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Parasitology > Nematodes > Flashcards

Nematodes Flashcards

1
Q

Nematode Features

A

-Unsegmented -Acoelomate (no body cavity) - Moult b/w stages (shed cuticle) - Most free-living (soil** and marine sediment)

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2
Q

Cuticle Characteristics

A
  • outer keratin-like
  • inner collagen
  • secreted by hypodermis
  • shed with each moult
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3
Q

Musculature Characteristics

A

-longitudinal muscles only (2 dorsal & 2 ventral groups)

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4
Q

Nervous System Characteristics

A
  • nerve rings (esophageal ring: dorsal, ventral, 2 lateral nerves and rectal ring)
  • Neurotransmitters: GABA & Acetylcholine (block=paralyse)
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5
Q

Digestive System Characteristics

A
  • Mouth
  • buccal capsule, leaf crown (gut feeders wafting), cutting plates, teeth
  • Dorsal Gutter
  • conduit for enzymes/anticoagulants from esophagus
  • Esophagus
  • Instestine (simple columnar ring, microvilli)
  • anus= female
  • cloaca= males
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6
Q

What is the Pseudocoelome? Funx?

A

-body cavity

  • no true lining
  • high hydrostatic pressure of pseudocoelomic fluid provides rigidity
  • work w/ muscles to funx as hydrostatic skeleton = S shaped locomotion
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7
Q

Excretory-Secretory System Characteristics

A
  • tubular
  • two lateral canals
  • open at ventral excretory pore level of esophagus
  • anterior 1/3 of worm
  • paired glands open onto pore
  • secretions = immunogenic
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8
Q

Mouth

A
  1. lips
  2. cephalic papillae
  3. amphids
  4. lancet
  5. teeth
  6. cutting plates
  7. long leaf crowns
  8. short leaf crowns
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9
Q

Male: Reproductive Features

A
  • Testes (single/tubular)
  • Spicules
  • elongate, pointed
  • assist in copulation (dilate vagina/sperm flow)
  • single or multiple
  • Copulatory Bursa
  • posterior expansion od cuticle
  • usually 3 lobes (1 dorsal, 2 lateral)
  • Bursal Rays
  • finger-like projections
  • Gubernaculum (gubernator=pilot)
  • dorsal plate on wall of spicule pouch
  • guides spicule
  • not all worms have
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10
Q

Female: Reproductive Features

A
  • 1-2 tubular ovaries
  • contain germinal cells
  • uteri
  • ovijector- muscular feature on some worms
  • vulval flap (worm identifier)
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11
Q
  1. Oviparous
  2. Ovoviviparous
  3. Viviparous
A
  1. only egg produced and released
  2. egg contains 1st stage larva when relseased
  3. eggs hatch inside felmale and L1 released
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12
Q

Basic Life Cycle

A
  • Egg > L1 > L2 > [L3] > L4 > adult (male/female) > egg
  • all free living stages feed on bacteria
  • 4 moults
    • shed cuticle
  • Indirect vs Direct
  • Routes of Transmission (oral, percutaneous, transplacental, transmammary)
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13
Q

Order: Rhabditida

Family: Rhabditidae

  • Features
A
  • rhabditiform esophagus
  • tiny nematodes
  • mostly free living
  • most feed on bacteria
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14
Q

Order: Rhabditida

Family: Rhabditidae

  • Genera
A
  • Micronema
    • free living, multiply in moist detritis
    • Halicephalobus gingivalis
      • nervous system
  • Rhabdias (stick)
    • parthenogenic female in lungs of snakes and frogs
  • Rhabditis strongyloides - hair follicle
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15
Q

Order: Rhabditidae

Family: Rhabditidae

  • Life Cycle
A
  • egg > L 1
  • L1 feeds on bacteria & moult > L2 moult >
  • L3
    • penetrate skin and migrate to lungs > parthenogenic female
    • develop on soil to free living M & F
      • copulate, eggs hatch within female
      • larvae develop to L3
      • released when female dies

***important pathogen in snakes and frogs

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16
Q

Order: Rhabditida

Family: Strongyloidae

Genus: Strongyloides (cylindrical appearance)

  • Species - Host - Site
A
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17
Q

Order: Rhabditida

Genus: Strongyloides

  • Life Cycle
A
  • parthenogenic female
  • eggs hatch in 6h
  • Prepatent Period: 5-12 days
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18
Q

Order: Rhabditida

Genus: Strongyloides

  • Autoinfection (S. stercoralis) Life Cycle
A
  • humans and dogs
  • eggs hatch inside host (SI)
  • L1>L3
  • L3 penetrates mucosal intestinal wall
  • travel through circulation> lungs> swallowed> adults lay eggs in SI
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19
Q

Order: Rhabditida

Genus: Strongyloides

  • S. ransomi & S. westeri
    • what species they infect and important modes of transmission?
A
  • S. ransomi -transplacental/ transcolostral
    • pigs
      • piglets infected in utero
  • S. westeri - transcolostral
    • horses
  • percutaneous infection w/ L3 migrating to mamary adipose tissue
    • activated and passed thorugh milk
    • shortened PPP: 2-5d
      • develop quickly into adults in piglets/foals etc
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20
Q

Order: Rhabditida

  • Strongyloides ransomi
    • Pigs
      • Pathogenesis
A
  • Invasive
    • dermatitis
  • Pulmonary
    • pneumonia
  • Intestinal
    • parasitic female burrow in SI
      • Dxa
      • < growth rate
  • Prenatal & transcolostral
    • primarily piglets see pathogenesis bc ingesting advanced stage larvae
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21
Q

Order: Rhabditida

  • Strongyloides papillosus
    • Pathogenesis
A
  • dermatitis
  • scratching
  • allopecia
  • death
  • malaborption/dxa

**free living

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22
Q

Order: Rhabditida

  • Strongyloides westeri
  • Strongyloides stercoralis
  • unnamed species- kangaroo

What is the host for each?

A
  • S. westeri (foals) > transcolostral dxa in 2 wks
  • S. stercoralis (dogs/cats) > weak immune response, 37 yr dormancy
  • Kangaroos > in stomach, causes mortality
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23
Q

Order: Rhabditida

Genus: Strongyloides

  • Diagnosis
A
  • smol eggs ( 20-30 x 40-55 um) - fecal float or colostrum
    • feces collected from rectum
    • cool feces to prevent hatching
  • Larvae - baermann technique (L1)
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24
Q

Order: Rhabditida

Genus: Strongyloides

  • Treatment & Control
A
  • Treatment
    • Albendazole & Levamisole
      • In feed days before parturition
    • Ivermectin
      • against adults, give 1-2wk before parturition
  • Control
    • free living population
    • remove moist areas
    • survive about 3 week
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25
Q

Order: Strongylida

  • General Taxonomy
A
  • Trichostrongyloidea ►abomasum/SI
  • Strongyloidea ► LI
  • Metastrongyloidea ► lungs
  • Ancylostomatoidea ►SI
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26
Q

Order: Strongylida

Family: Trichostongyloidea

  • General Life Cycle features
A
  • Direct
    • in feces : egg → L1-L2
    • → (L3) (infective stage) → L4 -male/female (both parasitic in host)
      • L3 exsheathed in rumen and enter duodenal mucosal glands > L4 > adult in lumen of abomasum/SI
    • L3 must be ingested in order to complete LC
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27
Q

Order: Strongylida

Family: Trichostongyloidea

  • Features
A
  • vestigial buccal capsule
  • copulatory bursa
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28
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

  • Genus: Trichostrongylus
    • common name?
A
  • black scour worm of sheep
  • hairlike worm
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29
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

  • Genus: Trichostrongylus
    • Species, Spicule & Distrbution
A
  1. T. colubriformis
    1. spicule: barb like tip
    2. summer rainfall areas
  2. T. vitrinus
    1. spicule: tapering end
    2. winter rainfall areas
  3. T. rugatus
    1. spicule: thick and disssimilar
    2. drier inland areas
  4. T. axei
    1. spicule: dissimilar and unequal
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30
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Trichostrongylus

  • Life Cycle
A

PPP= 18-21d

female lays: 10-100 eggs/day

L3 - overwinter

  • can become anhydrobic and become active when rehydrated
  • can survive harsh environment
  • development occurs in duodenum
    • ​**search in 1st 6 meters of SI
      • moult to L4 (5d)
        • moult to adult (10d)

Intra-epithelial parasite

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31
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Trichostrongylus

  • Pathogenesis
A
  • villous atrophy
    • decreased mitosis
    • inflammation and matted
    • increased permeability → loss of plasma proteins
  • protein loss
    • hypoalbuminemia -20% loss in wool produciton & growth rate
    • [globulin] increased bc of host immune resp.
  • < absorption of Ca & PO4
    • decr. absportion in duodenum
    • incr. Ca as compensation
      • hypophosphatemia
      • decreased osteoblastic activity
  • anorexia
    • esp. T. vitrinus
  • diarrhea
    • secrete parasympathetic analogues (increase parastaltic waves)
    • release inflam. mediators, ^ capillary/epithelial perm. = exudation
    • poor absorption, change in osmotic P
    • predispose to fly strike
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32
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Trichostrongylus

  • How does the host respond? (Immunity)
A
  • immune respose if > 5 mo
  • imunity theshold 3000 worms ​
    • against incoming L3 and expel exisiting
    • ++ baso, eosino, mast cells in lamina propria
      • histamine, cytokines, serotonin
      • eosinophils can kill larvae
    • goblet cell hyperplasia → ^ mucus
      • entangle worms and paralyses
    • cellular response : Th2 hypersensitivity 1
      • IL5- eosinophil
      • IL4,9,13- mast cell degran.
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33
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Trichostrongylus

  • Can you still have scouring in immune sheep?
A
  • yes
    • still have increased parastaltic movements and increased mucus from immune response
    • also won’t expell full worm burden
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34
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Trichostrongylus

  • Seasonal Patterns
    • Winter Rainfall Zones
A

T. vitrinus

  • autumn moist - larvae develop
    • larvae migrate up blades of grass in moisture
  • winter moist- short grass
    • sheep graze low to ground and ingest
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35
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Trichostrongylus

  • When is maximum intake of T. vitrinus?
A
  • mid winter (high winter rainfall zone)
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36
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Trichostrongylus

  • Seasonal Patterns
    • Summer Rainfall Zones
A
  • T. colubriformis
  • development begins w/ incr temp & moisture
    • spring
  • overwinter (L3 in environment)
  • pasture growth can dilute larvae and high temps reduce survival
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37
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Trichostrongylus

  • Maximum burden in N. Hemisphere?
A

Autumn

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38
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Trichostrongylus

  • When do you have maximum numbers of T. colubriformis?
A

Mid summer - summer rainfall zone

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39
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Trichostrongylus

  • Where do you see high numbers of T. rugatus?
A

dry areas

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40
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Trichostrongylus

  • When would Trichostrongylus worms cause mortalities?
A
  • >60,000 load (esp young sheep)
  • winter rainfall zones can have death mid winter
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41
Q

Trichostrongyles of ruminants

Abomasum : HOT

Small intestine : Not Too Cold

A

HOT

  • Haemonchus
  • Ostertagia
  • Trichostrongylus axei

Small Intestine

  • Nematodirus
  • Trichostrongylus
  • Copperia
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42
Q

Order: Strongylida

Family: Trichostongyloidea

Genus: Cooperia

  • Location? Common name? Infected species?
A
  • small intestine
  • “wire worm”
  • cattle/sheep
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43
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Cooperia

  • Recognition features?
A
  • Size; ~9mm
  • small cephalic vesicle
  • esophageal region - transverse cuticular striations
  • body- longitudinal cuticular ridges
  • spicules- wing like in middle region
  • no gubernaculum
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44
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

  • What genus and what are the recognition features?
A
  • Genus: Cooperia
  • Features
    • transverse striations on cephalic dilation
    • no gubernaculum
    • wing like spicules
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45
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Cooperia

  • Species of Cattle
A
  • Temperate (moderate pathogenicity)
    • C. oncophora (southern AUS)
    • C. surnabada
  • Sub-tropical (very pathogenic- world wide/N. AU)
    • C. pectinata
    • C. punctata
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46
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

  • Genus? Species? Infected animal species?
A
  • Cooperia
    • cattle
      • C. punctata
      • C. pectinata
      • C. onchophora
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47
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Cooperia

  • Species of Sheep
A
  • C. curticei
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48
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Cooperia

  • Life Cycle
A
  • Direct
  • L1 - hatches in environment & feed on bacteria
  • L3- retains L2 cuticle/withstand harsh conditions
    • ensheathment in rumen
    • burrows in mucosal glands
  • L4 - head in gland & body in lumen
    • HYPOBIOSIS - in summer
  • Adult - in lumen
  • PPP= 15d
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49
Q

What is hypobiosis?

A
  • temporary cessation in development inside host
    • summer isn’t great for free living stages (cooperia/nematodirus/ostertagia)
      • hypobiosis in summer months
      • resume development in late autumn
      • produce eggs when environment is suitable for development of eggs/larval stages
    • winter hypobiosis (Teladorsagia circumcincta/hemonchus)
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50
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Cooperia

  • Effect on host
A
  • villous atrophy
  • erosion of epithelium
  • burden of > 50,000 cause anorexia/dxa
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51
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Cooperia

  • Epidemiology
    • In Southern Australia, when do cattle pick up wire worms?
A
  • winter
  • (ingest during wet season (summer/winter))
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52
Q

Order: Strongylida

Family: Trichostongyloidea

Genus: Nematodirus

  • Common name? Infected host? Location?
A
  • Thin-necked intestinal worm
  • sheep/cattle
  • small intestine
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53
Q

Order: Strongylida

Family: Trichostongyloidea

  • What genus and what are the defining features?
A
  • Genus: Nematodirus
    • largest of the 3 SI Trichostrongyles (25mm)
    • coiled
    • cephalic vessicle
    • long thin spicules
      • join at posterior end
    • female - spine tail
    • VERY LARGE EGGS
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54
Q

Order: Strongylida

Family: Trichostongyloidea

  • Genus?
  • Egg/larvae features?
A
  • Nematodirus
  • L1-L3 occur INSIDE egg
  • need cold or drying to hatch
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55
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Nematodirus

  • Species (worm and host)
A
  • Sheep
    • N. spathiger
    • N. fillicolis
    • N. abnormalis
  • Cattle
    • N. helvetianus
  • Both (in N. America and Europe)
    • N. battus (most pathogenic)
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55
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

  • NAME THAT SPICULE
A
  • Nematodirus
    • N. filicollis
    • N. spathiger
    • N. battus
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56
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Nematodirus

  • Life Cycle & Pre Patent Period
A
  • L1-L3 inside egg
    • need drying or cold to hatch
  • L3 burrows in mucosal glands or coil aroud villi > moult to L4
    • L4 Hypobiosis common
  • adult in lumen
  • PPP= 18-21d
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57
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

  • Genus and Pathogenesis
A
  • Genous: Nematodirus
  • villous atrophy
  • erosion of epithelium (from coiling)
    • L3 burrow into crypts
  • dxa common
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58
Q

Order: Strongylida

Family: Trichostongyloidea SMALL INTESTINE

Genus: Nematodirus

  • Epidemiology
A
  • L3 with egg = resistance
  • can survive over summer
  • heavy infections can accumulate in lambing paddocks
  • greatest larval pick up = WINTER
  • strong immunity develops
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59
Q

Order: Strongylida

Family: Trichostongyloidea

  • What is the Trichostrongylus species found in the abomasum and what is the common name?
A
  • T. axei
  • “stomach hair worm”
  • primarily parasitic in CATTLE
    • can occur in sheep, horses, pigs, humans
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60
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • Pathogenesis of this worm
A
  • T. axei
    • damage to epithelium
    • protein lost in lumen
    • mucus produced > pH rises
    • 40,000 can kill little lamb
  • pathogenesis similar to O. ostertagei (T1)
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61
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

Genus: Trichostrongylus axei

  • Life Cycle and Epidemiology
A
  • direct LC
    • environmental part similar to other trichostongylus spp.
      • (L1-L2) in feces > (L3) ingested and exshealthed
    • host part similar to ostertagia spp.
      • L4- hypobiosis in abomasal glands
  • wide host range > important in mixed grazing
  • highly pathogenic
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62
Q

Order: Strongylida

Family: Trichostongyloidea

  • Genus? Location? Common name? Infected hosts and specific species ?
A
  • Hemonchus -barbers pole worm
  • Abomasum
  • sheep
    • H. contortus
  • cattle
    • H. placei
  • deer, camel
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63
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • Genus and Features?
A
  • Hemonchus
  • 2-3 cm long
  • red - barber pole in female
    • large vuval flap
  • lancet tooth in buccal capsule
  • prominent cervical papillae
  • asymmetrical dorsal rays
  • spicules with barbs
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64
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

Genus: Hemonchus

  • Life Cycle & prepatent period?
  • What is the infective stage?
A
  • direct LC
  • INFECTIVE STAGE: L3
    • exsheathment
    • burrows in abomasal glands to moult L4
  • L4 re-emerge in lumen
    • lancet tooth & sucks blood
  • Adult - feed on blood

PPP= 21d

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65
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

Genus: Hemonchus

  • 5 Effects on the Host
A
  1. microcytic hypochromic anaemia
    1. voracious blood suckers
    2. white eyes and mucosal membranes
  2. hypoproteinemia > bottle jaw
  3. NO DXA
  4. reduced exercise tolerance
    1. iron deficiency
  5. heavy infection > sudden death
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66
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • Why do you have anemia and edema associated with a Hemonchus infection?
A
  • Pick up low dose daily
  • trying to compensate blood loss
  • blood loss> protein loss
    • reduced oncotic P
    • edema > bottle jaw (localised) or anasarca (generalised)
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67
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • What type of rainfall area is most favorable for Hemonchus? When is L4 in hypobiosis?
A
  • Summer rainfall areas most common
    • maximum : Feb-March
    • hypobiosis in winter
  • less common in winter rainfall areas
    • summer too hot/winter too cold
    • if mild winter and wet summer > can be widespread
      • problems w/ pregnant ewes in autumn
      • problems w/ lambs in spring
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68
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

Genus: Hemonchus

  • Epidemiology
    • egg/day?
    • Eggs WONT hatch below what temperature?
A
  • high biotic potential - 5,000/10,000 egg/day
  • eggs wont hatch below 10ºC
  • labile larvae
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69
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • What worm “self cures” when threshold is reached?
A
  • Hemonchus
    • **similar to T1 sensitivity
    • eosinophil-based damage of worm on second exposure
  • also vaccine against gut wall proteins (of parasite)
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70
Q

Order: Strongylida

Family: Trichostongyloidea

Genus: Ostertagia

  • Location? Common name? Infected host?
A
  • Abomasum
  • Brown stomach worm
  • sheep, deer, cattle
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71
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

A

Ostertagia

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72
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

Genus: Ostertagia

  • Species found in sheep?
A
  • O. circumcincta **(main) (also Telodorsagia)
  • O. trifurcata
  • also Teladorsagia davtiani
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73
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

Genus: Ostertagia

  • Species found in cattle?
A
  • Ostertagia ostertagi
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74
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • T. circumcincta in sheep Life Cycle
A
  • Direct (free living similar to trichostrongylus)
    • L1-L3 in feces (2 wks)
    • L3 ingested > exsheaths in rumen
      • winter rainfall area
        • max: june/july
    • migrates to lumen of abomasal gland
    • moult > L4 > return to lumen
      • hypobiosis common (6 mo)
        • occus in spring
        • emerge in autumn
  • cause nodules in abomasum
  • PPP= 18-21d
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75
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • T. circumcincta effect on sheep?
A
  • laval migration to gland cells > hyperplasia & necrosis
    • reduced parietal and chief cells
      • red. acid and pepsin > pH rises (6)
    • hypoproteinemia
      • protein digestion stops
      • leaking plasma proteins into abomasum
    • ^plasma pepsinogen
      • ^ secretion & ^ permeability
    • hypergastrinemia
      • pouches w/o worms secrete more gastrin
    • anorexia
    • dxa (maldigestion)
      • nematodes promote gastrointestinal motility (parasympathomimetic)
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76
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • T. circumcincta GROSS effects on sheep?
A
  • areas of hyperplasia
    • raised pin point white foci
    • towards antrum and folds of fundus
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77
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • Where is T. circumcincta primary distribution?
A

High rainfall southern australia

  • mainly infects younger animals
  • immunity seen in older animals & worm burden expelled
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78
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • What happens to T. circumcincta worms and eggs in immune animals?
A
  • stunted/small and lower fecundity
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79
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • What GIN gives a “moroccan leather” appearance?
A
  • Ostertagia ostertagi in cattle
    • found in TEMPERATE areas
    • nodules in abomasum
      • same pathophysiology as in sheep
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80
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • 2 differences of O. ostertagi in cattle from sheep?
A
  1. fecal mass as a reservoir for larvae
    1. DUNG PAT = HOME
  2. inhibited larvae can emerge synchronously
    1. L4 resume development from hypobiosis
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81
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

Genus: Ostertagia

  • Why is the cattle dung pat a “helminthological time bomb”?
A
  • cow pat is ideal environ for development
  • crust on surface prevents desiccation of interior
    • aeration occurs and larvae dev. to L3 (ensheathed) in moist poo
    • if dry, crust prevents migration but L3 can still develop over summer
  • moisture> emerge onto herbage
  • picked up by cattle in autumn through spring
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82
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • What is Type 1 Ostertagiasis?
A
  • young animals
  • no immunity
  • occurs in spring - just a buildup of worms
  • dx w/ egg counts & plasma pepsinogen
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83
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • What is Type 2 Ostertagiasis?
A
  • larvae emerge synchronously (hypobiotic larvae)
    • can be induced by cooling larvae or removing adults
    • subtropical: hypobiosis does NOT occur
  • 2-4 yo animals
  • precipitated by stress (calving)
  • erratic occurance
  • occurs in autumn
  • dx w/ ^ plasma pepsinogen or ^gastrin
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84
Q

Order: Strongylida

Family: Trichostongyloidea ABOMASUM

  • Epidemiology of O. ostertagi?
A
  • EU: inhibited in winter
  • AUS: inhibited in summer
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85
Q

Order: Strongylida

Family: Trichostongyloidea

  • Name each genus
A
  • hemonchus
  • ostertagia
  • cooperia
  • trichostrongylus
  • nematodirus
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86
Q

Trichostongyles of Sheep

Abomasum & SI (5)

A
  • Abomasum
    • Hemonchus contortus
    • Teladorsagia circumcincta
    • Trichostrongylus axei
  • SI
    • Trichostongylus spp.
      • T. colubriformis
      • T. vitrinus
      • T. rugatus
    • Nematodirus spp.
      • N. spathiger
      • N. filicollis
      • N. abnormalis
      • N. battus
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87
Q

Trichostrongyles of Cattle

Abomasum & SI (5)

A
  • Abomasum
    • H. placei
    • O. ostertagi
    • T. axei
  • SI
    • Cooperia spp.
      • temperate
        • C. oncophora
        • C. surnabada
      • subtropical
        • C. pectinata
        • C. punctata
    • N. helvetianus
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88
Q

What sheep parasites have the largest economic impact in Australia?

A
  1. fly strike
  2. Lice
  3. Liver fluke
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89
Q

What cattle parasites have the largest economic impact in Australia?

A
  1. cattle tick
  2. buffalo fly
  3. internal parasites
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90
Q

3 assumptions about ruminant parasites?

A
  1. infections are always mixed
  2. all animals infected all the time
  3. control rather than eradicate
    1. erradication impossible
    2. would leave susceptible sheep/cattle
      1. no immunity
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91
Q

how do you target a parasite in the environment?

A
  • strategic drenching
  • pasture spelling
  • alternate grazing
  • rotational grazing
  • reduced stocking density
  • nematophagus fungi
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92
Q

How do you reduce parasites at the level of the host?

A
  • anthelmintics
  • vaccination
  • breed for resistance
  • nutrition
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93
Q

5 factors that influence worm burden

A
  • moisture
  • temperature
  • grazing factors
  • host factors
  • management factors
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94
Q
  • What is the importance of moisture in the epidemiology of trichostrongyloidosis?
A
  • development of L3 in feces
  • larvae migration to pasture
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95
Q

What is the effective rainfall for trichostrongylus movement on the pastures?

A

P/E > 0.3

(precipitation/evaporation)

* estimates for hemonchus = P/E > 1.0

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96
Q

What factors assist movement of trichostrongyles?

A
  • Lateral
    • heavy rains and floods
    • fungal spores (L3)
  • Vertical
    • films of moisture (up tip of grass blade)
    • ** stay at root when dry or increased temp
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97
Q

Effects of weather/moisture on trichostrongyles?

A
  • negatively geotropic
  • photophobic in strong light
    • sheep graze at dawn/dusk
  • when water dries out on grass > anhydrobic state
  • survival limited by lipid reserves
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98
Q

What happens to trichostrongylus eggs in lower temperatures?

A
  • slow egg hatching & development
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99
Q

What happens to trichostrongylus eggs in higher temperatures?

A
  • shorten survival times of L3 on pasture
  • also have quicker hatching and L3 development
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100
Q

What trichostrongylus species has the longest growth period (days) in low humidity?

A
  • T. rugatus
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101
Q

How can you epidemiologically assess Hemonchus?

A

bioclimatographs

* based on 10ºC min and rainfall

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102
Q

What grazing factors influence Trichostrongylus burdens in sheep?

A
  • sheep do NOT graze uniformly
    • use indicated by fecal deposits
    • larval distribution not uniform
  • sheep graze selectively
    • avoid certain plants/ contaminated areas
  • STOCKING DENSITY
    • ^sheep = ^poop
    • initially have a high burden but overgrazing will reduce #s bc of UV exposure
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103
Q

What are the HOST factors that influence Trichostrongylus burdens?

A
  • age
  • genetic susceptibility
    • can select for resistance
  • ​follow negative binomical distribution
    • only a few sheep will have large burdens
      • FEC can be skewed
        • must sample 10+ sheep
  • breed differences
    • merinos more susceptible than cross breed
  • Self-cure phenomenon
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104
Q

What causes “periparturient rise” in Trichostrongylus burdens in sheep?

A
  • “spring rise” in fecal egg count
    • ^FEC in ewes just prior to lambing & first 4-6wks of lactation
  • Due to:
    • re-emergence of inhibited larvae
    • relaxation of immunity
      • existing worm burden becomes more fecund
    • increased susceptibility to L3
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105
Q

What management factors influence Trichostrongylus burdens?

A
  • time of lambing/calving
  • grazing management
    • stocking density
    • quality and length of pasture
  • nutritional status
    • low BCS w/ low burden can be detrimental
  • strategic use of anthelmintics
    • FEC pre/post
      • CHECK EFFICACY
    • timing
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106
Q

Hypobiosis vs. Overwintering

A
  • hypobiosis
    • arrested development of L4 inside host
      • more common in AUS
  • overwintering
    • L3 in environment resistant to harsh winter
      • not very common in AUS bc not cold enough
107
Q

Factors supporting hypobiosis?

A
  • unfavorable climatic conditions
  • immune status of animal
  • density of GINs
108
Q

Factors supporting resuption of development of inhibited larvae?

A
  • hormonal changes
  • altered components of immune system
  • density of the parasite
    • young animals have more larvae
  • environmental temperatures
109
Q

How do you diagnose trichostrongyloidosis antemortem?

A
  • history “tail to mob”
  • symptoms/signs
    • scouring, anemia, poor BCS, dag score
  • clin path
    • fecal egg counts
    • fecal cultures
    • molecular ID
    • hematology, biochem and serology
  • pasture larval counts
110
Q

How do you diagnose trichostrongyloidosis postmortem?

A
  • total worm count
  • gross pathology
111
Q

Indirect method - fecal egg count

  • What does an FEC tell you?
A
  • determines # worm eggs per gram of feces (EPG)
    • estimate worm burden
  • strongyle-type eggs
    • trichostrongyle & strongyle eggs
  • req. measured amt. feces and floatation soln.
    • McMaster slide
  • useful in diagnosis of nematode infections <9mo
    • old animals dev. immunity
  • variability and degree of infection
  • indicates # female worms only
  • need 10+ samples
  • > 500 epg = pathogenic
112
Q
A

A. strongyle - type

B. nematodirus egg

113
Q

How does starving sheep or diarrhea influence FEC?

A
  • starving sheep
    • increase FEC by 50%
  • dxa
    • reduced FEC
114
Q

Fecundity of Trichostrongylus genera?

  • Hemonchus
  • Trichostrongylus/Ostertagia
  • Nematodirus
A
  • Hemonchus: 5,000- 10,000 eggs/female/day
  • Trichostrongylus/Ostertagia: 10-200 eggs/female/day
  • Nematodirus: 50 eggs/female/day
115
Q

3 Factors influencing fecal egg counts?

A
  1. host immunity = suppression
    1. resist estabilishment of infection
    2. deceased fecundity
  2. concentration of eggs in feces affected by digesta, dxa, fasting, feed quality, and size of host
  3. egg count higher in young sheep (esp. merinos)
116
Q
A

A. Ostertagia

B. Trichostrongylus

C. Haemonchus

D. Chabertia

E. Oesophagostomum

F. Cooperia

117
Q
A

A. Teladorsagia circumcincta

B. Trichostrongylus spp.

C. Hemonchus contortus

118
Q

Molecular ID of trichostongylus nematodes

  • Steps and benefit of MT-PCR?
A
  • Step 1: pre-amplification
    • isolation w/floatation (extract eggs)
  • Step 2: real time PCR
    • DNA based test for true ID
  • Data analysis
    • need to wait at least 1 week for larval culture
    • PCR takes 24-48hrs and reliable
119
Q

In diagnosing trichostongylosis what does a pasture larval count tell you?

A
  • direct quantification from pasture
    • # larvae/kg herbage
    • not reliable at low levels of contamination
  • collect in M pattern
  • introduce worm-free “tracer” animals
    • costly & time consuming
    • mimic grazing patterns of resident flock
120
Q

What is the most reliable (direct) method of assessing trichostrongylus burden?

A
  • total worm count
    • use 1-2 sheep from tail of mob
      • abomasum & SI assessment
    • ID genera and species
121
Q

What is the most pathogenic Trichostrongyloid?

A
  • hemonchus
    • fatal : 5,000-10,000
    • production loss : >2500
122
Q

What are the least pathogenic Trichostongyloids?

A

Ostertagia : produciton loss @ 50,000

Nematodirus : fatal burden 100,000

123
Q

7 control methods for trichostrongyloids?

A
  1. Grazing management
    1. Pasture spelling
    2. Crops
    3. Alt. grazing
  2. Anthelmintic drugs
    1. more effective in summer in S. Aus
  3. Nutrition
    1. resiliance > withstand normal produciton levels w/ good BCS
  4. Breeding
    1. resistance
  5. Use of vaccines
    1. barbervax (barbers pole worms)
  6. Biological control
    1. Duddlingtonia flagrans- nematode trapping fungi
  7. Integrated parasite management
    1. combination of all of the above
124
Q

When should you spell a paddock to control trichostrongyloidosis?

A
  • summer & harrow in summer
125
Q

How does crop integration control trichostrongyloidosis?

A
  • sowing crops reduces pasture contamination
  • drench onto stubble (Nov/Dec)
    • L3 will be on ground and eat just above
126
Q

Alternate grazing sheep with cattle and horses reduces contamination except for what worm?

127
Q

Factors affecting immunity to trichostrongyloidosis?

A
  • age/nutritional status of sheep
    • older and good BCS hastens immunity
  • previous exposure to worms
  • number of worm larvae on pasture
    • enough worms to activate response
  • reduced immunity
    • stress (weaning/transport)
    • pregnancy/lactation
    • sex
      • dry adult ewes > wethers > rams
128
Q

Trichostrongyles of horses?

A

T. axei in stomach

129
Q

Trichostrongyles of pigs?

A
  • T. axei - stomach (asymmectric spicules)
  • Hyostrongylus rubidus - stomach
    • adult pigs **free range not on concrete floors
    • LC
      • direct (similar ostertagia L3)
        • L3 in gastric glands (3rd and 4th moults)
      • hypobiosis
      • PPP= 21
    • Pathogenesis
      • dxa, weight loss
    • Control
      • concrete floor
      • Tx: fenbendazole, ivermectin, dormectin
130
Q

Trichostrongyles of cats?

A
  • Ollulanus tricuspis - stomach
    • female tail has 3 short cusps
    • viviparous
      • L1-L4 inside host
    • not very pathogenic
    • transmit in vomit
131
Q

Trichostrongyles of birds?

A
  • Amidostomum anseris (gizzard worm)
    • geese, duck, swan
    • site: junx of gizzard & proventriculus
    • highly pathogenic > massive necrosis
    • LC- direct; oral infection
  • Trichostrongylus tenuis
    • site: cecum
    • wide host range
      • controls wild grouse pop
      • pathogenic in domestic birds
    • nodular lesions & moralities in galliform birds
132
Q

Order: Strongylida

Family: Strongyloidea

  • Common name?
  • Usual site?
  • Features?
A
  • Stongyles
  • Large intestine
  • well developed buccal capsule w/ leaf crowns
  • males have bursa
133
Q

What is the main host and what is the general life cycle?

A

Genus: Strongylus

  • horses
  • L1-3 in feces
  • L3 on herbage
  • L3 migrates into intestinal gland
  • L4 emerges to lumen
  • final moult in lumen
  • PPP= long
  • +/- extra intestinal migration
134
Q

Order: Strongylida

Family: Strongyloidea

  • subfamily? & common name
  • genera in equine?
A
  • strongylinae
    • large stongyles - MIGRATORY
  • strongylus***
  • tridontophorus**
  • oesophagodontus
  • craterostomum
135
Q

Order: Strongylida

Family: Strongyloidea

  • common name
  • genera in equine
A
  • small strongyles - NON MIGRATORY
  • cyathostomum
136
Q
  • genus & species of the red worms/blood worms
  • location
A

A. Strongylus equinus

  • pointed teeth

B. S. vulgaris

  • ear shaped teeth

C. S. edentatus

  • no teeth
    location: cecum & colon
137
Q

Life cycle??

A
  • Strongylus vulgaris
    • direct
      • L1-L2 : dev. in feces feed on bacteria
      • (L3) : exsheathes SI/LI migrates into mucosa
        • development stops below 8C
      • L4: ascends to root of cranial mesenteric arteries
        • remain for several weeks
      • return to gut > moult to adult > enter lumen
        • feed on gut mucosa/blood
  • PPP= 6 mo
138
Q

Effects of “red worm” on host

A
  • migrating larvae
    • damage arterial wall/inflammation > fibrous tissue > thrombus > emboli/occulde vessels
      • intermittent colic
      • ischemia > infarct, gnagrene
    • “verminous arteritis” not aneurysm
  • adults
    • blood feeders > anemia, eosinophilia, leukocytosis
139
Q

When are Strongylus vulgaris larvae most abundant? When does larval development stop?

A
  • Larvae most abundant in spring
    • desiccated in summer
    • become egg laying females in autumn
    • winter reduces larval development
    • egg output max in spring
140
Q

When do horses develop immunity to Strongylus vulgaris?

A
  • As foals
    • become infected early in life
141
Q

No teeth in buccal capsule, common in AUS & larger than S. vulgaris…who am I?

A

Strongylus edentatus

  • buccal capsule wider than rest of body
142
Q

Life Cycle of S. edentatus

A
  • L3 exsheaths in cecum
    • burrows in gut wall
      • enter portal veins
        • migrate to liver (home for 8 wks)
          • migrate to subperitoneal tissue
  • L4 moult & return to gut lumen via mesentery
  • PPP= 10 mo
143
Q

where can you find S. edentatus?

A
  • liver, kidney, cecum, lung, testes
    • found post mortem
144
Q

3 teeth in deepest buccal capsule, not common in AUS, tropical species…who am I?

A

Strongylus equinus

145
Q

Life Cycle?

A

S. equinus

  • L3 exsheaths in cecum > migrates to gut wall
  • L4 migrate in subserous tissues of intestine
    • > peritoneal cavity > liver (6wks)
    • migrates via pancreas to gut

PPP= 8 mo

(pathogenesis similar to other strongylus spp.)

146
Q
A

Family: Strongylidae (large strongyles)

  • Genus: Strongylus (red worms)
147
Q

Tridontophorus features

A

3 teeth, numerous external leaf crowns

148
Q

Oesophagodontus features?

A

lancet like esophageal teeth

149
Q

Craterostomum features?

A
  • strong mouth
150
Q

Life cycle?

A
  • Triodontophorus serratus & T. brevicauda
  • L3 exsheaths in cecum > penetrate intestine
  • L4 moult > emerge into lumen > final moult in lumen
  • adults feed in groups= ulceration

PPP= 9 wks

151
Q

what large strongyle occurs in groups, causes ulceration & blood loss?

A

Triodontophorus

152
Q

how many of these worms will you see in a heathy horse?

A

small strongyles (cyathostominae)

occurs in large numbers (15,000)

153
Q

Life cycle?

A

Cyathostomum

  • L3 exsheaths in cecum & enters cecal glands
    • fibrous capsule (encysted) and L4 moult
      • hypobiosis of L3:
        • may be synchronous reemergence following removal of adults
        • seasonal or if adults in lumen
  • L4 reemerges to lumen and final moult
    • reemergance may be synchronous after killing off adults with moxidectin (ML)

PPP= 5 weeks (min)

154
Q

Diagnosis of Cyathostomum & effect on host?

A
  • diagnosis
    • eggs in feces > 300 epg pathogenic (McMaster chamber)
    • larval culture (otherwise cant differentiate bw large and small strongyles)
  • pathogenesis
    • adults poorly pathogenic
    • normally 115,000 larvae encysted
      • visible
      • large migration of larvae cause dxa & blood loss
155
Q

Difference in horse immunity of Strongyloides westeri vs Strongyles spp.

A

S. westeri - immunity develops in first 12 wks of age

Strongyles spp- develop immunity after 24 mo

  • large strongyles
156
Q

At what age do horses develop immunity to Cyathostomum (sm. strongyles)?

A

they dont develop immunity

  • horses commonly infected with several species
157
Q

why is dewormer not effective against Cyathostomum?

A
  • L3 encysted - only kills adults and majority are encysted
  • different to Trichostongylus in ruminants where L4 undergoes hypobiosis but can be killed by anthelmintics
158
Q

Strongyles of Ruminants

  • Family: Chabertiidae
    • Genus/Species?
    • Host?
    • Site?
    • Recognition features?
A
  • Chabertia ovina
  • sheep, cattle, goats
  • proximal colon > tissue feeder
  • globular bell shaped buccal capsule, no teeth, tiny leaf crown
159
Q

Ruminant strongyle Life Cycle?

A
  • similar to Tridonophorus (equine lg strongyle)
  • L1-L2: dev. in fecal pellets
  • L3: ensheathed> exsheath in SI
    • enters ileal mucosa (moults L4)
  • L4: returns to lumen and migrates to colon
  • final moult in LI

PPP= 8 wks

160
Q

Ruminant strongyle: tissue feeder…whats the pathogenesis?

A
  • Chabertia ovina
  • feed on mucosa > hemorrhage
  • excess mucus production
  • dxa
  • common temperate worm but in low numbers
    • pathogenesis = 200
  • strong immunity
161
Q

Family: Chabertiinae

  • Genus?
  • Host?
  • Site?
  • Regocnition features?
A
  • Oesophagostomum (nodule worm)
  • cattle, pigs, sheep
  • Cecum, colon > gut content feeders
  • cylindrical buccal capsule, leaf crowns, cervical collar
162
Q

Typical life cycle of Oesophagostomum?

A
  • L3 exsheaths in SI > penetrate mucosa of ileum/colon
  • moult L4 in nodule
  • L4 reemerges to lumen and final moult in LI

PPP= 5-6 wks

163
Q

Ruminant strongyle- nodule worm of cattle?

A
  • Oesophogostomum radiatum
    • no external leaf crown/sm. internal leaf crown
    • 2 parts of cervical collar
    • common in Northern AUS
    • LC typical of genus
164
Q

Pathogenesis of this gut feeder strongyle (ruminants)?

A
  • “pimply gut”
  • Susceptible (young) host
    • no rxn - normal maturation to adult
  • Resistant animals (T1 hypersensitivity)
    • intense inflam. rxn around nodule
      • filled with eosinophils & giant cells
      • larva kills > caseous lesion calcifies
  • adults irritate gut > ^ mucus, dxa
  • loss of plasma protein & Hb into gut
  • interfere w/ gut motility
  • anorexia
165
Q

when do cattle develop immunity to Oesophgaostomum radiatum?

166
Q

What where do you find this lesion in cattle and what causes it?

A
  • Cecum/Colon
  • Oesophagostomum radiatum (stongyles)
167
Q

Nodule worm of sheep (strongyle), less common now…who am I and where am I found?

A

Oesophagostomum columbianum

Location: colon

*very pathogenic in young worm w/ nodules frequent

168
Q

Very common strongyle of sheep in southern states, non-pathogenic, does NOT cause nodule formation.. who am I and where am I found?

A
  • Oesophagostomum venulosum
    • note single cervical collar
  • Location: cecum
    • some scouring and mucus production
169
Q

Nodule worm of pigs?

A

Oesophagostomum dentatum

  • note sing cervical collar
170
Q

Kidney worm of the pig…genus/species, location & distribution?

A

Stephanurus dentatus

  • teeth present in cup shaped buccal capsule
  • Location: perirenal fat in cysts attached to uteter
    • pass eggs in urine***
  • Distribution: limited to warm, moist areas in AUS
    • tropical and subtropical world wide
171
Q

What is the life cycle of Stephanurus dentatus?

A
  • Kidney strongyle of pigs
    • Eggs passed in urine***
    • L3
      • percutaneous
        • travel to liver via lymphatics or lungs/aorta
      • ingested/Earthworms as transport host
        • exsheathment > penetrate gut wall > mesenteric LN > moult L4
      • L4 passes to liver (portal system) > migrate in liver for 2-3 mo
      • Moult to adult > rupture or penetrate peritoneal cavity and migrate to perirenal fat but can go anywhere in the body
        • form fibrous capsule and connect with ureter & eggs pass through connection

Long PPP= 9 mo

172
Q

You find this egg in the urine of a pig…what effect does this have on the host?

A
  • Stephanurus dentatus
    • fibrosis in liver
      • white spots due to extensive migration of L4
    • abscesses in carcass/loss of organs
    • weight loss
    • elevated liver enzymes (ALT/AST)
173
Q
  • Genus/Species & common name?
  • Location?
  • Host?
  • Features?
A
  • Syngamus trachea (gape worm)
  • Location: trachea
  • Host: poultry & other birds
  • Features
    • up to 10 teeth in cup-shaped buccal capsule
    • small M joins F > Y shaped grossly
174
Q

What is the life cycle of Syngamus trachea (strongyle of birds)?

A
  • eggs coughed up and swallowed
  • L1-L3 within egg***
  • Bird can ingest
    • earthworm paratenic host
    • hatched L3
    • egg
  • L3 exsheaths and penetrates gut > portal circulation to liver> lungs
  • L3 moult L4 in lungs > migrate up airways to trachea

PPP= 2 wks

175
Q

Pathogenesis and diagnosis of Syngamus trachea?

A

Pathogenesis

  • causes excess mucus production
  • block airways w/ lg #s
  • respiratory distress (gaping)
  • blood feeders- hemorrhages in trachea

Diagnosis

  • eggs in feces are ellipsoidal w/ thick operculum at both sides
176
Q

Common name and site of Ancylostomatoidea?

A
  • hookworms
  • small intestine
177
Q

Superfamily Ancylostomatidae

  • ID subfamilies and features
A
  • Ancylostomatinae
    • 2-3 pairs of teeth at mouth opening
    • Genus: Ancylostoma
  • Bunostominae
    • cutting plates
    • Genera: Globocephalus, Uncinaria, Bunostomum, Gaigeria, Necator
178
Q

Life cycle of hookworms - Ancylostomatoidea?

A
  • Adult female lays 15,000 eggs/day
  • L1-(L3) dev. in feces
  • oral infection > moult L4 in mucosal gland> return to SI lumen > moult to adult
    • PPP= 2 wks
  • Percutaneous infection
    • circulatory or lymphatics > lungs > trachea > SI (longer PPP)
    • through tissues > milk
179
Q

What is this worm and who does it infect and important features of LC?

A

Ancylostoma caninum - dogs (SI)

  • oral infection
  • skin penetration
    • feet pads & enter venous blood > heart> lungs> swallow> SI (PPP= 5wks)
    • can stay in skeletal mm
      • transmammary/colostral infection important
        • PPP= 10-15 d
        • pups 2-3 wks (deworm every fortnight)
      • male dogs dead end host
180
Q

What are the 3 clinical forms of Ancylostoma caninum?

A
  • Peracute - neonate pups
    • pot belly
    • dont see many eggs bc woms havent fully developed
    • microcytic hypochromic anemia
    • death
    • black tarry faces
  • Acute- older/mature pups
    • may see anemia
  • Chronic- adult dogs
    • aysmptomatic
    • can see eggs
    • immunity develops following exposure
    • voracious blood sucker> anemia

***eosinophilic enteritis in man (through feet)

181
Q

Epidemiology of Ancylostoma caninum- where are they found, ideal larval development conditions, and what is a significant egg count?

A
  • northern AUS - warmer climates
  • shaded/sandy conditions best for larva
  • > 5000 eggs significant (relatively small in size)
    • dissimilar poles
182
Q

What is this parasite? Where can you find it? What does it cause in humans? In the desired host?

A
  • Ancylostoma braziliense
    • tropical/subtropical
    • less pathogenic but can cause hypoproteinemia & dxa
    • creeping eruption in humans
    • oral and percutaneous infection
      • erythematous inflammatory tracts w.in dermis
183
Q

What is this parasite? Host? Epidemiology? Pathogenesis?

A

Uncinaria stenocephala - dogs SI (Bunostominae)

  • L3 ingested - no extra-intestinal migration
  • common in cooler areas
  • less pathogenic - slight anemia
  • PPP= 15d
  • * eggs larger than Ancylostoma caninum eggs
184
Q

Hook worms of seals/sea lions? Important route of infection?

A
  • Uncinaria lucasi
    • N. hemi seals
    • larvae can penetrate skin (flippers) when on sand and transfer to pups transmammary
      • adult seals dont harbor adult nematodes just larvae
  • U. hamiltoni
    • anemia of Australian sea lions
185
Q

Hook worms of cats

A

A. Ancylostoma tubaeforme

B. Ancylostoma braziliense

C. Uncinaria stenocephala

186
Q

Hookworms of Ruminants

A
  • Bunostomum phlebotomum - cattle SI
  • Bunostomum trigonocepthalum - sheep SI

* mainly found in warms areas

* percutaneous infection > Lung > L4 > tracheal migration

* transcolostral

PPP= 7wks

187
Q

What is the effect of Bunostomum spp. on ruminants?

A
  • anemia
  • hypoproteinemia
  • dxa
  • 1000 burden fatal (young animals - transmam)
188
Q

African (S. American and Indo) hookworm of ruminants?

A
  • Gaigeria pachyscelis
    • feed on blood- severe anemia & death
    • low worm burden can be fatal (25 worms)
189
Q

Hookworm of pigs

A

Globocephalus spp.

  • tropical areas around the world except AUS
  • Path
    • anemia - blood feeder
    • weight loss
    • emaciation
190
Q

Metastrongyloidea- common name, site and recognition features?

A
  • Lung worms > lung
  • reduced buccal capsule & copulatory bursa
  • usually have slugs/snails as intermediate hosts
  • L1 have characteristic kinks in tail
    • dx by Baermann technique
191
Q

Describe Direct Life Cycle of Metastrongyloidea (lung worms) - what genus and what host?

A

Direct: (L1 passes in feces)

  • L1-L3 in feces > L3 ingested & exsheathment
  • migrate and moult L4 in mesenteric LN > lungs (final moult)
  • Host: ruminants, horse
  • Genus: Dictyocalus
192
Q

Describe Intermediate Host Life Cycle of Metastrongyloidea (lung worms) - what genus and what host?

A

Intermediate Host- L1 passed in feces

  • L1-L3 in molluscs /earthworms (snails/slugs)
  • L3 ingest IH
  • migrates via lymphatics to lungs (similar to direct)
  • Host: ruminants, pigs, cats
  • Genera: Protostrongylus, Muellerius, Metastrongylus, Aelurostongylus
193
Q

Describe Simple Direct Life Cycle of Metastrongyloidea (lung worms) - what genus and what host?

A

Simple Direct - L1 passed in feces

  • L1 infects definitive host (L1 passed in vomit)
    • also transmitted by licking
  • Host: dogs
  • Genera: Oslerus, Filaroides
194
Q

Name the larval tail!

(lungworms of sheep & name location)

A

A. Dictyocaulus filaria - bronchi

B. Protostrongylus rufescens - bronchioles

C. Muellerius capillaris - alveoli

195
Q

Sheep (in VIC- cool/moist) w/ chronic cough, increased mucus production, developed pneumonia, labored breathing and pronounced eosinophilia. What is this parasite?

A
  • Dictyocalus filaria
    • sm. buccal capsule
    • spongy spicule
196
Q

What is the life cycle of Dictyocalus filaria?

A
  • lungworm of sheep
  • Direct LC - L1 in feces
    • L3 ingested and exsheaths in abomasum
    • migrates and moults in mesenteric LN > Lungs > final moult to bronchi
  • PPP= 21d
197
Q

What effect will Dictyocalus filaria have on sheep?

A
  • damage epithelium
  • block airways- esp @ tracheal bifurcation
  • excess mucus
  • loss of mucocilliary escalator
  • interstitial pneumonia
  • detached alveolar macrophages > consolidation of lung lobules

*** immunity will develop following exposure

198
Q

This sheep had mild pneumonia w/ red/brown lesions at the dorsal surface of the lungs and worms found in bronchioles. What parasite is this? What is its Life Cycle?

A

Protostrongylus rufescens - striated spicule

  • Indirect - snails
    • L1 in feces
    • penetrates foot of snail (L1-L3 in snail)
    • sheep ingests snail and migrates via lymphatics > lungs (bronchioles)
199
Q

Several sheep in VIC had no pathogenic signs but their lungs had red/brown to grey/green lesions on the dorsal surface. Goats on the same farm had similar lesions but presented w/ severe respiratory pathogenesis. What is this parasite, what is the life cycle and how do you make the diagnosis?

A

Muellerius capillaris

  • L1 passes in feces
  • Indirect LC w/ snails & slugs as intermediate hosts

Diagnosis w/ larval culture - kinked tail

200
Q

What is the main lungworm of cattle? pathological effects?

A

Dictyocaulus viviparous

  • Direct LC- similar to D. filaria in sheep (temperate)
    • larval tail is a short spike
  • cough, laboured breathing, hypersensitivity rxn
  • disease mainly seen in calves
    • develop strong immunity
  • Pilobolus spores help L3 move along pasture
201
Q

What is the equine lung worm? Where is it found and what is the life cycle pattern? What features allow you to diagnose?

A

Dictyocaulus arnfieldi

  • trachea of donkeys, horses, etc - mild path.
  • Direct LC
  • DX: eggs passed in feces not L1
    • larvae have pointy tail
202
Q

What are the 3 main lung worms of pigs? LC & location? Effect on host?

A

Metastrongylus apri, M. salmi & M. pudendotectus

  • Location: bronchi
  • LC: Indirect
    • Eggs coughed up, swallowed & passed in feces
    • IH: earthworms (L1-L3) > pig ingests
    • L3 moults in mesenteric LN > L4 moults in lungs
  • Pathogenesis
    • resp. airway disease/obstruction
    • nodular formation of lungs & fibrosis
203
Q

In North America, white tailed deer have no clinical signs when infected with what lung worm? What is the lIfe cycle and who is the abnormal host? What happens to the abnormal host population when they are infected with this parasite?

A

Parelaphostrongylus tenuis

  • adult worms lay eggs in cranial venous sinuses > eggs carried to lungs & hatch to L1
  • L1 enters alveoli and via mucocillary escalator passed in feces
    • L1-L3 develop in snail - ingest L3 via snail
    • L3 exsheathment in abomasum migrate through wall
  • follow nerves> spinal cord (dorsal horns of grey matter) > subdural space> cranial venous sinuses
  • Abnormal host
    • moose, cattle, sheep
      • neurologic disease> fatal
204
Q

In NZ, red deer have no clinical signs to what lungworm? What is the LC and who is an abnormal host?

A

Elaphostrongylus cervi

  • occur in connective tissues & meninges
  • L1 enters blood & reaches lungs
    • IH: snail
  • abnormal host
    • other ruminants
    • neurological signs
205
Q

Winter in VIC (and other temperate zones) cats eat snails and many present with mild cough, weight loss, and eosinophilia. What parasite could cause this? Where are they found and what is the LC? How do you diagnose?

A

Aelurostrongylus abstrusus

  • Site: alveoli & blood vessels
  • LC: Indirect
    • L1 in feces > penetrates snail
    • L3 develops in snail and ingested
    • other transport hosts
      • rodents, lizards, birds
    • L3 penetrates gut wall> blood> lungs
  • PPP= 6 wks

Diagnose - larvae in feces - kinked tail

206
Q

What are the 3 lungworms of dogs and where are they found?

A

Angiostrongylus vasorum - pulm. artery

Oslerus osleri - trachea

Filaroides hirthi- alveoli

207
Q

What are the effects of Angiostrongylus vasorum in dogs? What is the LC and how can you diagnose?

A

Pathogenesis

  • mild cough,interstitial pneumonia
  • right ventricle/pulm. a.
    • edema, jugular pulse
    • congestive heart failure, liver, kidney

LC: Indirect PPP= 4-8wks

  • eggs released in pulm a > L1 migrates through lungs and passed in feces

Diagnose : barbers pole appearance

208
Q

Nodules and adult nematodes found in a trachea of a dingo, commonly transmitted to young through feed regurgitation. What is this parasite and what is the life cycle? How do you treat?

A

Oslerus osleri

  • LC: direct (L1 in feces or vomit)
    • adults migrate from lung to trachea > larvae penetrate duodenum > migrate to lung where all moults occur
    • PPP= 9wks
  • TX: fenbendazole @50 mg/kg/day for 7d
209
Q

Focal granulomatous lesions (looks neoplastic) were found on the lung parenchyma of a beagle. What is this parasite?

A

Filaroides hirthi

  • drect LC - L1 passed in feces
210
Q

This rat presented with no clinical signs but can cause pathogenesis in abnormal hosts. What is it and what are the effects?

A

Angiostrongylus cantonensis

  • LC- indirect
    • IH: snails, crabs & prawns and pass in snail slime
      • L3 penetrate gut> brain > L4 > pulm a final moult
  • Abnormal host
    • dog, cat, horse, zoo animals, humans
      • severe encephalitis (neuro)
      • eosinophilic meningitis
211
Q

What are the 6 characteristics of an anthelmintic?

A
  1. specturm of activity**
  2. administration
  3. safety margin**
  4. selective toxicity
  5. withdrawl period
  6. economical
212
Q

Why would you use a tertiarty benzimidazole (eg. Fenbendazole or Oxfendazole) over a primary benzimidazole (eg. Thiabendazole)?

A

1º - broad spectrum but not effective against inhibited larvae or Ostertagia.

3º- highly effective against Ostertagia, will kill hyperbiosed larvae and migrating S. vulgaris

  • Tertiary BZ’s also have a longer half life
    • ​modified side chains ^ metab
213
Q

MOA of Benzimidazoles

A
  • inhibits polymerization of tubulin
    • microtubules polymerised in nematode gut cells
  • OVICIDAL
214
Q

How do you administer benzimidazoles (BZs) how are they metabolized in ruminants?

A

Admin: oral“white” drenches

Metabolism (3º BZs widespread use)

  • form depot in rumen and absorbed
  • metabolised to sulphoxide in liver
    • sulphoxide: anthelmintic properties
  • sulphoxide to sulphone
    • sulphone: anthelmintic properties
  • metabolites diffuse across gut wall from blood to lumen
  • excreted in urine
    • ABZ excreted in bile
      • good for treating liver flukes
215
Q

When would you use benzimidazoles in ruminants?

A
  • kills all “strongyles”, trichostrongyles & lung worms
    • **fendendazole resistance in trichostrongylus of sheep
  • kills inhibited larvae & migrating larvae
  • non toxic (safety index > 10)
216
Q

When would you use benzimidazoles (BZs) in horses? What nematode is it not effective against?

A
  • Drug depot in large intestine
  • widespread use - kill adult strongyles & migrating S. vulgaris larvae
  • NOT effective against inhibited cyathostomes (encysted) & widespread resistance (sm. strongyles)
217
Q

What BZ do you use in cats/dogs? How do you administer and why?

A
  • Mebendazole
    • no “depot” so must give 3-5 days of doses bc cleared quickly
  • effective against adult nematodes
    • not effective against inhibited larvae (Ancylostoma)
218
Q

MOA of Imidazothiazoles- Levamisole?

A
  • acts on nervous system
    • cholinergic agonists at synaptic and extrasynaptic nicotinic ACh receptors (motor end plates) > ^ Na+ into cell
    • depolarisation causes spastic paralysis
219
Q

What drug class is broad spectrum and known as a “clear” drench? What’s it’s activity and pharmacokinetics? How do you administer?

A

Imidazothiazoles- Levamisole

Activity

  • All GINs & lung worms
  • NOT effective against inhibited larvae & flatworms
  • immunomodulation at low doses
  • Safety index: 5
  • NOT ovicidal

Pharmacokinetics

  • absorbed rapidly and excreted in urine 6 hrs

Administration

  • Oral, SQ, topical, intraruminal inj.
220
Q

Imidazothiazoles (Levamisole) has resistance to what nematode in sheep?

A

Trichotrongyles

221
Q

Do you use Imidazothiazoles (Levamisole) in horses?

A

No - causes excitement

222
Q

What are Imidazothiazoles (Levamisole) effective against in dogs/cats?

A

hookworms & lungworms

223
Q

MOA of Tetrahydropyrimidines (pyrantel & morantel)

A

nicotinic agonists- depolarise motor end plates in muscle (same as levamisole)

Safety index: 7

224
Q

Differences b/w Pyrantel tartrate, Pyrantel pamoate, and Morantel tartrate?

A

Pyrantel tartrate

  • white powder soluble in water- absorbs well orally in dogs, pigs and rats
    • in dogs excreted in urine

Pyrantel pamoate

  • yellow power insoluble in water- poorly absorbed in GIT and excreted in feces
  • safe in young/weak animals

Morantel tartrate

  • water soluble, rapidly absorbed & excreted in urine
  • used in ruminants against GINs not lungwoms
225
Q

What do tetrahydropyrimidines act against?

A
  • GINs
    • NOT lungworms
    • NOT inhibited larvae
226
Q

What is the use of Tetrahydropyrimidines in sheep/goats?

A
  • morantel tartrate
    • against common GIN
    • resistance in trichostrongyles
    • no activity against lungworms
227
Q

What is the use of Tetrahydropyrimidines in pigs?

A
  • Pyrantel tartrate against roundworms and nodular worm (Oesophagostomum spp.)
228
Q

What is the use of Tetrahydropyrimidines in dogs/cats?

A
  • Pyrantel pamoate - against hookworms (Ancylostoma & U. stenocephla) and roundworms
  • recommended for all ages (even preg)
229
Q

What is the use of Tetrahydropyrimidines in horses?

A
  • Pyrantel tartrate - lg & sm strongyles
    • not effective against encysted cyathostomes
      • & resistance reported
    • safe all ages
  • Pyrantel pamoate - lg strongyles and cestodes
230
Q

Why cant you use pyrantel, morantel and levamisole concurrently?

A

They all have similar mechanisms of action

231
Q

MOA of Macrocyclic lactones

A
  • MLs bind w/ high affinity to a GABA receptor (trigger Cl- influx)
  • hyperpolarization of neuron and prevents initiation/propagation of normal APs
  • flacid paralysis
    • somatic musculature > parasite unable to stay on host
    • pharyngeal pump > affects nutrient ingestion
  • Death of nematodes and arthropods
232
Q

What drug class is an endectocide?

A

MLs- act on all GINs and Arthropods

-safe (SI: 20) and effective @ low doses (not ovicidal)

233
Q

Pharmacokinetics of MLs? - administration, absorption/metab?

A
  • Admin: oral, injectable or pour-on
  • absorbed rapidly
    • short half life after oral admin
    • parenternal half life (ivermectin): 14d
    • moxidectin (cydectin) half life: 28d
      • can have long acting (SQ admin): 3 mo

*variability w. pouron bc inter-animal & host licking

234
Q

What is the use of Macrocyclic Lactones in sheep?

A
  • mainly oral - widely used
  • ivermectin resistance in trichostongyles
  • cydectin effective
235
Q

What is the use of Macrocyclic Lactones in cattle?

A
  • injectable and pour-on used
  • kills inhibited Ostertagia
  • resistance in Cooperia
  • **lactating dairy cows: use eprinomectin
    • ​0 withdraw w/milk & meat
    • pour-on
  • Dormectin used
236
Q

What is the use of Macrocyclic Lactones in horses?

A
  • oral
  • ivermectin kills 10% of inhibited cyathostomes
  • moxidectin kills 80%
    • resistance in cyathostomes
237
Q

What is the use of Macrocyclic Lactones in dogs/cats?

A
  • milbemycin & ivermectin - effective against heartworm larvae present in blood
  • selamectin - external and internal parasites
  • moxidectin - SC 55d before pregnancy
    • prevents nematode transmammary transmission in dogs
238
Q

What are the residual effects of MLs in the feces/environment?

A
  • persists in dung - kill arthropods
  • may have detrimental environ effects
239
Q

MOA of Organophosphates (Naphthalophos & Dichlorovos)

A
  • binds and inactivates AChE irreversibly > spastic paralysis due to non-inactivation of ACh
240
Q

What are OPs effective against?

A

Hemonchus (need high doses to kill Trichostrongylus and Ostertagia)

  • only used in sheep
  • used in combination where resistance is a problem
241
Q

MOA of Heterocyclic compounds (Piperazine)

A
  • agonist of GABA receptors - flaccid paralysis
    • hyperpolarisation of nerve endings
    • disloged from intestinal lumen
    • expelled from normal peristaltic action
242
Q

What is the action of Heterocyclic compounds (Piperazine)? (admin, tox, target?)

A
  • Narrow spectrum- ascarids & nodular worms
  • rapidly absorbed and excreted in urine
  • given orally
  • low toxicity - safe in all animals
243
Q

Besides targeting roundworms (Ascarids) what uses do Heterocyclic compounds (Piperazine) have in horses, dogs/cats and pigs?

A

Horses

  • pinworms and large strongyles (S. vulgaris)

Cats/Dogs

  • just ascarids

Pigs

  • Oesophagostomum spp.
244
Q

MOA of Salicylanilides (Closantel)

A
  • uncouples oxidative phorphorylation
    • act in mitochondria
245
Q

What is the action of Salicylanilides (Closantel)?

A
  • highly effective against blood feeders
    • cannot penetrate cuticle
    • eg. Hemonchus & Ancylostoma
  • narrow spectrum
  • Admin: orally - absorbed and binds to plasma proteins> persists 4-6 wks
  • Safety Index low : 5
246
Q

What is the drug of choice against Hemonchus contortus in sheep?

A

Salicylanilides (Closantel)

247
Q

MOA of Cyclic depsipeptides (Emodespside) & when is it used

A
  • MOA: flaccid paralysis by binding latrophlin receptors in parasitic nematodes
  • effective against most nematodes - used in cats
248
Q

MOA of Amino-acetonitrile derivatives (ADD’s - Monepantel)

A
  • binds nematode specific nicotinic ACh receptor - cannot close > Na+ influx = spastic paralysis
  • safe bc receptor only in nematodes (SI: 30)
  • mostly converted to sulphone in liver ( long halflife in plasma) and most passes in feces
  • effective against most GINs in ruminants except lungworms
249
Q

MOA of Derquantel? It’s toxic to horses and used in sheep what is the action?

A

MOA

  • nicotinic antagonist > flaccid paralysis
  • does NOT kill nematodes

Action

  • effective against Dictyocaulus
  • successful when combined with Abamectin
  • “medium spectrum”
250
Q

2 Advantages of Broad Spectrum Anthelmintics?

A
  1. makes admin easier against mixed infections
  2. treated animal will likely be cleared of untreated parasites
251
Q

What anthelmintics are recommended against encysted larvae?

A
  • fenbendazole & moxidectin
252
Q

What is the best deworming regimen for pups and pregnant bitches?

A

Pups

  • tx every 2 weeks pre weaning
  • tx every 4 weeks post weaning
  • tx every 3 months after 6 m/o

Preg

  • Fenbendazole 50mg/kg/day from 3 wks prepartum to 2-15 d postpartum
  • Moxidectin 1mg/kg given SQ on pregnancy day 55 prevents nematode transmammary transmission
253
Q

When do you see an increase in anthelmintic resistance?

A

-after “lag” period - increase in gene frequency

254
Q

What is double resistance?

A

When one genus of parasite (ostertagia) is resistant to one class of anthelmintic (BZs) while another genus (Hemonchus) is resistant to a different anthelmintic class (levamisole)

  • use drugs together to eliminate parasites
255
Q

What is multiple resistance?

A

When a single genus is resistant to 2 drug classes (eg. BZs and levamisole) - though uncommon

256
Q

What is side resistance?

A

when parasites develop resistance to one benzimidazole they are resistant to other benzimidazoles

257
Q

Where is anthelmintic resistance mostly a problem? What are the main parasites involved

A

sheep & goat (BZs and LEV especially)

  • Trichostrongylus, Ostertagia, & Hemonchus
258
Q

In cattle, what is Cooperia oncophora resistant to?

A

BZs & avermectins

259
Q

What are the factors that influence anthelmintic resistance?

A
  • polymorphism in nematode population
  • initial frequency of resistance alleles
  • number of genes involved
  • fecunditiy & length of life cycle
    • shorter LC = higher fecunditiy = higher chance of resistance
  • resistance gener dominant or recessive
  • treatment frequency & proportion of nematode population exposed to a drug
    • deworm only 70-80% of population
  • pharmacokinetic profile of drug
    • enough to remove parasite dont want subtheraputic
260
Q

What are 4 mechanisms of anthelmintic resistance?

A
  • Reduced drug uptake
  • Increased drug efflux
  • detoxification at its site
  • Altered target (binding site-receptor)
261
Q

What drug class has the least resistance to cyathostomins (small stongyles) in horses?

A

MLs (most resistance w/BZs and Pyrantel)

262
Q

How can you test for anthelmintic resistance?

A

Laboratory tests

  • egg hatching inhibition w/ BZs (ovicidal)
  • tubulin binding assays w/ BZs
    • no radioactivity = resistance
  • L3 paralysis test w/ LEV/ML
    • migration through mesh
  • larval development test = Drenchrite test

Field

  • Fecal egg count reduction test
    • test 2 dif. dewormers in sheep w/existing burdens
    • FEC > 250epg
    • resistance if less than 95% reduction
263
Q

What does the Drenchrite test tell you in terms of resistance?

A
  • isolate eggs from feces
  • determine level of resistance for BZ and LEV
264
Q

How can you manage anthelmintic resistance? (6)

A
  1. check timing & admin of drenches (2 summer)
  2. check mgmt practices
    1. pre/post trx FEC & pasture mgmt
  3. double doses?
    1. no use with BZs and temporarily effective w/LEV
  4. rotation and mixtures used (eg. BZ,LEV,ABA)
  5. Quarantine drenches for all introduced sheep
  6. use effective drench (eg. monepantel)

Parasitology (5 decks)

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