Presentation on theme: "Dicrocoelium dendriticum Presentation By Kristi Bjerke & Heather Lee."— Presentation transcript:
Dicrocoelium dendriticum Presentation By Kristi Bjerke & Heather Lee
Background Digenean trematode Part of the Dicrocoeliidae family of liver flukes Commonly known as the “lancet fluke” because of its bladelike shape. “small liver fluke”
Morphology 6-10 mm long 1.5-2.5 mm wide Pointed ends
Geographic Distribution Most of Europe and Asia North America South America Australia North Africa alkaline soils that are favorable environments for reproduction and survival of the intermediate hosts
Hosts Definitive Host: sheep, cattle, goats, pigs, other ruminants, occasionally dogs, horses, and rabbits, rarely humans –Lives in the bile duct and gall bladder Intermediate Host: snails, ants
Life Cycle Indirect Approximately 6 months Begins when a snail eats the parasite eggs The eggs have miracidia which hatch and then penetrate the snail’s intestinal wall. Within the digestive gland, the miracidia transforms into a mother sporocyst.
Life Cycle Cont. Mother sporocysts produce daughter sporocysts. Second generation daughter sporocysts develop into cercariae 3 months later, cercariae build up in the “lung” of the snail. The snail deposits the cercariae (5,000) in a slimeball.
Life Cycle Cont. An ant eats the slime ball. Metacercariae form within the ant’s abdominal cavity. They then encyst and become infective to the definitive host. One or two cercariae travel to the brain which causes a cataleptic cramp. The cramp paralyzes the ant on a tip of grass when temperatures get below 15ºC. This makes the ant more likely to be eaten by a ruminant.
Life Cycle Cont. After the ant is eaten, the metacercariae excyst in the gut of the definitive host. They migrate to the bile duct and then the gall bladder. Here they develop into mature flukes. The flukes reproduce via cross fertilization or hermaphroditism Eggs are released through the host’s feces.
Pathogenesis Hard to reproduce the life cycle in experiments In the field there is often infection with other types of parasites with similar symptoms
Pathogenesis continued No penetration of the gut wall, liver capsule, or liver parenchyma as in fasciolosis Clinical symptoms are not usually manifested even in heavy infections However they may show anemia, edema, emaciation,and in advanced cases, cirrhosis, and scarring of the liver surface
Diagnosis adult dicrocoelia recovered in the liver post mortem egg coprological (fecal) examination –Releasing of eggs can take 49-79 days upon infection
Newer Diagnostic Techniques Immuno-diagnostic techniques Immuno-flourescence precipitation Passive haemoagglutination test Complement fixation ELISA All try and detect anti- Dicrocoelium antibodies
Treatment Anti-helminthic drugs like benzimidazole and pro-benzimidazole derivatives As of 2002 no possible vaccines have been studied even though an anti-body dependent response has been found
Control Husbandry practices (don’t allow to graze at night or early in the morning) Try and control snail and ant populations (difficult/expensive) Test the soil to see whether it could be suitable for the intermediate hosts
References D. Otranto and D. Traversa. A review of dicrocoeliosis of ruminantsincluding recent advances in thediagnosis and treatment. Veterinary Parasitology 107 (2002) pp 317-335 http://workforce.cup.edu/Buckelew/dicrocoelium_den driticum_is_a_bi.htmhttp://www.ilri.org/InfoServ/Webp ub/Fulldocs/X5492e/x5492e04.htm http://www.spaltudaq.com/ http://commons.wikimedia.org/wiki/Image:Benzimidaz ole_simple_structure.png http://www.princetonol.com/groups/iad/bell/seddon.ht ml Janovy, John Jr. and Roberts, Larry S., Foundations of Parasitiology, 7th Edition, 2005