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Parasitology II > Cattle & Sheep GI Worms > Flashcards

Cattle & Sheep GI Worms Flashcards

1
Q

Cattle GI nematodes in north america?

A
  • increasing worm burdens & clinical disease as you go south
  • increasing worm burdens as you move towards coasts
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2
Q

Cattle GI nematodes in north america?

A

GI nematodes affect production of grazing animals but clinical disease is rare

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3
Q

What is the basic trichostrongyle lifecycle?

A
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4
Q

What is Ostertagiosis type 1?

A

Summer ostertagiosis (July-Oct)
- grazing calves (usually 1st season)
- ONSET MAY BE GRADUAL
- larvae acquired on pasture that grazing season
large numbers of adult worms (10-50k), HIGH FEC
- bright green watery D+
- high morbidity, low mortality (if treated)
- weight loss, anorexia

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5
Q

What is Ostertagiosis type 2?

A

Winter ostertagiosis (March-May)
- yearlings (can be off pasture)
- SUDDEN ONSET
- larvae acquired in past grazing season
- inhibited larvae emerge at once, LOW FEC
- depression, weight loss, anorexia
- hypoalbuminemia, submandibular edema
- low morbidity, high mortality

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6
Q

How do we diagnose ostertagiosis?

A
  • on herd, not individually
  • FEC/ post-mortem
  • serum pepsinogen (research)
  • in Europe: commercial Ab ELISA for bulk milk tank
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7
Q

What is the life cycle of Strongyloides papillosus?

A
  • unlike most GIN, transmit well off pasture
  • larvated eggs, relatively small
  • ingestion of L3 or SKIN PENETRATION
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8
Q

What is unique about the lifecycle of Osteragia ostertagi?

A
  • L4 MAY ENTER ARRESTED DEVELOPMENT (hypobiosis) to survive harsh weather conditions
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9
Q

What is unique about the lifecycle of Haemonchus placei?

A
  • L4 MAY ENTER HYPOBIOSIS
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10
Q

What is unique about the lifecycle of Cooperia spp.?

A
  • parasitic stages develop on surface of SI mucosa
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11
Q

What is unique about the lifecycle of Nematodirus spp.?

A
  • DEVELOPMENT TO L3 INSIDE THE EGG
  • EGGS OVERWINTER ON PASTURE, hatch when temp rises in spring
  • SHEDDING RARE IN ANIMALS > 6 MONTHS OF AGE (IMMUNITY)
  • pasture contamination predominantly from calves (adult cattle are not important to epidemiology)
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12
Q

What is unique about the lifecycle of Bunostomum spp.?

A
  • ingestion of L3 or SKIN PENETRATION of L3
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13
Q

What is unique about the lifecycle of Oesophagostomum spp.?

A
  • life cycle similar to trichostrongyles, except pre-adult larvae create nodules in large intestinal mucosa
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14
Q

What is unique about the lifecycle of Trichuris spp.?

A
  • direct life cycle, larvated eggs infectious, PPP 4-6 wks
  • transmits well off pasture (thick wall)
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15
Q

Basic epidemiology of GIN in cattle?

A
  • infection through ingestion of infective stages from PASTURE (build up of large amounts of L3 on pasture)
  • possible sources of springtime pasture contamination (overwintered eggs or larvae (esp. Nematodirus) on pasture; reactivation of hypobiotic larvae)
  • peak pasture contamination: 2nd half of grazing season
  • outcome of infection largely depends on immune status
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16
Q

What is the overall prevalence of GI nematodes of Cattle in Western Canada?

A
  • dry climate, cold winter, short grazing season
  • some L3s survive in the pasture, some overwinter as hypobiotic L4
  • most grazing cattle infected, burdens vary
  • BEEF CATTLE: subclinical production loss can be important, magnitude will depend on climate/stocking density/ production systems
  • DAIRY CATTLE: milking herds zero grazed, so not a major problem
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17
Q

How does ostertagiosis work in the gastric glands?

A
18
Q
A
19
Q

How do we diagnose GIN of Ruminants?

A
  • history: age, season, management (pasture, cow/calf, dairy)
  • clinical signs: anorexia, anemia, diarrhea, weight loss, or nothing obvious - production losses
  • FEC: eggs separated from fecal debris by floatation in saturated salt solution, trichostrongylid eggs are usually undistinguishable, NOT USUALLY V SENSITIVE MEASURE OF PARASITE BURDEN IN CATTLE, often pooled from 20-25 individual cattle or sheep
  • coproculture & morphology
  • molecular approaches (Nemabiome)
20
Q

How do we manage GI nematodes of cattle?

A
  • quarantine & treat prior to introduction of new stock
  • good husbandry: nutrition & concurrent disease
  • pasture management
  • anthelmintics
  • strategic treatments
21
Q

How are anthelmintics used for GI nematodes of cattle?

A
  • increasing problems w/ resistance
  • long acting anthelmintics, rumen boluses, residual effects (ML)
  • parasite control is usually not evidence based (pour on ML routinely given for ectoparasites & now how low effectivity due to resistance)
  • limited drugs available: ML (ivermectin) & Benzimidazoles
22
Q

How are strategic treatments used for GI nematodes of cattle?

A
  • depends on use & management
  • treat cows in spring to reduce pasture contamination
  • treat young animals in first grazing season 6-8 wks later
  • fall (housing) treatment to cows & calves for arrested larvae
  • TARGETED SELECTIVE TREATMENT (TST)
23
Q

Who are the GI nematodes of cattle?

A
24
Q

What symptoms do GI nematodes cause in Sheep?

A
  • bottle jaw, death, reduced production, anemia, weight loss, diarrhea
25
Q

What is parasitic gastroenteritis in sheep & who causes it?

A

reduced weight gain & D+
- Teladorsagia spp., Cooperia spp., Trichostrongylus spp., & Nematodirus spp.

26
Q

Who are the GI nematodes of sheep?

A
27
Q

What is haemonchosis in sheep & who causes it?

A

Acute anemia, edema, lethargy, & death
- Haemonchus contortus (“Barber’s Pole worm”)

28
Q

What is important about the various species of GI nematode infections in sheep?

A
  • OCCUR IN MIXED INFECTIONS - PGE
  • distinguishable features in L3s (corproculture) or adults (necropsy), to sp or genera
  • PATHOGENICITY varies w/ sp
  • EGG PRODUCTION varies w/ sp, environmental conditions, interactions btwn spp, etc.
29
Q

What is anthelminthic resistance?

A

heritable trait, present when w/in a population more individuals are able to tolerate doses of a drug that, in a normal population of the same sp, would be harmful

30
Q

What is important about GI nematodes of sheep?

A
  • same broad principles apply as w/ cattle
  • clinical disease is more common & widespread (worse in goats)
  • anthelmintic resistance is a HUGE GLOBAL PROBLEM
  • multiple nematode spp are involved, some are more pathogenic than others
31
Q

How do we control GI nematodes in sheep?

A
  • maximize overall heath, good nutrition & pasture management
  • breed resistant hosts
  • chemical treatments: limited availability of drugs
  • strategic treatments - monitor egg counts, identify sp whereever possible, no “one-fits-all”
  • targeted selective treatments to slow development of drug resistance
  • vaccination: barbevaxx (targeting intestinal antigens)
32
Q

How do we control GI nematodes in sheep with chemicals?

A
  • Benzimidazoles (off label use)
  • ML (Ivermectin is licensed in Canada)
  • Imidazothiazoles/ Tetrahydroxypyrimidines
  • salicylanilides (Closantel - licensed in Canada, targeted activity, used to be called Flukiver for flukes, now only for Haemonchus)
33
Q

How does anthelmintic resistance develop?

A
  • established when a population of worms is subjected to a treatment pressure, selecting for the individuals w/ resistant genotypes over time
34
Q

What are refugia?

A
  • susceptible subset of the population present on pasture, not expose d to the anthelmintic treatment, that will subsequently re-infect the flock
  • if the population of refugia is composed of susceptible worms, this will dilute the concentration of resistant worms on pasture after treatment
  • the larger the refugia population, the less selection pressure (resistants breed with susceptible & dilute resistant population)
35
Q

What are the factors that determine the rate of anthelmintic resistance development?

A
  1. underdosing
  2. length of time used
  3. frequency of treatment
  4. pasture management (open/closed flocks)
  5. size of in-refugia population
36
Q

How do refugia vary?

A
  • in temperate climates, most parasites are in refugia due to high survival on pasture (even so, overtime resistance will develop)
  • when there are few parasites in refugia (v clean pastures, v dry climates), resistance develops rapidly
  • treatments during spring in Canada are not recommended b/c low refugia (most are inside hosts) -> high selection pressure
37
Q

What action causes a strong selection for resistance?

A

treating animals & then moving to a clean pasture

38
Q

How do we diagnose AHR?

A
  • usually suspected when there is poor response to anthelmintic treatment
  • In-vitro tests - low specificity, time consuming
  • molecular markers of resistance - early stages
  • FEC reduction test (FECRT) is widely used to detect AHR
39
Q

What is the fecal egg count reduction test?

A

test, treat, re-test in 14 days
> % efficacy = [(pretreatment FEC - posttreatment FEC) x 100]/Pretreatment FEC
> drug resistance when FECRT is less than 95%
- ideally egg counts are done individually for at least 10-20 animals in a herd (can average pre & post treatment numbers)

40
Q

What are current recommendations & strategies to reduce AHR?

A
  • quarantine & anthelmintic treatment of purchased livestock
  • good nutrition & management (do not mix sheep & goats - share same parasites)
  • make informed choices on drug use
  • monitor resistance status (regular FECRT)
  • minimize & strategize anthelmintic use
  • targeted selective treatment (TST) - goal is to leave refugia, treat only those w/ high FEC, poor body condition, high FAMACHA scores (anemic)
41
Q

How can you use FEC to approach targeted selective treatment?

A
  • can used absolute fecal egg counts ex: treat all animals w/ FEC above threshold (ex: 200 EPG)
  • can also treat top proportions of shedders

Parasitology II (9 decks)

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