Liver parasitology Flashcards
(78 cards)
1
Q
List the nematodes which infest the liver in common domesticated species
A
- Capillaria hepatica
- Ascaris suum
2
Q
List the cestodes which infest the liver in the common domesticated species
A
- Echinococcus granulosus
- Echinococcus multilocularis
- Cysticercus tenuicollis
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
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
5
Q
What are the signs of infestation by Capillaria hepatica?
A
- Hepatomegaly/fibrosis
6
Q
Describe infestation by Ascaris suum
A
- Pigs
- Adults in SI
- Migrating larvae cause liver and lung pathology
7
Q
Describe the eggs of Ascaris suum
A
- All ascarid eggs look similar
- Round, thick shell, proteinaceous coating
- Very resistant in environment
8
Q
Describe the adults of Ascaris suum
A
- No buccal capsule
- 3 lips around anterior opening instead
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
10
Q
What causes the pathology in Ascaris suum?
A
Migration of the larvae
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
12
Q
How can infestation with Ascaris suum be diagnosed?
A
- FEC via McMaster
- Necropsy
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
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
15
Q
List the hosts of Echinococcus granulosus
A
- Definitive: canid
- Intermediate: herbivore
- Accidental: humans
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
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)
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
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
20
Q
What are the hosts of Echinococcus multilocularis?
A
- Definitive: dogs, cats, foxes
- IH: rodents
- Accidental: humans
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
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
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
24
Q
Describe Cysticercus tenuicollis
A
- Cystic stage of Taenia hydatigena
- Adults live in intestine of dogs
25
Describe the life cycle of Taenia hydatigena/ Cysticercus tenuicollis
- 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
26
Describe the clinical signs caused by Cysticercus tenuicollis
- Usually no clinical signs
- In very heavy infection may get depression and weakness
- In young aniamsl liver damage and peritonitis
- Liver condemned at slaughter
27
Describe the appearance of Cysticercus tenuicollis
- Cysticercoid
- One scolex
- Otherwise similar to E. granulosus
28
Describe the commercial importance of Capillaria hepatica
- Unknown importance, probably underestimated
- Problem in zoos
- Very zoonotic, spread by brown rats
- Rare in humans, but 50% fatality rate
29
Describe the commercial importance of Ascaris suum
- Significant economic importance
- Economic loss in older growing animals
- Rarely fatal, lowers carcass value
- Liver and intestine condemnation
- Reduced weight gain
30
Describe the commercial importance of Echinococcus granulosus and multilocularis
- Can infect humans
- Cysts decrease slaughter value of sheep carcass
- Can be fatal to humans
31
Describe the commercial importance of Cysticercus tenuicollis
Liver condemned at slaughter
32
List the prominent organs of adult trematodes
- Oral sucker
- Pharynx
- Oesophagus
- Intestine
- Caeca
- Ventral sucker
- Testes
- Ovaries
- Vitellaria
- Uterus (containing eggs)
33
What is the function of the tegument?
- Provides protection
| - Aids in gas exchange
34
What are the important families of Digenea?
- Dicrocoeliidae
- Fascioliidae
- Opisthorchiidae
- Schistosomiidae
35
Describe the digenetic trematodes
- 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
What are the important species of Fascioliidae?
- hepatica (30mm)
- gigantica (75mm)
- magna (100mm)
37
Describe the general fluke life cycle
- 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
Describe the morphology of flukes throughout their life cycle
- Each stage morphologically distinct
- Eggs golden, polar operculum
- Miracidium
- Redia
- Cercaria
- Encysted metacercaria
39
Describe Fascioloides magna in cattle/camelids
- Pathogenicity low
- Liver condemned at slaughter
- Eggs not passed
- Dead end host
40
Describe Fascioloides magna in sheep/goats
- Few pathogens can cause serious disease
- Due to extent of migration
- Eggs not passed
- Aberrant host
- Black pigmented adhesions ebtween liver and diaphragm
41
Describe Fascioloides magna in deer
- Adults encapsulated
- Usually no pathology
- Eggs passed
- Patent infection (deer true host)
42
Describe the migration of Fascioloides magna
- Migrate in liver
- If 2 flukes meet, stop migration, form capsule around themselves together
- Eggs still laid, found in faeces
43
Describe the immune response to Fascioloides magna
- 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
Describe the diagnosis of F. magna
- 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
Describe the treatment of F. magna
- 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
Describe the epidemiology of F. gigantica
- 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
Describe the diagnosis of F. gigantica
- Increased eosinophils in blood
- Increased serum IgG
- Find flukes on necropsy
48
Describe Dicrocoelium dendriticum
- Lancet/small/lesser fluke
- Very small
- Can kill and cause economic losses
- Indirect, via snail
- Host must ingest ants containing metacercaria
49
Describe the life cycle of Dicrocoelium dendriticum
- 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
Describe the clinical signs of Dicrocoelium dendriticum
- Usually subclinical
- Can cause signs in heavy infection, especially in sheep
- Anaemia, oedema liver fibrosis and hepatic damage
51
Describe Dicrocoelium dendriticum within the definitive host
- Does not penetrate liver capsule, tissue or gut wall
| - Antibody responses against adult protein secretions
52
Describe the epidemiological factors of Dicrocoelium dendriticum
- Eggs reistant
- Wild life may act as reservoirs
- Resistant to flukicides
53
Describe fish borne zoonoses
- 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
Describe Opisthorchis felineus
- Significant constant irritation leads to transformation of cells and thus causes cancer
- Snail first IH, fish second
55
Describe the signs of Opisthorchis felineus
- Diarrhoea
- Abdominal pain
- Constipation
- Jaundice
- Renal malfunction
56
How can Opisthorchis felineus be treated?
Common flukicides
57
How does infection with Opistorchis felineus occur?
- Ingestion of raw fish
- Metacercaria excyst in duodenum
- Travel through hepatopancreatic ampulla, enter bile duct
58
List the diagnostic tests for Opistorchis felineus
- ELISA
- McMaster
- Necropsy
- Plasma proteins
59
What are the layers of the tegument?
- Membranocalyx
- Plasma membrnae
- Muscle layer
- Cell body
- Tegument has surface pits and in cytoplasm have vesicles
60
Describe miracidia
- 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
Describe sporocyts
- 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
Describe rediae
- 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
Describe cercariae
- 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
Describe encysted metacercariae
- 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
What is the snail that acts as the intermediate host for fasciolosis
Lymnaea truncatula
66
Explain how the epidemiology of fasciolosis is determined by the biology of L truncatula and the climatic factors
- 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
Discuss the economic importance of Fasciola
- 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
Describe the pathology of acute fasciolosis
- 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
Describe the clinical signs of sub-acute fasciolosis
- 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
Describe the clinical signs of chronic fasciolosis
- 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
Describe the pathogenesis of fasciolosis
- 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
Describe the immunity to fasciolosis
- 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
Describe the diagnosis of fasciolosis
- 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
What is the clinical presentation of fasciolosis dependent on?
- 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
Describe the treatment of fasciolosis
- 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
Describe the control of fasciolosis
- Need to control IH (pesticides)
- Isolate and treat all new animall brought in from outside
- Fence off wet areas
- Increase soil drainage
-
77
What is Black disease caused by?
Ingestion of Clostridium novyi in soil
78
Describe infection with Clostridium novyi
- 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
