Cattle & Sheep GI Worms Flashcards
Cattle GI nematodes in north america?
- increasing worm burdens & clinical disease as you go south
- increasing worm burdens as you move towards coasts
Cattle GI nematodes in north america?
GI nematodes affect production of grazing animals but clinical disease is rare
What is the basic trichostrongyle lifecycle?
What is Ostertagiosis type 1?
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
What is Ostertagiosis type 2?
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
How do we diagnose ostertagiosis?
- on herd, not individually
- FEC/ post-mortem
- serum pepsinogen (research)
- in Europe: commercial Ab ELISA for bulk milk tank
What is the life cycle of Strongyloides papillosus?
- unlike most GIN, transmit well off pasture
- larvated eggs, relatively small
- ingestion of L3 or SKIN PENETRATION
What is unique about the lifecycle of Osteragia ostertagi?
- L4 MAY ENTER ARRESTED DEVELOPMENT (hypobiosis) to survive harsh weather conditions
What is unique about the lifecycle of Haemonchus placei?
- L4 MAY ENTER HYPOBIOSIS
What is unique about the lifecycle of Cooperia spp.?
- parasitic stages develop on surface of SI mucosa
What is unique about the lifecycle of Nematodirus spp.?
- 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)
What is unique about the lifecycle of Bunostomum spp.?
- ingestion of L3 or SKIN PENETRATION of L3
What is unique about the lifecycle of Oesophagostomum spp.?
- life cycle similar to trichostrongyles, except pre-adult larvae create nodules in large intestinal mucosa
What is unique about the lifecycle of Trichuris spp.?
- direct life cycle, larvated eggs infectious, PPP 4-6 wks
- transmits well off pasture (thick wall)
Basic epidemiology of GIN in cattle?
- 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
What is the overall prevalence of GI nematodes of Cattle in Western Canada?
- 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
How does ostertagiosis work in the gastric glands?
How do we diagnose GIN of Ruminants?
- 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)
How do we manage GI nematodes of cattle?
- quarantine & treat prior to introduction of new stock
- good husbandry: nutrition & concurrent disease
- pasture management
- anthelmintics
- strategic treatments
How are anthelmintics used for GI nematodes of cattle?
- 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
How are strategic treatments used for GI nematodes of cattle?
- 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)
Who are the GI nematodes of cattle?
What symptoms do GI nematodes cause in Sheep?
- bottle jaw, death, reduced production, anemia, weight loss, diarrhea
What is parasitic gastroenteritis in sheep & who causes it?
reduced weight gain & D+
- Teladorsagia spp., Cooperia spp., Trichostrongylus spp., & Nematodirus spp.
Who are the GI nematodes of sheep?
What is haemonchosis in sheep & who causes it?
Acute anemia, edema, lethargy, & death
- Haemonchus contortus (“Barber’s Pole worm”)
What is important about the various species of GI nematode infections in sheep?
- 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.
What is anthelminthic resistance?
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
What is important about GI nematodes of sheep?
- 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
How do we control GI nematodes in sheep?
- 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)
How do we control GI nematodes in sheep with chemicals?
- 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)
How does anthelmintic resistance develop?
- established when a population of worms is subjected to a treatment pressure, selecting for the individuals w/ resistant genotypes over time
What are refugia?
- 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)
What are the factors that determine the rate of anthelmintic resistance development?
- underdosing
- length of time used
- frequency of treatment
- pasture management (open/closed flocks)
- size of in-refugia population
How do refugia vary?
- 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
What action causes a strong selection for resistance?
treating animals & then moving to a clean pasture
How do we diagnose AHR?
- 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
What is the fecal egg count reduction test?
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)
What are current recommendations & strategies to reduce AHR?
- 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)
How can you use FEC to approach targeted selective treatment?
- can used absolute fecal egg counts ex: treat all animals w/ FEC above threshold (ex: 200 EPG)
- can also treat top proportions of shedders
