Fasciolosis Flashcards
Alimentary Tract Trematode
Fasciolosis
Trematode–> Digenea –>Fasciola–> Hepatica (the liver fluke)
- Trematodes are divided into 2 groups
- Trematoda: monogenea (ex: fish ectoparasites), Digenea (MAIN FOCUS: more important economically and socially)
- Digenea includes: Fasciola, Dicrocoelium, Paramphistomum (emergingly common), Schistosoma (common, zoonotic, from amazon)
Monogeneans
- Ectoparasites of fish
- DIrect Life Cycle
- Oral Sucker to Feed
- Haptor Organ with sucker and hooks to feed
Digeneans
- All digenea are parasitic
- Small dorso-ventrally flattened worms- majority are worms withsimple anatomy & no segmentation
- No coelom (secondary body cavity), but they are filled with mesodermal parenchyma. No segmentation
- No blood vessels, simple ladder nervous system
- Possess two suckers: Oral sucker for attachment & contains the mouth
- Ventral sucker for attachment
- Muscular pharynx allows for parasite to pump food into blind ending gut: Waste either diffuses through the parasite or goes back out mouth
- Most= hermaphrodites (cross as well as self-fertilization occurs)
Fasciola Hepatica
(Liver Fluke)
- Hermaphrodite
- Large part of this parasite has been devoted to reproduction
Trematodes
(Nutrient Uptake)
- Can absorb nutrients from env’t
- Trematode gut is not only organ for food uptake
- The (in)tegument is highly active in nutrient uptake: Highly active outer layer
- The epidermis is essentially a single cell (a syncytium)
- Actin spines- help the worms to anchor themselves
- Vitellary Glands- produce the cells–> eggs, Cirrus- the male sex organ
Life Cycle
(Environment:Egg)
Environment: Egg
- Hatching requires water and light
- Persistence:
- Can last 5-8 months (overwintering is possible)
- in silage aprox. 30 days, in hay eggs do not survive (dry out)
- –> Miracidium (first motile stage)–> actively burrows into intermediate host
Egg: 150 um: About the biggest parasite eggs you will come across (strongyle egg is 80um). Has operculum (“cap”)–> Will develop into larval parasite
Miracidium (1st motile)
Sporocyst (1mm)
Redia (1-3mm)
Cercaria (1mm)
Metacercaria (0-2mm)
Intermediate Host: Mud Snail
(Galba truncatula)
- Sporocyst- Non-environmental, Motile, Asexual replication
- Redia- Non-environmental, Asexual replication
- Cercaria–> environmental, motile- swims to vegetation, loses tail & encysts to become encysted metacercaria,
- Peristence of Redia/ Cercaria- several months (overwintering is possible)
Egg develops in water and hatches (hatching requires water and light) to release miracidium which then penetrates the snail. Swims through water to find intermediate host (mud snail)
- goes through a round of asexual replication in the snail
- once in the snail, mother sporocyst produces a daughter rediae
- The rediae is filled with cercariae before it leaves the snail
Cercaria –> can leave snail,
Exit snail and attach to vegetation, encysts, These survive for a long time!!-encysted metacercariae will be consumed by next host (definitive host)
Environment
(Metacercariae)
Persistence: Several months (overwintering is possible)
- In hay still infective (4-6 months), in silage ~12 days
- Miracidium (from egg in faeces) –> metacercariae ~ 6-7 weeks- but can remain in snail for longer if environmental conditions aren’t right*
- -Cercaria are shed from snail (intermediate host)*
Host Animals
(sheep, cattle, rabbits, horses and humans)
- Ingestion of encysted metacercaria–> excystation & migration –> liver
- PPP= ~ 8-12 weeks (Metacercariae –> eggs)
- Patent period = 9 months (cattle) or >years (sheep) : Depends on the species, how long it can stay alive?
- Up to 5,000-20,000 eggs per fluke per day: High level of contamination to the environment
- It can infect a variety of host and cause different effects
Types of Infection
- Acute- Sudden death, Sept - Nov (usually), Large, haemorrhagic liver, >1000 imm. Flukes –> No eggs.
Parasites are not completing their life cycle
- Sub-Acute- not actual immediate death. Rapid weight ↓, Oct-Dec, Large, haemorrhagic liver, >500 flukes (imm/adult) –> Some eggs. Because they are not killing the host, some will become adults
- Chronic- Progressive weight ↓, Jan – March, Small, distorted liver & Bottle jaw, >250 adult flukes –> Eggs
- Subclinical- ↓Production: ↑ Beef finishing times, ↓ milk yield & wool quality,↓ Reproductive performance? –> Eggs produced. Much lower infection levels
Migration and Pathology
- Migration to Liver- Migrating Immature fluke–> most of the damage- slowly develop & grow as they migrate (0.1cm–> 1cm), once in the bile duct, continue to grow –>3.5cm
- Ingested: migrates through intestine, through peritoneum , into the liver, migrates through the liver and feeds on secretions—> can cause hemmorhage in the liver
- see increases in GDH and yGT, use to diagnose
- at end of migration, makes it to bile duct and continues to grow
- feeds on secretions
- Damages parenchyma tissue & causes haemorrhage/ necrosis (necrotic tracts) –> release of glutamate dehydrogenase (GDH) & y glutamyl transpeptidase (yGT)- can act as diagnostic markers
- Black Disease in Sheep- (infectious necrotic hepatitis) Secondary infection caused by migrating flukes–> necrosis of the liver parenchyma (anaerobic, survive best in those conditions), any bacteria present at low level are then able to flourish (Clostridium novyi type B)–> toxins produced which cause the problems
Pathogenesis –> bottle jaw, In Liver: necrotic tracts & haemorrhage –> post necrotic scarring –> shrinkage of infected parts of liver & hypertrophy of infected parts, peribiliary & monolobular fibrosis (Different levels of fibrosis between animals. starts 16-24 weeks post-infection-mech. unknown)
If animals doesn’t die, you will see scarring after this necrosis
Epidemiology
Disease Manifestation- determined primarily by number (and rate) of metacercariae ingested
- Rapid ingestion of large numbers = acute (warmer, wetter months),
Slow ingestion of small numbers = chronic
BUT…
- Host species-specific susceptibility:
- Sheep= most susceptible & will remain infected longer (due to ↓ fibroblastic potential in liver)
- Sheep are the most susceptible and exhibit symptoms and die. Sheep tend not to clear the infection, they stay infected. Cows tend to clear the fluke eventually
- Don’t really see much in accordance to immune responses that kills parasite, more just a high Ab count
Sheep> Cattle> Pig
If we control the snail, we can control the life cycle!
Influence of Season/Weather
- In UK: Normally see infected animals shedding eggs in Spring –> Acute disease: (metacercaria encysted by september) September to November OR Chronic disease: January of following year onwards (Classic case in UK)-peak november for acute
- In West Ireland: Warmer Winter (>10 degrees)–> ↑ snail survival –> ↑ overwintering parasites –>↑ risk of disease –> Winter snail infection dominant & there’s a greater snail population earlier next summer.
- Acute disease: August to November OR Chronic disease: November onwards
- Encyst earlier and infect earlier!!
- Cold Winter –>↓ snail survival–> ↓ overwintering parasites –>↓ risk of disease- Summer snail infection dominant
- Warm Winter: enhanced snail survival, more overwintering parasites, increased risk of disease, winter snail infection dominant
- Wet Summer: Enhanced parasite & snail survival–> ↑ snails –>↑ risk of disease
- Dry Summer: ↓ parasite & snail survival –> ↓ snails –>↓ risk of disease
Try to predict the F. hepatica challenge of farms by considering the season, their clinical history with F. hepatica & the long-term weather forecast
Diagnosis
- Faeces- only see eggs during the patent period, won’t ID acute disease (repeated faecal examinations). Larger eggs! That will tell you if there are adults. No use with acute disease though–> dont produce eggs
- Post mortem examination- bit late by this point
- Blood parameters- Hypoalbuminaemia, anaemia, hepatic enzymes (Increase in response to damage of liver)
- Serology- Serum ELISA, milk ELISA, haemagglutination test
- Molecular methods- PCR, DNA-hybridisation.
Stimulate an immune response even if it isnt a strong immune response-can recover parasite DNA as well
- Area that is very wet, wet fields, can already build suspicion
- Need to use sedimentation for these guys
Control
Immunity
- sheep= unprotected, cattle= develop some immunity & pigs moreso
–chance of developing a vaccine based on natural immune response –> not good
- Cattle- Develop partial resistance > 12 weeks after primary infection (hyperplasia of bile ductepithelium, fibrosis, calcification of bile ducts entombs & kills adult flukes)-See calcification of bile duct–> starving off and killing adult flukes
- High antibody levels- these don’t generate much protection
- Recombinant vaccine in development (~70% protection) targets early stages of life cycle –> partial protection, to be used as a part of combined packet of control
- Based on secreted parasite proteins
- if you use to vaccinate sheep you can see partial increase (70%)
- not a sterile protective response, can help move from acute to chronic
- easier to manage
- Chemotherapy:
- Targeting parasites- These have limited time of efficacy BUT Triclabendazole can target all stages (Only one to really remember, most effective at killing ALL stages of the fluke)-Other drugs have varied level of efficacy of other stages
- If you think it is chronic, you might choose albendazole, If acute, you use Triclabendazole
- Targeting snails (molluscicides)- Specific, effective & ↓mammalian toxicity but commercial failure, no longer availbale. Commercial failure because people don’t want to use them on the fields in this kind of climate
KEY: CONTROL THE SNAILS
- Integrated anti-Fasciola Control: if we expect this to be a summer issue
- Kill over-wintered adult flukes using targeted chemotherapy pre-turnout –> ↓ spring egg output
- Minimise snail numbers & at the end of season use a broad-range drug (triclabendazole)
Fewer parasites, fewer snails, far less levels of infection
If there is already prevalent evidence for acute infection, target young flukes!
Rarely give meds pre-emptively
Fasciola Hepatica
(egg)
Hepatica Fasciola Life Cycle
