Cestodes Flashcards
Cestodes-tapeworms
Structure
Segemented body: body is like a ribbon and it’s composed of segmenets
Hermaphrodite: only need one worm to get eggs in feces
No alimentary canal: nutrient uptake via tegument (tegument is highly absorptive)
Adult cestode
Scolex or head: suckers=organs of sttachment- usually cestodes live in SI, suckers combat peristalsis
rostellum= concentric rings of hooks
armed cestode= has hooks
Chain of segments or proglottids (strobila)
Segments bud from neck
more posterior segments get passed out in feces
Tapeworm segments
a mature segment contains organs of reproduction (mid-body)
A gravid segment contains eggs ONLY (tail end)- ready to be passed out in feces
Taenia gravid segement
Segements are continually budded from the neck region
Organs of sexual reproduction is present in the mature segment
Disappear as proglottid matures and moves down the chain until the uterus is full of eggs (gravid)
Uterus+eggs is what we find in feces of infected individuals.
Taenia egg
radially striated eggshell: thick, protective, can live for many years
hexacanth= 6-hooked embryo or onchosphere
Never see all 6 hooks at once because they’re never all in the same plane.
Cestode life cycles
ALWAYS INDIRECT
Final host contains adult tapeworm (often in small intestine) and passes out eggs
IMH ingests eggs, hatch and larval stage encysts (usually migrates through IMH)
Final host eats the cyst containing the head of the future tapeworm
Head latches on ot the SI wall and starts to bud segmenets.
Cestode larval stages in IMH
no L1, L2, L3 etc
Just egg, larval stage and adult
in IMH, larval form=metacestode
Usually found in tissues
cysticerucs, coenorus, cysticercoid, hydatid (all names for metacestode/larval forms)
Family taeniidae
final host: man/cat/dog small intestine (adults always in small intestine)
IMH: mammal- larval stages are encysted
Scolex is armed (except T. saginata)
Adults are relatively non-pathogenic
Taenia saginata
Final host- man
get t. saginata from undercooked beef
5-15 metres long
unarmed- head has no hooks
IMH= cow
Metacestode/larval form= cysticercus bovis: small fluid-filled cyst containig a single scolex.
Life cycle of T. saginata
Adults in SI (man)–> because worms are SO big, pass many segments per day containing millions of eggs–> resistant eggs–> ingested by susceptible bovine
In bovine, onchopheres released in abomasum, penetrate SI wall–> travels to skeletal muscle and encysts
Cysticercus bovis= cysts in IMH 1mm when it 1st encysts, over 12 weeks grows to 1cm.
Meat gets ingested by man–> latching onto SI stimulates worm to grow–> adults in SI.
T. saginata epidemiology
Resource poor settings: sanitation, long-living eggs, high-level of infection in cattle (can be 30-60%), inadequate cooking of meat (due to expense of fuel)
Europe/Australia, etc: low incidence in cattle <1%; role of birds in spreading infection? hypothesis is that seagulls hanging around sewage tx plants can defecate out eggs; eggs are long-lived
Can get cysticercosis “storms” i.e. use of human sludge as fertilizer
T. saginata diagnosis
not very pathogenic- usually the only clinical sign is appearance of gravid segments in feces.
diagnosis via meat insepction: masseter, heart, tongue, IC mucles and diaphragm.
T. saginata control
Meat inspection: >25 cysts, condemn, <25 cysts, chill infected carcasses (-10c for 10 days). If, however, those 25 or fewer cysts are distributed around the body, carcasse gets condemned.
Cooking meat: 57 degrees C will kills cysts
Restrict use of human sludge to cultivated fields or no cattle grazing for at least 2 years
Hygiene/sanitation.
Taenia solium
Final host: man
IMH: pig (normal pork tapeworm) or Man (eggs can be ingested by human and form cyst in human)
Eggs are infective for man: accidental ingestion of eggs; auto infection via reverse peristalsis (tapeworm in SI, gravid segmenets that fall off end go back to stomach and reactivate)
Cysticercus cellulosae (analagous to cysticercus bovis in T. saginata)
Life cycle similar to T. saginata
T. solium pathology
adult tapeworm= no pathology
Cysticerci=serious disease–> encysts in CNS or eye
Major problems in latin america.
T. solium epidemiology
Close association man/pig–> increased number of infections in rural areas
unrestricted access of pigs to human waste
poor meat inspection
T. solium control
Mass treatment to kill adult worms in humans
e.g. albendazole or praziquantel (really effective against tapeworms)
Detection and tx of carriers
health education
mass tx of pigs: oxfendazole
meat inspection
pig corralling
vaccination of pigs
T. solium control- issues
cuultural considerations- i.e. home slaughter in some cases
costs and long term sustainability of control
efficacy of vaccines: recombinant proteins from egg (antigens from egg)
prototype vax for t. ovis, saginata, solium and E. granulosus
Taenia multiceps
seen in UK- lifecycle between dog and sheep
Final host: dog
Adult worm ~100cm long
IMH: sheep
Cyst in sheep= coenorus cerebralis (multiple heads; often found in brain of sheep)
Causes “gid” in sheep= altered gate
Taenia hydatigena
Final host: dog
Adult worm: ~500cm long
IMH: sheep
cystic form in sheep: cysticercus tenuicolis (single head)–burrows through sheep liver and encysts on surface
Common in abattoir: persistent cause of condemnation of livers (usually lambs)
Taenia ovis
similar to T. saginata
Final host: dog
Adult worm ~200cm long
IMH: sheep
Cyst in sheep: cysticerus ovis–causes sheep measles
Relatively common in abattoirs
First recombinant vaccine against helminth parasite
T. ovis vaccine
progressed through all trials
registered for use in NZ
never marketed
important as prototype for vaccines against t. solium, t. saginata and e. granulosus.
Taenia taeniaeformis
Final host: cat
adult worm ~60cm long
IMH: mouse, rat
cyst in mouse/rat: cysticercus fasciolaris
Dipyldium caninum
Can infect dogs, cats, humans
V. common parasite in dogs; prevalent in animals that aren’t well looked after
Dipylidium caninum life cycle
Adults in SI of dog/cat/man 50cm–> 3 weeks post infection, gravid segments shed–>eggs ingested by flea/louse IMH
Cysticercoid in haemocoel (body space of flea/louse)
cysticercoid=tiny solid cyst with single head
Ingestion of flea/louse by dog/cat–> head latches in SI
Adult worms have different shaped segments
Has rostellum with hooks and suckers
IMHs for Dipylidium caninum
Fleas: larvae, not adults, adult mouthparts can’t ingest eggs
important IMH (flea larvae): Ctenocephalides canis, Ctenocephalides felis, Pulex irritans
Lice: all stages–Tricodectes canis
Diagnosis of D. caninum
active motile segments, elongate shape (rice grain)
DOUBLE GENITAL PORE: little holes in sides of tegument where eggs can be released from
EGG PACKETS: can tease segment apart in saline and egg packet will pop up
nb: don’t usually see eggs in feces because they’re enclosed
double genital pore and egg packets are diagnostic features
Distinguishing features of taenia and dipylidium
Double genital pore in dipylidium and presence of egg packets
also, in d. caninum, segments looks like rice grains and have motile segments
Why do we need to distinguish? Control
Taenia= praziquantel
Dipylidium: praziquantel + flea/lice tx
Echinococcus granulosus granulosus
Final host: dog, wild canids
Site: SI
IMH: ruminants, pig, man
Zoonotic
Echinococcus granulosus equinus
final host: dog, red fox
Site: SI
IMH: horse/donnkey
not zoonotic
Echinococcus sp.
small ~6mm
scolex plus 3-4 segments
in SI of dog
gravid segment is usually about 1/2 length of the whole worm.
Eggs similar to taenia: 6 hooks, radially striated, passed in dog feces.
Life cycle of echinoccocus
Adults in SI of dog (Final host)–> gravid semgents shed 1 per week–> egg resistant (thick, striated egg shell)
Egg ingested by IMH–> onchosphere released and penetrates SI well–> hydatid cyst in IMH liver/lungs 6+ months post infection
Hydatid cysts can form anywhere in the body but usually found in liver/lungs. Hydatid cysts have protoscoleces.
Cysts ingested by final host–> adults in SI
Tiny worm takes ~7 days for next segment to become gravid, however SI likely has thousands of worms in an infected dog.
PPP= 40-50 days from ingestion of cyst to eggs shed in feces.
Pathology of echinnococcus
Pathology is associated with cystic stage not the adult worm
E. granulosus sp. hydatid cysts
Horses and cattle (cattle not natural IMH): 90% of hydatids in liver
Sheep: 70% in lung, 25% in liver
most cysts in cattle are sterile- don’t have all heads of future tapeworms in hydatid
Hydatid cyst in IMH
Cyst wall: thick
Germinal epithelium: cells similar to stem cells
Protoscoleces bud off from germinal epithelium- this process just carries on happening. Liver/lung constrains cyst size, but if cyst is in peritoneal vaity, cyst can get quite big.
Hydatid sand: protoscoleces or heads of future tapeworm. This is what you would see if you took an aspirate from it.
E. granulosus diagnosis
IMH: abattoir
Final host: fecal egg count; copro-antigen test (picks up antigen released by parasite); copro-PCR (picks up DNA released by parasite)
In sheep, see clincal signs if cyst is in a weird place i.e. brain/pancreas
E. granulosus pathogenesis
Mostly well tolerated in IMH unless cyst is in an unusual site
Most cases detected in abattoir
not pathogenic in dog final host
always of significance in humans
Epidemiology of echinococcus
E. granulosus sylvatic cycle: host- wild dog, IMH- ruminant- maintained by predation/carrion feeding
E. granulosus domestic cycle: host-dog, primary IMH- sheep (hydatid more infective from sheep)– Man becomes infected from dog (i.e. man is IMH instead of sheep)
E. equinus (not v. common in UK, but rather from european imports): host-dog/red fox– equine abattoirs/hunting kennels–maintained by feeding hunting dogs on equine viscera.
E.g. granulosus
IMH depends on local animal husbandry
in UK, sheep is most important, but elsewhere can be camels or reindeer.
E.g. granulosus zoonotic infection
Man is accidental IMH
Most common in sheep farming areas
Requires close man-dog contact
Man becomes infected via ingestion of onchospheres from water, foodstuffs or coat of dog
Control of hydatid disease
break cycle by: regular deworming of dogs with praziquantel, proper disposal of infected carcasses, deny access of dogs to abattoirs, hygiene to control human infection.
E.g. granulosus in Australia
introduced with sheep
spread from domestic animals into dingoes as final host and wild marsupials as IMH- sylvatic cycle established
cycle re-introduced to domestic dogs in some areas by hunters allowing dogs to feed on offal from wildlife.
Control: praziquantel, dried dog food too, better diagnosis (ELISA to detect copro-Ag), education
Echinococcus multilocularis
final host: dog, cat, wild canids
IMH: lemings, voles, man
Life cycle similar to E.g. granulosus
Important zoonosis
Prevalent in europe
E. multilocularis life cycle
similar to granulosus
Adults in SI (fox)–> gravid segments shed in feces–> eggs resistant to -50C–> ingested by rodent IMH–> embryo released, penetrates SI wall–> usually goes to liver via hepatic portal vein where embryo rapidly vesiculates (sits in liver and forms big vesicles). IMH usually gets sick, can’t run as fast
rodent+cyst ingested by fox
Pet passport and human cases
Dogs and cat must be treated against E. multilocularis 24-48 hours prior to returning to UK (praziquantel)
Human cases: 15% prevalence in parts of china and tibet
urban foxes in zurich and stuttgart infected, prevalence rates 20-47%
no +ve foxes in recent UK survey
E. multilocularis in humans
Causes alveolar echinococcosis
potentially fatal
if untreated, long asymptomatic periods (5-15 years) followed by clinical signs
tx: liver transplant, section or albendazole
Alb+ surgery improves 10 year survival rates from 6-25% to 80-83%
Horse cestodes
Anoplocephala perfoliata**
Anoplocephala magna
Paranolocephala mamillana
Site: small and large intestine
IMH: orbatid forage mites
Anoplocephala perfoliata
prevaelence 14-81%
High prevalence at temperate climates
Ulcerations at site of attachment of parasites–> risk factor for ileo-caecal colic.
A. perfoliata have suckers and lappets just underneath sucker. not sure what lappets do, but maybe they’re sensory organelles? either way, very characteristic for A. perfoliata
Segements are MUCH wider than long.
Anoplocephala perfoliata life cycle
Adults at ileo/caecal junction–> eggs pased in feces–> ingested by forage mite IMH–> forms cysticercoid in mite
Infected mite ingested by horse–> attaches to gut wall in horse–> adults at ileo/caecal junction
PPP=6-10 weeks
A. perfoliata and colic
Horses with tapeworms are more likely to suffer colic
80% of 20 cases of ileal impaction colic were tapeworm associated
22% of 95 spasmodic colic cases were tapeworm associated
Treat with PZQ +/- ivermectin
A. perfoliata diagnosis
FEC: low sensitivty, high specificty
Eggs are misshapen- odd-looking- have pyriform appartus. In fresh specimen, looks like a stalked mushroom and embryo sits on top.
ELISA and Corp-Ag PCR.
