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Echinoccous Granulosus
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Topics Introduction Habitat Morphology Life cycle Pathogenesis
Clinical diseases Lab diagnosis Treatment
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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.
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Habitat: Morphology: >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.
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Scolex: is spherical, has 4 oral suckers and a rostellum with hooks arranged in two rows. Neck: Short and thick
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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.
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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]
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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.
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invaginated evaginated Phase contrast cyst
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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.
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Pathogenecity: Spleen[3-4%] brain[3%] bones[1%]
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%]
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Inguinal region kidney Brain adrenal
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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
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Cuticle layer, laminated hyaline membrane.
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.
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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.
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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”.
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Evolution of hydatid cyst:
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Histopathology: Lung Liver
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Hydatid fluid: secreted by germinal layer of cyst
colour: clear colourless or pale yellow specific gravity: low varies from 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.
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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.
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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!
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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.
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contraindicated due to accidental spilling of contents
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. Diagnostic Findings The diagnosis of echinococcosis relies mainly on findings by ultrasonography and/or other imaging techniques supported by positive serologic tests. In seronegative patients with hepatic image findings compatible with echinococcosis, ultrasound guided fine needle biopsy may be useful for confirmation of diagnosis; during such procedures precautions must be taken to control allergic reactions or prevent secondary recurrence in the event of leakage of hydatid fluid or protoscolices. Antibody Detection Immunodiagnostic tests can be very helpful in the diagnosis of echinococcal disease and should be used before invasive methods. However, the clinician must have some knowledge of the characteristics of the available tests and the patient and parasite factors associated with false results. False-positive reactions may occur in persons with other helminthic infections, cancer, and chronic immune disorders. Negative test results do not rule out echinococcosis because some cyst carriers do not have detectable antibodies. Whether the patient has detectable antibodies depends on the physical location, integrity, and vitality of the larval cyst. Cysts in the liver are more likely to elicit antibody response than cysts in the lungs, and, regardless of localization, antibody detection tests are least sensitive in patients with intact hyaline cysts. Cysts in the lungs, brain, and spleen are associated with lowered serodiagnostic reactivity, whereas those in bone appear to more regularly stimulate detectable antibody. Fissuration or rupture of a cyst is followed by an abrupt stimulation of antibodies. A patient with senescent, calcified, or dead cysts is generally found to be seronegative. Cystic echinococcal disease (Echinococcus granulosus). Indirect hemagglutination (IHA), indirect fluorescent antibody (IFA) tests, and enzyme immunoassays (EIA) are sensitive tests for detecting antibodies in serum of patients with cystic disease; sensitivity rates vary from 60% to 90%, depending on the characteristics of the cases. Crude hydatid cyst fluid is generally employed as antigen. At present, the best available serologic diagnosis is obtained by using combinations of tests. EIA or IHA is used to screen all specimens; a positive reaction is confirmed by immunoblot assay or any gel diffusion assay that demonstrates the echinococcal “Arc 5.” Although these confirmatory assays give false-positive reactions with sera of 5% to 25% of persons with neurocysticercosis, the clinical and epidemiological presentation of neurocysticercosis patients should be rarely confused with that of cystic echinococcosis. A commercial EIA kit is available in the United States. Antibody responses have also been monitored as a way of evaluating the results of treatment, but with mixed results. Following successful radical surgery, antibody titers decline and sometimes disappear; titers rise again if secondary cysts develop. Tests for Arc 5 or IgE antibodies appear to reflect antibody decline during the first 24 months postsurgery, whereas the IHA and other tests remain positive for at least 4 years. Chemotherapy has not been followed by consistent declines in antibody titers. Consequently, the usefulness of serology to monitor the course of disease is limited; imaging techniques provide a more accurate assessment of the patient’s condition. Alveolar echinococcal disease (Echinococcus multilocularis). Most patients with alveolar disease have detectable antibodies in serologic tests using heterologous E. granulosus or homologous Echinococcus multilocularis antigens. With crude Echinococcus antigens, nonspecific reactions create the same difficulties as described above, however, immunoaffinity-purified E. multilocularis antigens (Em2) used in EIA allow the detection of positive antibody reactions in more than 95% of alveolar cases. Comparing serologic reactivity to Em2 antigen with that to antigens containing components of both E. multilocularis and E. granulosus permits discrimination of patients with alveolar from those with cystic disease. Combining two purified E. multilocularis antigens (Em2 and recombinant antigen II/3-10) in a single immunoassay optimized sensitivity and specificity. These antigens are sold in a commercial EIA kit in Europe, but not in the United States. As in cystic echinococcosis, Em2 tests are more useful for postoperative follow-up than for monitoring the effectiveness of chemotherapy.
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Hooklet of Echinococcus spp.
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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 Observations made for next 30 mins and after 1 to 2 days.[A wheal response occurring at the injection site within 20 minutes is considered positive. (Immediate hypersensitivity). Delayed hypersensitivity reaction usually read after hours. [2] The test is positive in about 90% of cases of hydatid disease affecting the liver, but positive in less than 50% of patients with hydatid disease elsewhere in the body; false positive results are also common. Precaution – Being a type I hypersensitivity reaction, anaphylactic reaction tray must be kept ready before carrying out the test.Consequently, serological tests are now generally used.
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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.
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TREATMENT SURGERY CHEMOTHERAPY CYST PUNCTURE PAIR Treatment
Cystic Echinococcosis In the past, surgery was the only treatment for cystic echinococcal cysts. Chemotherapy, cyst puncture, and PAIR (percutaneous aspiration, injection of chemicals and reaspiration) have been used to replace surgery as effective treatments for cystic echinococcosis and, for some cases, no treatment but a conservative “watch and wait” approach is best. Treatment indications vary with cyst characteristics, including cyst type, location, size, and complications. Surgery may be the best treatment for liver cysts that are secondarily infected or cysts located in the brain, lungs, or kidney. Liver cysts larger than 7.5 cm are likely to have biliary communication; surgery may be the best option for these cysts. Many abdominal cysts can be treated by injection of protoscolicidal chemical solutions into the cyst, followed by evacuation, prior to further manipulations and extirpation of cysts. For some patients, chemotherapy with benzimidazoles is the preferred treatment. Patients with small cysts or multiple cysts in several organs can be treated successfully with albendazole. Approximately one third of patients treated with chemotherapy with benzimidazole drugs have been cured of the disease and even higher proportions, between 30-50%, have responded with significant regression of the cyst size and alleviation of symptoms. Both albendazole 10 to 15 mg/kg body weight per day (max 800 mg orally in two doses) and, as a second choice for treatment, mebendazole mg/kg body weight per day continuously for several months have been highly effective. Additionally, chemotherapy can be very effective when used in conjunction with surgery. Albendazole has been administered to patients prior to surgery for the intended purpose of facilitating the safe surgical manipulation of the cysts by inactivating protoscolices, altering the integrity of the cysts membranes, and reducing the turgidity of the cysts. A third treatment option, PAIR (percutaneous aspiration, injection of chemicals and reaspiration), has been shown to be effective. This option is indicated for patients with relapse after surgery, failure of chemotherapy alone, or who refuse surgery. Albendazole400 mg orally twice a day for 1-6 months (ADULTS); mg/kg/day (max 800 mg) orally in two doses for 1-6 months (CHILDREN); Praziquantel may be useful preoperatively or in case of spillage of cyst contents during surgery Alveolar Echinococcosis Alveolar echinococcosis requires chemotherapy with or without surgery; radical surgery is the preferred approach in suitable cases. Effective treatment involves benzimidazoles administered continuously for at least 2 years and patient monitoring for 10 years or more since recurrence is possible. This has inhibited progression of alveolar echinococcosis and reduced lesion size in approximately half of treated cases. Intermittent treatment with albendazole is not recommended.
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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 The disease can be prevented by periodic deworming of dogs, improved hygiene in the slaughtering of livestock including proper destruction of infected offal, and public education campaigns. Vaccination of livestock with an E. granulosus recombinant antigen (EG95) offers encouraging prospects for prevention and control. Small-scale EG95 vaccine trials in sheep indicate high efficacy and safety with vaccinated lambs not becoming infected with E. granulosus.
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Hymenolepis nana
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TOPICS CLASSIFICATION EPIDEMIOLOGY TRANSMISSION MORPHOLOGY LIFE CYCLE
MODES OF INFECTION CLINICAL SYNDROMES DIAGNOSIS TREATMENT PREVENTION MCQ’S
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CLASSIFICATION Kingdom: Animalia Phylum: Platyhelminthes
Class: Cestoda Order: Cyclophyllidea Family: Hymenolepididae Genus: Hymenolepis Species: Hymenolepis nana
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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.
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TRANSMISSION : Ingestion of eggs from contaminated hands .
Ingestion of infected rat fleas ,beetles as they contain cysticercoid in their haemocele.
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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
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ADULT WORM
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SCOLEX Shows a knob like rostellum Bears a ring of hooklets.
They possess 4 suckers.
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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 eggs. There are 3 round testis and bilobed coaresly granular ova that lie in the posterior part of each proglottid.
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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 The mnemonic for non bile stained eggs is "A HEN" laid non bile stained eggs Ankylostoma duodenale Hymenolepsis nana Enterobius vermicularis Necator Americans
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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.
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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.
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CLINICAL SYNDROMES Asymptomatic H.nana causes HYMENOLEPIASIS/ HYMENOLIPIDOSIS. Heavy infections : abdominal discomfort diarrhoea anorexia pruritis Hyper infection : autoinfection in immuno compromised pts. With heavy worm burden
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DIAGNOSIS Adult worm or proglottids are rarely seen in stools.
Demonstration of typical eggs with 6 hooked embryo & polar filaments.
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Egg of H. nana Egg of H. diminuta
Eggs of Hymenolepis nana. These eggs are oval and smaller than those of H. diminuta, with a size range of 30 to 50 µm. On the inner membrane are two poles, from which 4-8 polar filaments spread out between the two membranes. The oncosphere has six hooks. Eggs of Hymenolepis diminuta. These eggs are round or slightly oval, size 70 – 85 µm X 60 – 80 µm, with a striated outer membrane and a thin inner membrane. The space between the membranes is smooth or faintly granular. The oncosphere has six hooks. There are no polar filaments extending into the space between the oncosphere and the outer shell. Egg of H. nana Egg of H. diminuta
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TREATMENT DRUG OF CHOICE : PRAZIQUANTEL
single dose of 25mg/kg. body weight. ALTERNATIVE : Niclosamide Nitazoxanide
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PREVENTION & CONTROL Improved sanitation & proper disposal.
Personal hygeine. Control of arthropod vectors
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Thank you!
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