Flukes Flashcards
Fluke classification
Phylum- Platyhelminthes
Class- Trematoda
Sub class- Digenea
Family- Fasciola
Fasciola hepatica
Final host- most mammals (significantly sheep and cow)
Disease- Fasciolosis, found most often in temperate regions of the world
IMH- small brown amphibious snail, Galba truncatula
Fasciolosis
Zoonosis and can cause severe illness in man
~2.4 million people infected world wide, but not very common in UK (associated with eating watercress)
Fasciola hepatica body plan
Has ventral and oral sucker (to keep in place) as well as spines in cuticle to keep it in place
Hermaphrodite
Acute fasciolosis
Usually detected in autumn/early winter and occurs 2-6 weeks post ingestion of >200 metacercariae. Due to migration of juvenile flukes, causing liver damage and hemorrhage. Usually present with sudden death, or weak with pale mucous membs, dyspnoea, palpable liver, and abdominal pain
Sub acute fasciolosis
Usually detected in late autumn/winter and occurs 6-10 weeks post ingestion of 500-1500 metacercariae caused by juvenile migration and adult flukes in bile duct. They feed on blood and damage the biliary mucosa, inducing inflammation which results in liver damage and manifests as rapid/severe hemorrhagic anemia with hypoalbuminaema, pale mucous membranes, enlarged liver, and may see SM edema
At PM- rupture of subcapsular haemorrhages rare
Chronic fasciolosis
Late winter/early spring and occurs 4-5 months post ingestion of 200-500 metacercariae. Caused by adult flukes feeding in bile ducts which results in anemia, hypoalbuminaemia, and cholangitis which manifests as progressive loss of condition, emaciation, pale mucous membranes, bottle jaw, and ascites.
Productivity losses- fewer multiples, and reduced weight growth in lambs
Bovine fasciolosis
Chronic disease- Productivity loss, calcification of bile ducts, and enlarged GB
Immune response- limits primary infection and inhibits secondary infection
Ovine diagnosis of F. hepatica
Clinical signs/seasonal occurrence
PM identification
eggs
Bovine diagnosis of F. hepatica
Eggs
Test for glutamate dehydrogenase gama glutamyl transpeptidase, indicator of biliary damage
ELISA
Fasciolosis epidemiology
Availability of snail habitat-Breed May-October and like muddy areas or slow moving shallow water, rushes indicate slightly acidic pH
Moisture- Increases snail habitat, and also make it easier for miracidium to find snail. Cercaria needs film of water as well.
Temperature- Need mean day/night temp of >10oC (15oC)
Summer infection of G. truncatula
Optimal period for parasite development in snail is May to October.
Snails infected by miracidia in late spring/summer are derived from overwintered eggs or eggs from carrier animals. Leads to an increase in metacercariae on pasture August to October
Winter infection of G. truncatula
Snails become infected my miracidia in autumn, conditions are sub-optimal and development stops over winter and development resumes over spring.
Metacercariae are produced May to June
Not really that important in UK
Meteorological forecasting
Used to predict the risk and severity of disease outbreaks (National Animal Disease info Service)
Rainfall data calculated as Mt index based on rainfall, evapo-transpiration and number of wet days/mo
Acute treatment
Triclabendazole and move to clean pasture
Resistance seen in some areas, so rotate drugs
Subacute treatment
Closantel and Nitroxynil. Move to clean pasture
Chronic treatment
Range of drugs
Control via snail population
Drainage to take away habitat and disrupt LC
Fence off saturated pasture
Move sheep to drier pasture when under threat
Mulluscicide (not in UK)
Treat and quarantine new arrivals
Treat cattle- same para, but dont show clinical signs, can give to sheep
Control via anthelmintics
Reduce burden- October for acute, and January for chronic
Reduce pasture contamination April/May
Rotate drugs
Will continue to be a problem bc of carriers, drug resistance, hard to eradicate snails, and global warming is making it harder to predict
Optimal period for snail development
May to October
Fasciola gigantica
Final hosts are mammals, and causes fasciolosis
Tends to be found in tropic/sub tropic regions (esp Africa and S. Asia)
More pathogenic than F. hepatica with longer PPP
Host is aquatic snail
F. gigantica epidemiology
Miracidia hatch in beginning of wet season to infect snails while cercaria are shed from snail at beginning of and during dry season, causing disease at end of dry/beginning of next wet season
Encyst on aquatic plants or water
In snail during wet, and in mammal during dry season
PPP 13-16 weeks
F. gigantica control
Anthelmintics Snail control (molluscicide usually impractical), but can fence permanent water sources, pump water through troughs, and parasitic castration
Dicrocelium dendriticum
Main host- sheep, cattle, horse, rabbits
IMH- land snail/ and (formica)
Found world wide and affects bile ducts/ GB
Enslaver parasite bc may encyst in ant brain, causing it to clim herbage and clamp on with its jaw to increase chances of getting eaten
D. dendriticum pathogenesis
Heavy infection in older sheep
Fibrosis and distention of bile ducts
Progressive cirrhosis
Weakness, anemia, and emaciation
Can cause productivity loss by decrease in wool production, premature aging, and reproductive losses
D. dendritiucum epidemiology
IMH independent of water and eggs can survive for months creating large reservoir of infection, making control difficult
Treat with albendazole
Paramphisomatidae
Rumen flukes that care conical maggot shaped
Adults are in rumen/reticulum
IMH- aquatic snail Planorbis and Bulinus
World wide distrobution, especially in tropics, sub-tropics, and S. US (emerging disease in UK)
Paramphistomum cervi and P. microbothrium
Paramphistom pathology
Juveniles excyst in duodenum and attach to mucosa as plug feeders causing pathology, causing necrosis and haemorrhage-erosion of duodenal mucosa (gastroenteritis)
Blood can be found in diarrhea, will strain but nothing is produced. Sometimes, intestinal mucosa can come out with parasite attached which is diagnostic
After about 6 weeks migrate to fore stomach as adults
PPP- 7-10 weeks
Paramphistom diagnosis
Clinical signs-
Foetid diarrhea, anemia, hypoalbuminaemia, intense thirst, anorexia- gives high potential for mortality
Diagnosis- PM wiht juveniles in duodenum
Fecal egg count doesn’t help much
Paramphistoma treatment
Oxyclozanide
Schistomatidae
Parasite of all domestic animals, even problem in humans, but mainly affects sheep and cattle in tropics, sub tropics, and S. Europe
IMH- aquatic snail, Bulinus and Physopsis
Major species are bovis, japonicum, and matthei
Male is larger than female, and they mature in his gynaecophoric canal
Egg is elongated with a terminal spine
Shistosoma pathogenesis
There is an inflammatory response against the eggs in veins, mucosa, and liver leading to granuloma formation
Acute Schistosoma pathogenesis
Mucosal hemorrhage, anemia, hypoalbuminaemia, hepatosplenomegaly
Clinical signs- anemia, diarrhea (mucous and blood tinged), thirst, anorexia, and emaciation
Chronic Schistosoma pathogenesis
Marked granuloma of intestine and cirrhosis as well as reduced productivity
Schistosoma diagnosis
Clinical signs/infected water source
Granulomatous lesions and adults in mesenteric veins
Eggs
Shistosoma epidemiology/treatment
Related to prevalence of snail
Clean water source
Drugs- praziquantel, albendazole (gradually increase, because abrupt killing can lead to embolism)
