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Echinoccous Granulosus

Echinoccous Granulosus. Topics. Introduction Habitat Morphology Life cycle Pathogenesis Clinical diseases Lab diagnosis Treatment. Introduction:. E. granulosus tapeworm formally called “Tenia echinococcus”, causes hydatid disease or echinococcosis.

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Echinoccous Granulosus

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  1. Echinoccous Granulosus

  2. Topics • Introduction • Habitat • Morphology • Life cycle • Pathogenesis • Clinical diseases • Lab diagnosis • Treatment

  3. Introduction: E. granulosus tapeworm formally called “Tenia echinococcus”, causes hydatid disease or echinococcosis. • History: Hydatid cyst is recognised since the time of Hippocrates. Adult worm was discovered by Hartmann in 1965, Goez described larva in 1782.

  4. Habitat: >Man harbours the larval form. > Adult worm lives in the intestine of dog and other carnivorous animals. Hence its also called as the “dog tapeworm” Morphology: It’s a small tapeworm{3-6mm} Consists of a scolex, neck and strobila of 3 proglotttids.

  5. Scolex: is spherical, has 4 oral suckers and a rostellum with 28-40 hooks arranged in two rows. Neck: Short and thick

  6. Strobila: 3 segments:- 1st segment is immature, 2nd is mature and the 3rd is gravid which is the biggest and measures 3-8mm in length and 0.6mm in breadth.

  7. Egg: Morphologically similar to Taenia > Ovoid, 32 to 36um long and 25-32um wide. > Has 2 layers, an outer shell surrounding the inner embryophore. Fully developed egg has 3 pairs of hooklets within the embryophore. Eggs are excreted in the faeces of canine animals [dog,fox,jackal]

  8. Larval form: Embryos develop into cyst [hydatid] in the intermediate host, which contain many brood capsules and small protoscolices. Protoscolex contains a scolex which represents future head of worm,remains invaginated within vesicular body. After entering into definitive host, scolex evaginates, attaches to mucosa with rostellar hooklets and develops into an adult worm.

  9. invaginated evaginated Phase contrast cyst

  10. Epidemiology: • Host: dogs are definitive hosts and herbivores [man,cattle,sheep] are intermediate hosts. • Tranismission: definitive host get infected by eating contaminated meat. Humans get infected by ingestion of eggs passed in dog faeces. 3. Distribution: Latin america, Arab, North Africa, Middle east and South east asia. Andra Pradesh and Tamil Nadu in India.

  11. Pathogenecity: • In dogs: no disease • In humans: hydatid cyst or disease, grows slowly and several years[5-20yrs]. 10% of cases terminate fatally. • most cysts occur in liver[70%] and lungs[20%] • cysts in other sites[10%] include: Spleen[3-4%] brain[3%] bones[1%] Pelvic organs[2%] head and muscles[1-3%]

  12. Inguinal region kidney Brain adrenal

  13. Evolution of hydatid cyst:the wall of cyst consists of 3 layers, 2 inner layers are secreted from embryo and outer layer is produced by host. • Germinal layer [endocyst]: Innermost vital thin layer, consisting of a number of nuclei embedded in protoplasmic mass. Functions: • formation of outer laminated layer • production of brood capsule with protoscolices • secretion of hydatid fluid

  14. 2. Laminated layer [ectocyst]: Cuticle layer, laminated hyaline membrane. Derived from parasite and composed of mucopolysaccharide material which is tough, elastic[1mm thick]. Looks like white of “hard boiled egg”. 3. Adventitial layer [pericyst]: Fibrous layer that results from cellular reaction with host. May become calcified or sclerosed.

  15. Development of brood capsules: small knob-like excrences protude into the lumen of the . cyst from germinal layer Excrescencs enlarge ,become vacuolated & filled with fluid to form “ Brood capsule” Protoscolices arise from inner layer of brood capsule Brood capsule detaches from germinal layer, escapes free into the fluid filled cyst cavity.

  16. Mature cyst contains about 1million protoscolices & • may detach from germinal membrane and float free in the cyst together with the brood capsule to form the “hydatid sand” The cyst may further form “daughter and grand daughter cysts”, Or may rupture into tissues or circulation, the spilled protoscolices may produce “secondary cysts”.

  17. Evolution of hydatid cyst:

  18. Histopathology: Lung Liver

  19. Hydatid fluid: secreted by germinal layer of cyst • colour: clear colourless or pale yellow • specific gravity: low varies from 1.005-1.010. • reaction: slightly acidic, pH 6.7 • chemical composition: NaCl, sodium sulphate, sodium phosphate, sodium and calcium salts of succinic acid. • antigenicity: antigenic, used for immunological tests. • toxicity: highly toxic, when comes out causes anaphylactic symptoms.

  20. Fate of hydatid cyst: • spontaneous recovery in some patients. Scolies die and fluid is gradully absorbed. • cyst may get calcified following injury to its wall • spontaneous evacuation of cyst may occur following inflammation reaction • cyst of liver may rupture into pleural cavity or lungs producing disseminated hydatid lesions. • may rupture to body cavity leading to disseminated and widespread growth of hdatid cysts.

  21. Clinical syndromes: Cyst grows slowly to 4cm diameter at end of 1st year, brood capsules and scolices begin to appear. Most remain symptomless for many years. • Hepatic liver cyst: hepatic enlargement, more frequent in right lobe of liver. Rupture of cyst may lead to severe symptoms and allergic manifestations. 2. Lungs cysts: cough dysponea and chest pain, rupture can cause haemomptysis, pneumonia pneumothorax. 3. In vital organs[ spleen, heart, brain] or bones, fatal!

  22. DIAGNOSIS: • Radiological findings: • X-ray: can only detect presence of cyst. • Ultrasound, CT scan & angiography can provide the first evidence of a cyst’s presence.

  23. 2) Exploratory cyst puncture: aspiration of cyst contents may reveal the presence of protoscolices [hydatid sand]. • contraindicated due to accidental spilling of contents • 3) Serologic tests: • Antibody detection: ELISA, indirect immunoflorescence test, latex agglutination,IHA. • Antigen detection: double diffusion and counter immunoelectrophoresis technique.

  24. Hooklet of Echinococcus spp.

  25. 4) Casoni test: immediate hypersensitivity skin test introduced by Cosoni in 1911. Antigen: hydatid fluid collected from human or animal cyst and sterilised by Sietz or membrane filtration. Test: sterilised fresh hydatid fluid[0.25ml] injected intradermally on one arm & equal volume of saline on other hand as control. Result:in a positive reaction large wheal(5cm diameter) with multiple pseudopodia

  26. Remarks: • False positive and false negative cases may occur. Nonspecificity being the major limitation. • Diagnostic sensitivity is limited in patients having intact or hyaline cysts. • The antigen may sensitize the patient leading to production of antibody and anaphylactic reaction. • > therefore rarely used these days for diagnosis.

  27. TREATMENT • SURGERY • CHEMOTHERAPY • CYST PUNCTURE • PAIR

  28. Prevention: i) Education: regarding transmission of infection and role of canines in life cycle. ii) personal hygiene:washing of hands and utensils in areas inhabited by dogs iii) Dogs should not be fed viscera of slain animals

  29. Hymenolepis nana

  30. TOPICS • CLASSIFICATION • EPIDEMIOLOGY • TRANSMISSION • MORPHOLOGY • LIFE CYCLE • MODES OF INFECTION • CLINICAL SYNDROMES • DIAGNOSIS • TREATMENT • PREVENTION • MCQ’S

  31. CLASSIFICATION • Kingdom: Animalia • Phylum: Platyhelminthes • Class: Cestoda • Order: Cyclophyllidea • Family: Hymenolepididae • Genus: Hymenolepis • Species: Hymenolepis nana

  32. EPIDEMIOLOGY DISTRIBUTION: • Worldwide • Infection more in warmer climates S.AMERICA & AFRICA • Crowded areas, such as India and China • More common in children than in adults.

  33. TRANSMISSION : Ingestion of eggs from contaminated hands . Ingestion of infected rat fleas ,beetles as they contain cysticercoid in their haemocele.

  34. MORPHPLOGY • ADULT WORM: Small thread like worm. • 1-4 cm long; max. 1mm width. • Often found in large numbers(1000 to 8000) • Life span is 4 –6 weeks. • Dwarf tape worm

  35. ADULT WORM

  36. SCOLEX • Shows a knob like rostellum • Bears a ring of hooklets. • They possess 4 suckers.

  37. STROBILA About 200 proglottids; mature proglottids are broder than long(0.22×0.8mm). • Genital sac lies on one side of strobila. • Uterus consists of a sac like structure with lobulated walls filled with 80-200 eggs. • There are 3 round testis and bilobedcoaresly granular ova that lie in the posterior part of each proglottid.

  38. EGGS • Colorless, oval or sub spherical 45*35 mm. • Egg ,has two membranes : a.outer thin and colorless. b.inner embryophore. • Space b/w them has – . yolk granules . polar filaments. • Oncosphere 3pairs of hooklets • Egg floats in salt solution

  39. MODES OF INFECTION H. nana has 3 modes of infection: (1) Indirect 2-host cycle involving rodents as primary definitive hosts and grain beetles, fleas, or other insects that feed on contaminated rodent droppings as intermediate hosts. (2) Oral-anal cycle in which eggs are passed from one human to another or recycle externally in a single host.

  40. 3) INTERNAL AUTOINFECTION: Eggs hatch within the gut and initiate a 2nd generation without ever exiting the host. This results in massive numbers of worms nausea vomiting diarrhea abdominal pain weight loss and nonspecific systemic symptoms.

  41. CLINICALSYNDROMES • Asymptomatic H.nana causes HYMENOLEPIASIS/ HYMENOLIPIDOSIS. • Heavy infections : abdominal discomfort diarrhoea anorexia pruritis • Hyper infection : autoinfection in immuno compromised pts. With heavy worm burden

  42. DIAGNOSIS • Adult worm or proglottids are rarely seen in stools. • Demonstration of typical eggs with 6 hooked embryo & polar filaments.

  43. Egg of H. nana Egg of H. diminuta

  44. TREATMENT • DRUG OF CHOICE : PRAZIQUANTEL single dose of 25mg/kg. body weight. ALTERNATIVE : Niclosamide Nitazoxanide

  45. PREVENTION & CONTROL • Improved sanitation & proper disposal. • Personal hygeine. • Control of arthropod vectors

  46. Thank you!

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