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Parasitology > Nematodes > Flashcards

Nematodes Flashcards

1
Q

What does nema mean?

A

Thread

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2
Q

What are some features of nematodes?

A

Unsegmented, acoelomate, moults between stages

Most are free living 70% abundant in soil and marine sediments

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3
Q

What are the two origins of nematodes?

A

Plant parasitic nematodes

Free-living soil nematodes

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4
Q

General characteristics of nematodes

A

* unisexual- therefore separate sexes

* females are usually longer than males

* size varies drastically 1 mm- 9 meters

*body is covered by cuticle (produced by hypodermis)

*digestive system- mouth, oesophagus, intestine, anus

* Pseudocoelome- maintains a high hydrostatic pressure to help them move

* fluid is important in terms of movement of these worms

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5
Q

What is the cuticle? When is it shed?

A

Outer layer- keratin, inner layer- collagen

Cuticle is shed during moulting

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6
Q

Hypodermis

A

Found under the cuticle- secretes cuticle

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7
Q

Muscles in nematodes

A

Only longitudinal muscles (no circular- which would help with movement)

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8
Q

What is the hydrostatic skeleton?

A

Pseudocoelomic fluid and muscles function as a hydrostatic skeleton- S-shaped locomotion. 3 things together help nematodes to move

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9
Q

Nervous system of nematodes

A

2 ganglia (bunches of nerves)

anterior- oesophageal ring (dorsal, ventral, and two lateral nerves)

posterior- rectal ring

AcH and GABA (neurotransmitters- which are important targets for drugs to control)

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10
Q

Excretory- secretory system

A

Tubular

Two lateral canals

Open at ventral excretory pore

paired glands open into pore

Secretions of glands- immunogenic (produces an immune response)

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11
Q
A

Dorsal nerve

cuticle

ovary

pseudocoelom

intestine

excretory canal

uterus

muscle

hypodermis

ventral nerve

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12
Q

Cephalic region = head, lips, etc

A

P= papillae

I= inner

O= outer

C= cephalic

A= amphids

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13
Q

Lips can be replaced by what?

A

Hooks or teeth (probolae)

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14
Q

What are the papillae for?

What are the amhids for?

A

touch, taste (pore-like)

taste (slits)

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15
Q

Lancet or cutting plate

A

What they use to suck blood

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16
Q
A

a. leaf crown
b. buccal capsule (teeth and dorsal gutter)
c. dorsal gutter (takes enzymes and other substances produced at the base of the buccal capsule to the mouth- for example anticoagulants produced because they suck blood)

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17
Q

Hypodontus macropi

A

Colon or kangaroos

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18
Q
A

Hypodontus macropi- colon of kangaroos

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19
Q

Oesophagus

A

Acts like a pump with various valves that prevent back movement of food. 6 different shapes.

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20
Q

Male reproductive organs

A

Testis, tubular in nature, ejaculatory duct with muscle- for semen

Copulatory bursa- expansion of cuticle

Spicules- copulatory organ- usually in pairs.

Gubernaculum- cuticle plate present on the dorsal surface

Telamon- cuticle plate present on the ventral surface

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21
Q

Female reproductive system

A

1 to 2 tubular ovaries, uteri, ovijector (musclar part of uterus), and vulval flap (important for taxonomy)

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22
Q

Oviparous

A

Produces eggs with embryonic material (size helps to ID nematode)

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23
Q

Ovoviviparous

A

Eggs containing larvae

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24
Q

Viviparous

A

Eggs hatch within female reproductive organs and only larvae come out

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25
Q

Basic life cycle of nematodes

A

Egg- L1- L2-{L3}-L4-L5- adults

i.e. L2 retains cuticle, L3 is usually infective stage

L5 and adults are the same

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26
Q

When do nematodes feed on bacteria?

A

All free living stages. (some adults feed on bacteria but also feed on blood, tissues, body fluids, gut contents)

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27
Q

Direct life cycle vs. Indirect life cycle

A

One host- no involvement of IH

Indirect- involvement of IH for completion of life cycle

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28
Q

Rhabditida (order) general characteristics

A

* very small

* abundant

* most are free living

* most feed on bacteria

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29
Q

Life cycle of Rhabditida

A

egg, L1-L4, adults (male/female)

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30
Q

What are the most important genera of rhabditida?

A

Stronglyoides, Rhabditis, Micronema “accidental” parasites

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31
Q

Strongyloides examples

A

S. papillosus- ruminants- small intestine

S. ransomi- pigs- small intestine

S. westeri- horses- SI

S. stercoralis- dog, cat, man- SI

S. cati- cat- SI

S. fuelleborni- primates- SI

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32
Q

Strongyloides papillosus life cycle

A

* Adult female lives in small intestine

* Genetically she produces eggs (parthenogenetic female)- eggs are passed in faeces

* L1

* THEN after development of L1 - eggs hatches and releases L1 quickly (6 hours)

* rhabditiform oesophagus in L1 (copus and istomus: narrow tube- posteriorly enlarges- BULB)

* L2 (rhabditiform oesophagus)

* If temperature is warm (>34C), cannot survive in the env. THEN

* L2 develop into L3 which has a different type of oesophagus- folidiform strongyliform

* L3 is then INFECTIVE STAGE - THEN GOES INSIDE THE HOST (only female at this stage)

* Infect host through 2 routes: by penetrating the skin or oral route

* goes to predilection site- small intestine- migration through the blood stream (goes to the heart, lungs, and through mucociliary escalator, up to pharynx, then ingested and swallowed–> small intestine)

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33
Q

Parthenogenesis

A

Does not need a male. Mitotically she produces eggs. Eggs are passed in faeces.

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34
Q

Homogonic vs. Heterogonic life cycle

A

Homogonic- Only female is involved in producing eggs (this is when L3 becomes infective if the temperature is unsuitable and it will find a host)

Heterogonic- when temp and conditions are suitable in the environment for development of free living stages, L2 will produce L3 which will have rhabidiform oesophagus, then will produce L4 which will produce L5 (adults) therefore both male and female (another way to produce eggs)– **all would have rhabidiform oesophagus**

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35
Q

How fast to strongyliform eggs hatch?

What is the prepatent period?

A

6 hours. Prepatent period (when the animal gets infected until when the female starts to produce eggs): 5-12 days.

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36
Q

Internal and external Auto-infection with Strongyliform sterocoralis

A

Internal- When eggs are laid by females, they travel through the intestinal tract, they can develop and hatch within the intestinal tract. Then L1-L2-L3 within the intestinal tract. L3 can then pentrate intestinal mucosa and through circulation it comes back into the intestine. Female then starts to produce eggs.

External- L3 will come out and penetrate through perianal area

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37
Q

Prenatal infection (S. ransomi)

A

Transcolostral or transmammary transmission. S. ransomi (pigs) and S. westeri (horses). Adult animals are infected through skin penetration- L3 rather than going into the intestinal tract and developing into parasitic female. L3 goes into muscles through circulation and just stay there and go into dormancy. When female pigs become pregnant and before farrowing, dormant L L3 becomes active- temporary immunocompromisation around parturition. So L3 becomes active and can pass through placental. Or when piglets are born can become infective through contaminated milk as well.

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38
Q

When can the prepatent period become shorter?

A

Prenatal or trans-mammary infection- L3 have already gone through some development within the mother. Therefore the prepatent period becomes 2-4 days.

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39
Q

Pathogenesis of strongyloidiasis (S. ransomi (pigs))

A

* Invasive (when penetrating)- dermatitis

* Migrating through lungs- respiratory signs i.e. pneumonia

* Large number of parasitic female worms in SI- development of diarrhoea, reduced growth rate

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40
Q

Pathogenesis of S. papillosus in calf

A

* Major disease problem

* Prenatal & transcolostral infection

* larvae survive for 3 weeks

* Must eliminate moist conditions in environment

* Good hygiene otherwise they thrive

* Nematodes only cause problems if they are present in large numbers (hundreds or a few thousand- not many)

* dermatitis, alopecia

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41
Q

Pathogenesis of S. westeri in foals

A

Transcolostral infection important diarrhoea in foals 2 weeks old

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42
Q

Pathogenesis of S. stercoralis in man

A

Can remain dormant for 37 years auto-infection can occur, secondary infection in AIDs cases

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43
Q

Pathogenesis of S. fuelleborni in primates

A

Serious pathogen in great apes- zoonotic

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44
Q

Pathogenesis in unnamed species in kangaroos

A

Occurs in stomach, causes mortality in young captive animals

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45
Q

Diagnosis and treatment of strongliform

A

Eggs- faecal flotation

Larvae- Baermann technique (funnel attached to a rubber tube and a sieve- small quantity of faeces and fresh water- the larvae will move out of faeces into fresh water and due to gravity- so they will end up at the bottom to collect larvae)

In vitro culture (eggs will develop and would be able to see rhabidiform oesophagus)

Serodiagnosis- ELISA

**Another way- Auto-infection you would see larvae in the faeces**

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46
Q

Treatment of strongliform

A

Ivermectin

Oxibendazole

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47
Q

Micronema

A

Normally in the environment, but sometimes can become pathogenic- “accidental” parasites

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48
Q

Order Strongylida Features

A

* no similarities with Strongyloides

* Strongylos- means round and compact

Features:

* Buccal capsule

* Male nematode has a copulatory bursa

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49
Q

What are the four important families of Strongylida?

A

Trichostrongyloidea, Strongyloidea, Metastrongyloidea, Ancylostomatoidea

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50
Q

What are Trichostrongyloidea?

A

Abomasum, small intestine

Trichostrongyles

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51
Q

Where are Strongyloidea found?

A

Strongyles are found in the large intestine

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52
Q

Where are Metastrongyloidea found?

A

Lungworms are found in the lung

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53
Q

Where are Ancylostomatoidea found?

A

Hookworms are found in the small intestine

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54
Q

General life cycle of order Strongylida?

A

Egg, L1 and L2 (in faeces), L3 (infective), L4- male/female (in host)

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55
Q

Trichostrongyloidea features

A

* Vestigial (under developed) buccal capsule

* Copulatory bursa

* usually found in small intestine or abomasum/ stomach

* direct life cycle

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56
Q

Why are trichostrongyles of ruminants important?

A

Cause production losses of cattle (found in the small intestine, abomasum, and air passages)

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57
Q

Trichostrongylus

A

Very small, first six meters of SI esp. in small ruminants.

Black scour worm, affects sheep.

T. colubriformis- sheep, goats- duodenum

T. vitrinus- sheep, goats- duodenum

T. rugatus- sheep, goats- duodenum

T. axei- sheep, cattle, goats, pigs, horses, humans- stomach, abomasum

** look for excretory pore for identification**

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58
Q
A

T. colubriformis (spicules)- barb-like tip

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59
Q
A

T. vitrinus (spicules)- tapering end

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60
Q
A

T. rugatus- thick and dissimilar

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61
Q
A

T. axei- dissimilar and unequal (spicules)

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62
Q

Distribution of Trichostrongylus

A

Higher rainfall areas (east coast- southern QLD, southern WA, East coast)

Main sheep raising areas

Species differ in regions e.g. T. columbiformis in summer rainfall areas, T. vitrinus in cooler, moist areas, T. rugatus in dry areas

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63
Q

What conditions does T. colubriformis like?

A

Summer rainfall zones (throughout the world, AUS too)

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64
Q

What conditions do T. vitrinus?

A

Cool, moist regions of the world. Important in sheep in central Victoria.

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65
Q

What conditions do T. rugatus like?

A

Likes a dryer environment. WA for example.

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66
Q

Life cycle of Trichostrongylus

A

* eggs laid in faeces

* L1 hatches (it developed in the egg)

* L1 (has to shed protective covering- moulting) & L2 (does not shed it’s protective layer) develop in faeces (in the environment)

*After feeding- develops into L3 is the infective stage- animals are grazing- they are quite active and motile- they move towards grass- they can travel horizontally and vertically to ensure that when sheep is grazing they will be eaten

* L3 within the host undergoes exsheathment- within the rumen

* L3 migrates to SI and then penetrates epithelial cells (within epithelial cells it develops into L4)

* L4 after damaging epithelial cells- goes into the rumen and becomes an adult

** INTRA EPITHELIAL DEVELOPMENT IS THE KEY**

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67
Q

What’s the most important nematode in Southern Australia?

A

Trichostrongylus

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68
Q

What is the prepatent period for Trichostrongylus?

A

21 days

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69
Q

When does the moult from L3 to L4 occur with Trichostrongylus? When does the moult to adult occur?

A

5 days

Moult to adult occurs at 10 days

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70
Q

What is the pathogenesis of Trichostrongylus?

A

Villus atrophy (flattened, picture shows at 21 days after infection), protein loss, reduced absorption of Ca and PO4, anorexia, diarrhoea

PRODUCTION LOSSES

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71
Q

How does Trichostrongylus cause hypoproteinaemia?

A

* Breaks in epithelium and increased permeability of capillaries leads to

* leakage of plasma proteins into gut, 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

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72
Q

Trichostrongylus reduction in absorption of Calcium and PO4

A

Less absorption in duodenum so body tries to compensate, but lower intestine cannot compensate.

Blood Calcium concentration has be maintained within a narrow range. And a balance between Ca and PO4

**Reduced bone growth**

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73
Q

What is one big effect of Trichostrongylus?

A

Anorexia. Always occurs. Mechanism unknown. Almost 90% reduction in a study.

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74
Q

How does diarrhoea develop with Trichostrongylus?

A
  1. Release parasympathetic neurotransmitters, act locally on GI tract and increase motility
  2. Whatever the animals are eating is not being properly digested and absorbed, therefore it just goes out

**Heavy infection hindquarters become soiled- how severe? “dag score” 0-5… can lead to myasis

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75
Q

How does the host respond to Trichostrongylus infection?

A

* Immune response only if > 5 months old AND there must be >3000 worms in order to see an immune response

* often young animals are infected

* if immune system kicks in rarely you will see 100% expulsion of worms

* Cell mediated immunity and usually local- hypersensitivity type I reaction

* Aniaml is second time infected- local immune response, release of certain local mediators leads to increased parastaltic movements and eosinophils release certain substances that damage cuticle of worm

* And increased production of mucus– it “entangles” worms– increase motility therefore they are expelled

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76
Q

Seasonal patterns of Trichostrongylus

A

Winter rainfall zone- infection occurs in winter

Summer rainfall zone- infection occurs in summer

Northern hemisphere- winters too cold- development occurs in spring

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77
Q

How many worms would cause mortality?

A

< 10,000 worms, you wouldn’t really see mortality from the worms themselves

High rainfall during winter- mortality number increased. Less rainfall then less mortalities in 5 year period

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78
Q

Genera Cooperia

A

“wire worm”- cattle (can also affect sheep, but primarily cattle)

Found in the small intestine

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79
Q

Cooperia features

A

Size ~9 mm

Small cephalic vesicle (inflation around head)

Oesophageal region- transverse cuticular striations

body- longitudinal cuticular ridges

spicules- wing- like expansion in the middle region with ridges

NO GUBERNACULUM

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80
Q

COOPERIA that affect cattle

A

C. oncophora, C. surnabada- temperate

C. pectinata, C. punctata (“cattle bankrupt worm”)- sub tropical

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81
Q

Cooperia that affect sheep

A

C. curticei (vary in pathogenicity)

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82
Q
A
  1. C. punctata
  2. C. pectinata
  3. C. oncophora
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83
Q

Life Cycle of Cooperia

A

Direct

* eggs are produced by female which are present in the anterior half of small intestine, then passed in faeces

* In the environment eggs develop into L1, then hatch releasing L1, L1 feeds on bacteria in the environment, then develop into L2

* after moulting then L2 feeds on bacteria in the env. and then develop into L3 (no moulting)

* L3 is the infective stage (no moulting)- when animals are grazing L3 are present on the pastures and they will ingest the larvae

* After ingestion they will undergo exsheathment in rumen then move towards small intestine

*within small intestine they penetrate mucosal glands, undergo moult, and then develop into L4

* then L4 go back into lumen and become adults (braced against villi)

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84
Q

What is the prepatent period of Cooperia?

A

2 weeks

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85
Q

What is hypobiosis?

A

Sometimes at the L4 stage Cooperia can arest at this stage. Temporary cessation in development of Cooperia within the host

Why? If the environmental conditions are going to be harsh for free living stages in the environment, they stop development until the conditons become suitable.

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86
Q

What are the effects of Cooperia on the host?

A

Villus atrophy, erosion of epithelium

Usually effects younger animals who pick them up on pasture. Older animals develop some sort of immunity. Older animals act as carriers.

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87
Q

What is the epidemiology of Cooperia?

A

Ingest larvae during wet season (summer or winter)

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88
Q

When is the highest presence of adult Cooperia in the animal?

A

IN THE ANIMAL: Late autumn to winter (winter months)

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89
Q

Nematodirus, who do they affect? Location?

A

Sheep, cattle

Small intestine

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90
Q

Features of Nematodirus.

A

Size ~25 mm

Coiled

Cephalic vesicle

Long thin spicules

Female with spiked tail

Very large eggs

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91
Q

What’s helpful about Nematodirus in terms of deciding infection?

A

Large eggs

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92
Q
A
  1. N. filicollis
  2. N. spathiger
  3. N. battus
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93
Q

Species of Nematodirus that affect sheep

A

N. spathiger

N. fillicollis

N. abnormalis

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94
Q

What is the most pathogenic Nematodirus in the world? Where?

A

N. battus- not in AUS- sheep and cattle- Europe

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95
Q

What Nematodirus affects cattle?

A

N. helvetianus

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96
Q

Life cycle of Nematodirus

A

Direct

Free living L1-L3

* when the eggs are passed in the faeces, the development of L1, L2, L3 occurs within the egg in the environment

* Infective stage possibility 1- egg containing L3- hatching occurs sometimes at that stage in the environment- ingest eggs containing L3

* possibility two of infectious stage- ingesting L3 that has just hatched

* Eggs need cold or drying to hatch (eggs first need cold conditions, then warm conditions to hatch i.e. winter into spring- infection of sheep usually occurs during late spring, early summer)

** Hypobiosis- COMMON- occurs at L4 stage**

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97
Q

What is the prepatent period of Nematodirus?

A

21 days

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98
Q

Nematodirus Effects on the host

A

Villus atrophy (actually wraps around the villi)

Erosion of epithelium

Diarrhoea

Hypoproteinaemia

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99
Q

Haemonchus (trichostrongyles)- common name, who does it infect? What does its name mean? Location?

A

“Barber’s pole worm”- sheep, cattle, deer, camel

haem- blood, onchus- tooth

Abomasum

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100
Q

Species of Haemonchus and who they infect?

A

H. contortus- sheep (rarely cattle)

H. placei- cattle (rarely sheep)

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101
Q
A

Haemonchus

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102
Q

Haemonchus features

A

2-3 cm long

Red

Tooth in buccal capsule

prominent cervical papillae

“barbers pole” in female

female with large vulval flap

asymmetrical dorsal ray

spicules with barbs

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103
Q

Life cycle of Haemonchus

A

Direct

Development of free living stages are similar to cooperia

Once L3 (infective stage) is picked up, after exsheathment, after L3 burrows into the space of abomasal mucosal glands- they do not enter the lumen, they enter the space between glands. L3 then undergoes moult. Then L4 comes out from that space. Then starts feeding using lancet on the abomasum mucosa. Later on they undergo another moult and become adults.

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104
Q

What is the prepatent period for Haemonchus?

A

21 days

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105
Q

What are the effects on host of Haemonchus?

A

* L4 and adult feed on blood

* ingest 0.05 ml/worm/day

* ANAEMIA most important- hypochromic, microcytic anaemia (because there is a large number of worms present, the body cannot compensate, it can only compensate up to a certain limit- sometimes we can see immature RBCs in the circulation because there is an urgent need and the maturation of RBCs is incomplete)- hypochromic because there is not enough saturation with haemoglobin

* Hypoproteinaemia- “bottle jaw”

* listless, exercise intolerance

* DO NOT CAUSE DIARRHOEA
* heavy infections- sudden death

** VORACIOUS BLOOD SUCKERS**

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106
Q
A

Haemonchus

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107
Q

Epi of Haemonchus

A

* High biotic potential-5-10,000 eggs/ day

* eggs will not hatch below 10C (they are subtropical organisms)

* Larvae NOT resistant to desication (dry, hot conditions)– so not an important parasite in Southern VIC because during winter temperatures are too low and during summer conditions are hot and dry

108
Q

Where do Haemonchus reside in AUS?

A

Summer rainfall areas (sometimes VIC, but usually not)

QLD and NSW- tropical, sub tropical, here in VIC whenever we have wet summer- we see this problem. Sometimes around Perth.

109
Q

Immunity and Haemonchus

A

No immunity against Haemonchus, however “self- cure” when threshold reached resulting in immunity labile. Vaccine against gut wall proteins. Type I HS- cell mediated response, local, sensitized mast cells are brought in. Certain vasoactive amines, histamine, eosinophils- release certain mediators that directly affect the cuticle of the worm. Other vasoactive amines will increase the motility of the intestinal tract, so temporarily there is relief to the animal– the second time they are infected- they are expelled. When the animals are infected a third time, it does not happen (he said “it’s quite weird”)

110
Q

What is the vaccine to Haemonchus?

A

Barbervax- introduced last year. 75-95% protection particularly in young animals, used with anthilmetics. At least 5 subcut injections to young lambs during their first grazing season in areas where haemonchus are a big problem (WA and QLD)

111
Q

Ostertagia- common name? Who does it affect?

Features?

A

Brown stomach worm, sheep, cattle, and deer

Size about 9 mm

Location: abomasum

Features:

* cervical papillae

* spicules terminate in 3 stubby hooked processes (male worms)

* small vulval flap (female worms)

112
Q
A
  1. O. circumcincta
  2. O. trifurcata
113
Q

What species of Ostertagia affect sheep and goats?

A

Ostertagia circumcincta, Ostertagia trifurcata, and Teladorsagia davtiana

114
Q

What species of Ostertagia affect cattle?

A

Ostertagia ostertagi

115
Q

Life cycle of Ostertagia

A

Direct

Free living stages are similar to Haemonchus, Cooperia, etc.

Infective stage is L3 after infection differences

L3 undergoes exsheathment in rumen, once it reaches abomasum, actually penetrates the lumen of the gastric glands.

Moults to L4, L4 returns to Lumen

** HYPOBIOSIS COMMON (6 months)** L4– within the host

116
Q

What is the prepatent period for Ostertagia?

A

21 days

117
Q

Effect of Ostertagia on host?

A

Nodules in abomasum

leads to necrosis of cells and presence of inflammatory cells- so parietal and chief cells are destroyed therefore not enough acid production therefore increased pH in the abomasum

pH rises to 6

protein digestion stops

LEADS TO DEVELOPMENT OF DIARRHOEA

plasma pepsinogen rises

hypergastrinaemia (increased plasma gastrin concentration)

hypoproteinaemia

anorexia

** if one area is infected, then acid production will be reduced in that area- but in areas with normal tissue will try to compensate and produce more acid. As well as increased plasma pepsinogen and plasma gastrin level**

118
Q

What age does Ostertagia normally infect?

A

Younger animals, though older animals act as carriers

Older animals develop immunity- worm burden expelled and remaining worms small and produce few eggs

119
Q

Hypobiosis of Ostertagia

A

Winter rainfall zone inhibition of L4 within abomasum during summer season therefore hypobiosis. But as we moved in late autumn and winter- less hypobiosis and during winter we wont see any hypobiosis.

** Larvae become inhibited in spring, emerge in autumn**

120
Q

Ostertagia in cattle effects on host

A

Most important nematode in cattle in temperate areas of the world (O. ostertagi)

* basic life cycle similar to Ostertagia in sheep

* causes nodules in abomasum

* severe infestation gives “morocco leather” appearance

* same pathophysiology of sheep

**BUT differences in cattle: faecal mass serve as a reservoir for larvae AND inhibited larvae can emerge synchronously leading to diarrhoea, emaciation, and even death**

121
Q

Cattle dung pat importance with what?

A

Ostertagia

“Helminthological time bomb”

*Can protect larvae for a long period of time in harsh conditions

*Water content and temperature within dung pat play crucial role in hatching of eggs and the development of larvae (outside may be dry but inside is moist)

*larvae can survive for extended periods in faecal pat

*emerge following rain

(L3 can withstand much harsher conditions than L1 and L2)

122
Q

Type 1 Ostertagiasis

A

Young animals, no immunity, pasture for the first time in the spring, diagnose with egg counts, plasma pepsinogen.

Clinical picture and type of animals infected are very similar to sheep.

123
Q

Type 2 Ostertagiasis

A

Larvae emerge synchronously

Occurs in relatively older animals 2-4 years old

Precipitated by stress (calving)

Erratic in occurrence (some years, few cattle affected)

Occurs in autumn

Diagnose with plasma pepsinogen

124
Q

What happens with Ostertagia when you remove the adults? What do nematodes avoid?

A

Larvae can emerge

Nematodes avoid the harshest conditions

125
Q

Where does hypobiosis not occur?

in what age animal does more hypobiosis occur?

When does hypobiosis occur in Australia vs. Northern Hemisphere

A

In sub-tropical regions, hypobiosis does not occur (in europe, hypobiosis occurs during winter)

Older animals- more hypobiosis occurs

Hypobiosis occurs during summer in AUS, during winter in Northern Hemisphere

126
Q

Trichostrongylus axei- common name? Who does it infect?

A

Stomach hairworm

Sheep, cattle, horse, pig, man

127
Q

Trichostrongylus axei- primary host?

Location?

Features?

A

Primarily parasitic in cattle

Abomasum/ stomach (interepithelial)

Size 6 mm

Spicules- unequal, dissimilar (male worms)

128
Q

Trichostrongylus axei life cycle and pathogenesis?

A

Direct- similar to Ostertagia

Pathogenesis: damages epithelium, protein lost into lumen, mucus produced, pH rises, 40,000 can kill a lamb

129
Q

Trichostrongyles

A

Haemonchus (first two)

Ostertagia

Cooperia

Trichostrongylus

Nematodirus

130
Q

What is the significance of trichostrongyles in small ruminants (southern AUS)?

A

Total cost= 369 millions (decreased income 310 million + increased expenses = 59 million)

Internal parasites are at the top of the list– then fly strike, then lice

131
Q

What influences pathogenic effects?

A

Season, number of worms, animal’s health status. There is always a burden, but it becomes higher and lower depending on the season. Eradication is impossible. If we eradicate them it actually makes the animals susceptible and large scale outbreaks. Best thing to do is control.

132
Q

What are some control methods?

A

Anthelminics, vaccination, breeding for resistance, nutrition

OR

pasture spelling, rotational grazing, reduced stocking, nematophagous fungus

133
Q

What are the factors that impact the free living nematode?

A

Moisture, temperature, grazing factors, host factors, management factors

Can help you predict which parasites would be where

Parasite burden varies depending on the year.

134
Q
A
135
Q

Moisture

A

Needed for development of L3 in faeces

Needed for larvae to migrate onto pasture

effective rainfall- P/E > 0.3 (growing season) roughly correlates with larvae on pasture (Precipitation/ Evaporation)

Lateral movement (by themselves) limited (<0.5 m) & assisted by heavy rain and floods

Vertical movement- films of moisture can ascend up to 7 cm

Negatively geotropic, respond to light intensity, become anhydrobiotic (when there is not enough water) on grass (when droplet of water dries on grass), survival limited by lipid reserves

136
Q

Temperature

A

* mild AUS temperatures have little effect except Haemonchus >10C

* low temp can slow egg hatching and development in some species (T. colubriformis, T. vitrinus, T. rugatus)

* high temperatures shorten survival times of L3s on pasture

* interaction with humidity

* significant in tropical climates

137
Q

What is the effect of humidity and temperature on nematodes?

A

T. vitrinus loves cold and moist conditions (VIC)

T. rugatus- cool and dryer conditions

Note the relationship between humidity and temperature

138
Q

Connection of rainfall, evaporation, and effective rainfall

A

Good rainfall, connected with evaporation, therefore changes in effective rainfall. Effects distribution of larvae on the pasture

139
Q

Grazing factors

A

* sheep do not graze uniformly in the paddock

* avoid certain plants, avoid contaminated areas, distribution of pellets and larvae in paddock not uniform

* Type of vegetation affects larval survival: height, species (microclimate)– LARVAE will be more likely to be picked up with SHORTER grass

* Stocking rate

  • initially higher stocking rates
  • lead to heavier contamination
  • very heavy stocking rates may reduce infections (DUE TO OVER GRAZING! So the parasites are exposed to sunlight)!
140
Q

Host factors that influence epidemiology

A

Age- young animals are more susceptible to Trichostrongyle nematodes

* genetic susceptibility

  • skewed worm burdens and faecal eggs counts (most have low FEC, but some have high- very individual)
  • can select for resistant sheep

* breed differences

  • merinos more susceptible than cross breeds
141
Q

Host factors epi of trichostrongyloidosis:

Periparturient rise or spring rise in FEC- why?

A

“periparturient rise” or “spring rise” in FEC- an increase in number of egg output around parturition. Why? Because pregnant animals have compromised immune system which allows L4 to resume development and then they moult to adults and the females start producing eggs. Also, the establishment of infection by L3 when they are picked up (which is abnormal in adults- the immune system can normally fight it)

* Relaxation of immunity

* Increase prolactin 5 weeks before parturition and then decline until weaning

* Increased susceptibility to L3s

* re-emergence of inhibited larvae

* increased fecundity

*important interaction with time of lambing in AUS

142
Q

Management factors that influence ep

A

* timing of lambing- esp. autumn lambing- so lambs go on pastures in winter in AUS therefore exposure to heavy burdens of larvae because abundance of L3 on pasture during winter months

* grazing management is important- e.g. farmer doing alternate grazing. First cattle grazes and then farmer allows ssheep to graze on same paddock. Most of the species of nematodes are host specific. If sheep pick up cattle specific, they will just pass through.

* Rotational grazing- farmers allow sheep to graze

* nutritional status of animals- poor condition are more susceptible to infection and in malnourished animals would be impacted worse

* strategic use of anthelminics- based on good epi knowledge.- consider anthelminic resistance

143
Q

Arrested development/ hypobiosis

A

Don’t know the exact cause but unfavourable climatic conditons and immune status (as animals get older they become immune) of the animal can likely cause this.

It is temporary cessation of dev. during L4 stage

Factors supporting the resumption of development:

* hormonal changes

* alterations in the components of immune system during the PRR

* density dependence of parasite

** self cure phenomenon

** anthelmintic resistance

144
Q

Sheep died during winter on a farm in SE South AUS. Lambing on this farms commenced mid-May. Approx 20% of one flock of merinos was scouring and their condition had deteriorated. FEC 230 epg was obtained from a bulk sample of faeces from 10 ewes. Sheep were not drenched. Despite supplementary feeding, the condition deteriorated and 6 ewes died in 6 weeks. One ewe had 53K worm count in abomasum. 76 cows had grazed paddock earlier this year- they had not been drenched.

A

Possible species: T. ostertagia, haemonchus, T. axei

(T. axei is the answer.)

What in vitro methos will you use?

Faecal culture, then characterizing them looking at the length, etc.

What type of management practice(s) could have exposed sheep to nematode parasites this year?

Cattle and sheep grazing on the same paddock- this can be useful sometimes but in this case T. axei can impact both.

145
Q

10 wk old Yorkshire terrier. Died after 3 weeks of intermittent diarrhoea. Clinical symptoms at 7 weeks. In SI

A
  1. What parasite can cause such clinical presentation in young

Strongylidies stercoralis

  1. what are the possible routes of transmission for this parasite?

Percutaneous, ingestion, transmammary transmission

  1. Can the owner of the pick it up? YES
  2. What implications can have on the owner if has autoimmune disease?

This parasite could therefore last for years.

146
Q

Diagnosis of Trichostrongyloidosis

A

Antemortem

  • history
  • signs/ symptioms
  • clinical pathology including
    1. faecal egg counts
    2. faecal cultures
    3. molecular ID of trichostrongylid nematodes
    4. haematology, biochemistry and serology

* pasture larval counts

Postmortem

* total worm count

* gross pathology

147
Q

Antemortem diagnosis of trichostrongyloidosis

A

* history “tail to mob”

* symptoms/ signs (scouring, anemia, poor body condition)

* dag score on the breech of scouring sheep (0-5)

* clinical pathology including : FEC

148
Q

Faecal Egg Counts

A

* FECs are useful for the diagnosis of nematode infections in sheep and cattle under the age of about 9 months (this is because as animals get older they become relatively immune- if worms are present they will be in hypobiosis of L4- therefore you would NOT see eggs in the faeces)

* variability and degree of infection and (light, moderate, heavy)

* give rough guide only > 500 epg pathogenic

* fecundity of worms:

Haemonchus 5000-10,000 eggs/ female/day

Trichostrongylus 10-200 eggs/ female/day

Nematodirus 50 eggs/ female/day

** sheep FECs are more reliable than cattle **

* indicates presence of female worms only neglects males and inhibited larvae (limitation)

** need more than 10 samples when we take FECs because there is a large variation in individual FEC

149
Q

Why is FEC helpful?

A

Shows that treatment is working

150
Q

What is the cut off that a mob should be dewormed?

A

> 500 epg in faeces then recommend deworming. But in certain conditions. Sometimes 150 epg in faeces, say animal condition is poor. Assess the situation. What species of parasite is present? (fecundity of worms varies) Another question you need to consider when advising.

151
Q
A
152
Q

FECs limitations

A

Host immunity may suppress egg production

Concentration of eggs in faeces affected by digesta, diarrhoes, fasting, feed quality, size of host

Egg counts in young sheep, in mernios are higher

Can be carried out in the field

Difficult to ID eggs to genus and species level- have to do faecal culture

153
Q

Faecal cultures

A

ID of nematode larvae

Permits determination of the composition of worm burdens

Cultures require an incubator set at 25-27C which limits its use in the field

154
Q

Haematology, biochemistry, and serology diagnosis of trichostrongyloidosis

A

e.g. Haemonchus- anemia

Look at PCV, Hb, RBC, WBC

* plasma pepsinogen, gastrin, Ca and PO4, total serum proteins

ELISA- osteragiasis (limited use)

155
Q

FAMACHA

A

For Haemonchus contortus ( developed for goats in South Africa)

Measures levels of anemia or blood loss and treatment decision based on these levels.

Important due to anthelmintic resistance. So you only treat the animals that really need treatment. Try to delay the development anthelmintic resistance by selected treatment

Not much in AUS- because we have massive flocks- so labour intensive. <1000 animals would be fine.

156
Q

Pasture larval counts

A

Direct quantification from pasture

* estimate no. of larvae/kg of herbage

* slow

* does not detect low levels of contamination

* non random distribution of larvae in paddock makes sampling difficult

* can be useful in comparing paddocks

157
Q

Introduction of worm-free “tracer” animals

A

Mimic the grazing patterns of the resident flock

* costly

* time consuming

* not all ingested larvae develop in adults

158
Q

Total worm counts

A

Gold standard

Count number of parasites in abomasum and small intestine

* direct assessment

* can ID genera and species

* can only do 1 or 2 counts

* usually animals from tail of mob

* pathogenicity affected by host age and nutritional status

159
Q

Pathogenicity in sheep

A
160
Q

How do you control trichostrongyloidosis?

A

* Paddock spelling- effective over summer, not effective after autumn break, harrowing in summer

* Crops- sowing to crops reduces contamination, use of stubbles

* Alternate grazing- alternating sheep and cattle reduces contamination (except for T. axei)

  • goats and sheep have same parasites
  • horses and kangaroos may be of use

* Anthelmintic drugs- timing of treatments

  • more effective in summer in southern AUS (during summer pasture L3 count is low, so larval pick up is low- so animals will have low burden after tx)
  • winter treatments have limited effects
161
Q

When do you treat using anthelmintics?

A
162
Q

Which nematode has a vaccine?

A

Haemonchus (used in combination with anthelmintics)

163
Q

What is the most useful technique to control nematodes inside the host?

A

Anthelmintics

164
Q

Smart Grazing

A

Merino weaners- go to winter pastures- dev. heavy infections. In order to dev. relatively safe pastures for merino weaners- this technique was developed in VIC.

Oct, Nov, Dec, Feb, March

Select a paddock with good height (medium height) in beginning of NOV FIRST treat wethers and then move onto this pasture. Why wethers? Almost a year age, relatively resistant to these parasites- so they don’t develop huge burdens.

2.5-3x the normal stocking density

Allow animals to graze for 1 month during november.

During that period, overstocking, grass will become very short. Larvae present on pasture will be exposed to sunlight and killed. At the end of NOV, destock the paddock and move these animals to another paddock. Then leave paddock for 2 months (DEC and JAN). Essentially paddock spelling.

Then in the beginning of FEB, you treat the wethers. Bring them back to the same pasture TREAT THEM FIRST. Then allow them to graze on the same pasture for one month again.

** then at the end of FEB, destock the paddock and then during MARCH you keep it destocked.

NOW prepared for merino weaners in the winter.

165
Q

T. axei

A

Not host specific- horses and pigs- present in the stomach

166
Q

Hyostrongylus rubidus

A

Stomach of pig. Larvae develop in gastric glands. Diarrhoea, wet loss, can control when pigs are reared on concrete floors

167
Q

Ollulanus tricuspis

A

Stomach of cat.

Minute nematode 1mm

Female has a tail with 3-4 short cusps

Viviparous (L3 develops within uterus)

Not very pathogenic

Transmitted through vomit- another cat eats the vomit

168
Q

Amidostomum anseris

A

Gizzard worm in birds

* ducks, geese, swans

* junction of gizzard and proventriculus

* larvae penetrate gizzard lining

* highly pathogenic

169
Q

Trichostrongylus tenuis

A

Found in caecum, wide host range, nodules and mortalities in galliform birds.

Controls wild grouse populations

170
Q

What is the superfamily of strongyles (common name)? Where are they normally found?

A

Strongyloidea.

Large intestine.

171
Q

What are the main features of Strongyloidea? Mainly found? Hosts?

A

Bursa in male, large buccal capsule, leaf crown

Main location: large intestine

Hosts: horses, ruminants, pigs, birds, elephants, macropodid marsupials

172
Q

What is the PPP for Strongyloidea? Life Cycle?

A

Long

Moults +/- extra migration

L1-L3 in faeces

L3 on herbag

L3 migrates into intestinal gland

L4 emerges to lumen

Final moult in lumen

173
Q

Important genera of Strongyloidea in horses

A

Strongylus, Triodontophorus, Oesophagodontus, Craterostomum (all part of subfamily- Strongylinae)
- “large strongyles”- globular buccal capsule

Subfamily- Cyathostominae- Cyathostomum (genera) “small strongyles”- cylindrical buccal capsule

174
Q

Strongylus are also called?

A

Red-worms, blood worms

S. vulgaris, S.edentatus, S. equinus, S. asini (all horses except S. asini- donkey, zebra - not in AUS)

175
Q

Strongylus vulgaris size

features that distinguish

A

14- 24 mm

2 teeth present in the buccal capsul

Dorsal gutter- duct like structure base of buccal capsule near opening of oesophagus- opens at the mouth.

176
Q

Life cycle of Strongylus vulgaris

A

Direct.

L1 and L2 in faeces

L3 dev. stops below 8 C

After exsheathment penetrate gut wall and moult from L3 to L4

L4 enters capillaries, arterioles, and arteries ultimately go towards cranial mesenteric artery. Going against the flow of the blood. They stay in cranial mesenteric artery 3-4 months. After that L4 starts migrating back into the intestinal wall. Forms nodules there. In nodule undergoes final moult where L4 moults into adult. Adult enters into lumen of the large intestine.

Extra intestinal migration- the PPP is longer- usually 6 months.

(no IH)

177
Q

Strongylus vulgaris effect on host

A

Migration of larvae and blood feeding patterns of adult worms.

Effect on host based on migrating larvae:

* damages arterial wall, thrombus formation lesion “verminous arteritis,” not an aneurysm (bulging and thinning of blood vessels– but here it is thickening of blood vessels and bulging- not “true” aneurysm), thrombi occlude arteries which can lead to ischaemia because parts of the large intestin will not get blood supply, intermittent colic to infarction (when there is a heavy burden in horses = colic)

Effect on host based on adult blood sucking:

* blood feeders (1 female worm can suck 10 mL of blood per hour!), lesions continue to bleed, anaemia, eosinophilia, elevated white cell count

178
Q

Strongylus vulgaris Epi

A

Common, cosmopolitan- prevalence was 85% now 25% in VIC due to broad spectrum anthelmintics

* larvae most abundant on pastures in spring, desiccated in summer, winter stops larval develop

* Larvae can survive inches of snow- horses become infected when they graze during spring (northern hemisphere infection spring to autumn); in VIC- infection will occur from autumn AND spring- summer here is hot and dry- so not conducive for dev of L3 on the pastures

* Foals develop immunity

* Peak egg laying occurs 10 months after infection- almost an annual cycle

* foals develop immunity

* Overwintering- survival of larvae on pasture over winter (terminology used in northern hemisphere)

179
Q

Strongylus edentatus Features- include size?

A

Buccal capsule is wider anteriorly than posteriorly, no teeth in buccal capsule, very common species, larger than S. vulgaris (2.3-4.4 cm)

180
Q

Life Cycle of S. edentatus. PPP?

A

After ingestion- L3 exsheathment- penetrate gut wall. Through Portal Veins they travel to the liver. In the liver they moult from L3 to L4. L4 migrates extensively within the liver parenchyma. Migration can last from 2-3 months within the liver. Then L4 penetrates egg capsule and comes into peritoneal cavity. From there they can go to any organ in the peritoneal cavity (kidneys, intestines, etc.) A few months in the peritoneal cavity. L4 then penetrate gut wall back into the lumen. Form a nodule (same as S. Vulgaris). Under go moult to adult- enter the lumen of the large intestine. Adults feed on blood. (same as S. vulgaris).

PPP= 10 months

181
Q

S. edentatus effect on host

A

Mainly horses.

Aberrant larvae found in many organs, migrating larvae cause lesions, adults cause anaemia.

182
Q

Strongylus equinus features

A

3 teeth in buccal capsule, deepest buccal capsule, tropical species

183
Q

Life cycle of S. equinus

PPP?

Effect on host?

A

L3 exsheaths in caecum, L3 migrates into gut wall (moults into L4), penetrate guts wall and goes all the way through into the peritoneal cavity and then penetrates the liver (6-7 weeks in the liver), from the liver it comes back again into the peritoneal cavity and penetrates pancreas, then back to peritoneal cavity and then back to gut. Undergoes final moult then adults god into the lumen of the large intestine.

PPP= 8 months

Effect on host is anaemia.

184
Q

Tridontophorus features, life cycle, PPP, pathogenic effects

A

3 teeth, there are different species but only need to know genus name.

Does not undergo extra intestinal migration. Once the horses are infected with L3, after exsheathment, L3 penetrate gut wall, undergoes moult within gut wall, from L3 to L4, then L4 comes back into the lumen. in the lumen it undergoes final moult. PPP is shorter=9 weeks

Pathogenic effects= Graze on epithelial lining of gut. parasites tend to feed in clusters- they can cause ulcers when they are feeding together. Ulcers can lead to diarrhoea. This also causes blood loss.

185
Q

Cyathostominae (subfamily) general information

A

Small strongyles

13 genera, 51 species worldwide

All have cylindrical buccal capsule

Occur in large numbers (15,000)

* 1 horse can be infected with 15 different species of small strongyles at once, for example. Numbers can be 200,000-300,000 where you’d start to see effects on host.

* do not have globular buccal capsules like large strongyles. They have more cylindrical buccal capsules.

186
Q

Cyathostomum (genus) Life Cycle, two unique facts?

A

Strongyle of equines.

Life Cycle:

(as usual L1-L3 in environment)

Ingested.

L3 exsheatment in caecum, L3 penetrates gut wall, then undergo moult in the gut wall- they form a cyst, L4 comes back into the lumen, undergoes final moult, adults start feeding on gut contents.

*** adult worms are not feeding on the blood!!***

HYPOBIOSIS- important. At L4 stage within the gut wall, Seasonal pattern, following removal of adults, emergence may be synchronous. (NOT LIKE THE LARGE STRONGYLES- they do not undergo hypobiosis)

187
Q

When you give broad spectrum anthelmintics, what can happen with Small Strongyles? Who else is affected? What two drugs are effective against inhibited small strongyles?

A

A drug can be effective on adult worms. Sort of a vaccum in the large intestine. Hypobiotic larvae emerge synchronous of L4. This can lead to diarrhoea. 200,000-300,000 larvae emerging synchronously- this can be fatal.

Inhibited larvae of all trichostrongyles are quite susceptible to currently used broad spectrum anthelmintics. Ostertagia will be killed. BUT for inhibited larvae of small strongyles of horses- only two drugs in HIGH DOSES can kill- while all others can’t kill inhibited larvae- Fenbendazole (0.3-0.4 mg/kg- 1 treatment is enough) and Moxidectin (10 mg/ kg body weight for 10 days).

188
Q

Cyathostomum effect on host

A

* adults feed on gut content, not pathogenic, very large numbers (10^6) cause diarrhoea, normally 115,000 larvae encysted, visible from external surface, massive emergence causes severe diarrhoea

189
Q

Diagnosis of Cyathostomum

A

Find eggs in faeces, use McMaster chamber (egg counting chamber with 3 pockets like we used in class), >300 epg pathogenic, larval culture to ID genera (faecal culture)

190
Q

Horse age and the relationship between age and important nematodes. Main reason this occurs?

A

Become infected in different ways.

At different ages, different parasites effect horses.

Look at 12-16 weeks of age- parasite in horses which is most important Strongyloides westeri (can become infected through the milk–> transmammary transmission)

12-28 weeks- most important is Parascaris equorum *thick shelled eggs- unique. (become infected through the milk)

after 16 weeks- gradually increasing curve- Strongyles- horses become infected when they are start grazing.

191
Q

Chabertiidae (Family), Chabertiinae (Subfamily), Chabertia (Genera)

Features, including size

Location

Hosts

Life cycle, include PPP

A

Small, cylindrical buccal capsule, tissue feeders

Bell shaped buccal capsule with no teeth

Size 1.5-2.0 cm

Tiny leaf crown (teeny tiny around the mouth compared to strongyles which are larger)

Location: Colon (first coil)

Hosts: sheep, goats, cattle

LC: Animals ingest L3, after exsheathment L3 penetrates gut wall, enters mucosal glands, moults to L4, L4 returns to lumen, migrates to LI, final moult in LI

PPP=8 weeks

192
Q

Chabertia ovina effects on host

What happens in older animals?

Geographical area? General climate elsewhere than AUS?

What number is pathogenic?

How many eggs/day can females lay?

A

Tissue feeders, feed on mucosa, cause haemorrhage, EXCESS MUCUS PRODUCTION, DIARRHOEA, cosmopolitan parasite but more prevalent in TEMPERATE areas (Southern states in AUS), strong immunity develops, usually only few worms present

200 is pathogenic

Females lay 3000 eggs/ day (eggs are very similar to trichostrongyle eggs- you can’t really tell the difference based on egg morphology- need to do faecal culture to ID genus)

Eggs of “strongyle” type

* Older animals develop immunity

193
Q

Genus Oesophagostomum

Common name?

Hosts? Sites?

Feature?

LC?- PPP?

A

Common name: nodule worms because they form nodules in large intestine

Feature: Cephalic vesicle

LC: Direct.

Sheep and Cattle- caecum and colon

PPP= 5-6 weeks L3 migrates into glands in SI or LI, L4 emerges and migrats to LI

194
Q

Oesophagostomum radiatum

Common name

Location

Features

A

Common name: nodule worm of cattle

Location: caecum/ colon

Features: cylindrical buccal capsule, small leaf crown only internal- very tiny, no external leaf crown, cervical collar in 2 parts (cuticle inflation called cephalic vesicle)

LC typical of genus

195
Q

Oesophagostomum radiatum effect on host

What kind of reaction? What happens to older animals?

A

Primarily in tropical and subtropical regions of the world.

Susceptible (young) animals- young more susceptible. When calves are exposed for the first itme. After ingestion of L3, undergo exsheathment and penetrate gut wall. Undergo moult to L4 and form nodules.

The severe reaction occurs when these animals are exposed the second time. Then you have a hypersensitivity type reaction (size of nodule increases due to HS rxn). Large number of nodules in the large intestine.

Nodule filled with eosinophils, larva killed, caseous lesion calcifies. Nodules cause Hb and plasma proteins to leak into gut when they rupture. This can lead to loss of proteins, haemorrhage. Leads to DIARRHOEA (interfere with gut motility- the nodules).

Sometimes nodules can become caseated and calcified (chronic situation).

Strong immunity by 12 months of age.

196
Q

Oesophagostomum columbianum

Common name

Location in body

Geographical region

Host

A

Nodule worm of sheep

Colon

Tropical and subtropical regions

197
Q

Oesophagostomum venulosum

Pathogenic or non-pathogenic?

Host?

Location?

Geography?

A

Location: caecum

Non-pathogenic, some scouring

Very common in sheep

Prolific egg layers

Typical strongylid eggs

QLD and Northern NSW

198
Q

Oesophagostomum columbianum story

A

In 1930s a massive problem- Aussies dev. drenching gun to control these parasites. Tried oral, tried anal. At one time a massive problem causing losses in tropical and sub-tropical parts of the country.

199
Q

Oesophagostomum dentatum

Host and common name

A

Nodule worm of the pig

200
Q

Oesophagostomum quadrispinulatum

host; generally what is it?

A

Significant pathogen in pigs

201
Q

Stephanurus dentatus

common name

location

distribution

A

The kidney worm of pig

Location: peri-renal fat in cysts attached to ureter (can be found in the pelvis of the kidney as well, as in pic)

Distro: limited to warm, moist areas in AUS; tropical and subtropical areas worldwide

Morphology- cup shaped buccal capsule; at the base of the cup- sometimes up to 6 teeth

202
Q

Stephanurus dentatus life cycle (and PPP)

A

Eggs are passed in the urine***

L3 ingested or can penetrate skin

Migrate to liver via portal system– depends on the route of entry– (3 days) or aorta ((8-40 days)- through the blood it goes into heart, lungs, and then back to the liver)

Migrate in liver L3 to L4 and to Adult–> for 2-3 months

Migrate to perirenal fat or area (near kidney)

Form a cyst around them and make a connection with the ureter- females start to produce eggs- and eggs are passed in the urine again

May migrate anywhere in body

PPP= 9 months (varies depending on the route of the portal system– does it take the short route to the liver or the long route through the aorta– heart, lungs, and then to the liver)

203
Q

Stephanurus dentatus effect on host

Diagnosis

A

Fibrosis in liver, abscesses in carcass, organs condemned at slaughter, weight loss (weak, anorexic in piglets)

Diagnosis: eggs in urine, elevated liver enzymes

204
Q

Syngamus trachea

Common name

hosts

location

features

A

The gape worm

Hosts: poultry, many other birds

Location: trachea

Features: cup shaped buccal capsule, up to 10 teeth, pair appear Y-shaped grossley

205
Q

Syngamus trachea Life Cycle, PPP

Effect on host

A

**Worms are present in trachea but they are passed through the faeces.**

**Involvement of paratenic host– 3 possibilities for birds to become infected**

Eggs coughed up, swallowed, L1-L3 within egg

**L3 in Molluscs OR oligochaetes (earth worms, snails, or slugs) paratenic hosts (no development of the parasite, just transport)**, L3 ingested

Migrate to trachea via liver than lungs

PPP=2 weeks

* Effect on host: Cause excess mucus production, block airways, respiratory distress- birds start “gaping” (open mouthed breathing), blood feeders

* Diagnosis- eggs in faeces (ellipsoidal thin-shelled eggs with a thick operculum at both sides- looks like a stick on both sides of the egg- the picture only shows one side it appears)

206
Q

Case Studies from Practical 2 for nematodes

A

* Merinos- efficacy- determine it if we have pretreatment and after treatment faecal egg counts so we can see the difference. But based on the results it is a 100 percent efficacy because we don’t see anything. Breed is important (merino breed is quite suceptible)

207
Q

Ancylostomatoidea (superfamily) features- common name- location- hosts?

A

Hookworms

Features: head bent dorsally, large buccal capsule, teeth or cutting plates, bursa in male, infect the host either orally or by skin penetration

Location: Small Intestine

Hosts: dogs***, cats, ruminants, pigs, humans

208
Q

General LC of Ancylostomatoidea

A

eggs passed in faeces–> L1–> (L3) (retains the cuticle)–> skin penetration OR ingestion

If skin penetration–> lungs/ trachea–> small intestine (undergoes moult)

If Ingestion–> intestinal wall–> small intestine

209
Q

How many teeth are in the Ancylostoma caninum vs. Ancylostoma braziliense?

A

3 pairs of teeth (A. caninum)

1 pair of teeth (A. braziliense)

210
Q

Ancylostoma caninum general, life cycle, and PPP (2 options)

A

* females lay 15,000 eggs/ day

* skin penetration important

* transmammary infection important

Eggs passed in faeces–> L1 (hatches, feeds on bacteria in env)–> L2 (feeds on bacteria)–> (L3) sheath of L2 is not shed- infective stage–> host becomes infected through a number of ways. L3 ingested, after ingestion goes to small intestine moults there and develops into adult. OR some larvae ingested can penetrate mucosa of GIT and go through blood– heart, lungs, coughed up, ingested, and swallowed and go back to small intestine where they develop into adults. OR second route of entry- L3 penetrates skin of the host. After entry L3 through circulation goes through heart, lungs, mucociliary escalator, pharynx, swallowed, small intestine– and again final moults– Adult.

** PPP can be 2-3 weeks ( no extra intestinal migration)

***PPP can be 4-5 weeks if there is extra intestintal migration

211
Q

When A. caninum infects adult dogs, what is the difference?

A

Adult dogs mostly infected via skin penetration, enters into circulation, they go into different muscles instead of SI and they become dormant. If this is a female dog, when it becomes pregnant, these larvae before developing they become activated. They go to SI and they go into circulation as well. Then the pregnant bitch can transmit infections TWO WAYS: when the pup is born (sucking the dam)– they are infected through contaminated milk. These encysted larvae are being passed in the milk. Pups become infected when they are having milk. These parasites can also cross placenta- pups can become infected while they are still in the uterus

***PPP through milk transmission= 2 weeks– L3 is already at advanced stage within the adult animal. When they are passed through milk- they do not undergo any extra migration. Young pups infected in the first 2-3 weeks of their life.

212
Q

Pathogenic Effects of Ancylostoma caninum

A

* PERACUTE HOOK WORM INFECTION Anaemia (like Haemonchus contorus in sheep) they are voracious blood suckers. 1 female can suck up to 1 ml/day. If you ahve a 1-2 week old pup with 50-100 worms of A. caninum- they can kill the pup. (immune system isn’t responding, haematopoeisis is not effective with such a loss of blood- cannot cope, microcytic hypochromic anaemia)

* Bloody diarrhoea (red, tarry coloured)

* CHRONIC hookworm infection- usually occurs in older dogs. Usually do not develop clinical signs unless they are immunocompromised then they could also develop anaemia due to this parasite

* If animals survive, they develop good immunity

* ZOONOTIC importance- eosinophilic enteritis in man. Walking on beach barefoot- end up with abdominal pain. RECALL tropical areas.

213
Q

A. caninum Epi and Diagnosis

A

* These parasites occur in tropical and sub-tropical areas of the world- for the dev. and free living stages- we need moist and warm conditions.

* Less common in southern Australia

* sandy or loam areas ideal for larvae

Diagnosis:

* eggs in faeces (2-8 blastomeres inside)

* if the egg count is high >5000 epg- suspect heavy burden

* in order to differentiate between <65 micrometers (Ancylostoma vs. unicinaria (colder climates as well))

214
Q

Ancylostoma braziliense general (summary)

A

* Not as voracious blood suckers, but they also have zoonotic importance

* L3 penetrate human skin- they form special lesions (creeping eruption)- they remain in subcutaneous tissue

* Tortuous erythematous inflammatory tracts within dermis associated with severe pruritis

* Common in tropical and sub tropical regions

* Less pathogenic - can cause hypoproteinaemia and diarrhoea

215
Q

Uncinaria stenocephala

A

Hookworms of dogs.

* Common in cooler areas

* L3 are ingested

* no extra-intestinal migration

* Less pathogenic

* eggs > 65 microns

* if pressent in large numbers- diarrhoea, hypoproteinaemia

216
Q

Uncinaria lucasi and U. hamiltoni

A

Hookworms of seals/sea lions

* Serious pathogen in northern hemisphere seals

* transmammary transmission most important route of infection

* larvae penetrate skin

* can go into muscles and stay there– when females give birth to pups- these encysted L3 will become activated from muscles and pass in the milk and therefore affect pups

217
Q

Hookworms of cats

A

Ancylostoma tubaeforme, Ancylostoma braziliense, Uncinaria stenocephala

218
Q

Hookworms of ruminants (cattle- where? sheep- where?) Features?

A

Summary : There are 2 main species that- skin penetration and transmammary- young animals can cause clinical signs. More than 1000 = death of animals. Anaemia, hypoproteinaemia, and diarrhoea.

Bunostomum phlebotomum- cattle, small intestine

Bunostomum trigonocephalum- sheep, small intestine

Features: transmammary transmission and skin penetration. Found mainly in warmer areas. Transcolostral infection (common way for calves to become infected- they can die from this parasite).

PPP= 7 weeks.

219
Q

What hookworm affects sheep, goats, and wild ruminants in Indonesia and South America, and Africa?

A

Gaigeria pachyscelis

Voracious blood suckers. Anaemia and death

25 nematode infection- fatal

220
Q

Hookworms of pigs

A

Globocephalus spp.

Distribution- occur in tropical areas of the world (unknown if in AUS)- in PNG

Anaemia, weight loss, emaciation

221
Q

Two important hookworms in humans

A

Ancylostoma duodenale- 2 pairs of teeth

Necator americanus

222
Q

Metastrongyloidea (superfamily)- common name, features?

A

Lungworms

Features: small buccal capsule, reduced bursa (not well developed), mainly found in respiratory system** (or connected to it- vascular and nervous system associated with respiratory tract)

223
Q

Life cycle of Metastrongyloidea (3 options)

A

** L1 passed in faeces ** primarily occur in the respiratory system or sometimes blood vessels associated or NS. But L1 is passed in faeces. This suggests that when the adults are present in resp system. When they lay eggs within lungs or trachea- the eggs develop there and then hatch. Then these L1 travel up the trachea to pharynx and then swallowed- they pass through the GIT and come out in faeces. Suggests they are quite strong because they survive enzymes of the GIT.

** 3 OPTIONS- simple direct life cycle

L1 come out in the env. with faeces–> dev to L2 and (L3)–> when animal becomes infected while grazing– once ingested exsheathment in GIT– penetrates mucosa of SI– goes to mesenteric LNs– undergo moults there and go to the lungs through Lymphatics or circulation and they become an adult in the lungs

Host: ruminants and horse GENUS: Dictyocaulus

2nd OPTION:

INDIRECT LIFE CYCLE

L1 passed in feaces–> L1 penetrates foot of snail or slug or other IH– dev. from L1 to L3 occurs within the IH– final host becomes infected when they eat the IH (mollusc or earthworm). L3 exsheaths, penetrates intestinal mucosa, goes to the lungs via circulation

Host- ruminants, pigs, and cats Genera- Protostrongylus, Muellerius, Metastrongylus, Aelurostrongylus

3rd OPTION:

DIRECT LIFE CYCLE

L1 infects the definitive host, host becomes infected when they ingest the vomit- after ingestion of L1– L1 penetrates mucosa and all the moults from L1 to adult.. All the moults occur in the lungs. Penetrate the mucosa go to lungs via the lymphatics– undergo moults in the lungs (4 moults there) and become adults.

Host- dogs; Genera: Oslerus, Filaroides

DIAGNOSIS: Baermann technique, larvae with distinctive morphology

224
Q

Lungworms of sheep (3) and site

A

Dictyocaulus filaria- bronchi

Protostrongylus rufescens- bronchioles

Muellerius capillaris- alveoli

225
Q

How do you ID lungworms of sheep?

A

Posterior section

226
Q

Dictyocaulus filaria features, life cycle, PPP

A

very long! 10 cm in length

* if such long parasites are present in the hundreds in trachea= blockage

* do not have well developed buccal capsule

* spongy spicules

Life Cycle:

SIMPLE DIRECT (L1-L3 occurs in the environment, sheep and goats become infected when grazing ingest L3– L3 undergoes exsheathment in abomasum, penetrates mucosa of SI– mesenteric LNs– undergoes moult twice in mesenteric LNs– then adult worms via lymphatics go to the lungs– then within lung parenchyma– alveoli- bronchioles– bronchi. Post mortem- you will find them at the bifurcation of the trachea. BRONCHI= LOCATION (predilection site)).

PPP= 21 days (typical of trichostrongyle nematodes)

227
Q

Dictyocaulus filaria effects on host

A

* Excess mucus production

* Blockage of airways

* Damage epithelium

* Loss of mucociliary escalator

* Interstitial pneumonia (excessive fluid)- alveoli filled with fluid- lead to consolidation of lung lobes

228
Q

Dictyocaulus filaria clinical signs

Diagnosis

Climate

A

If you have 10-20- no clinical signs

If you have hundreds= then you will see clinical signs, chronic cough, difficulty breathing, secondary bacterial infections

Eosinophilia

DEATH if hundreds of thousands- severe infections

COOLER CLIMATES
Find L1 in faeces and looking at characteristic features

229
Q

Protostrongylus rufescens- features, location, LC?

A

Occurs in Bronchioles

Looks red

65 mm long

LC:

L1 passed in faeces, penetrates foot of snail or slugs, L1-L3 in slug, different types of snail that serve as IH (Cernuella is main one). Sheep ingests snail. L3 exsheathment in SI or abomasum, penetrate SI mucosa via lymphatics go to lungs and undergo two moults.

230
Q

Protostrongylus rufescens pathogenic effects

A

* Mild pneumonia

* Most infections subclinical (small numbers present in lungs)

231
Q

Protostrongylus stilesi

A

Lungworm of sheep

Can cause death in Rocky Mountain Sheep

Transcolostral transmission

232
Q

Muellerius capillaris feature, LC, pathogenic effects, climate

A

Lungworm of sheep

Tiny coiled worms in alveoli

LC: INDIRECT LIFE CYCLE. L1 with kinked tail, snail & slug intermediate hosts

Pathogenic effects: high prevalence, virtually non-pathogenic in sheep, can be highlypathogenic in goats. Lesions: GREYISH TO GREENISH.

TEMPORATE AREAS.

233
Q

Lungworm of cattle

A

Dictyocaulus viviparus (“husk”- name for infection)

* major pathogen of cattle

* cough, laboured breathing, hypersensitivity reaction

* Disease mainly in calves (younger than 9 months)

* Develop strong immunity

* X- irradiated larvae provoke immunity (** a parasite with which a vaccine has been developed BUT WITHDRAWN due to problems with shelf life and efficacy)

LARVAE CAN MOVE ON PASTURES: horizontally and vertically- rain and floods. But all SPORANGIA OF Pilobolus. Larvae can travel with the fungi.

234
Q

Lungworm of equines- host, LC (unique start),

A

Dictyocaulus arnfieldi

* In trachea of horses, donkeys, and other perissodactyls

Natural host of donkeys- but they dont’ develop clinical signs- horses can though

DIRECT LIFE CYCLE. Main differential point (because same as other Dictyocaulus spp.)

* Starts from lung– pharynx– swallowed– passed through GIT– egg containing larvae (NOT L1!). SEE EGG CONTAINING L1.

Diagnosis: Baermann technique, larva with pointed tail

235
Q

Lungworms of deer

A

Parelaphostrongylus tenuis

* White tailed deer (North America)

* Adults present in cranial venous sinuses of the brain

* Eggs are laid present in the sinuses- through blood they go into lungs– hatch there and then L1 through mucociliary escalator– trachea– swallowed– passed in faeces (L1). Then LC is INDIRECT. Penetrates foot of snail or slug– IH– dev. from L1-L3… deer becomes infected when grazing. L3 then goes into abomasum after exsheathment. L3 then penetrates the mucosa- comes into peritoneal cavity- starts moving towards the nerves– goes back to the spinal cord– following the nerves. Travels all through the spinal cord– and then back to the cranial sinuses (undergoes two moults there).

DEER- NO CLINICAL SIGNS. Problem occurs when domestic life stock or other animals are grazing in the same paddock where the deer is grazing. Ingest infected IH– then they develop neurological signs…. in its natural host it causes no problem- but with an accidental host- neurological signs depending on the part of the brain affected.

**In abnormal host- moose, cattle, sheep. Produce fatal neurological disease.

236
Q

Elaphostrongylus cervi

A

parasite of Red deer from NZ

* we do not know if it is in AUS

* Occurs in connective tissues and meninges

No clinical signs in normal host- but if they occur in ruminants= neurological signs

237
Q

Lungworm of cats, general, LC, effect on host, diagnosis

A

Aelurostrongylus abstrusus

Occurs in alveoli- they are tiny

VERY COMMON.

LC is INDIRECT. Snail and slugs are IH. Paratenic host- rodent, birds, and reptiles. When the cat eats the paratenic host. Larvae enters bloodstream to reach lungs.

Within the final host- the moults occur in lungs. After eating either IH or PH- final host infected– moults to L5 in lungs. L3 penetrate intestinal wall–> lymphatics–> lungs

Pathogenic effects:

* generally subclinical, mild cough, weight loss, eosinophilia

* diagnosis: looking at the tail of the larvae (Baermann for larvae), differentiate from Strongyloides cati by shape of tail.

238
Q

Lungworms of pigs (3), Location, LC, effects on host

A

Metastrongylus apri, M. salmi, M. pudendotectus

Location: large worms found in bronchi

Life cycle: INDIRECT. Eggs are passed in faeces, ingested by IH (earthworm), egg hatches to L1. Dev from L1-L3 within earthworm, pigs become infected when they ingest earthworm containing L3. Within the pig, L3 exsheathment, penetrate gut wall–> mesenteric lymph nodes–> L4 final moult in the lungs.

Effects on host: resp. airway disease, obstruct airways. Transmit swine influenza virus (in egg).

239
Q

Lungworms of dogs (3)- name them and where

A

Angiostrongylus vasorum- pulmonary artery

Oslerus osleri- trachea

Filaroides hirthi- alveoli

240
Q

Angiostrongylus vasorum (geography, location in the body, host, LC, PPP, clinical signs)

A

Lungworm of dog. Right ventricle or pulmonary artery

Common in Europe, uncommon in AUS

INDIRECT LC.

L1 in faeces, snail IH. L3 penetrates mucosal wall and goes to the lungs.

PPP= 4-8 weeks

Clinical signs:

Mild, cough, interstitial pneumonia

CAN CAUSE CONGESTIVE HEART FAILURE (in severe cases)

In chronic cases- dependent organs- liver and kidney can be affected due to congestive heart failure (not by parasite).

241
Q

Oslerus osleri- host, location, LC, effects on host, PPP

A

In nodules in trachea

Lungworm of dog

LC:

DIRECT (or simple direct??) Infective stage L3.

can lead to obstruction in airways

PPP= 18 weeks

Effects on host- airway obstruction, common in dingoes

242
Q

Filaroides hirthi

A

Mainly associated with beagles

Tiny worm in alveoli

LC: DIRECT, L1 passed in faeces

Effects on host: granulomatous type lesions within lung parenchyma, chronic lesions- tend to be more neoplastic TYPE (not neoplasia). Fatal with incurrent disease BUT infection is usually inapparent

243
Q

Angiostrongylus cantonensis- host? LC?

A

Features:

Found in pulmonary arteries of rats.
INDIRECT LC.

Does not cause major pathogenic effect in rats. BUT ZOONOTIC IMPORTANCE.

QLD and NSW- found. Humans can become infected– neurological signs. Vegetables, salad, and prawns can become contaminated and this how humans contract. Within humans- they can be present in the brain or other organs (picture of eye).

Again, natural host, no clinical signs but in accidental hosts- yes.

244
Q

Prior history of a bitch tells us that the puppies were infected with nematodes, how would you treat? 2 possibilities have shown efficacy.

A

1) high doses of Fenbendazole

at day 40 of pregnancy- administer HIGH DOSE (50 mg per kg of BW) everyday until whelping. More than 90% of larvae will be killed.

When they are encysted- they are not susceptible to treatment.

2) If you give two treatments of ivermectin (.5 mg per kg BW)- 2 weeks prior to whelping– second dose one week after whelping. Will also kill encysted larvae into circulation

245
Q

What do anthelmintics treat?

A

Helminths: Nematodes, cestodes, tapeworms, flatworms

246
Q

Test for evaluating efficacy of an athelmintic

A

Faecal egg count reduction test (FECRT)

controlled test: control and treated groups (slaughter and total worm count WITH CONTROL GROUP)

Critical test: treated animals act as controls (most reliable)

247
Q

What does spectrum of activity mean?

A

What parasites is it effective against? Broad spectrum: anthropods and nematodes

vs. narrow spectrum

248
Q

Characteristics of an anthelmintic

A

* Spectrum of activity

* administration

* safety margin (ratio of toxic dose and effective dose- wide margin is safer)

* Selective toxicity (need larger doses or the host can metabolize the drug rapidly)

* withdrawal period (when dealing with production animals- how long does it take for the drug to leave the system)

* economical

249
Q

What is an effective anthelmintic?

A

If it can reduce the worm burden up to 99%

250
Q

Benzimidazoles

A

Developed in 1961- the first one

Benezene ring and imidazole ring- it affects the parasite by inhibiting the polymeratization of the tubulin cytoskeleton of any cell–> leading to damage of the parasite

e.g. Oxibendazole- cleared rapidly, not effective against many parasites, req high dose

NOWADAYS- metabolites are effective against parasites– TERTIARY BZ’s!!! HIGHLY EFFECTIVE AGAINST OSTERTAGIA

** DRUG HAS A DEPOT EFFECT in ruminants: give a tertiary BZ to a sheep- in rumen- converted to sulphoxides of this drug-is absorbed from rumen into the blood–> comes back into the rumen–> sulphoxide is changed into sulphones–> absorbed and comes back–> some passed into GIT and kills the parasite (metabolites having an anthelmintic effect)–> 3 FOLD EFFECT– CALLED DEPOT effect– only ruminants and horses (because of the caecum)

* mostly excreted through urine- some are excreted in bile- SOME are effective against liver flukes. These drugs can KILL THE EGGS OF PARASITES so= OVICIDAL!!!

** not water soluble– administered primarily orally

Ruminants- 3BZs used widely- inhibited migrating larvae and inhibited larvae

** In sheep WIDESPREAD RESISTANCE IN TRICHOSTRONGYLES OF SHEEP!!!

* Only one drug from this class is effective against inhibited larve of horses– small strongyles.

251
Q

Use of BZs

A
252
Q

Imidazothiazoles- Levamisole

A

Spastic paralysis

253
Q

Imidazothiazoles- Levamisole: activity, pharmakokinectics, safety margin

A

Not safe!

254
Q

Imidazothiazoles- Levamisole- Use

A

widespread resistance

Causes excitement in horses- so not used!

Dogs and cats- hookworms and lungworms

255
Q

Tetrahydropyrimidines- Morantel, Pyrantel

A
256
Q

Tetrahydropyrimidines- Morantel, Pyrantel USE

A

In horses- also effective against cestodes or tapeworms.

dogs and cats- hookworms and ?? in young pups

257
Q

Macrocyclic Lactones

A

From a fungus

Mode of action: paralysis by binding to GABA gated Cl-ion channels in neurons

258
Q

Macrocyclic Lactones mode of action

A

No AP= flaccid paralysis

259
Q

Macrocyclic Lactones- activity, pharmacokinetics, safety index

A
260
Q

Macrocyclic Lactones Use

A

Limited resistance in trichostronglyes

Cattle- resistance only to Cooperia

Horses- resistance in cyathostomes (no studies done in AUS)

261
Q

Organophosphates- mode of action, activity, use

A
262
Q

Heterocyclic compounds

A

Narrow spectrum anthelmintic

263
Q

Salicylanilides

A

Affects oxidative phosphorylation within mitochondria

Narrow spectrum anthelmintic

Very effective against parasites that suck blood e.g. Haemonchus

264
Q

Octadepsipeptides- Emodepside

A

Only binds to specific receptors present in worms- nematodes

265
Q

Amino-acetonitrile derivatives (AADs)- Monepantel

A

Most recent

When an organism is resistant to all major classes of anthelmintics- when they also gave Monepantel- can kill 99% of worms.

266
Q

Derquantel

A

Marketing stunt of a company- not really effective- “medium spectrum”- combined with ivermectin then effective.

267
Q

Anthelmintics for small strongyles in horses, deworming regimen for young dogs and pregnant bitches

A

Horses- small strongyles: ONLY Fendendazole and Moxidectin

Deworming regimen for young dogs and pregnant bitches:

* hookworms… when pups become infected through mammary transmission PPP is shorter. Repeat anthelmintics every fortnight until pups are weaned because the parasites become mature quickly until the age of approx 3 months. After 6 months of age- pups should be dewormed every month. After weaning source from the dam is gone.

Pregnant bitches- once they become infected they remain infected up to 6-7 litters- cannot 100% eliminate larvae from adult animals. You can try to reduce the burden. So before and after whelping = treat

Parasitology (6 decks)

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