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Parasitology > Flukes > Flashcards

Flukes Flashcards

1
Q

Flukes, phylum, class, sublcass

A

Phylum: platyhelminthes

Class: trematoda

Subclass: Dignea (Flukes)

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2
Q

Fasciola (Liver flukes)

A

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)

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3
Q

Fasciolosis- zoonosis

A

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.

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4
Q

Fasciola hepatica

A

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

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5
Q

Life cycle of liver fluke (fasciola hepatica)

A

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

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6
Q

Pathogenesis of Fasciola hepatica

A

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.

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7
Q

Acute phase liver at PM

A

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.

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8
Q

Subacute fasciolosis pathogensis

A

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.

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9
Q

Chronic fasciolosis pathogenesis

A

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

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10
Q

Bovine fasciolosis

A

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)

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11
Q

Diagnosis of fasciolosis

A

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.

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12
Q

Factors in epidemiology of fasciolosis

A
  1. 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
  2. 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.

  1. 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.

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13
Q

Summer infection

A

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.

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14
Q

Winter infection of snails:

A

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)

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15
Q

Forecasting fasciolosis

A

can use weather forecasting to predict risk and severity of disease outbreak. warm, wet conditions confer risk.

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16
Q

Treatment of fasciolosis

A

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

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17
Q

Control of fasciolosis- reduction of snail population

A

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

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18
Q

Control of fasciolosis- prophylactic use of anthelmintics

A

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.

19
Q

Fluke families of major importance

A

Fasciolidae

Dicrocoeliidae

Paramphistomatidae

Schistosomatidae

20
Q

Fasciolidae

A

fasciola (liver flukes)

Fasciola hepatica

Fasciola gigantica

Final host: most mammals

Disease: fasciolosis

21
Q

Fasciola gigantica

A

Distributed in tropical and sub tropical regions

*africa

*southern asia (buffalo and cattle)

USA (south and hawaii)

Middle east

Southern europe

22
Q

Differences between fasciola spp.

A

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

23
Q

F. gigantica epidemiology

A

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.

24
Q

F. gigantica life cycle

A

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.

25
Q

Control of F. gigantica

A

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)

26
Q

Dicrocoeliidae

A

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)

27
Q

Life cycle of dicrocoelium dendriticum

A

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.

28
Q

Dicrocelium dentridicum as “enslaver”

A

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.

29
Q

Pathogenesis of Dicrocoelium dendriticum

A

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.

30
Q

Epidemiology of dicrocoelium dendriticum

A

IMH are independent of water

eggs survive for months on pasture

large reservoir of infection

control is difficult

treatment: netobimim (albendazole)

31
Q

Paramphistomatidae (rumen flukes)

A

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

32
Q

Paramphistomes

A

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

33
Q

Paramphistomum life cycle

A

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.

34
Q

Paramphistomum pathogenesis

A

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.

35
Q

Paramphistomes- clinical signs, diagnosis, tx

A

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

36
Q

Epidemiology of paramphistomes

A

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

37
Q

Schistosomatidae

A

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.

38
Q

Schistoma: adult worms

A

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

39
Q

Schistoma egg

A

egg secretes toxins which cause pathology.

Terminal spines act only as an anchor

40
Q

Life cycle of schistosoma

A

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.

41
Q

Schistosoma pathogenesis

A

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.

42
Q

Diagnosis of schistosoma

A

based on clinical signs/infected water source

couple to demonstration of granulomatous lesions and adults in mesenteric veins

demonstration of eggs.

43
Q

Schistosoma epidemiology and control

A

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.

Parasitology (12 decks)

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