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GI > Liver parasitology > Flashcards

Liver parasitology Flashcards

1
Q

List the nematodes which infest the liver in common domesticated species

A
  • Capillaria hepatica

- Ascaris suum

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2
Q

List the cestodes which infest the liver in the common domesticated species

A
  • Echinococcus granulosus
  • Echinococcus multilocularis
  • Cysticercus tenuicollis
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3
Q

Describe infestation by Capillaria hepatica

A
  • Rats, mice, rabbits, hares, dog, cat, horse, squirrel, muskrat, beaver, antelope, human
  • Rodents and lacomorphs are most important reservoirs
  • Eggs similar to trichuris eggs (bipolar plug, one side more curved than the other)
  • Adults 13-25mm long
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4
Q

Describe the life cycle of Capillaria hepatica

A
  • Rodent ingests infective eggs in soil
  • Eggs hatch, L3-adults development on route through intestine and liver via HP vein
  • Adults mate, produce eggs, die in liver causing pathology
  • Rodent ingested by carnivore
  • Eggs pass out in faeces and embryonate on ground
  • Eggs can be released from the carnivore, or when rodent dies and decomposes
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5
Q

What are the signs of infestation by Capillaria hepatica?

A
  • Hepatomegaly/fibrosis
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6
Q

Describe infestation by Ascaris suum

A
  • Pigs
  • Adults in SI
  • Migrating larvae cause liver and lung pathology
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7
Q

Describe the eggs of Ascaris suum

A
  • All ascarid eggs look similar
  • Round, thick shell, proteinaceous coating
  • Very resistant in environment
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8
Q

Describe the adults of Ascaris suum

A
  • No buccal capsule

- 3 lips around anterior opening instead

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9
Q

Describe the life cycle of Ascaris suum

A
  • Ingestion of eggs containing L2
  • Eggs hatch to L2 in intestine
  • Migrate to HP vein and liver (L3)
  • Migrate to heart and lungs (L4)
  • Coughed up and swallowed (adult develops in intestine)
  • Eggs in faeces
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10
Q

What causes the pathology in Ascaris suum?

A

Migration of the larvae

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11
Q

Describe the immune response to Ascaris suum

A
  • Adult pigs dominant Th2 response, IL-4, IL-5, IL-13 and eosinophils in blood and tissue containing larvae
  • IgA and IgG in colostrum recognises A. suum antigens
  • After 6 weeks have multiple exposure to parasite and tus strong disease resistance
  • Colostrum adn milk antibody have protective effect
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12
Q

How can infestation with Ascaris suum be diagnosed?

A
  • FEC via McMaster

- Necropsy

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13
Q

How can infestation with Ascaris suum be prevented?

A
  • Eggs resistant, viable up to 11 years in environment
  • Avoidance difficult in outdoor units, easier indoors
  • Susceptible to albendazone, piperazine, pyrantel, ivermectin
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14
Q

Describe the genus Echinococcus

A
  • Part of Cyclophyllidae order
  • Scolex has sucker and/or hooks
  • Hexacanthlarvae (larval head has 6 hooks)
  • Larvae in egg only have head without body
  • Once hatch, begin germination and form chain of segments
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15
Q

List the hosts of Echinococcus granulosus

A
  • Definitive: canid
  • Intermediate: herbivore
  • Accidental: humans
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16
Q

Describe the life cycle of Echinococcus granulosus

A
  • Embryonated egg in faeces
  • Ingested by humans or sheep/goat etc
  • Oncosphere hatches, penetrates intestinal wall
  • Forms hydatid cyst in liver, lungs etc
  • Canid ingests cysts in organs of IH
  • Protoscolex forms from cyst
  • Scolex attaches to intestine
  • Develops to adults in small intestine
  • Egg shed in faeces
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17
Q

Describe the clinical signs of Echinococcus granulosus

A
  • Usually non in sheep
  • Cysts on slaughter
  • No sign in dogs
  • In human cysts may take up to 20 years before siings appear (large cysts filled with fluid can be anywhere in the body)
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18
Q

Describe the diagnosis of Echinoccus granulosus

A
  • In dogs: ELISA, dot blot of copro antigen, arecoline can be used to flush adults from intestine
  • In IH: ELISA
  • In humans: MRI and CT scans
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19
Q

Describe the treatment of Echinococcus granulosus

A
  • No effective human treatment except removing cysts
  • Course of albendazole will shrink cyst
  • For dogs regular worming with praziquantel
  • Reduce contact with sheep carcasses
  • Do not allow dogs to lick face, can also transmit infection to humans
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20
Q

What are the hosts of Echinococcus multilocularis?

A
  • Definitive: dogs, cats, foxes
  • IH: rodents
  • Accidental: humans
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21
Q

Describe the life cycle of Echinococcus multilocularis

A
  • Ingestion of embryonated eggs by rodents/humans
  • Oncospheres hatch
  • Multiple hydatid cysts form per egg ingested
  • Dog/cat ingests rodent
  • protoscolex released from cyst
  • Scolex attaches to intestine
  • Adult in small intestine
  • Shed eggs in faeces
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22
Q

Describe the differences between Echinococcus granulosus and multilocularis

A
  • M. more dangerous - one egg can lead to many cysts
  • M. highly invasive
  • M. cysts metastasise more easily
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23
Q

Describe the effects of Echinococcus multilocularis in humans

A
  • Can cause alveolar hydatidosis, usually fatal
  • Moves from tissue to tissue
  • Often misdiagnosed as tumour
  • Infection through ingestion of eggs
  • Leads to gelatinous inflammation
  • Destructive impact on tissue
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24
Q

Describe Cysticercus tenuicollis

A
  • Cystic stage of Taenia hydatigena

- Adults live in intestine of dogs

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25
Q

Describe the life cycle of Taenia hydatigena/ Cysticercus tenuicollis

A
  • Eggs passed out of intestine of dog
  • Sheep ingests eggs
  • Migrate via portal vein to mesentery, peritoneum and liver where cysts form
  • Dog ingests cysts from liver of sheep
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26
Q

Describe the clinical signs caused by Cysticercus tenuicollis

A
  • Usually no clinical signs
  • In very heavy infection may get depression and weakness
  • In young aniamsl liver damage and peritonitis
  • Liver condemned at slaughter
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27
Q

Describe the appearance of Cysticercus tenuicollis

A
  • Cysticercoid
  • One scolex
  • Otherwise similar to E. granulosus
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28
Q

Describe the commercial importance of Capillaria hepatica

A
  • Unknown importance, probably underestimated
  • Problem in zoos
  • Very zoonotic, spread by brown rats
  • Rare in humans, but 50% fatality rate
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29
Q

Describe the commercial importance of Ascaris suum

A
  • Significant economic importance
  • Economic loss in older growing animals
  • Rarely fatal, lowers carcass value
  • Liver and intestine condemnation
  • Reduced weight gain
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30
Q

Describe the commercial importance of Echinococcus granulosus and multilocularis

A
  • Can infect humans
  • Cysts decrease slaughter value of sheep carcass
  • Can be fatal to humans
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31
Q

Describe the commercial importance of Cysticercus tenuicollis

A

Liver condemned at slaughter

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32
Q

List the prominent organs of adult trematodes

A
  • Oral sucker
  • Pharynx
  • Oesophagus
  • Intestine
  • Caeca
  • Ventral sucker
  • Testes
  • Ovaries
  • Vitellaria
  • Uterus (containing eggs)
33
Q

What is the function of the tegument?

A
  • Provides protection

- Aids in gas exchange

34
Q

What are the important families of Digenea?

A
  • Dicrocoeliidae
  • Fascioliidae
  • Opisthorchiidae
  • Schistosomiidae
35
Q

Describe the digenetic trematodes

A
  • Have features in common
  • Leaf-like, flat, prominent attachment organs (oral and ventral suckers)
  • Rest of body made up of mainly reproductive organs
  • Tegument covering external surface
  • Feed on host by pumping of muscular pharynx
  • Gut with 2 caecae lined with cells for nutrient uptake
36
Q

What are the important species of Fascioliidae?

A
  • hepatica (30mm)
  • gigantica (75mm)
  • magna (100mm)
37
Q

Describe the general fluke life cycle

A
  • Always indirect
  • Metacarcaria ingested by ruminant
  • Excyst in stomach/duodenum
  • Migrate through wall of duodenum, via blood to liver
  • Adult fluke reaches sexual maturity in liver
  • Eggs shed in manure
  • Eggs hatch to miracidium, covered in cilia, move to water
  • Invade snail tissues, transport to sporocysts and rediae
  • Released into water as cercariae
  • Find water on plants etc, form capsule around themselfs = encysted metacercaria
38
Q

Describe the morphology of flukes throughout their life cycle

A
  • Each stage morphologically distinct
  • Eggs golden, polar operculum
  • Miracidium
  • Redia
  • Cercaria
  • Encysted metacercaria
39
Q

Describe Fascioloides magna in cattle/camelids

A
  • Pathogenicity low
  • Liver condemned at slaughter
  • Eggs not passed
  • Dead end host
40
Q

Describe Fascioloides magna in sheep/goats

A
  • Few pathogens can cause serious disease
  • Due to extent of migration
  • Eggs not passed
  • Aberrant host
  • Black pigmented adhesions ebtween liver and diaphragm
41
Q

Describe Fascioloides magna in deer

A
  • Adults encapsulated
  • Usually no pathology
  • Eggs passed
  • Patent infection (deer true host)
42
Q

Describe the migration of Fascioloides magna

A
  • Migrate in liver
  • If 2 flukes meet, stop migration, form capsule around themselves together
  • Eggs still laid, found in faeces
43
Q

Describe the immune response to Fascioloides magna

A
  • Increased blood eosinophils
  • Increased eosinophil and plasma cell infiltrate in tissues in which flukes have migrated
  • Serum IgG specific for E/S products of F. magna detected in sheep and goats
44
Q

Describe the diagnosis of F. magna

A
  • Eggs in faeces via McMaster (not in sheep or goats)
  • Sedimentation not flotation
  • Plasma enzymes signal liver or bile duct damage e.g. gamma-glutamyltransferase
  • General on condemnaation of liver or following necropsy
  • ELISA
45
Q

Describe the treatment of F. magna

A
  • All treat adults and juveniles
  • Triclabendazole, albendazole, mebendazole+closantel, levamisole+triclabendazole, praziquantel
  • Available as combination fluke and worm drenches
  • Pour-on products developed for use in cattle
46
Q

Describe the epidemiology of F. gigantica

A
  • Chronic fasciolosis in cattle, buffalo less suceptible
  • Acute, often fatal disease in sheep
  • Secere economic loss in weight gain adn milk
  • Life cycle same as F. hepatica but snail species different
  • Order of susceptibility: sheep>cattle>buffalo
  • Biphasic immune response to liver flukes
  • PPP64 days in cattle, 95 days in buffalo
47
Q

Describe the diagnosis of F. gigantica

A
  • Increased eosinophils in blood
  • Increased serum IgG
  • Find flukes on necropsy
48
Q

Describe Dicrocoelium dendriticum

A
  • Lancet/small/lesser fluke
  • Very small
  • Can kill and cause economic losses
  • Indirect, via snail
  • Host must ingest ants containing metacercaria
49
Q

Describe the life cycle of Dicrocoelium dendriticum

A
  • Eggs passed in faeces by host
  • Eggs eaten by land snail
  • Develop to cercaria
  • Leave as cercaria and stick together in slime balls
  • Brown ants eat slime balls (2nd IH)
  • Ingests cercaria
  • Encystation within ant to metacercaria
  • Ant climbs up grass, eaten by host
50
Q

Describe the clinical signs of Dicrocoelium dendriticum

A
  • Usually subclinical
  • Can cause signs in heavy infection, especially in sheep
  • Anaemia, oedema liver fibrosis and hepatic damage
51
Q

Describe Dicrocoelium dendriticum within the definitive host

A
  • Does not penetrate liver capsule, tissue or gut wall

- Antibody responses against adult protein secretions

52
Q

Describe the epidemiological factors of Dicrocoelium dendriticum

A
  • Eggs reistant
  • Wild life may act as reservoirs
  • Resistant to flukicides
53
Q

Describe fish borne zoonoses

A
  • Affects 300 million humans worldwide
  • About 17 million affeted with trematoeds from family Opisthorchiidae
  • Opistorchis felineus (cats, dogs, humans), O. veverini (cats, dogs, humans)
  • Clonorchis sinesis (gall bladder cancer, cats, dogs, humans)
54
Q

Describe Opisthorchis felineus

A
  • Significant constant irritation leads to transformation of cells and thus causes cancer
  • Snail first IH, fish second
55
Q

Describe the signs of Opisthorchis felineus

A
  • Diarrhoea
  • Abdominal pain
  • Constipation
  • Jaundice
  • Renal malfunction
56
Q

How can Opisthorchis felineus be treated?

A

Common flukicides

57
Q

How does infection with Opistorchis felineus occur?

A
  • Ingestion of raw fish
  • Metacercaria excyst in duodenum
  • Travel through hepatopancreatic ampulla, enter bile duct
58
Q

List the diagnostic tests for Opistorchis felineus

A
  • ELISA
  • McMaster
  • Necropsy
  • Plasma proteins
59
Q

What are the layers of the tegument?

A
  • Membranocalyx
  • Plasma membrnae
  • Muscle layer
  • Cell body
  • Tegument has surface pits and in cytoplasm have vesicles
60
Q

Describe miracidia

A
  • Ciliated larva which develops in the egg
  • May be fully developed when passed, or develop outside host
  • Contains germ balls
  • Ig IH is aquatic snail, hatches out, seeks and penetrates snial (not in F. hepatica!)
  • if IH is terrestrial, stays in egg and is eaten by snail
61
Q

Describe sporocyts

A
  • Sack in snail containing germ balls
  • Germ balls divide by asexual multiplication
  • Some transform into next stage (daughter sporocysts, rediae or cercariae)
  • Final larval stage must develop to next larval type or leave snail to continue cycle
62
Q

Describe rediae

A
  • Larval stage in snail with precursor gut and oral sucker
  • Contains germ balls
  • Some germ balls develop into more of the same and others transform into next larval stage (daughter rediae or cercariae)
63
Q

Describe cercariae

A
  • Mobile larva without germ ball
  • Leaves snail to find next host to penetrate
  • Or encysts in or on another host or as substrate to be eaten by final host
  • Usually dies within 24 hours of release if not proper place
  • Variety of tail morphologies
64
Q

Describe encysted metacercariae

A
  • Larval stage is end-stage cercaria
  • Tail shed, juvenile fluke within resistant wall secreted by fluke
  • Rarely may form on snail in which cercariae were produced, on vegetation or on/in some other hosts
  • Has to be eaten by final host for infection to occur
65
Q

What is the snail that acts as the intermediate host for fasciolosis

A

Lymnaea truncatula

66
Q

Explain how the epidemiology of fasciolosis is determined by the biology of L truncatula and the climatic factors

A
  • Availability of suitable snial habitats
  • Temperature (above 10 degreesC)
  • Need thin film of moisture
  • In spring overwintered metacercariae emerge
  • Infect snails
  • Cercaria shed from snails
  • Snails can hibernate
  • Snails infected in summer by carrier animals or over wintered eggs
67
Q

Discuss the economic importance of Fasciola

A
  • Hepatic parasite of ruminants
  • Responsible for significant economic loss
  • Loss of meat, milk, wool production and liver condemnation
  • Associated with poor production and anaemia
68
Q

Describe the pathology of acute fasciolosis

A
  • Sudden death Aug-Oct
  • Signs of liver damage incl haemorrhage
  • Liver damage due to larval migration to bile ducts and gall bladder
  • Liver enzymes in plasma/albumin and globulin concentration
69
Q

Describe the clinical signs of sub-acute fasciolosis

A
  • Rapid loss of body condition
  • Poor fleece condition
  • Depression
  • In-appetance
  • Inability to stand
  • Non-clinical diagnosis by liver enzymes/protein concentration in pasma and immature fukes in bile duct and gall bladder
  • Occurs in winter
70
Q

Describe the clinical signs of chronic fasciolosis

A
  • Very poor body and fleece condition
  • Bottle jaw may be apparent
  • Death may occur during lambing
  • Non-clinical diagnosis by eggs in faeces adn adult flukes in bile duct
71
Q

Describe the pathogenesis of fasciolosis

A
  • Juveniles migrate through liver until locate bile ducts where they mature
  • Severe disease when many ME are ingested over short period of time resulting in liver haemorrhage/anaemia
  • Usually small amounts ingested over longer period of time, liver function compromised by fibrosis
72
Q

Describe the immunity to fasciolosis

A
  • Stron parasite specific IgG1, IgE
  • Prolonged eosinophilia
  • large quantities of IL-4 and Il-10 bu not IFN-y
  • Dominant Th2 response
  • Infected animals undergo extreme immuno-modulation
73
Q

Describe the diagnosis of fasciolosis

A
  • FEC
  • Standard sedimentation technique followed by examination under microscope
  • Clinical exam
  • Differential blood count
  • Serum conentrations of liver enzymes AST, GGT, GLDH
  • Progess in antibody based diagnostics (ELISA kit, cathepsin L1 based kit)
74
Q

What is the clinical presentation of fasciolosis dependent on?

A
  • Dose of metacercariae
  • Rate of uptake of metacercaeria
  • Final worm burdens
  • Routine treatment of animals
  • Parasite drug resistance
  • Animal condition at onset of infection
75
Q

Describe the treatment of fasciolosis

A
  • If flukes present, treat with triclabendazole in Sept/Oct adn aain in Jan if FEC is positive
  • Treat agains adult only stages in May/June to prevent pasture contamination
  • Do not use same treatment Sept/Oct and May/June
  • Treat additionally in wet years
76
Q

Describe the control of fasciolosis

A
  • Need to control IH (pesticides)
  • Isolate and treat all new animall brought in from outside
  • Fence off wet areas
  • ## Increase soil drainage
77
Q

What is Black disease caused by?

A

Ingestion of Clostridium novyi in soil

78
Q

Describe infection with Clostridium novyi

A
  • Cattle and sheep
  • Animal ingests spores of Clostridium novyi in soil
  • Non-pathogenic in oxygen rich environment
  • In liver rapidly mutliply in area of necrosis caused by migrating flukes
  • Produce tissue toxins which cause severe damage to liver
  • Usually no signs, animal suddenly dies
  • Misdiagnosis as acute fasciolosis

GI (31 decks)

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