Week 3

Question 1

Answer 1

Trematodes (Flukes), Platyhelminths (flatworms)

Question 2

What are Digenea?

Answer 2

Parasitic Trematodes (Flukes)- Playhelminths (flatworms)

Parasites of vertebrates (internal); two/ indirect host life cycle

Question 3

Answer 3

Cestodes (Tapeworms), Platyhelminths (flatworms)

Question 4

What are features of Platyhelminthes?

Answer 4

* Flattened, and mm- m!

* bilaterally symmetrical

* Tegument (role in diffusion, like a semi ectoderm skin layer)

* Triploblastic (3 layers- ectoderm, mesoderm, endoderm– one of the first with these 3 layers), acoelomate (solid mesoderm)

* Hermaphroditic (male/female reproductive organs in the same organism)

* Flame cells (protoephridium)- early forms of kidney tubules

* Cephalisation- first signs of brains- aggregation of nerve cells

* Blind ended (trematodes) or no gut (cestodes)– i.e. tapeworms have no gut… blinded means there is no anus but they have a gut

* Cephalisation

Question 5

Digenea

Answer 5

(Platyhelminthes)

* >6000 species

* Indirect life cycle- IH host

• generations of sexual (definitive host) and asexual (larval- intermediate host) generations in alternate hosts

* 2+ hosts

Question 6

Answer 6

Digenea, Platyhelminthes

Question 7

Answer 7

Digenea, Platyhelminthes

Question 8

Answer 8

Digenea, Platyhelminthes

Question 9

Digenea features (adult worms)

Answer 9

* Non-segmented

* Suckers (oral, ventral or posterior)

* Spines (tegument)

* Digestive tract; usually no anus

* Mostly hermaphrodies (monoecious); some dioecious (two different sexes)– except schistosomes

Question 10

What are the 4 layers of a flatworm?

Answer 10

* Protective layer

* ectoderm disappears during penetration of definitive host

* microvilli on the surface- role in protection, nutrient absorption, and metabolism (increased surface area, golgi apparatus, and ER)

4 layers:

1. Tegument
2. Muscle Layer
3. Sub-tegument
4. Parenchyma– if no body cavity, you will know it is a flatworm

Question 11

Answer 11

Digestive system of a flatworm (platyhelminth)

Question 12

Answer 12

Reproductive System of a platyhelminth (flat worm)

* Testes, ovaries, vitallaria glands (yolk), ootype (egg is shaped)

Question 13

What is the life cycle of a Digenea?

Answer 13

* Definitive host: humans- adults live in bile duct spews out eggs–> eggs come out in faeces–> embryonated (miracidium is in there) hatch–> release miracidium–> eaten by snail OR penetrates snail–> asexual cycle occurs producing thousands of offspring from one egg–>(next stage that comes out is the cercariae- motile form) asexual forms exit the snail and penetrate second IH OR metacercariae form go into a cystic form ingested by the definitive host

(some differences occur like no metacercariae in schistocytes)

Question 14

Distinguishing feature of all trematode eggs

Answer 14

* Spine assists with motility- helps them get through blood vessels into the bladder and out through the faeces

Question 15

What is a miracidium?

Answer 15

** looking for snail!! So many sensory nerve endings!!

* Aquatic- ciliated epithelium

* Highly sensory- must find a snail

-light, temp, salinity, chemotaxis (secretions snail), negative geotaxis

* Retractable apical papilla

• sensory nerve endings
• apical galnds- enzymes for penetration
• muscular contractions
• = penetration snail ( ALL OF THIS HELPS WITH PENETRATION)

Question 16

Answer 16

Ciliated ectoderm lost during penetration (of snail, for example)- become diphoblastic

Question 17

Answer 17

Question 18

Cercariae

Answer 18

Question 19

Metacercariae

Answer 19

Metacercariae are encysted within the second IH (snail–> ant–> cat eats the ant)

Question 20

Life cycle of Fasciola spp.

PPP? How long does the life cycle take?

Answer 20

* adult in bile duct–> sexual production of eggs excreted into faeces–> eggs are unembryonated when passed (not infective, just blastocyst sgages there– need the proper environment to start embryonating and to produce miricidium) (wet and at least 10 C for embryonation to start)–> 2-3 weeks for miracidium to be formed and hatch, egg is attracted to water–> miracidium has cilia and swims and looks for snail host and actively penetrates–> undergoes asexual multiplication 1000-4000 cercariae per miracidium–> latch onto vegetation and form resistant free living metacercaria–> definitive host eats plants and metacercaria–> metacercaria hatch and penetrate GI tract and migrate through into the peritoneal cavity–> parenchyma of the liver as juveniles and mature in 4-6 weeks into adults

PPP= 3 months (but in total 6 month life cycle outside the host as well)

Question 21

Morphology of F. hepatica

Answer 21

Question 22

Answer 22

Question 23

How do you identify Lymnaea snails?

Answer 23

1. Clockwise spiral
2. No cover to the hole in the shell
3. Triangular ears

L. lessoni is not an IH in Australia

Question 24

Pathogenesis of Flukes (cattle vs. sheep)

Answer 24

* Acute Phase (usually seen in sheep)

* Chronic Phase (usually seen in cattle, because they have some immunity to Fasciola so unlikely to see massive infections all at once)

(Sometimes seen in organs other than the liver)

* Clostridium novyi adds to the problem (Black disease)- Sudden death in sheep

* If the animal lives through acute phase– mature to adults and live in the bile ducts– cause inflammation and subsequent fibrosis of bile ducts. The parasites themselves get calcified. Animals and humans produce gal stones. Cirrhosis of the liver ensues (no albumin production which = hypoalbuminamia, wasting, etc.)

Question 25

How does Acute Fascioliasis occur?

Answer 25

\* Occurs seasonally and acutely- late spring/ early summer in temperate regions OR drought conditions in areas with dry summer so you see it in early AUTUMN where the sheep search for water sources (haven't been there before so naive) \* Massive intake of metacercariae over short time (500-2000) ON PLANTS \* Traumatic hepatitis, haemorrhage (because of spines of the juvenile flukes migrating through the liver) \* Clostridium novyi toxaemia (opportunistic in conditions produced by haemorrhage and hepatitis, capillaries burst), resulting in "black disease" (Necrotic hepatitis) \* Anaemia, abdominal pain, sudden death

Question 26

Answer 26

Acute Fascioliasis

Question 27

Answer 27

Subacute fascioliasis

Question 28

Answer 28

Question 29

Answer 29

Chronic Fascioliasis

Question 30

Diagnosis of Fascioliasis

Answer 30

\* History and clinical signs \* Serology- may not be adults yet, so no point in looking at poo- antibody test can diagnose acute fascioliasis \* Faecal egg counts \* Post-mortem \* Look for the Lymnaea snails \* CBC/biochem: anaemia (due to chronic infection), elevated liver enzymes, hypoproteinaemia

Question 31

Answer 31

Aberrant migration to lungs of fascioliasis

Question 32

Economic significance

Answer 32

\* Production losses- 60-80 million p.a.- reduced production and quality wool/ milk, low lambing rates, poor growth and feed conversion, sudden death \* Drenching- 10 million (specific drugs) \* Condemnation of livers at abattoir

Question 33

What three things do you need for Fasciola to flourish? What months would you see it in a temperate climate (winter rainfall area)? What about summer rainfall climate? Tropics??

Answer 33

1. Rainfall \> 50 mm, temp \> 10 C 2. Parasite 3. Freshwater, shallwo, stagnant, pond, trickle streams, irrigation channels \*\* Not in WA or NT \* Eggs start to embryonate in spring--\> 2-3 weeks develop and hatch (egg came from previously infected cattle)--\> goes into snail approx 3 months before metacircariae encysted on vegetation--\> early summer sheep and cattle infected expect to see acute disease 5-6 weeks later when juveniles have caused destruction in the liver (JANUARY!! Early to mid summer, consider acute fascioliasis if in a temperate region... CHRONIC would be a few months later--\> MARCH/ APRIL-- takes time for liver to get cirrhosed) \*\* Reversed in a summer rainfall area \*\* The whole YEAR! Control needs to be regular

Question 34

Treatment and Control of Flukes

Answer 34

\* Fence off the area from grazing where snails are present, sufficient water and supplementary feed so they don't need to go to those areas in drought \* Draining marshy pastures \* Building dams \* Strategic flukicidal treatments \* 5 in 1 vaccines (Clostridium novyi is included- treat before summer) \* Triclabendazole (oral; pour on formulations also available)-- the best as it will kill flukes at all ages (do not use in winter as do not want to encourage resistance- possibly Closantel) \* Closantel plus oxfendazole (specific for haemonchus as well-- and flukes 6-14 weeks old)

Question 35

Strategic anthelmintic treatment

Answer 35

Depends where you're working, but generally: \* Winter to kill flukes: reduce pasture contamination with eggs as snails emerge in later winter/spring- CLOSANTEL \* Mid summer- Jan/Feb- kill immature flukes acquired over early summer- TRICLOBENDAZOLE \* April/ May- kill flukes if Jan/Feb dose was not effective against immature flukes- CLOSANTEL