Flukes Flashcards

1
Q

What is Fasciola Hepatica? What are the finals hosts? Significant hosts? Disease caused? Distribution?

A
  1. Liver fluke
  2. Most mammals
  3. Sheep/ Cattle
  4. Fasciolosis
  5. Temperate regions
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2
Q

What phylum are the flukes in? Class?

A

Platyhelminths

Trematoda

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3
Q

What is the IMH for Fasciolosis?

A

Amphibious Galba truncatula (small brown snail)

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4
Q

Describe the life cycle of F. hepatica. What is the PPP?

A
  1. Adults eggs are passed in the feces. These eggs contain quinone which gives them its yellow coloring and provides stability allowing enrivonemntal resistance.
  2. Embryonation of the egg occurs in the presence of H20, 22 degrees Celsius and will occur in 9 days. In the presence of light the embryo will hatch from the egg.
  3. The embryo will form into the ciliate motile MIRACIDUM which has a small window of time (~24 hrs) to find a host.
  4. The MIRACIDUM penetrates the amphibious Galba truncatula and the MIRACIDUM develops into the bag like SPOROCYST.
  5. The SPOROCYST takes 6-7 weeks to deveop into the asexul REDIA which produce daughter REDIA.
  6. REDIA will develop in the CERCARIA in the right conditions (warm, wet, light conditions).
  7. The CERCARIA will exit the snail and enter the environment maturing into METACERCARIA which encyst in the environment into the vegetation (resistant) until ingested by grazing via the sheep or cattle.
  8. Excystation of the METACERCARIA is induced by C02 and bile.
  9. Juvenile flukes will penetrate the liver parenchyma.
  10. Adults will enter into the bile ducts and gall bladder.
  11. The PPP is 10-12 weeks.
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5
Q

Identify this image. Describe these parasites. What functional characteristics do they have?

A

These are F. hepatica.

They are flat, cone like anteriorly.

They have 2 suckers and a spine on their cuticle:

  • Ventral: allows to keep bounds to bile ducts.
  • *-Oral Sucker:** allows intial adhesion to bile ducts.
  • *-Cuticle spine:** assists in stabilization in the bile ducts.

They are hermaphroditic therefore self fertilizing

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6
Q

Acute Fasciolosis:

When is it detected? When does it occur post ingestion? What is it caused by? What does it result in? What does it manifest as?

A

Detected in Autumn-Early Winter.

Occurs 2-6 weeks post ingestion.

Caused by migration of juvenile flukes through the liver parenchyma.

Results in: Liver Damage & Hemorrhage

Manifests as: Pale MM, Suddent death, dyspnoea, ascites, palpable liver, abdominal pain.

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7
Q

What would you expect in Acute phase liver @ PM.

A

Enlarged hemorrhagic liver.

Rupture of the sub capsular hemorrhage.

Fibrinous exudate over the ventral lobe.

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8
Q

Subacute Fasicolosis:

When is it detected? When does it occur post ingestion? What is it caused by? What does it result in? What does it manifest as?

A

Detected in late autumn-winter

Occurs: 6-10 weeks post ingestion

Caused by: Migration of juvenile flukes and feeding of adults on bile duct mucosa causing inflammation.

Results in : Liver parenchymal damage, Cholangitis, blood loss

Manifests as: Rapid/ severe hemorrhagic anemia, ascites, hypoalbuminemiea, Pale MM, may see SM edema (bottle jaw)–more common with chronic fasciolosis.

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9
Q

Chronic Fasciolosis:

When is it detected? When does it occur post ingestion? What is it caused by? What does it result in? What does it manifest as?

A

Detected: Late Winter-Early spring

Occurs: 4-5 months post ingestion

Caused by: Adult flukes feeding in the bile ducts.

Results in: Cholangitis, Anemia, hypoalbuminemia.

Manifests as: SM edema (bottle jaw), Progressive loss of body condition, emaciation (losing blood decreased nutrition), Pale MM.

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10
Q

How would you diagnose Ovine Fasciolosis?

A

Clinical signs/ seasonal occurence.

PM indentification of flukes

Eggs in feces.

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11
Q

How would you diagnose Bovine Fasciolosis?

A

Eggs in feces

Test for glutamate dehydrogenase: (increases with liver parenchymal damage)

Test for Gamma-glutamyl transpeptidase: This is an indicator of biliary damage.

ELISA

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12
Q

What occurs in Chronic Bovine Fasciolosis?

A

Usually assoc. with younger live stock.

Will see:

  1. Productivity loses.
  2. Calcification of bile ducts
  3. Gall bladder enlargement.

Immune Response:

Limits primary infections and inhibits the secondary infection.

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13
Q

Fasciolosis Epidemiology:

  1. Snail Habitat
  2. Temperature
  3. Moisture
  4. Optimal period of the year for all of these factors to coincide and allow the proliferation of fasciolosis.
A
  1. Snails (amphibious) thrive on shallow, muddy, slow moving water. Water at the edge of banks and ponds.
  2. Moisture (rainfall) increases the likelihood of the MIARCIDIUM finding the snail host because it increases its habitat. Remember there is a small window (24 horus) for the MIRACIDIUM to find a host)
  3. A mean day/ night temp of > 10 degrees celsius is essential for snail breeding, larval development, and hatching.
  4. MAY-OCTOBER
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14
Q

What is Summer Fasciolosis?

A

Snails infected by MIRACIDIUM in late spring/ summer derived from over-winterd eggs and eggs from carrier animals.

Will take approx two months before CERCARIA erupt.

Therefore will get an increase in METACERCARIA on pasture from August to October.

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15
Q

What is Winter Fasciolosis?

A

Snails become infected by MIRACIDIUM in August.

Due to the drop in temperature the snails hibernate and thefore the larvae undergo hypobiosis.

They are reactivated in Spring and development resumes.

METACERCARIA are released into pasture in May-June. NOT AS IMPT. AS SUMMER INFX.

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16
Q

What are some methods of controlling Fasciolosis?

A
  1. Drainage
  2. Fence off saturated pasture.
  3. Move sheep to drier pasture.
  4. Molluscicide
17
Q

Fasciola gigantica:

Distribution?

A

Tropical & Sub tropical regions.

18
Q

What are the differences between F. hepatica & F. gigantica regarding size, pathology, IMH?

A

F. Hepatica are 30mm in size whereas F. gigantica are 75mm in size (2x the size–GIGANTICA BIGGER)

F. gigantica are more pathogenic

F. gigantica have an Aquatic Snail IMH v. Amphibious.

19
Q

F. gigantica epidemiology and life cycle and PPP

A
  • MIRACIDIA hatch at the beginning of the wet seaon, infect snails, & develop by end of wet season.
  • CERCARIA leave the snail at the beginning of and during the dry period
  • METACERCARIA encyst on aquatic plants or water.
  • Disease occurs at end of dry season beginning of wet.

** Wet Season:**

  • Development within the snail
  • @ end of wet- metacercaria encyst on aquatic plants/ H20 surface

Dry Season:

  • Development within the mammal.
  • @ end of dry- Disease occurs, MIRACIDIA hatch and infect snails.

**PPP= 13-16 weeks. v 10-12 of F. hepatica. **

20
Q

Control of F. gigantica.

A

Similar to that of F. hepatica.

21
Q

Dicrocoeliidae

Dicrocoelium dendriticum:

Distribution?

Main hosts?

Site?

IMH?

A

Worldwide distribution

Main hosts: Sheep, cattle, horses, rabbits

Site: Bile Ducts/ Gall Bladder

IMH: Land Snails/ Ants

22
Q

D. dendriticum life cycle

A
  1. egg is fully embryonated when laid.
  2. hatching only occurs when ingested by suitable land snail.
  3. Inside the IMH it develops from MIRACIDIUM -> SPOROCYST-> CERCARIA. This development process takes approx 90 days.
  4. CERCARIA are ejected with slimeball.
  5. Infected vegetation eaten by ant which encompasses the slime ball.
  6. METACERCARIA encyst in the ant’s abdomen.
  7. The ant is accidentally ingested by mammal host.
  8. Excystation of the METACERCARIA occurs in the duodenum and migrates to the liver via the bile ducts.
  9. Mature flukes in the bile duct for 10-12 weeks then produce eggs which are excreted via the anus.
23
Q

Dicrocoelium dendriticum pathogenesis.

What are the clinical symptoms?

Productivity loses?

A

Will get heavy infections in older sheep.

Pathogenesis:

Fibrosis, Distension of bile ducts, progressive cirrhosis.

Clinical symptoms:

Weakness, Anemia, Emaciation.

Productivity loses:

Decreased wool production, premature ageing, repro losses.

24
Q

Dicrocoelium dendriticum epidemilogy:

IMH habitat

Egg surival

Tx:

A
  1. Dry habitiat (no water)
  2. eggs survive for months
  3. Albendazole
25
Q

What are paramphistomidae?

What are the two species?

What are their sites of infection?

IMH?

A

Rumen Flukes

Rumen/ Reticulum

  • p. cervi
  • p. microbothrium

Aquatic snails:

  1. Planorbis
  2. Bulinus
26
Q

Where do the juvenile paramphistomidea reside?

A

The excyst in the duodenum, attach to mucosa, cause the pathology.

27
Q

What is the paramphistomum life cycle and PPP?

A

Snail stages as Fasciola (4 weeks)

Metacercaria are ingested

Excyst in duodenum where juveniles attach to intestinal wall and feed (6 weeks)

Adults migrate to forestomachs

PPP: 7-10 weeks

28
Q

Paramphistomum: pathogenesis

A

Is due to Juvenile intestinal phase of infection-
attach to duodenal mucosa

Which causes Necrosis & haemorrhage-
erosion of duodenal mucosa

Results in Gastroenteritis- marked by
oedema, haemorrhage & ulceration

Adults cause little harm

29
Q

Paramphistomes:

Clinical signs?

Diagnoses?

Tx?

A
  1. Clinical signs:
    - Foetid diarrhea
    - Anemia
    - Hypoalbuminemia
    - Intense thirst & anorexia
    - Potential for high mortality.
  2. Diagnoses:
    - PM (juveniles in duodenum)
    - Fecal egg count of limited value
  3. Treatment:
    - oxyclozanide
30
Q

Paramphistomidae Epidemiology:

A

Tropics/ Sub tropics:

  • Similar to F. gigantica
  • Transmitted by aquatic snails
  • Associated with flooding
31
Q

SCHISTOSOMATIDAE

Species affected?

IMH?

Major species of schistosomatidae?

A

Parasites of all domestic mammals

Cattle and Sheep in tropics, sub-tropics & S. Europe

IMH: aquatic snails (Bulinus and Physopsis)

Major species:

  • Schistosoma bovis,
  • **S. japonicum **
  • S. matthei
32
Q

Identify this species image.

A

Schistosomatidae egg

33
Q

Schistosoma: pathogenesis

A
  • Inflammatory response against eggs in veins, mucosa & liver
  • Leading to granuloma formation - intestinal mucosa and liver
  • Acute: mucosal haemorrhage, anaemia, hypoalbuminaemia hepatosplenomegaly
  • Clinical signs: anaemia, diarrhoea (mucous & blood tinged), thirst, anorexia, emaciation
  • Chronic: marked granuloma of intestine and cirrhosis/periportal fibrosis of liver, reduced productivity
34
Q

Schistosoma: diagnosis

A

Based on clinical signs/infected water source

Coupled to demonstration of granulomatous lesions and adults in mesenteric veins

Demonstration of eggs

35
Q

Schistosoma: epidemiology/control

A

Epidemiology is related to prevalence of aquatic snail

Clean water source - controlled movement of cattle

Drugs - praziquantel, albendazole