TREMATODES REVIEWER

Cards (59)

  • Trematodes are also called Platyhelminths
  • They are flat leaf shaped helminthes.
  • They are mostly hermaphrodites except for Schistosoma which have separatemale and female species.
  • They are commonly associated with aquatic fauna likesnails, mollusks and fish.
  • Blood trematodes?
    S hematobium
    S mansoni
    S japonicum
    S intercaltum
    S mekongi
  • Hepatic trematodes?
    Facciola hepatica
    Fasciola gigantic
    Clonorchis sinensis
    Opisthorchis felineum and viverrini
  • Intestinal trematodes?
    Fasciolopsis buski
    Metagonimus yokogawi
  • Lung trematodes?
    Paragonimus westermani
  • General Morphological features of Trematodes
    (a) Have conspicuous suckers, hence termed “Flukes”
    (b) No body cavity
    (c) Oviparous - release only eggs
    (d) Eggs of all Flukes except Schistosoma are operculated
    (e) Most commonly found in tissue sections
    (f) Sexes are separate and eggs non-operculated
    (g) Male - female paired together
    (i) Cercarial dermatitis, tissue reaction - thrombosis on death
    (j) Expulsion of eggs - eosinophilic granuloma, fibrosis, TCC
    (k) Splendore - hoeppli bodies.
  • General Morphological features of Trematodes
    (h) Eggs differentiated on basis of spine
    i. S haematobium- terminal spine
    ii. S japonicum – no spine
    iii. S. mansoni- lateral spine
  • SCHISTOSOMIASIS
    The Schistosoma derive their name from the fact that the males body is split and forms a gynecophoral canal in which the female worm rests.
  • SCHISTOSOMIASIS
    Schisto (Split)
    soma (body).
  • SCHISTOSOMIASIS?
    The adult worm of schistosoma live in the venous plexus of the definitive host.
  • SCHISTOSOMIASIS
    The inhabit the venous plexus of the urinary bladder (Sheamatobium, intestines) (S japonicum and S mansoni).
  • Morphology
    Schistosoma Japonicum Egg
    i. 70-100 x 50-65 microns.
    ii. Oval to rounded, nonoperculate egg.
    iii. Contain developed miracidium.
    iv. Note: Lateral knob.
  • S mansonii adults
    i. Adult male 0.6-1.4 × 0.11 cm. in size.
    ii. Grossly tuberculate integument.
    iii. Note: Ventral gynecophoral canal.
    iv. Intestinal ceca unite early, united intestinal long.
    v. 7(3-13) small testes situated dorsal and posterior to the ventral sucker.
  • S haematobium Adult
    i. Adult female measure 2.0-2.5 × 0.025 cm.
    ii. Cylindrical shape with pointed ends
    iii. Smooth integument.
    iv. The oral and ventral suckers near the anterior end are of equal size.
    v. Elongate ovary situated in posterior half of body.
    vi. Long,voluminous uterus contains 20-30 ova
  • S haematobium egg?
    i. 112-170 × 40-70 microns.
    ii. Large, spindle shaped with rounded anterior and conical posterior end.
    iii. Yellowish-brown, nonoperculate egg.
    iv. Contains developed miracidium.
    v. Note: Terminal spine.
  • Schistosoma cercaria?
    i. Elongated, pear-shaped body with round ends
    ii. Long tail with a terminal furca.
    iii. Tactile hair are distributed over the body and tail.
  • LIFE CYCLE OF SCHISTOMA SPECIES?
    Schistosoma pass their life in two hosts
  • LIFE CYCLE OF SCHISTOMA SPECIES?
    Man is the definitive host
  • LIFE CYCLE OF SCHISTOMA SPECIES
    • The mollusksor the snails are the intermediate host.
    • Ova from the sexually mature worms are passed in the intestinal tract or the urinary bladder.
    • The ova are passed in the urine or the stools into fresh water bodies.
    • The miracidium hatch from the ova immediately or after a short period of incubation.
    • The miracidium infects the first intermediate host the snail.
    • Within the snail or mollusks the miracidium transforms into sporocysts
    • The sporocysts develop into second generation sporocysts (in schistosomes).
    • Miracidium develops into tailed larvae called cercaria.
  • LIFE CYCLE OF SCHISTOMA SPECIES
    • The cercaria mature and leave the snail and become free living in water
    • In case of schistosoma the cercaria have a forked tail. They infect the man by penetrating the skin of humans who are in water.
    • The immature worm enters the blood stream and eventually reach the veins near the intestines and urinary bladder.
    • The worm reaches sexual maturity in these venous plexus of the intestines and urinary bladder.
  • PATHOLOGY?
    (a)Penetration of skin by metacercaria
    Skin penetration may not be apparent.
    Human and some non human species of Schistosoma cause cercarial dermatitis (swimmers itch).
    This manifests with papules, macules, vesicles and intense itching
  • PATHOLOGY?
    b) Migration and maturation of immature worms
    • There are general toxic and allergic symptoms including urticaria with eosinophilia, fever, abdominal pain and tender hepatosplenomegaly.
    • This is known as Katayama or snail fever.
  • PATHOLOGY?
    c) Damage by eggs in tissue
    Resulting damage depends on the severity of the parasite load.
    An inflammatory granuloma forms with epithelial, giant plasma and eosinophil cells and fibroblasts (Hoeppli reaction).
    There is subsequent fibrosis and calcalcification.
    Such damage may be local and/ or ectopic.
  • PATHOLOGY?
    d) Urinary schistosomiasis
    • It is caused by Schistosoma haematobium.
    • The initial toxic and allergicsymptoms are not marked.
    • The urinary bladder and the ureter are typicallyinvolved with hyperemia and terminal hematuria, dysuria and increasedfrequency of micturation, papules, papillomata and ulceration.
  • PATHOLOGY?
    d)urinary schistosomiasis
    • Hypertrophy of the bladder can later lead to contraction.
    • There may be cystitis and calculusformation.
    • This may be followed by calcification and squamous cell carcinoma. Fistula may develop.
    • There can also be hydroureter and hydronephrosis.
    • Ectopiclesions are less severe than in other species of Schistosoma.
    • GenitalSchistosomiasis may lead to lumpy semen, haematospermia or wart like lesionson the vulva.
  • PATHOLOGY?
    e) Intestinal schistosomiasis
    • It is caused by Schistosoma mansoni.
    • There are marked initial toxic and allergicsymptoms.
    • The large intestine and the rectum are typically involved withpolyposis, papules, abscesses, ulcers , papillomata, fistulae and ova in stools.
    • The bladder is sometimes involved with pathology similar to urinary Schistosoma above.
    • There can also belesions in the brain, spinal cord and lungs.
  • PATHOLOGY?
    e) Intestinal schistosomiasis
    • There can be ectopic lesions.
    • The liver is frequently involved(receiving the eggs via the portal vein) with inflammatory reaction and fibrosisleading to periportal (pipe-stem) fibrosis with portal hypertension.
    • This maymanifest with oesophageal varices, splenomegaly and ascitis.
  • PATHOLOGY?
    f) Oriental schistosomiasis
    • This is caused by Schistosoma japonicum.
    • There are marked initial toxic andallergic symptoms which can lead to myocarditis and death.
    • Intestinal lesionare similar to those with S mansoni infection and the small intestine is involved.
    • The liver is involved as in S mansoni infection and hepatic lesions are similarand may lead to portal hypertension.
    • The brain may also be become involved.
  • PATHOLOGY?
    5. Laboratory Diagnosis:
    • Eosinophili may be present.
    • Ova found in terminal urine by Nucleopore filtrationor after centrifugation.
    • Ova may also be found in semen.
    • Ova may also be foundin faeces directly or using formol- ether concentration, rectal scrapings orbiopsies.Serology.
    • ELISA tests (using soluble egg antigen) are useful 6-12 weeks postexposure. In many chronic cases, the diagnosis will be made on serology alone.
  • CLONORCHIS SINENSIS?
    These are leaf shaped and flat helminthes. They are hermaphrodites. Twentyeight million people are infected worldwide.
  • CLONORCHIS SINENSIS?
    Morphology
    a)12-20 x 3-5 mm. in size.
    b)Flat, elongated, aspinous, flabby, tapering anteriorly and somewhat rounded posteriorly.
    c) Note: Lancet appearance.
    d) Small, slightly lobate ovary anterior to the branched testes
  • Life Cycle of Clonorchis species?
    • Ova from the sexually mature worms are passed in the intestinal tract.
    • The ova are passed in the stools into fresh water bodies.
    • The ova are ingested by the snail sand the miracidium hatch from the ova in the first intermediate host the snail.
    • Miracidium develops into cercaria.
    • The cercaria leave the snail.
    • Free swimming cercaria encyst in the fish which is the second intermediate host.
    • Cercaria develop into metacercaria and reach the muscles of the fish.
  • Life Cycle of Clonorchis species?
    • The fish may be eaten by the dogs and cats which serve as the animal reservoir of the disease.
    • Humans get infected by consuming under cooked fish.
    • Encysted metacercaria release the immature worm in the duodenum.
    • The immature worm penetrates the intestinal mucosa and reaches the portal circulation through which it reaches the liver.
    • In the liver the worm lodges in the intrahepatic bile ducts where it reaches sexual maturity
  • CLONORCHIS SINENSIS Pathology and Clinical features?
    • Adult flukes inhabit the distal bile duct with epithelial proliferation, surrounding inflammatory reaction and ascending cholangitis.
    • Sometimes there is secondary bacterial infection with jaundice and septicemia.
    • There can also be eosinophilia.
    • All this can lead to thick, dilated fibrous ducts with adenomata of epithelium, bile duct stenosis and cholangiocarcinoma.
  • CLONORCHIS SINENSIS Pathology and Clinical features?
    • Many cases are asymptomatic.
    • Acuteinfection may lead to tender hepatomegaly.
    • Chronic infection can result inanorexia, low-grade fever, epigastric pain and tender hepatomegaly
  • Laboratory Diagnosis of Clonorchis Sinensis?
    The ova are found in the feaces and in the bile duct (via duodenal aspiration or‘string test’)
  • FASCIOLIASIS?
    • The fluke is found in all sheep- rearing countries. About one million people areinfected worldwide.
    • F.gigantica reside in bile ducts. Larvae might get “lost”