Parasitology 2 Flashcards

1
Q

What makes a arachnida, the features and the two parts of the body

A
  • 4 pairs of legs (3 pairs in larva)
  • no antennae
  • no wings
  • body divided into 2 parts
    1. gnathosoma (= capitulum)
    [modified for specialised feeding]
    2. idiosoma (= the rest)
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2
Q

Features of Ixodoidea

A

Ticks

  • obligate parasites - neeed blood meal
  • most of life cycle is spent off host (in most cases)
  • variable host specificity (specialist (like a certain host - parasitise one host) / generalist)
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3
Q

What is the mouth piece of the tick and how does it work

A
  • Flanked by palps - length and shape differentiate between species
  • Tip of hypostome structures called chelicerae (cut into host)
    ○ Saliva is secreted which acts as a cement that lodges tick onto host via hypostome
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4
Q

What are the 3 distinct features you look for with ticks and the variations

A

1) anal groove
- present, posterior or anterior
2) Festoon - present ‘ornate’, doesn’t have then ‘inornate’
3) with or without eyes
- located near the edge of the scutum in females and near the second leg on the side in males

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5
Q

Tick life cycle at what stage how many legs

A
  • larva (6 legs)
  • nymph (8 legs) - looks like mini adult
  • male and female (8 legs) - males tend to be more colourful, scutum is the whole back unlike females
    ○ When female drink blood they can expand rapidly - can drink lots of blood
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6
Q

What are the 3 types of tick lifecycles

A

1) 1 host tick, feed as larvae moults to nymph feeds then moult to adult
2) 2 host tick
1. first host
- Larvae feed become nymphs and then leave the host
- Lymph feeds and engorged nymphs will drop and find next host
2. second host)
- Become an adult and reproduce
- Females drop off and lay eggs
3) 3 host tick
2. Hatch into 6 leg larvae
3. 1st host, feed moult to lymph
4. 2nd host feed, moult to adult
5. 3rd host feed and reproduce
6. Female drop off and lay eggs - repeat

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7
Q

how do ticks get onto their host

A

Hunting
- Move up stick or blade of grass
- Tendrils on legs that allow you to grasp onto what walks by
- Questing - move around there legs
Are also about to see if have eyes, detect CO2 - very good hunters

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8
Q

What is the generalised soft tick lifecycle

A

Multiple hosts and lymph stages
- Need to have a blood meal between lymph stages moult
- Can be huge problem for poultry
1) 1st host Larvae moult into 1st lymph stage
- Between stages stay in environment - constantly leaving the hosts and infest the environment
○ Chicken coops are the perfect area
2) 2nd host (can be the same host), feed, moult to 2nd lymph stage
3) 3rd host, feed, moult
4) Can be repeated 7 times depending on the species
5) Finally adult and reproduce

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9
Q

List 6 effects ticks have on their host

A
  1. blood loss (tick can take 5ml of blood) - if have thousands on animals - losing litres of blood
  2. irritation, hypersensitivity
  3. damage hide - industry issue, production
  4. reduce growth rate of host
  5. produce toxins (can lead to paralysis)
  6. transmit protozoans*
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10
Q

List the 3 main differences between Ixodidae and Argasidae

A
Family Argasidae
“soft ticks”
- no scutum
- mouthparts underneath
- rapid feeders (hours)
○ Allows them to parasitise so many hosts 
Family Ixodidae
“hard ticks”
- scutum present
- mouthparts anterior
- slow feeders (days)
○ If producing a toxin the longer the feed the more concentrated the toxin
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11
Q

Argas persicus common name, type and distinctive features

A

the fowl tick
- soft tick
- reddish tick
- mouthparts concealed
- distinct patterned margin to body - IMPORTANT DISTINCTION
○ Colouring more concetrated at margin of anterior side

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12
Q

What is the lifecycle of argas persicus, how long can it survive

A
  1. eggs laid in cracks
  2. hatch in 3 weeks
  3. larvae feed for 5-10 days - unusual for soft ticks normally rapid
  4. moult in crevices
  5. nymphs feed in 2h
    - nymph and adult nocturnal - if check chickens during the day won’t see, may see larval stages (due to long stage of feeding)
    - larvae survive for 3 months without food
    - adults survive for 3-5 years without food - just burn it down (chicken coop)
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13
Q

What is the pathogenesis, diagnosis and treatment for argas persicus

A

1) Death due to paralysis from larvae
2) anaemia
3) irritation
4) reduce egg production
5) transmit: ○ Borrelia anserina (tick fever) and
○ Aegyptianella pullorum
Diagnosis :
- find larvae on birds
- find adults in sheds
Treatment :
- organophosphate spray
- kerosene emulsion - burn the chicken coop as adults can last 3-5 years

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14
Q

Ornithodoros common names, where found, where live, host species, effect on host

A
“tampan ticks”
- Or. moubata in Africa
- Or. gurneyi in Australia
○ live in sand
○ feed on any host species
○ cause painful bites
○ transmit Q fever
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15
Q

Otobius megnini common name, where found, hosts, where found on host

A

spinose ear tick

  • in North America, Africa
  • adults free living
  • larva & nymph live in ear - painful, balance is off
  • horses, cattle, dogs
  • found recently in WA
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16
Q

Ixodes what features are unique, are they native and list the 2 main examples and what they cause

A
  • long palps
  • anal groove in front of anus
  • native ticks
    I. holcyclus and I.cornuatus cause paralysis
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17
Q

Ixodes holocyclus lifecycle, host, seasons and what sex found on host

A
  • 3 host tick
  • on native mammals
    ○ Bandicoots are common host
  • life cycle takes 18 months
  • larvae & adults in spring
  • nymphs mainly in autumn
  • males rarely found on host
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18
Q

Ixodes holocyclus effect on host, which hosts most susceptible, when do clinical signs develop

A
  • all stages cause irritation & paralysis
  • sheep, dogs & cats most susceptible: 1 female tick will kill a dog
  • calves & foals also susceptible : 4 female ticks can kill a calf
  • can affect humans (homophilic tick)
  • females engorge for up to 21 days
  • signs develop on days 5-6 - detect in domestic species at this time
    ○ ascending motor paralysis - die from paralysis of respiratory muscles
  • intense vasoconstriction
  • native & domestic animals can develop immunity - if doing tick checks
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19
Q

Ixodes holocyclus treatment and distribution

A
  • find & remove tick - very tiny, larval ticks look like a grain of sand (ears, underneath neck, under arm and legs)
  • acaricidal wash
  • hyperimmune serum
    Other species - *Dermacentor variabilis and D. andersoni cause paralysis (North America)
    Distribution
  • Unsure of exact distribution - more commonly around coast
  • Can occur in Melbourne
    Can be transported by human activity
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20
Q

Boophilus features list 4

A
  • short palps with ridges
  • pale legs - in comparison to the body
  • anal groove behind anus, difficult to see
  • engorged female has “waist” (sometimes)
    ○ Sometimes look like they have a belt
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21
Q

Boophilus microplus common name, where found, hostss

A

the cattle tick

  • occurs in Central & South America, Southeast Asia
  • introduced into northern Australia, goes into Queensland and down into northern NSW
  • major cattle disease in northern Aust.
  • host specific but occurs occasionally on horses, sheep, dogs & pigs
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22
Q

What is the lifecycle of Boophilus microplus

A
  • 1 host tick
  • life cycle takes 22 days
    1) eggs hatch
    2) “seed ticks” climb up grass
    3) attach to passing cattle via questing
    4) Moult to larvae & nymph remain on host
    5) Moult to adult and reproduce
    6) female ticks drop off after 18-37 days, most on day 22
    ○ drop off mainly in early morning
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23
Q

Boophilus microplus what are the 5 effects on the host

A

the cattle tick
1) irritation - ticks removed by grooming
2) damage to hides - loss of 25% of value
3) anaemia - each tick takes 1-5 ml blood
○ Resulting in anorexia (reduced appetite)
4) reduced growth rate and milk production
5) transmit protozoans**
○ Babesia
○ Anaplasma
○ Theileria

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24
Q

Boophilus microplus distribution in 1) southern limits 2) dry tropics and 3) wet tropics

A
○ Temperature humidity
1) at southern limits (SE Qld):
○ uniform rainfall and cool winters
§ winters suppress tick development
○ takes 3-4 generations in spring to build up again
2) dry tropics
○ temp. never limiting
○ dry winters
§ tick numbers increase in wet season
3) wet tropics
○ temp. never limiting
○ rain in all months
○ ticks all year round
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25
Q

Dispersal and survivial of Boophilus microplus on the soil

A

cattle tick
- larvae accumulate around site of egg mass
- can migrate short distances (<1m)
- can be blown up to 30m
- cattle avoid heavily infected areas
- can “spell” paddocks to control ticks
○ depending on climate, harder with warm weather and high humidity
- in summer 50% live 2 weeks, 10% live 4 weeks
- can be up to 11 weeks in cool weather

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26
Q

List 3 ways to control Boophilus microplus and which breed most resistant

A

the cattle tick
very good at developing resistance
1) chemicals
2) growth regulators - flurazuron
- zebu cattle naturally more resistant so require less
3) vaccine - ticks grow poorly and have low fecundity (not laying as many eggs)
- 70% effective, need 2 vaccinations

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27
Q

What are the features of the Haemaphysalis

A
  • anal groove behind anus - others in front

- lateral projections on palps

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28
Q

H. longicornis common name, is it native, hosts, where occur and effects on host

A
  • introduced into Australia
  • common in SE Asia
  • occurs on cattle & other hosts (eg., horses, dogs)
  • 3 host tick
  • occurs in eastern Australia
    ○ common in eastern Victoria
  • causes anaemia and hide damage
    ○ vector of Babesia gibsoni of dogs
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29
Q

List the 3 Features of Rhipicephalus

A

1) anal groove behind anus
2) basis capituli projects - projections (the neck where the mouth parts connect)
3) forked first coxa

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30
Q

R. sanguineus common name, is it native, where common, what are the 2 effects on host

A
brown dog tick”
- common in tropical countries
- introduced
- common in northern Australia
- uncommon but present in Melbourne
- causes anaemia and irritation
- vector of Babesia canis of dogs
○ Rocky mountain fever - kills children
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31
Q

Aponomma & Amblyomma features list 3 and list hosts

A

1) long mouthparts like excytoes
2) anal groove behind anus (unlike excytoes)
3) often brightly coloured
Hosts
- important on cattle in Africa and USA
- most Australian species occur on reptiles (one on wombat, one on echidna, one on kangaroos)

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32
Q

Features of arachnids and the two areas of the body

A
○ ticks and mites (parasitic)
- 4 pairs of legs (3 pairs in larva)
- no antennae
- no wings
- body divided into 2 parts 
1. gnathosoma (= capitulum)
[modified for specialised feeding] - chelicera - cutting
2. idiosoma (= the rest)
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33
Q

Features of mites, mouth parts, lifecycle. type of parasites, where found

A
  • abundant, most free-living
  • lack rows of teeth on hypostome
  • have capitulum with palps and chelicerae
  • life cycle : egg, larva (with 6 legs), can have several nymphs (proto-, deuto-, trito- depending on lifecycle), adults
    ○ Similar to ticks
  • can be : intermittent parasites in nests or burrows, or permanent parasites
  • can be on: skin, in ears or respiratory system
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34
Q

List 4 generalised effects on hosts of mites

A
  1. blood loss
    - Only in heavy infestation
  2. Irritation
    - Can lead to hypersensitivity
  3. hair loss
    - Mange mites
  4. vectors of disease
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35
Q

In terms of spiracles where are they found on mesostigmata, trombidiformes and sarcoptiformes

A

Orders of the mites
Mesostigmata - Spiracles between coxae
Trombidiformes - Spiracles on capitulum (mouth parts)
Sarcoptiformes (no spiracles - respiration through body wall)

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36
Q

Ornithonyssus spp common name features, host, lifecycle and effect on host

A
  • common on wild birds
  • found in bird nests
  • referred to as “starling lice” - not lice but can feed on bees
  • feed on birds while in nest
  • some remain on birds all the time
  • blood feeders
  • not host specific***
    ○ Not able to reproduce but can bite other hosts
    Effect on host
    1. cause severe anaemia
    2. reduced egg production
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37
Q

Dermanyssus gallinae common name, general features, hosts, lifecycle and effects on host

A
  • triangular anal plate* important
  • parasite of birds & mammals
  • life cycle : eggs, larva, 2 nymphs, adults
  • eggs laid in crevices (like the chicken coop, hoping on and off the chickens, can use the same host but need to come off and go back on for a feed between life stages) - life cycle 7 days
  • nocturnal
  • blood feeders
    Effect on host :
    1. anaemia
    2. irritation
    3. transmit Borrelia anserina - (Spirochaetosis in birds)
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38
Q

Varroa destructor what order, what causes, and what leads to

A

honey bee mite
- causes varroosis
○ sucks hemolymph
- most pronounced economic impact on beekeeping industry
- contributing factor to colony collapse disorder
- Transmit viruses and bacteria

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39
Q

Order TROMBIDIFORMES s.o. PROSTIGMATA common name and main features

A
  • referred to as “trombiculids” fuzzy ones)
  • stigma on capitulum
  • feather-like setae
40
Q

Genus Trombicula

A

Trombidiform mites from Trombidiforme order
- referred to as “trombiculids
- only larvae are parasitic
○ Need microscope to see them - different to ticks
- attach in clusters
- transmit scrub typhus (Rickettsia australis)
- Causes painful bites with high irritation
- T. sarcina causes “black soil itch” in Qld
○ causes extreme itching, inflammation
○ reddish larvae revealed in papules microscopically

41
Q

features of demodex canis, physical, lifecycle, transmission

A
  • vermiform (wormlike)
  • legs very short at front of body
  • Localisation : hair follicles
  • feed on cytoplasm
    Life cycle :
    1. egg, larva, 2 nymphs, adults
  • (all stages in hair follicles)
    Transmission :
  • contact during suckling as spend all the time on the hair
    ○ Puppies affected often from mum
  • Host specific
    ○ May see some transmission but don’t last long, need to be in very close contact
42
Q

Demodectic mange how develop disease, what age affected, what can it lead to and clinical signs

A
  • all dogs infected
    ○ only some develop disease, high stress, immunocompromised
    ○ short-haired dogs with CMI deficiency (cell mediated immunodeficiency)
  • mainly 6-10 months of age
  • predilection sites eyes, ears muzzle
  • secondary infection with Staph. albus
  • infection of follicles leads to hair loss & hyperkeratosis (thickening of the keratin
  • Disease can be : localised (head or limbs) or generalised (anywhere)
  • squamous or pustular (2°infection)
43
Q

How to diagnose demodectic mange, what does it suggest

A

NEED TO DIFFERENTIATE BETWEEN SARCOPIC MANGE - not as inflamed as sarcoptic
do deep skin scraping to determine between
Suggests underlying disease - need to find that

44
Q

demodectic mange what is the treatment for the 2 types of infection and what causes an issue

A

Treatment :

  1. Localised infection - resolve spontaneously
    - rotenone-based insecticide ointment
  2. Generalised infection - extended, aggressive therapy
    - benzoyl peroxide shampoo - first
    - Amitraz dip (Mitaban) - second
    - high-dose oral ivermectin, oral milbemycin oxime, topical moxidectin, injectable doramectin - third
    * *breeds with mutations in their MDR1 genes have an increased risk of toxicity
    - Dog breeds - collies, Shetland sheepdogs,
45
Q

Psorergates ovis common name life cycle, transmission, where found and seasonal occurance

A

The sheep itch mite
life cycle : egg, larva, 3 nymphs, adults (5 weeks)
Transmission : contact (suckling, shearing - other animals in contact with fleece)
Predilection sites : sides, between hip & shoulder near mid-line
Seasonal occurrence : most abundant in winter

46
Q

Psorergates ovis common name, effect on host, diagnosies and treatment

A
sheep itch mite 
Effect on host : 
1. hypersensitivity causes irritation,
2. rubbing, “pulled wool” 
- not all sheep affected and spreads slowly in mob
○ Unlike damilimia 
Diagnosis : skin scraping
Treatment : none, amitraz, OP’s, ivermectin; will not eliminate mites
- Separate and cull affected sheep
47
Q

List the 3 species within genus cheyletiella, main features, effect on host

A
C. parasitivorax rabbits
C. yasguri dogs
C. blakei cats
Features : claw on palp
Effect on host :
	1. mild mange
	2. often around head
	-  “walking dandruff”
	- can bite humans, doesn't sexually reproduce
48
Q

Sarcoptes scabiei features, lifecycle and transmission

A
  • triangular scales on dorsum - used for identification
  • wide host range
    ○ strains on specific hosts (eg. “var. canis”) - definitive host
  • can survive but not reproduce on other hosts
    Life cycle :
  • lives in superficial layers of skin
  • lay eggs in tunnel
  • larva and 2 nymphal stages
  • life cycle 10-17 days
  • mites survive for few days off host
  • transmission by contact
49
Q

Sarcoptes scabiei

Pathogenesis :

A
  • burrowing mites cause irritation
  • intense pruritus (itching)
  • hyperkeratosis
  • alopecia
  • lesions begin on face, extend over body
  • Only need a couple of mites to cause damage and not just immunocompromised (unlike Demodex)
  • 2º infection, pustules
  • self-inflicted trauma
  • Extreme hypersensitivity**
50
Q

Sarcoptes scabiei host and diagnosis

A
Host
- canine “specific”
- same variety on dogs and foxes
- dog mites can cause lesions on humans
- self-limiting
Diagnosis :
- deep skin scrapings to get the burrowing female and eggs - need to differentiate between demodex
- can be difficult to find mites
- response to treatment - indicator
51
Q

Sarcoptes scabiei treatment, control and other hosts that can be affected

A

Treatment :
- selamectin, topical moxidectin/imidacloprid
- Corticosteroids - prevent inflammation temporary but make the mange mites worse DON’T USE
- Can take up to 3 months to get over
Control:
- routine use of fipronil, topical moxidectin, selamectin
Other hosts affected
- Pigs, camels, ferrets, wombats, humans
- Subspecies preferences for different host - all have the same pathogenicity

52
Q

How to tell the difference between psorptes and chorioptes

A

Psoroptes - jointed pedicles and more defined caruncle

Chorioptes - simple pedicles (not jointed) - smaller caruncle

53
Q

Otodectes cynotis common name, host, effect on host, diagnosis and treatment

A
  • common ear mite of dogs and cats
    ○ also occurs in foxes and rabbits
  • causes scabs in external ear canal - very painful, don’t remove
  • hosts shake heads and rub ears
  • transmitted by contact, often while suckling
    Diagnosis : with otoscope, unreliable
    *examine exudate under microscope
    Treatment : topical moxidectin/imidacloprid and selamectin
54
Q

Psoroptes ovis common name, where live, what feed on, lifecycle, pathogenesis and is it present in australia

A
  • live under scabs
  • feed on tissue fluids, cause serous exudate
  • life cycle 9-10 days
  • high biotic potential - can reproduce very quickly, perfect environment
  • irritation, scabs, hypersensitivity
  • starts on shoulders and back, spreads over whole body
  • in latent cases can occur in ears, inguinal folds, interdigital spaces
  • most abundant in cool weather
  • can have emaciation & high mortality
  • eradicated from Australia
55
Q

Psoroptes cuniculi common name, hosts, what does it cause to what effect and treatment

A

ear mite
Hosts : rabbit, horse, goat, maybe alpaca
- causes “ear mange”
○ may spread onto face
- common in lab rabbits, if one gets it all gets it with close contact
- causes irritation, shaking of head, self-mutilation - extremely painful
- mites can “eat” the ears
Treatment: Avermectins (treat before removing crusts - painful!)
- If you wait awhile scabs can lift off the animal

56
Q

Chorioptes bovis what is it, what does it cause, hosts, where occur and treatment

A

A mite

  • causes chorioptic mange
  • cattle, sheep, goats, horses
  • occurs mainly on legs, belly
  • commonly seen in housed sheep & cattle
  • referred to as “barn itch” (can cause scrotal mange in rams)
  • Treatment - should be able to treat
57
Q

Nematoda generally features

A
  • insegmented
  • acoelomate - don’t have true body cavity
  • moults between stage
  • most are free-living abundant in soil, marine sediments other are parasitic
  • separate sexes (females generally longer than males)
  • body covered in cuticle
  • females have cloaca
58
Q

nematodes body wall layers, muscles and how move

A

Cuticle of body wall shed during moulting
- outer layer keratin
- inner layer collagen
Hypodermis -> secretes cuticle
Longitudinal muscles -> pseudocoelomic fluid and muscles function as hydrostatic skeleton

59
Q

Nematode nervous system what are the 2 main nerves and other major nerves, nerve rings and neurotransmitters

A

Main - anterior and posterior nerve brain
- 4 major nerves between, ventral, dorsal and 2 lateral
Nerve rings - oesophageal and rectal
Neurotransmitters - ACh and GABA -> drug targets

60
Q

Digestive tract of nematodes what are the structures and the membrane type

A

Mouth, pharynx/oesophagus, Intestine, anus cloaca

Simple columnar epithelium with microvilli

61
Q

What are Amphids, Lancet and Leaf crowns all examples of and function

A

Mouth structures
Amphids - sensory structures
Lancet - pointed projection at end of mouth to help worm penetrate into mucosa in which it sucks blood
Leaf crowns - gut content feeders, direct food into the mouth

62
Q

What are copulatory bursa, spicules, telamon and gubernaculum all examples of and function

A
Male reproductive structures 
Copulatory bursa 
- Extension of the cuticle that helps guide the spicules
Spicules - Expand female copulatory organs 
Telamon - ventral surface
Gubernaculum - dorsal surface 
- Before copulatory bursa
FUNCTION 
- Direct spicules during copulation
- Important for identification
63
Q

What are the 3 reproductive types of nematodes and 4 main routes of transmission

A
  1. Oviparous - eggs
  2. Viviparous - larvae
  3. Ovoviviparous - eggs contain the 1st larval stages
    Routes of transmission:
    • Oral
    • Percutaneous
    • Transplacental
    • Transmammary
64
Q

Order Rhabditida what type of oesophagus, size, freeliving or parasitic, sexes and how many larval stages

A

Rhabditiform oesophagus
tiny nemotodes
Most species free-living (parasitic if oesophagus changes from rhabditiform to filariform (females only))
L1-4

65
Q

Genus stronglyoides what is the lifecycle

A
  1. Present in intestines
  2. Females produce eggs
    - Only the females are parasitic
  3. Eggs passed out in the faeces
  4. Present in environment
  5. Hatch quickly within 6 hours
  6. EITHER
    - PARASITIC - Homogenic lifecycle (only female produce eggs)
    - Egg hatches into L1 - L2
    ○ Rhabditiform oesophagus
    ○ L3 - filariform oesophagus
    § Penetrate skin of sheep and move into heart, then pumped into lungs and start migrating towards the airways, through mucociliary clearance go to pharynx where swallowed and goes into the digestive system
    § L3 moults to L4 which moults to L5 females
    - NON-PARASITIC - heterogonic lifecycle (both sexes are involved in the production of eggs
    ○ Egg hatches L1 - L4 all have rhabditiform oesophagus
    ○ Free living, not infective
66
Q

Genus strongyloides what are the 2 main forms of the life-cycle and what determines which one is taken

A

1) Parasitic - Homogenic lifecycle
2) Non-parasitic - heterogonic lifecycle
Determination
1) sexes - only female can be parasitic
2) Type of oesophagus - Rhabditiform (free living) or Filariform (parasitic)
3) temperature - more than 34 degrees parasitic lifecycle otherwise free-living

67
Q

Genus stronglyoides what occurs with auto-infection, prenatal and trans-colostral infection and which species involved in this

A

1) Auto-infection can occur (Strongloides sercoralis )
○ Hatch with intestinal tract and then develop from L1 - L3, through circulation and parasitic lifecycle without going into the environment
Strongloides sercoralis
2) Prenatal infection - S. ransomi
3) Trans-colostral (mammory) infection - S. ransomi & S. westeri (horses)
○ L3 penetrates the skin doesn’t undergo normal route but go into tissues around the mammary gland - stay for a long period of time
§ If in males, the male will be the dead-end host - parasite will die with the host
○ When partition occurs for females, activate dormant L3 -> Pass through the milk - infect the neonates

68
Q

Genus stronglyoides where most commonly found and PPP

A

small intestines

PPP = 5-12 days (short) depending on if parasitic or free-living lifecycle

69
Q

Stronglyoides ransomi host, 3 main groups of clinical signs, transmission and climate most effective

A
Pigs 
1.  Invasive - dermatitis
2.  Pulmonary - pneumonia
3.  Intestinal – parasitic female burrow in small intestine- diarrhoea - reduced growth rate
Prenatal and transcolostral infection 
Most susceptible in moist conditions
70
Q

Stronglyoides papillosus host, what can lead to

A

ruminants
calf
- Heavy infections in young animals can result in death
- Also leads to dermatitis

71
Q

Genus stronglyoides diagnosis and treatment

A
Diagnosis
• Eggs - faecal flotation
• Larvae - Baermann technique - recover larvae from faeces 
• In vitro culture
• Serodiagnosis – ELISA
Treatment
• Ivermectin
• Oxibendazole
72
Q

Strongylida what are the 4 superfamilies their common names and usual site

A

1) Trichostronglyoidea - trichostronglyes - abomasum, small intestines
2) Strongyloidea - strongyles - large intestine
3) mestastronglyoidea - lungworms - lungs
4) ancylostomatoidea - hookworms - small intestines

73
Q

What are the 2 main features of order strongylida

A

1) Buccal capsule - some well-developed or vestigial - identification
2) Male nematode has a copulatory bursa - that’s why called bursate nematodes

74
Q

Superfamily Trichostongloidea list 4 main features

A
  • vestigial buccal capsule
  • copulatory bursa
  • usually found in small intestine or abomasum/stomach
  • direct life cycle
75
Q

what is the most important nematode of sheep in south-east Australia

A

Trichostrongylis (black-scour worm) - sheep

76
Q

Genus Trichostrongylus common name, where found and distribution of species

A
  • Black scour worm, hairlike worm
    Small intestines generally duodenum (axei in abomasum)
    • higher rainfall areas
    • main sheep raising areas
    • species differ in regions
    ○ T. colubriformis in summer rainfall areas
    ○ T. vitrinus in cooler, moist areas
    ○ T. rugatus in dry areas
    • same principles apply elsewhere in world
77
Q

Genus Trichostrongylus lifecycle with 3 different stages

A

HOST STAGE
1) Adult in small intestines (duodenum) - both female and males present
2) Females produce eggs that are passes in faeces
DUNG STAGE
3) Within environment L1 develops within egg outside
4) Hatch into L1 - feed on bacteria in the environment (faeces)
5) Develop into L2 - feed on bacteria again
6) Develop into L3, cuticle from the L2 doesn’t leave as go into L3
- Protect from harsh conditions of environment - remain infective during winter (overwintering)
PASTURE STAGE
- Move side to side on the pasture
- Sheep pick up from the pasture stage
HOST STAGE
- Exsheathment - disintegration of the cuticle from L2
- L3 moves to the duodenum
- Penetrates the epithelial cells where develop into L4 - adult worms

78
Q

List 5 effects Trichostrongylus has on host

A
  1. villus atrophy
  2. protein loss
  3. reduced absorption of Ca and PO4
  4. anorexia
  5. Diarrhoea
79
Q

Describe how Trichostrongylus leads to Hypoproteinaemia and what associated wtih

A

breaks in epithelium and increased permeability of capillaries lead to
• leakage of plasma proteins into gut - whenever is being eaten isn’t be digested •hypoproteinaemia/hypoalbuminaemia associated with up to 20% reduction in wool production and reduced growth rate
• globulin concentration in blood rises as host mounts immune response

80
Q

Describe how get decrease in Ca and PO4 abosrption with Trichostrongylus and what result in

A

• absorption occurs in duodenum
- flattened villi in intestine cannot compensate so decrease absorption of Ca and PO4
• blood Ca conc. has to be maintained within narrow range
- So compensatory increased by removing calcium from the bone into the blood
- Results in reduced bone growth
• see hypophosphataemia - very low - no compensatory methods to increase

81
Q

Describe anorexia and diarrhoea in sheep with trichostrongylus infection

A

Anorexia
• feed intake reduced
• mechanism not known
• major effect on growth rate
- Different species of infection causes a different rate of decrease
Diarrhoea
• parasites secrete analogues of parasympathetic transmitters
• increase frequency & strength of peristaltic waves
• together with poor absorption, leads to diarrhoea

82
Q

What is involved with the immune response in sheep infected with trichostrongylus

A
  • Immunity mainly TH2 response however can still get scouring in immune sheep
  • Increase mucus production - natural barrier to prevent infection - LOCALLY
    ○ Contains mucin defences - anti-microbial and pro-inflammatory response
    ○ Helps bring certain immune cells such as macrophage, eosinophils, dendritic cells, plasma cells
    ○ Discharge histamine, serotonin, cytokines - lead to expulsion of nematodes
    ○ Eosinophils can kill the larvae
    ○ Type 1 hypersensitivity reactions involved
83
Q

Cooperia common name, hosts, location, size and general features

A

(wire worm - as a thin worm)
Hosts: cattle, sheep
Location: small intestine
Features:
• size - ~9 mm
• small cephalic vesicle
• oesophageal region - transverse cuticular striations
• body - longitudinal cuticular ridges
• spicules - wing-like expansion in the middle region with ridges
• no gubernaculum - tubular structure at posterior end not present

84
Q

What are the 4 Cooperia species within cattle and what zones present in, which is more pathogenetic

A

C. oncophora, C. surnabada - temperate zones (south east)
C. pectinata, C. punctata (“cattle bankrupt worm”) - sub-tropical
More pathogenetic, cause enteritis in young calves

85
Q

Cooperia list the 10 steps in the lifecycle, parasitic or free-living

A

Free living and parasitic lifecycle together - NEED TO BE PARASITIC

  1. Eggs passed in faeces within environment
  2. L1 - hatches out of the egg
  3. Feed on bacteria in environment
  4. Develops to L2, eats bacteria
  5. Develops L3 - INFECTIVE STAGE
  6. Animals infected during grazing (L3)
  7. Exshealthment in rumen then small intestine
  8. Burrow in mucosal glands and develop - different
  9. Develop into L4 and move back to rumen and small intestine
  10. Final moult occurs there
86
Q

Cooperia what is the PPP and what is important within the lifecycle, describe

A

PPP = 15 days - pre-patent period
HYPOBIOSIS - prominent
- L4 stage can temporarily stop development
- Ensure survival of free-living stages within the environment in harsh conditions (hot and dry conditions)
○ When come into cooler weather, autumn will start development again and turn into adult worms to create eggs that then are exposed to environmental conditions that are more favourable
○ Therefore in Southern Hemisphere undergo hypobiosis in summer

87
Q

What are the 5 effects on host and epidemioogy of Cooperia

A
Effects on host: - same as thrichostrongylus
1) villus atrophy
2) erosion of epithelium
3) Diarrhoea
4) hypoproteinaemia,
5) anorexia
Epidemiology:
- ingest larvae during wet season (summer or winter)
88
Q

Nematodirus common name, host, location, size and features

A
Thin-necked intestinal worm"
Host: sheep, cattle
Location: small intestine
Features:
• size ~25 mm
• coiled
• cephalic vesicle
• long thin spicules
• female with spiked tail
• very large eggs**
89
Q

List the 5 species of Nematodirus, host and zones found and which most pathogenic

A

1) N. spathier - Sheep - temperate
2) N. filicollis - sheep - t
3) N. abnormalis - sheep - dry zone
4) N. battus - sheep/cattle - dry not in Aus - most pathogenic
5) N. helvetianus - cattle - dry

90
Q

Nematodirus what are the 5 steps in the lifecycle

A

1) Eggs passed in the faeces
2) L1-L3 in egg - all free living stages (in the environment) are developing within the egg
- need drying or cold to hatch, spring is the main stimulus after long winter or rain
3) Pick up L3 while grazing
4) L3 burrows in mucosal glands, or coil around villi and moult to L4
5) adult in lumen

91
Q

Nematodirus what is important about lifecycle, PPP and 3 main effects on host

A
HYPOBIOSIS - common
- L4 again can stop development 
PPP = 21 days 
Effects on host:
• villus atrophy - adult worms make loop around villi (coiled) 
• erosion of epithelium
• diarrhoea
92
Q

Haemonchus common name, location, size and features

A
(haem - blood; onchus – tooth; barber’s pole worm)
Location: abomasum
• 2-3 cm long - LARGEST IN ABOMASUM
Features:
• red
• tooth in buccal capsule - sucks blood 
• prominent cervical papillae
• “barber’s pole” in female
• female with large vulval flap
• asymmetrical dorsal ray
• spicules with barbs
93
Q

Haemonchus list the 5 steps in the lifecycle and PPP

A

Free living part the same as intestine species
1) Animals infected by eating L3
2) After exshealthment
3) L3 burrows in abomasal glands moult to L4 - NOT INSIDE LUMEN
4) L4 re-emerge to abomasum lumen and starts to feed on blood
5) Moult to adult and continue sucking blood
• PPP = 21 days

94
Q

Haemonchus list 4 effects on host

A

1) L4/adult feed on blood - ingest 0.05ml/worm/day, anaemia, high burden sudden death
2) microcytic, hypochromic anemia
3) Hypoproteinaemia - ucks out protein and open wounds that lead to further loss of protein -> low oncotic pressure in the blood -> leakage of fluid into extracellular space -> accumulate in dependent parts of the body -> “bottle jaw”
4) reduced excercise tolerance
DOESN’T CAUSE DIARRHOEA

95
Q

Haemonchus epidemiology what rely on, egg hatching, increase when in summer and winter, is it present in Victoria

A

Epidemiology = RAINFALL AND TEMPERATURE
• high biotic potential - 5-10,000 eggs/day
• eggs will not hatch below 10ºC - larvae not resistant to desiccation
Summer rainfall - increase in spring, max in Feb (decline as hypobiotic)
Winter rainfall - summer too hot, winter too cool, increase in spring and autumn
Not major issue in Victoria as temperate zone

96
Q

Haemonchus immunity, what age most common, what response activated and possible control

A

“self-cure” when threshold reached
1) Primarily occurs in young lambs - 9-12months
2) As they age they develop immunity
3) Hypersensitivity type 1 is activated, previously exposed sheep during secondary exposure, degranulation of eosinophils
- Smooth muscle contraction, vasodilation, influx neutrophils - production in chemicals such as peroxidases that destroy the worms
○ LOCAL RESPONSE
Control
Vaccine against gut wall proteins