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PARASITOLOGY - 2 > 5 – Cattle GIN > Flashcards

5 – Cattle GIN Flashcards

1
Q

What is the disease caused by GIN?

A
  • Parasitic gastroenteritis
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2
Q

GIN are very common in ruminants

A
  • Clinical disease mostly in young animals
    o ‘only the tip of the iceberg’
  • Sub-clinical diseases cause major production loss
  • Diagnosis relies on quantitative fecal egg counts
  • Control has relied on regular use of broad spectrum anthelmintic
    o *resistance is a MAIN CHALLENGE
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3
Q

Subclinical production loss

A
  • Reduced appetite and grazing/feed intake
  • Increased loss of protein into gut!
  • *more than $2billion a year!
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4
Q

Parasitic gastroenteritis (PGE)

A
  • Predominantly a disease of young stock, poorly fed animals, animals with concurrent disease
    o Adult animals gradually develop acquired immunity
  • IF clinical effects: diarrhea and failure to thrive
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5
Q

What is the most important nematodes in grazing ruminants?

A
  • Trichostrongyles
    o Direct lifecycle
    o Infective L3
    o PPP 21 days
    o Commonly occurs in MIXED infections
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6
Q

Cattle GI nematodes prevalence and distribution in NA and Canada

A
  • As go south: increase worm burdens and clinical disease
  • As go toward coasts: increase worm burdens
  • *Canada: affect production of grazing animals, but clinical disease is RARE
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7
Q

What is basic Trichostrongyle life cycle?

A
  • Worms mature in digestive tract where adults lay eggs
  • Eggs passed in feces
  • Free living stage (L1 and L2)
  • Infective L3 develop in 1 week
    o Remain infective for weeks to months
  • *larvae migrate following rainfall
  • Cattle ingestion infective L3 while grazing
  • Immature worms migrate into mucosa
    o L4 to immature to adult
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8
Q

What are the parasites of the bovine abomasum?

A
  • Ostertagia ostertagi
  • Haemonchus placei
  • Trichostrongyuls axei
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9
Q

Ostertagia ostertagi

A
  • MOST important nematode species in cattle in Canada and northern US
  • L4 may enter arrested development to survive harsh weather conditions
  • *’morocco leather’
  • *Ostertagiosis
  • 1cm in length, reddish in colour
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10
Q

What happens to an infective gastric gland with Ostertagia ostertagi?

A
  • parasites cause damage to parietal cells=not production of HCl
    o pepsinogen does NOT become pepsin
  • rupture of intercellular junctions leading to leakage of plasma proteins=HYPOPROTEINEMIA
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11
Q

What contributes to increase of abomasal pH with Ostertagia ostertagi?

A
  • Reduced pepsinogen to pepsin conversion
  • Reduced protein digestion
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12
Q

What does increase of adomasal pH contribute to with Ostertagia ostertagi?

A
  • Bacterial overgrowth (putrid smell)
  • Increase blood pepsinogen
  • Malabsorptive diarrhea, anorexia
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13
Q

How do you diagnosis Ostertagia ostertagi?

A
  • Serum pepsinogen
  • Antibodies in bulk milk
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14
Q

What are the 2 types of Ostertagiosis syndromes?

A
  1. Type I: summer ostertagiosis (July-October)
  2. Type 2: witner ostertagiosis (March-May)
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15
Q

Type I: summer ostertagiosis (July-October)

A
  • Grazing calves: usually 1st season
  • *onset may be GRADUAL
  • Larvae acquired on pasture
  • Large number of adult worms, HIGH FEC
  • Bright green watery diarrhea
  • High morbidity, low mortality
  • Weight low, anorexia
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16
Q

Type 2: winter ostertagiosis (March-May)

A
  • Yearlings (can be off pasture)
  • SUDDEN ONSET
  • Larvae acquired in past grazing season (hypobiotic larvae)
  • Inhibited larvae emerge at once, LOW FEC
  • Depression, weight loss, anorexia
  • Hypoalbuminemia, submandibular edema
  • Low morbidity, high mortality
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17
Q

How do you diagnose ostertagiosis?

A
  • On herd, NOT individually
  • FEC/post-mortem (Trichostrongyle type eggs)
  • Serum pepsinogen (research)
  • In Europe: commercial Ab ELISA for bulk milk tank
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18
Q

Haemonchus placei

A
  • Barber pole worm
  • BLOOD SUCKER
  • L4 may enter hypobiosis
  • Low abundance in Canada (more important in warmer regions)
  • *NO DIARRHEA
  • *FFC can be low (PPP) or very high!
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19
Q

What are the clinical signs of Haemonchus placei, hyperacute?

A
  • Sudden death due to HAEMORRHAGIC ANEMIA
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20
Q

What are the clinical signs of Haemonchus placei acute?

A
  • Anemia
  • Bottle jaw
  • Ascites
  • Dark feces
  • Anorexia
21
Q

What are the clinical signs of Haemonchus placei, chronic?

A
  • Weight loss
  • Weakness
  • Anorexia
22
Q

How do you diagnose Haemonchus placei?

A
  • L3 coproculture
  • PCR
    adults at necropsy
23
Q

How do you treat Haemonchus placei?

A
  • Increasingly difficult
    o Multi-drug resistance H. controtus, emerging in H. placei
24
Q

Can Haemonchus spp. and Trichostrongylus axei infect co-grazed sheep or horses?

A
  • H. placei: NOT transmissible to horses or sheep
    o Own H. contortus=pathogenic in sheep
  • T. axei: transmibble to BOTH sheep and horses
25
Q

What are the parasites of the bovine small intestine?

A
  • Cooperia spp.
  • Nematodirus spp.
  • Trichstrongylus spp.
  • Bunostomum spp.
  • Strongyloides papillosus
26
Q

Cooperia spp.

A
  • Common and sometimes dominant GIT in cattle
  • Adults 1 cm long
  • Contributes to PGE as part of MIXED INFECTION
  • Parasitic stages develop on SURFACE of SI mucosa
  • Inappetence and reduced weight gain
  • *increasing AHR in NA
  • *dose-limiting species for anthelmintics
27
Q

Cooperia punctata

A
  • More pathogenic
  • Increasing abundance in Northern USA, Central/Eastern Canada
28
Q

Cooperia oncophora

A
  • Mild pathogen
  • Temperate areas
  • VERY COMMON in Canada
29
Q

Nematodirus helvetianus

A
  • Development of L3 inside the egg
  • Eggs overwinter on pasture
    o Hatch with temperature rising in spring
  • *shedding rare in animals >6 months of age (IMMUNITY)
  • Pasture contamination predominantly from calves
  • *acute diarrhea in YOUNG CALVES on pasture
  • Clinical disease occasionally seen in Canada
30
Q

What is the PPP of Cooperia and Nematodirus spp.?

A
  • 3 weeks
31
Q

Where does translation occur for Cooperia and Nematodirus spp?

A
  • Cooperia: L1 hatches out of egg and undergoes translation to L3 free on pasture
  • Nematodirus: L1-L3 develops within the egg
  • *Nematodirus eggs survive better on pasture overwinter (large=provide nutrients and shelter)
32
Q

Bunostomum spp.

A
  • Hookworm: BLOOD FEEDERS
  • Ingestion of L3 OR SKIN PENETRATION by L3
  • Rare in Canada!
    o More in warmer and wetter regions
33
Q

Bunostomum spp. eggs

A
  • Typical Trichostrongyle type egg despite NOT being Trichostrongyle nematode
34
Q

Stongyloides papillosus

A
  • Only ADULT females are parasitic
  • Warm and wet regions of world
  • NOT seen in W. Canada
  • Unlike most GIN, transmit well off pasture
  • *larvated eggs: relatively small
  • Ingestion of L3 OR SKIN PENETRATION
35
Q

What is the life cycle of Strongyloides papillosus?

A
  • Adult females in small intesting
  • Larvated eggs in fecesor L3 in colostrum (trans mammary)
    o L1 to L2 to L3
     Free living adult (heterogonic cycle), ingested or ‘lays eggs’
     Skin penetration (homogonic cycle)
36
Q

Strongyloides papillosus eggs

A
  • Larvated eggs in: cattle, sheep, horse and pigs
  • (dogs: shed larvae directly)
37
Q

What are the parasites of the bovine large intestine?

A
  • Oesophagostomum spp.
  • Trichuris spp.
38
Q

Oesophagostomum spp.

A
  • Nodular bowel worm
  • Life cycle similar to Trichostronglyes
    o Except pre-adult larvae create NODULES in large intestinal mucosa
  • *limited pathogenicity
  • Nodules in LI associated with larvae
39
Q

Trichuris spp.

A
  • Whip worm
  • Host-specificity
    o T. globulosa=cattle
  • Direct life cycle
    o Larvagted eggs infectious
    o PPP 4-6 weeks
  • Transmits well off pasture (thick wall)
  • Very mild pathogen
  • Commonly seen during fecal egg counts in Canadian cattle: incidental finding
40
Q

What is the basic epidemiology of GIN in cattle?

A
  • Infection thru ingestion of infective stages from PASTURE
    o Build up large amounts of L3 on pasture
  • Possible sources of springtime pasture contamination
    o Overwintered eggs or larva spp. on pasture
    o Reactivation of hypobiotic larvae
  • *peak pasture contamination: 2nd half of grazing season
  • *outcome of infection largely depends on IMMUNE STATUS
41
Q

What is the diagnosis of GIN in ruminants based on?

A
  • History: age, season, management
  • Clinical signs: anorexia, anemia, diarrhea, weight loss or nothing obvious
    o *production losses
  • *FEC, coproculture+morphology, molecular approaches (Nemabiome)
42
Q

Fecal egg counts (FEC) for diagnosis of GIN in ruminants

A
  • Eggs separated from fecal debris by floatation in SATURATED SALT SOLUTION
  • Trichostrongylid eggs are usually undistinguisable
  • NOT usually very sensitive measure of PARASITE BURDEN in cattle
  • Often pooled from 20-25 individual cattle or sheep
43
Q

What is Nemabiome?

A
  • Universal primer targeting a conserved region in most species
  • DNA sequencing using barcods
  • *compare sequences generated to a reference database
44
Q

What about western Canada and GIT nematodes?

A
  • Dry climate, cold winter, short grazing season
  • Some L3s survive in pasture, some overwinter as hypobiotic L4
  • Most grazing cattle infected, burden vary
45
Q

Western Canada beef cattle and GIT nematodes

A
  • Subclinical production loss can be important
    o Magnitudes will depend on climate/stocking density/production systems
46
Q

Western Canada dairy cattle and GIT nematodes

A
  • Milking herds zero grazed=not a major problem
47
Q

How do you manage GIT nematodes of cattle?

A
  • Quarantine and treat prior to introduction to new stock
  • Good husbandry: nutrition and concurrent disease
  • Pasture management
48
Q

Anthelmintics for GIT nematodes of cattle

A
  • Long acting, rumen boluses, residual effects (ML)
  • Parasite control usually NOT evidence-based
    o Pour on ML routinely given for ectoparasites, now LOW effectivity due to resistance
  • Limited drugs available: ML (ivermectin) and Benzimidazoles
49
Q

Strategic treatments for GIT nematodes of cattle: depends on use and management

A
  • Cows in spring to reduce pasture contamination
  • Young animals in first grazing season 6-8 weeks later
  • Fall (housing) treatment to cows and calves for arrested larvae
  • *target selective treatment (TST)

PARASITOLOGY - 2 (13 decks)

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