Trematodes Flashcards

1
Q

What is a platyhelminth?

A

flatworm

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2
Q

What are the 3 classes of flatworms that are trematodes (flukes) and what are their main features

A

Monogenea

  • marine, freshwater parasites
  • one host LC

Digenea

  • internal parasites of vertebrates
  • 2/indirect host LC

Aspidogastrea

  • marine, freshwater internal parasite of molluscs, arachaic fish and turtles
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3
Q
A

A: Ovaries

B:Oral Sucker

C: testes

D: ventral sucker

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4
Q

Name 5 general features of platyhelminthes?

A
  1. flat
  2. bilaterally symmetrical
  3. tegument - role in diffusion
  4. acoelomate
  5. hermaphroditic
  6. “flame cells”
  7. “cephealisation”- suck up juices
  8. blind ended (trematodes) or no gut (cestodes)
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5
Q

Features of the order Digenea life cycle?

A

indirect LC

generations of sexual (adult) and asexual (larval) generation in alternate hosts

2+hosts

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6
Q

What is the veterinary significance of trematodes?

A
  • acute and chronic fascioliasis
  • paraphistomiasis
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7
Q

what is the medical significance of trematodes?

A
  • schistosomosis
  • fish borne liver flukes
    • clonorchiosis
    • opisthorchiosis
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8
Q

What are 5 featues of adult digenea?

A
  • non segmented
  • suckers (oral, ventral, posterior)
  • +/- spines on tegument- suck nutrients along body wall
  • digestive tract; ususally no anus - open
  • mostly hermaphrodites (monoecious) some dioecious (shistosomes)
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9
Q
A

A: monoecious

B: dioecious

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10
Q

What are the funcitonal systems of trematodes?

A
  • tegument
    • extension of cytoplasm
    • microvilli- large SA
    • rich in mitochondria, vacuoles and ER- actively metabolising and absorbing nutrients
      • syncytium
    • may have spines
  • muscle later
  • subtegument
    • reticulate, neruomuscular and anchoring layers
  • parenchyma
    • digestive tract
    • osmoregulatory system
    • nervous
    • reproductive
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11
Q
A

Parenchyma -digestive system

A: oral sucker

B: ventral sucker

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12
Q
A

A: nervous system

B: osmoregulatory system : protonephridial “flame cells”

C: flame cells

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13
Q
A
  1. testes
  2. cirrus
  3. seminal receptacle
  4. mehlis’ gland - produces final shell

A: ovary

B: testes

** as eggs matures they get thicker and darker

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14
Q

General Digenean Life Cycle

Aquatic Hatching vs Terrestrial Hatching

A

Aquatic Hatching

  • Fasciola
    • eggs dont contain fully developed larva when passed in feces
    • hatching dependent on light and increased temperature
  • Schistosome-type
    • egg fully developed in miracidium when passed in feces or urine
    • hatching spontaneously in water - IH is aquatic

Terrestrial

  • Dicrocoelium type
    • egg containing the miracidium is ingested by IH and hatches under the inflence of grinding of snails gizzard/enzymes
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15
Q

General Digenean Life Cycle

* larval development

A
  • miracidium (chemotactically attracted to snail and burrows into foot)
  • IH = asexual reporduction
    • sporocyst > rediae (paraphistomes and fasciola) > cercaria
  • Cercaria released from snail = actively motile
  • metacercaria
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16
Q

Egg features- Slide 15 L 7

A.B.C.D.

A

A. Dicrocoelium

B. Schistosoma

C. Schistosoma

D. Fasciola

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17
Q

Features of Miracidium

A
  • Aquatic -ciliated
  • sensory to find snail -chemotaxis, light, salinity
  • retractable apical papilla - sensory, enxymes for penetration
    • PENETRATE SNAIL
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18
Q

When does the sexual cycles of the digenean occur?

A

When the DH ingests the metacercaria or cercaria penetrates DH > adult fluke

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19
Q

what is a sporocyst?

A
  • asexual reproductive stage - binary fission > daughter sporocyst/rediae
  • sac like structure with germinal cells within snail
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20
Q

Features of the Cercariae

A
  • escape from snail
  • active swimmer - tail
  • may penetrate host (DH or 2IH)
  • mechanical head movement and protease enzymes force entry
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21
Q

What are examples and features of free, second aquatic and second terrestrial IH metacercaria?

A

free = (fasciola/paramphistomes) - encyst on vegetation along waterways

second aquatic IH= (paragonimus- crab, Clonorchis, Diplostomum) - encyst in the tissues of 2IH and then ingested by DH

Second terrestrial IH = (Dicrocoelium) - cercaria released in a slim ball thats ingested by an ant, ant is digested by DH

** modify host behaviour

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22
Q

Life Cycle of Fasciola

A

> 6 Month Life cycle

  1. eggs in feces into water - 2-3 wks to embryonate and hatch at > 10*
  2. Miracidium in water > penetrate LYMNAEA snail (IH)
  3. Asexual repro in snail > cercaria
    1. 1000-4000 cercaria per miracidium
  4. metacercaria encyst on vegetation
  5. ingested by DH - immature fluke migrates in liver (4-6 wks)
  6. mature adults in bile ducts
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23
Q

What are 2 species of Faciola and where are they found?

A

Fasciola hepatic - worldwide (wide, leaf life)

Fasciola gigantica (tropical liver fluke) - Asia, Africa (long w/shoulders)

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24
Q

Main morphology of Fasciola hepatica?

A
  • large, leaf like, broad (anterior)
  • Conical projection @ anterior end
  • Caeca highly branched
  • spines on tegument
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25
Q

How can you identify the lymnea snai?

A
  • clockwise spiral
  • long conical spiral
  • triangular tenticles
  • found near standing or slow flow bodies of water - fresh water
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26
Q

What is the common pathogenesis of fasciola sp in sheep?

A

metacercaria ingested > juvenile flukes

  • through intestinal wall to peritoneal cavity > penetrate liver capsule > migrate in liver paranchyma (sometimes aberrant sites- lung)
  • this is the acute phase - 4-6 weeks
  • disruption of liver function and promote clostridial spore germination
    • Black disease: acute toxemia (clostridium) = FATAL

no natural protective immunity

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27
Q

What is the pathogenesis of fasciola in cattle?

A
  • Metacercaria ingested > juvenile flukes through instinal wall > peritoneum > liver paranchyma migration
  • Adult flukes establish in bile ducts
    • hypertrophy of bile duct epithelium
    • calcification of parasite & bile stones
    • fibrotic response & wasting
    • Chronic phase = > 6 weeks
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28
Q

What happens if an animal ingests 500-2000 metacercaria over a short period of time?

A

traumatic hepatitis, hemorrhage

Clostridium novyi toxemia >necrotic hepatitis “black disease”

anemia, abdo pain, sudden death

* L 8 Slide 10 for post mortem findings

29
Q

What are the clinical signs and gross findings of an animal with chronic fascioliasis?

A
  • cirrhosis of liver
  • biliary calcification > thick nodular ducts
    • anaemia
    • bottle jaw, ascites
    • diarrhea
    • wasting
    • autumn, early winter
30
Q

How do you diagnose fasciolosis?

A
  • history & clinical signs
  • FEC
    • think shelled, large tan operculate
    • SEDIMENTATION
  • Serology (ELISA IgG)
    • 4-6 wks sheep ** juveniles dont shed eggs
    • 6-8 wks cattle
  • Post mortem
  • CBC/ Biochemistry
    • anaemia
    • elevated liver enzymes
    • hypoproteinemia

things to condider

* differential : hemonchus contortus

31
Q

What is the economic significance of fasciola?

A
  • production loss
    • reduced milk/wool quality
    • low lambing rates
    • poor growth/ feed conversion
    • sudden death
  • drenching costs
  • condemn livers
32
Q

What are the epidemiological factors of Faciola hepatica?

A
  • Parasite + snail + rainfall (>50mm) + temp >10*
  • freshwater, shallow, stagnant, irrigation channel, pond
  • All AUS states except WA & NT
    • QLD- all year
    • VIC- spring and autumn

* when snails are most abundant there is the highest parasite load

September (eggs) – 2 mo– > mid November (cercaria) – 6wks –> January (juvenile)

33
Q

What 2 factors increase infection pressure of faciola?

A
  • winter rainfall areas - snails breed and eggs hatch in spring
    • metacercaria in early/mid dec
  • grazing habits
    • summer rainfall - sheep graze near water in winter
    • winter rainfall - sheep graze near water in summer
34
Q

How do you treat faciola?

A
  • trichlabendazole (oral or pour on) - works on all life stages
  • Clostantel + oxfendazole/albendazole - adult life stages (when in bile duct)
35
Q

How can you control faciola?

A
  1. Fence off snail prone areas
  2. drain marshy pastures
  3. build dams
  4. flukicidal trx (depend on climate/rain)
    1. Aug/Sept - late winter
      1. reduce pasture contamination w/eggs as snails emerge in late winter
    2. Jan/Feb - mid summer
      1. kill immature flukes over summer
    3. April/May
      1. kill flukes if Jan/Feb was ineffective against immature flukes
  5. 5-1 vax
36
Q

what is the giant intestinal fluke : pathogenesis and LC features?

A
  • Fasciolopsis buski
    • Asisa : malabsorption > stunting and dxa
    • metacercaria on watercress > ingested by pigs or humans
37
Q

What are the 1st IH, 2nd IH and DH of Paramphistomidae?

A

Snail (1st) IH : planorbids

2nd IH: free metacercaria

DH: ruminants, horses, pigs, humans

38
Q

What are the 1st IH, 2nd IH and DH of Dicrocoeliidae?

A

Snail (1st) IH: Cionella spp

2nd IH: ant

DH: ruminants, pigs, horses, humans

39
Q

What are the identifying features of paramphistomes?

A
  • fleshy pear shaped
  • juvenile flukes are smal
  • large vental sucker at posterior end
  • ovaries behind testes - hermaphrodites
40
Q

What is the vector of paramphistomes?

A

Planorbid aquatic snails

41
Q

What is the life cycle of Paramphistomes? Differences from Faciola?

A
  • LC and epidemiology similar to Fasciola (aquatic & free metacercaria)
  • immature flukes in DUODENUM for 3-4 wks
  • migrate to reticulum and rumen - ADULTS
  • PPP = 2-3 mo
42
Q

Juvenile and Adult pathogenesis of paramphistomes

A
  • wks 4-8 = juveniles move from duodenum to rumen/retic
    • atrophy of villi
    • enteritis
    • reduced weight, milk production, ill thrift w/ moderate infection
    • pin prick appearance of duodenum
  • adults cause no harm
  • light infections - asymptomatic
43
Q

in drought conditions, weaner sheep are introduced to a new paddock and have watery dxa and dehydrated. The sheep that died were found to have an infection of 70,000 juvenile worms in duodenum. The older sheep on the property seem uninfected. What is the trematode?

A

paramphistomes

*exposure = increased immunity

weaners most susceptible - drought, movement and stress

44
Q

How do you diagnose paramphistomes?

A
  • History
    • temperature (10*), rainfall (15mm rainfall), grazing conditions, age group affected, drench history
  • Clinical signs
  • post mortem - enteritis and open rumen for adults
  • eggs in feces? - sedimentation (large eggs with operculum)
45
Q

When do you treat paramphistomes with closantel and oxyclozanide?

A
  • Adults in rumen
    • late winter
    • reduce contamination of pasture
  • Juveniles in duodenum
    • summer to autumn
    • treat/prevent clinical disease
      • can treat monthy bc can cause disease rapidly

fence and drain affected areas

46
Q

What are the important features of the Dicrocoelium dendriticum life cycle?

A
  • Embryonated eggs shed in feces
  • IH = cionella terrestrial snal (3 mo)
    • miracidia > cerceriae
  • cercariae released from slime ball > ingested by ant
  • 2IH = ant > ingested by DH on blade of grass
  • juveniles migrate up bile duct to become adults
    • calcification of bile ducts (mildly pathogenic)
    • liver condemation

PPP= 3 mo

not in AUS

47
Q

Its hard to treat dicrocoelium dendriticum but what compounds can you use?

A

benzimidazoles (albendazole) at high dose or Praziquantel

48
Q

What are the fish borne liver flukes found in asia? What clinical signs would you expect to see?

A

Family: Opisthorchidae

  • Opisthorchis and Clonorchis

Signs

  • asymptomatic
  • gall bladder stones
  • cholangitis, jaundice
  • Cholagiocarcinoma
49
Q

What are the fish borne small intestinal flukes found in SE asia & china? What clinical signs would you expect to see?

A

Heterophyidae and Echinostomatidae

Clincal signs

  • asymptomatic or enteritis/gastritis and ulceration
    • dxa, upper gastric pain (ddx peptic ulcers)
50
Q

What is the life cycle of fish borne liver and intestinal flukes?

A
  • eggs passed in feces w/ miracidium
  • IH = aquatic freshwater snail
  • free swiming cercariae penetrates 2IH = fish
  • fish w/ metacercariae is ingested by DH (human, dog, cat, pig)
  • Adult flukes in bile duct
51
Q

What are 3 risk factors of fish borne flukes?

A
  • traditaional dietary practice of eating raw, pickled or fermented fish
  • poor sanitation
  • uncontrolled reservoir host population
52
Q

features of fish borne fluke eggs

A

Lecture 9 slide 20

53
Q

features of audlt fish borne flukes

A

lecture 9 slide 21

54
Q

how do you control fish borne flukes ( liver= opisthorchis & chlonorchis) (intestinal = heterophyidae & echinostomatidae)

A
  • Monitor and chemotherapy
    • praziquantel for humans
  • education
    • alter eating practices - cook fish or free @ -20* for > 24hr
    • indoor defication
    • dont feed dogs/cats raw fish
55
Q

What is the life cycle of Paragonimus sp?

A
  • eggs coughed/swallowed & passed in feces
  • miracidium penetrate snail (1IH)
  • free swiming cercaria penetrate 2IH (crabs)
    • Paratenic Host = pigs
  • metacercaria ingested (eat pig or crab) by DH (dog/cat)
  • aults migrate through diaphragm into alveolar sacs and in lung paranchyma
56
Q

What is the epidemilogy and clinical signs of Paragonimiasis? How do you treat?

A
  • endemic to SE asia, america and africa
  • Canids and felids eeservoirs
  • pulmonary form
    • cough, hemoptysis (form cysts in lung)
    • “non responsive tuberculosis”
  • 30% extra pulmonary > brain, abdo
    • juvenile forms wander

treat = praziquantel

control= cook crabs

57
Q

What are the “blood flukes”? Are they in australia?

A

Schistosomas

  • human pathogens not in AUS (in SE Asia, Africa)
58
Q

What is the adult morphology of schistosoma?

A
  • oral and ventral suckers
  • split body
  • dioecius
  • in-copula (female in gynecophoric groove of male)
59
Q

what is the schistosoma life cycle?

A
  • eggs in feces
    • s. mansoni, s. japonicum, s. hematobium
  • eggs in urine
    • s. japonicum, s. hematobium
  • hatch and release miracidum > penetrate aquatic snail (sporocyst)
  • cercaria released (forked tail for swimming) > pentrate skin of human
  • enter circulation and migrate to portal blood in liver
  • paired adults migrate to mesesnteric venules of bowel/rectum or venous plexus of bladder
60
Q

Snail intermediate hosts of schistosoma

A

lecture 10 slide 7

61
Q

What are the risk factors of S. japonicum?

A

risks

  • rice farm
  • fishing
  • swimming

zoonosis

  • wter buffalo, cattle, pigs, dogs, cats
62
Q

What is the clinical differences between acute and chronic schistosomiosis?

A

Acute

  • self limiting cercarial dermatitis (swimmers itch) - 24h
  • delayed hypersensitivity response (3-4 wks)
    • TH1 proinflam response
    • hypereosinophilia
    • fever, arthralgia, bronchiopneumona, urticaria or angioedema

Chronic

  • eggs laid in venules of bladder/distal colon > eggs penetrate using spine and proteolyic enzymes to enter lumen and be passed
  • some eggs lodge in organs causing granulomas >> intestines, liver, bladder, brain
  • portal & pulm hypertension & ascites
  • dysuria, hematuria, calcification
  • worm antigens in circulation
    • nephrotic synndrome
    • ab -mediated glomerulonephritis
  • anemia, stunted children
  • HIV/AIDS co-infection complications
63
Q

How do you diagnose schistosomiasis?

A
  • history/clinical signs
  • eggs in feces/urine
    • SPINES
  • serology
64
Q

Treat w/ praziquantel, improving sanitaion and access to clean water, molluscicidal treatment - are possible control measures for what trematode?

A

Schistosoma - blood flukes

65
Q

What is Cercarial dermatitis? Is it in australia?

A
  • swimmers itch is in australia
    • from aquatic birds
    • skin penetration of wrong host
      • self limiting hypersensitivity reaction (multiple exposures)
66
Q

What are 2 species of schistosoma that infect cattle in africa and middle east and are found in the venules of mucosa (mesenteric and hepatic)

A

S. bovis and A. matthei

67
Q

What is the schistosoma that infects pigs in SE asia and India and are found in the nasal veins

A

S. nasale

68
Q

Young animals with high burdens of visceral schistosoma - what are the clinical signs?

A
  • pathophysiology and trx similar to humans
  • dxa, hematuria, ascites, wating
  • severly affected deteriorare rapidly and die w/in a fee mo
  • severe phebitis and thrombosis of mesenteric veins (see lecture 10 slide 17)