Flukes Flashcards
Flukes, phylum, class, sublcass
Phylum: platyhelminthes
Class: trematoda
Subclass: Dignea (Flukes)
Fasciola (Liver flukes)
Fasciola hepatica= main liver fluke in UK
Final hosts: Most mammals
Significance: sheep and cattle
Disease: fasciolosis
Distribution: temperate regions, worldwide (if tropical tend to be at higher altitudes)
Fasciolosis- zoonosis
F. hepatica can cause severe illness in man
estimated 2.4M people infected worldwide
>60% of population infected in some communities in bolivian highlands
not very important zoonosis in UK- associated with eating watercress and chewing of Qat.
Fasciola hepatica
IMH: galba trunculata- amphibious snail
Final site: maturity in bile ducts/gall bladder
small, brown, 1.0cm
Appearance of adults f. hepatica: leaf shaped, browny ,gray color 2-3 cm in length. fairly flat, cone in anterior part.
Ventral sucker holds in place, and oral sucker is what they attach with.
Spines on cuticle help hold in place- prevent being swept out in the bile
No male or female version- parasite is hermaphroditic
Life cycle of liver fluke (fasciola hepatica)
Adult flukes mature in bile ducts 4 weeks–> egg in feces (quinone tanned yellowish- provides some sort of stability in envrionment, but eggs don’t like dessication)–> embryonation: water/22 degrees C ~9days–> light induced hatching–> operculum (at one end) opens–> MIRACIDIUM
Miracidium penetrates the mud snail. translucent cilia around egg– locates snail and penetrates inside snail and develops to SPOROCYST. After 6-7 weeks in snail and multiplication (600x)- germinal centers in sporocyst give rise to REDIA (x2) via asexual repro (pirogenesis)
Redia goes to CERCARIA if conditions are right (light, warmth, rainwater), otherwise, go through asexual repro as redia to form more redia.
Cercaria leaves the snail–> resitant METACERCARIA encysted on grass–> gets ingested.
Metacercaria= juvenile fluke. Once ingested, it burrows across intestinal wall, goes through liver capsule and migrates through parenchyma to bile ducts.
Excystation is induced by presence of CO2 and bile. Juvenile flukes stay in liver parenchyma for 6-8 weeks.
Adult flukes mature in bile ducts (4 weeks).
PPP=10-12 weeks
(6 to 8)+4= 10-12 weeks
Pathogenesis of Fasciola hepatica
Acute fasciolosis
detected: autumn/early winter
Occurs: 2-6 weeks post ingestion of >2000 metacercariae
Caused by: massive # of flukes, migration of juvenile flukes through the liver capsule/parenchyma
Results in: liver damage and hemorrhage
Manifest as: sudden death/ may find weak animals with pale mucous membranes, dyspnea (thought to be caused by pressure on diaphgram), palpable liver, ascites and abdominal pain.
Acute phase liver at PM
enlarged hemorrhagic liver
subcapsular hemorrhage- capsule often ruptues–> see blood-stained ascites
fibrinous exudate over ventral lobe
Flukes ~1mm in size at this stage
See necrotic migration tracts of juvenile flukes in ventral lobe of liver.
Subacute fasciolosis pathogensis
detected: late autumn/winter
occurs: 6-10 weeks post ingestion (cf. 2-6 weeks post ingestion in acute) of 500-1500 metacercariae
Caused by: juvenile migration and ADULT flukes in bile ducts (adults feed on blood/bile–> mostly inflammatory reaction in bile ducts)
Adults: feed on blood and damage biliary mucosa–> induce inflammation
Result: liver damage- parenchyma, plus cholangitis
Manifest as: rapid/severe hemorrhagic anemia with hypoalbuminemia, pale mucous membranes, enlarged liver, may see SM oedema (bottle jaw)/ascites
Liver at PM: rupture of subcapsular hemorrhage rare.
Chronic fasciolosis pathogenesis
slow, emaciating disease
detected: late winter/early spring
occurs: 4/5 months post ingestion of 200-500 metacercariae
Caused by: adult flukes feeding in bile ducts- no fresh juveniles migrating because it’s too late in the year/cycle
Results in: anemia, hypoalbuminemia, cholangitis
Manifest as: progressive loss of condition, emaciation, pale mucous membranes, SM oedema, ascites
PM of liver: pale, firm, smaller ventral lobe marked by fibrosis, thickened, distended bile ducts
Subclinical: productivity losses- fewer multiple births, reduced weight growth in lambs
Bovine fasciolosis
often a disease of young stock
Chronic disease: productivity loss, calcification of bile ducts, gallbladder englargement
Immune response: limits primary infection, inhibits secondary infection
Cattle have good IR: can mount good IR, limit primary, prevent secondary (sheep don’t do this)
Diagnosis of fasciolosis
Ovine: clinical signs/seasonal occurence
PM/ID of flukes
Demonstration of eggs
Bovine: demonstration of eggs; test for glutamate dehydrogenase (released with parenchymal damage in liver- suggestive of migrating fluke)
gamma glutamyl transpeptidase- marker for biliary damage
ELISA
NB: don’t often do bovine PM for this because cows don’t really die often from fasciolosis.
Factors in epidemiology of fasciolosis
- availability of snail habitat: permanent habitat, muddy areas/slow moving shallow water; edges of ponds, banks of streams and ditches; rushes indiciate slightly acidic pH. Snails breed May to October
- Moisture: critical for snail and other life cycles
Rainfall>transpiration= increase of snail habitat (i.e. puddles form)
Miracidium: not hardy, transient life cycle, needs moisutre, needs to find a snail with a few hours
Increased: snail breeding, production of larval stages in snail and egg development.
- temperature: need mean day/night temp >10C
snail breeding- one snail has 100,000 descendants in one year
larval development in snail
stimulus for egg development/hatching
These factors only suitable during May-October, however this has been extended in recent years, NB: spring infection.
Summer infection
optimal period for snail development/ parasite development is may to october
Snails infected by miracidia in late spring/summer derived from overwintered eggs or eggs fromc arrier animals. This increases metacercariae on pasture August to October= summer infection of snails.
Winter infection of snails:
snails become infected by miracidia in autumn
conditions sub-optimal and development stops over winter- arrested development within the snail
Development resumes in the spring and metacercariae are produced May to June (early summer)
not as important as summer infection (in UK)
Forecasting fasciolosis
can use weather forecasting to predict risk and severity of disease outbreak. warm, wet conditions confer risk.
Treatment of fasciolosis
Acute: (very young flukes) Triclabendazole and move to clean pasture
Subacute: Closantel (not effective against young, but treats immature adults) and Nitroxynil (treats adults) and move to clean pasture
Chronic: range of drugs
Resistance to triclabendazole in Eire, Scotland and Wales
Control of fasciolosis- reduction of snail population
Drainage
fence of saturated pasture
Move sheep to drier pasture when under treatment
Molluscicide (often v. toxic to fish): none licensed for use in UK
treat and quarantine new arrivals
treat cattle
Control of fasciolosis- prophylactic use of anthelmintics
Reduce fluke burden: october (acute), january (chronic)
Reduce pasture contamination: april/may (june)
rotate drugs (annually)
will continued to be a constraint on livestock productivity because of: carriers, drug resistance, snail eradication being difficult and global warming.
Fluke families of major importance
Fasciolidae
Dicrocoeliidae
Paramphistomatidae
Schistosomatidae
Fasciolidae
fasciola (liver flukes)
Fasciola hepatica
Fasciola gigantica
Final host: most mammals
Disease: fasciolosis
Fasciola gigantica
Distributed in tropical and sub tropical regions
*africa
*southern asia (buffalo and cattle)
USA (south and hawaii)
Middle east
Southern europe
Differences between fasciola spp.
F. gigantica has a similar structure to hepatica but is a little more than twice as large and more slender.
F. gigantica is more pathogenic
IMH are aquatic (not amphibious) snails
F. gigantica epidemiology
Miracidia: hatch at beginning of wet season, infect snails and developed by end of wet season
Cercaria: shed from snail at beginning of dry season
Metacercaria: encyst on aquatic plants or on surface of water– picked up by animals at drinking holes
Disease occurs at end of dry season/beginning of next wet season.
F. gigantica life cycle
Wet season: Miracidia hatch and infect sails–> develop within the snail
Dry season: Cercariae shed from snail and enyst on aquatic plants or on surface of water–> ingested and develop within mammal
PPP= 13-16 weeks.
Control of F. gigantica
Anthelmintics: similar to F. hepatica- triclobendizoles
Snail control: molluscicide usually impractical; fence permanent water sources; pump water to troughs (careful not to bring snails with you); parasitic castration
Parasitic castration: fluke=enchinostoma of ducks
Aggressive echinostoma will invade a snail instead of F. gigantica.
Problem: ducks that carry echinostoma carry schistosomes which affect people (dermatitis)
Dicrocoeliidae
Dicrocoelium dendriticum
Distribution: worldwide (Europe, UK, USA)
Main hosts: sheep, cattle, horses, rabbits
Site: bile ducts and gall bladder
Intermediate hosts: land snails/ants (formica)
Life cycle of dicrocoelium dendriticum
Mature flukes in bile duct of final host (sheep) –> produce eggs–> Eggs fully embryonated when laid (shell quinone-tanned)–> hatch only on ingestion by suitable terrestrial snail)
Hatch as miracidium–>Two sporocyst stages–> cercaria–> slimeballs formed with cercariae–> slimeballs released and stick to vegetation.
Infected vegetation eaten by ants. In ant, cercaria–>metacercariae–> encyst in ant abdomen.
Sheep eats ant, metacercaria encysts in duodenum and migrate to liver via bile duct. No invasion of parenchyma.
Dicrocelium dentridicum as “enslaver”
enslaver parasite
encystation of metacercariae in ant brain
ant climbs herbage and remains, clamping its jaws into grass. Increases chances of transmission i.e. sheep ingests ant when grazing.
Pathogenesis of Dicrocoelium dendriticum
Heavy infection in Older sheep: fibrosis of and distented bile ducts, progressive cirrhosis
Clinical signs: weakness, anemia, emaciation
Productivity losses: decreased wool production, premature ageing, reproductive losses.
Epidemiology of dicrocoelium dendriticum
IMH are independent of water
eggs survive for months on pasture
large reservoir of infection
control is difficult
treatment: netobimim (albendazole)
Paramphistomatidae (rumen flukes)
conical, maggot shaped flukes of ruminants
Adults in rumen and reticulum
Paramphistomum=common genus
Paramphistomum cervi and paramphistomum microbothrium
Aquatic snails (planorbis and bulinus) as IMH
Paramphistomes
Worldwide distribution: tropics, sub-tropics, southern USA
emerging disease in the UK
Juveniles: excyst in duodenum, attach to mucosa (plug feeders), cause pathology
Adults in rumen
Paramphistomum life cycle
Snail stages as in fasciola (4 weeks)
Metacercaria are injested
Excyst in duodenum where juveniles attach to intestinal wall and feed (6 weeks)
Adults migrate to forestomachs
PPP=7-10 weeks.
Paramphistomum pathogenesis
Due to: juvenile intestinal phase of infection: attachment to duodenal mucosa
Which causes: necrosis and hemorrhage- erosion of duodenal mucosa
Results in: gastroenteritis- marked by oedema, hemorrhage and ulceration
Adults cause little pathology.
Paramphistomes- clinical signs, diagnosis, tx
Clinical signs: fetid diarrhea, anemia and hypoalbuminemia, intense thirst and anorexia, potential for high mortality (up to 90%)
Diagnosis: post mortem (juveniles in duodenum)
FEC of limited value
TX: oxyclozanide
Epidemiology of paramphistomes
tropics/subtropics: similar to F. gigantica, transmitted by aquatic snails, associated with flooding
In the UK: reported in 2007 in wales/western england and scotland; dairy and suckler cattle rather than young stock
Schistosomatidae
parasites of all domestic mammals
cattle and sheep in tropics, subtropics and S. Europe
IMH are aquating snails (Bulinus and physopsis)
Major species: schistosoma bovis (problem more in sheep than cattle); s. japonicum and S. matthei
japonicum and matthei are zoonotic.
Schistoma: adult worms
Pair of adult worms
Male is bigger and thicker with gynaecophoric canal. Male has ventral and oral sucker
Female lies in that groove of male, has ventral sucker
Schistoma egg
egg secretes toxins which cause pathology.
Terminal spines act only as an anchor
Life cycle of schistosoma
Males and females come into contact in liver. Female lay eggs in walls of the venules of mesentery (sometimes walls of bladder or nasal passages). Eggs migrate through the blood vessels to the intestinal lumen. Eggs in feces
Eggs contain mature miracidia passed in feces. Hatch very quickly. Miracidia attack snail.
Within snail, go through 2 rounds of sporocyst formation: miracidia to sporocyst–> daughter sporocysts
Cercariae outside of snail–> quite aggressive and swim towards sun, warmth and surface of water (cercariea have forked tails)
Cercariae ram their way through skin using collagenase and hyaluronidase enzymes
Reach lymph nodes–>go to heart–>lungs–> heart–> liver.
Schistosoma pathogenesis
Inflammatory response against EGGS in veins, mucosa and liver
Lead to granuloma formation in intestinal mucosa and liver
Acute: mucosal hemorrhage, anemia, hypoalbuminemia, hepatosplenomegaly
Clinical signs: anemia, diarrhea (mucus and blood tinged), thirst, anorexia, emaciation
Chronic: marked granuloma of intestine and cirrhosis/periportal fibrosis of liver, reduced productivity.
Diagnosis of schistosoma
based on clinical signs/infected water source
couple to demonstration of granulomatous lesions and adults in mesenteric veins
demonstration of eggs.
Schistosoma epidemiology and control
Epidemiology is related to prevalence of aquatic snail
clean water source- controlled movement of cattle
Drugs: praziquantel, albendazole
Praziquantel is paraticularly effect but if parasites are killed/ died in CV system, they can form emboli which leads to death of the final host.
