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37 Cards in this Set
- Front
- Back
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Class of Flukes? Phylum? |
Class = TREMATODA Phylum = PLATYHELMINTHES
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Fasciola hepatica - Final host? IMH? Significant in what species? Disease? Zoonotic? |
Final host = Most mammals IMH = Galba truncatula (Amphibious small brown snail) Significance = CATTLE & SHEEP Disease = Fasciolosis Zoonotic = Yes! Can cause severe illness in man! |
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Where are the adult fasciola hepatica located? |
BILE DUCTS (Gall bladder) |
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Leaf-shaped trematodes with oral sucker and a central sucker. |
FASCIOLA HEPATICA |
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Describe the life cycle of liver fluke (fasciola hepatica): |
1. Eggs passed in feces (yellow, tannish color), but need to embryonate before infective 2. Embryonation occurs in about 9 days; required temps ~22C & light for hatching into infective miracidium. 3. Miracidium penetrates mud snail (Galba truncatula); requires watery environment for motility toward snail 4. Miracidium sporocysts to redia after about 6-7 weeks in the snail (multiplies x600 in the snai= pedogenesis) 5. Light, warmth and rainwater triggers the fluke to leave the snail in Cercaria form 6. Cercaria transforms to resistant metacercaria form and encysts on grass, awaiting to be ingested by a grazing mammal 7. Once ingested, excystation is induced by CO2 and bile, juvenile flukes in liver parenchyma 6-8 weeks & adults mature in bile ducts by 4 weeks. * PPP = 10-12 weeks |
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Pathogenesis of acute, subacute and chronic fasciolosis? |
** ACUTE FASCIOLOSIS 2-6 weeks post ingestion of >2000 metacercariae * Detected autumn/early winter CAUSED BY: Migration of juvenile flukes RESULTS IN: Liver damage and hemorrhage CLINICAL SIGNS: sudden death, weak animals with pale mucous membranes, dyspnoea, palpable liver, ascites, abdominal pain ** SUBACUTE FASCIOLOSIS: 6-10 weeks post ingestion of 500-1500 metacercariae CAUSED BY: Juveniles migrating & ADULTS IN BILE DUCTS (feed on blood and damage biliary mucosa, inducing inflammation) RESULTS IN: Liver damage (parenchyma, plus cholangitis), bile ducts & blood loss CLINICAL SIGNS: Rapid/severe hemorrhagic anemia with hypoalbuminemia, pale mucous membrane, enlarged liver, some edema or ascites ** CHRONIC FASCIOLOSIS 4-5 months post ingestion of 200-500 metacarcariae CAUSED BY: Adults feeding in bile ducts RESULTS IN: Anemia, hypoalbuminemia, cholangitis CLINICAL SIGNS: Progressive loss of condition, emaciation, pale mucous membranes, submandibular edema ("Bottle jaw"), ascites |
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Acute fasciolosis disease symptoms caused by . . .? Results in? Clinical signs? |
CAUSED BY: Migration of juvenile flukes RESULTS IN: Liver damage and hemorrhage CLINICAL SIGNS: sudden death, weak animals with pale mucous membranes, dyspnoea, palpable liver, ascites, abdominal pain |
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Describe a PM Liver of an animal who suffered with acute fasciolosis. |
- Enlarged hemorrhagic liver - Rupture of sub-capsular hemorrhages - Fibrinous exudate build up on fascia - Necrotic migration tracks of juvenile flukes |
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Chronic parasitic disease resulting in productivity loss, calcification of bile ducts and gall bladder enlargement. |
BOVINE FASCIOLOSIS (liver fluke; fasciola hepatica) - Immune response limits primary infection & inhibits secondary infection |
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How would you diagnose liver fluke in ovine? Bovine? |
OVINE: - Clinical signs/seasonal occurrence - Eggs in feces - PM & identification of flukes
BOVINE: - Eggs in feces - Test for glutamate dehydrogenase - Y glutamyl transpeptidase - ELISA
* Same parasite causing disease in sheep and cattle |
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Describe the epidemiology of fasciolosis (fasciola hepatica). |
SUMMER infection of snail (galba truncincta): Optimal period for snail development/parasite development is MAY-OCT (snail breeding season) - Snails infected by miracidia in late Spring/Summer, derived from overwintered eggs or eggs passed in feces of hosts - Inc metacercariae on pasture Aug-Oct WINTER infection of snail (less imp): - Snails infected by miracidia in Autumn - Conditions sub-optimal & development stops over winter, and resumes in Spring - Metacercariae produced May-June |
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Liver fluke infections in sheep have been rising each year.
True or False? |
TRUE |
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Treatment protocols for Acute Fasciolosis? Subacute? Chronic? |
ACUTE = Dose with Triclabendazole & move to clean pasture!
SUBACUTE = Closantel, Nitroxynil dose & move to clean pasture
CHRONIC = range of drugs can be given but should rotate to avoid further resistance. |
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Faciola hepatica resistance to ___________________ has been shown in Scotland and Whales. |
TRICLABENDAZOLE |
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Control methods for fasciola hepatica? |
- Drainage of fields - Fence off saturated pasture - Move sheep to drier pasture when under threat - Treat & quarantine new arrivals - Prophylactic use of anthelmintics (dose in Oct & Jan) |
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What are the four fluke families of major importance? |
1. Fasciolidae - Fasciola hepatica, giagantica 2. Dicrocoeliidae 3. Paramphistomatidae 4. Schistosomatidae |
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Fasciola gigantica distribution? |
Tropical & Sub-tropical regions (Africa, S Asia) |
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Differences between Fasciola gigantica and hepatica? |
F. GIGANTICA - Much bigger (75mm) compared to F. Hepatica (30mm) - More pathogenic - IMH are AQUATIC SNAILS (not amphibious) |
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Epidemiology of F. gigantica? |
- Miracidia = hatch at beginning of wet season, infect snails & develop by the end of wet season - Cercaria = shed from snail at beginning/during dry season - Metacercaria = encyst on AQUATIC plants or in water - Disease symptoms = end of dry season or beginning of next wet season |
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PPP of F. gigantica? |
PPP = 13-16 weeks |
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Control of F. Gigantica? |
1. ANTHELMINTICS - similar to F. hepatica 2. Snail control - Fencing permanent water sources - Pump water to troughs |
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Dicrocoelium dendriticum distribution? Hosts? IMH? Predilection site? |
DISTRIBUTION: Worldwide (Europe, UK, USA) MAIN HOSTS: Sheep, cattle, horses, & rabbits IMH: Land snails & ants PREDILECTION SITES: Bile ducts & gall bladder |
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Lice cycle of dicrocoelium dendriticum? |
1. Yellow, brown egg is fully embryonated when laid. 2. Snails eat the eggs and once inside the snail, the eggs hatch. 3. Cercariae ejected with slimeball release from snail 4. Slimeballs eaten by ants and the metacercariae encysts in abdomen of ant 5. Then moves to the brain of the ant and controls it to move to the ends of grass, ready to be eaten by host mammal = ENSLAVER PARASITE 6. Within the host mammal, excystation in duodenum and migrate to liver via bile duct 7. In bile ducts, fluke develop to adults, begin reproducing and perpetuating the cycle. |
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Pathogenesis of Dicrocoelium dendriticum results in heavy infections of older sheep. Clinical signs? PM signs? |
CLINICAL SIGNS: - Weakness - Anemia - Emaciation - Productivity losses (dec wool production, premature aging, repro losses) PM SIGNS: - Fibrosis of & distended bile ducts - Progressive cirrhosis |
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Treatment of dicrocoelium dendriticum? |
ALBENDAZOLE |
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Conical, maggot-shaped flukes of ruminant rumens. |
PARAMPHISTOMATIDAE (Rumen fluke) - Paramphistomum cervi & P. microbothrium
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Paramphistomes distribution? Hosts? IMH? Cause of pathology? |
DISTRIBUTION: Tropics, sub-tropics, S USA, emerging in UK HOST: Ruminants IMH: Aquatic snails CAUSE OF PATHOLOGY: Juveniles, attach to mucosa of rumen (plug feeders) |
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Life cycle of paramphistomums? |
Snail stages same as Fasciola species - Metacercaria are ingested - Excyt in duodenum where juveniles attach to intestinal wall and feed (6 weeks) - Adults migrate to forestomach and reproduce PPP = 7-10 weeks |
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Pathogenesis of paramphistomums? |
Juveniles attach to mucosa of duodenum, causing intestinal infection - Causes necrosis and hemorrhage/erosion of duodenal mucosa - Results in gastroenteritis causing clinical signs of edema, hemorrhage, & ulceration - Adults cause little harm |
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Clinical signs of paramphistomes? |
- Fetid diarrhea (smelly) - Anemia & Hypoalbuminemia - Intense thirst & anorexia - Potential for high mortality |
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Diagnosis of paramphistomes? Treatment? |
DIAGNOSIS: - PM (juveniles in duodenum) - FEC = limited value
TREATMENT: - OXYCYLOZANIDE |
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SCHISTOSOMATIDAE major species? distribution? Hosts? IMH? |
MAJOR SPECIES: - Schistosoma bovis, S. japonicum & S. matthei
DISTRIBUTION: Tropics, subtropics & S. Europe
HOSTS: - All domestic mammals, cattle and sheep
IMH: Aquatic snails |
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Life cycle of schistosomes? |
1. Eggs shed in feces 2. As soon as eggs touch water, miracidia emerge and infect snails 3. WIthin the snails transform from sporocyst to cercariae, which emerge from the snail. 4. Cercariae then attack skin of host mammal & within 15 minutes enter the blood circulation of the host mammal 5. Enter lymph glands and continue to circulate around the heart, lungs and liver 6. Eggs laid in mesenteric vessels and eventually tear through the BVs and into the gut cavity to be passed in feces |
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Inflammatory response against eggs in veins, mucosa and liver, which lead to granuloma formation on intestinal mucosa and liver - Which parasite pathogenesis is this? |
SCHISTOSOMA |
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ACUTE VS CHRONIC SCHISTOSOMA PATHOGENESIS? |
ACUTE: - Mucosal hemorrhage, anemia, hypoalbuminemia & hepatosplenomegaly - Clinical signs: diarrhea (mucous & bloody), thirst, anorexia, emaciation
CHRONIC: - Marked granuloma of intestine & cirrhosis/periportal fibrosis of liver - Reduced productivity |
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Diagnosis of schistosoma infection? |
- Eggs in feces - Clinical signs/infected water source (coupled to demonstration of granulomatous lesions and adults in mesenteric veins) |
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Epidemiology, control and treatment of schistosomas? |
EPIDEMIOLOGY: - Related to prevalence of aquatic snails
CONTROL: - Clean water source available - Controlled movement of cattle
TREATMENT: - Praziquantel, albendazole |
