weight gains

25
Q

Treatment of Cooperia spp

A

-increasing resistance in North America cattle, especially avermectans (macrocyclic lactones)

-dose limiting species for anthelmintics

26
Q

Cooperia punctata vs. cooperia oncophora

A

C. punctata: more pathogenic, increasing abundance in N. USA, central/eastern canada

C. oncophora: mild pathogen, temperatre areas, very common in Canada

27
Q

Nematodirus helvetianus

A

-small intestines
-development to L3 inside the egg
-eggs overwinter on pasture, hatch with rising temperature in Spring
-shedding rare in animals older than 6mths of age so pasture contamination predominantly from calves

-acute diarrhea in young calves in pasture
-clinical disease occasionally seen in Canada

28
Q

Bunostonum spp

A

-small intestine
-hookworm (ancylostomatidae): Blood feeders
-ingestion of L3 or skin penetration by L3
-rare in Canada, more in warmer and wetter regions

29
Q

Strongyloides papillosus

A

-small intestine
-only adult females are parasitic
-warm and wet regions of World; not in W. Canada
-unlike other GIN, transmit well off pasture
-larvated Eggs, relatively small
-ingestion of L3 or skin penetration

30
Q

Strongyloides papillosus life cycle

A

PPP:10days
1. adult females in cattle
2. Larvated eggs released in feces
3. Develop into L3 filariform larvae
4. Homogonic cycle: L3 larvae are ingested by cattle or undergo skin penetration
Heterogonic Cycle: L3 become free-living adults and can produce more larvated eggs

31
Q

Oesophagostomum spp

A

-nodular bowel worm
-large intestines
-life cycle similar to trichostrongyles, except pre-adult larvae create nodules in large intestinal mucosa
-limited pathogenicity

32
Q

Trichuris spp

A

-whipworm
-small intestines
-host specific, T. globulosa in cattle
-transmits well off pasture due to thick egg
-mild pathogen; commonly seen during fecal egg counts in Canadian Cattle as incidental finding

33
Q

Pasture contamination of GI nematodes in cattle

A

Infection is through ingestion stages from Pasture (build up of L3 larvae)
-springtime pasture contamination due to overwintered eggs or larvae, and reactivation of hypobiotic larvae

34
Q

Peak pasture contamination

A

Occurs during 2nd half of grazing season

35
Q

Diagnosis of GI nematodes

A
  1. History: age, season, management (pasture, cow/calf, dairy)
  2. Clinical signs: anorexia, anemia, diarrhea, weight loss, or nothing obvious but production loss
  3. Fecal eggs counts-separated by flotation in saturated salt solution
    *not very sensitive
    *usually pooled from 20-25 individual cattle
  4. Coproculture and morphology, and molecular approaches
36
Q

Nemabiome

A

-universal primer targeting a conserved region in most species
-compare sequence generated to a reference database

37
Q

GI nematodes in Western Canada

A

-dry climate, cold winter, short grazing season
-Some L3s survive in pasture, some overwinter as hypobiotic L4
-mostly affects grazing cattle but burdens vary

38
Q

Beef vs. Dairy cattle in Western Canada

A

Beef: subclinical production loss, magnitude will depend on climate/stocking density/production systems

Dairy: milking herds zero grazed so not a major problem

39
Q

Management of GI nematodes

A

-quarantine and treat prior to introduction of new stock
-good husbandry: nutrition and concurrent disease
-pasture management

40
Q

Anthelmintics for GI nematodes in cattle

A

-increasing resistance
-long acting anthelmintics, rumen boluses, residual effects
-limited drugs: macrocyclic lactones and benzimidazoles

41
Q

Strategic treatments

A

-cows in spring reduce pasture contamination
-young animals in first grazing season 6-8wks later
-fall housing treatment to cows and calves for arrested larvae
-Targeted selective treatment

Parasitology #2 (12 decks)

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