logging in or signing up Cysticercosis and Hydatid disease rka10 Download Post to : URL : Related Presentations : Let's Connect Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 596 Category: Entertainment License: All Rights Reserved Like it (0) Dislike it (0) Added: September 05, 2011 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Cysticercosis & Hydatid Disease: Cysticercosis & Hydatid DiseaseCysticercosis: Cysticercosis Caused by pork tape worm T. Solium – Human – definitive host Pigs – Intermediate Host Infection with adult tape worm – Taeniasis Solium Infection with larval form in tissues - CysticercosisCysticercosis: Cysticercosis T. Solium exists world wide but most prevalent in Latin America, Sub Saharan Africa, South East Asia, Eastern Europe Cysticercosis occurs in industrialised nations as a result of immigration of infected persons from endemic areasAetiology, Pathogenesis: Aetiology, Pathogenesis Adult tape worm lives in upper jejunum About 1000 proglottids and produces upto 50000 eggs Groups of 3 to 5 proglottids released in faeces Eggs are infective to humans and animals Survive in environment for several monthsAetiology, Pathogenesis: Aetiology, Pathogenesis After ingestion by intermediate host, larvae are activated, penetrate the intestinal wall, carried to many tissues with a prediliction for striated muscle of neck, trunk, tongue Within 60 to 90 days, encysted larval stage developsAetiology, Pathogenesis: Aetiology, Pathogenesis Humans acquire intestinal tapeworm by ingestion of undercooked pork containing cysticerci Human cysticercosis caused by ingestion of Taenia Solium eggs from contact with a tape worm carrier. Auto infection can also occurClinical Manifestations: Clinical Manifestations Intestinal infections may be asymptomatic. Rarely epigastric discomfort, nausea, sensation of hunger, weight loss and diarrhoea. Fecal passage of proglottids may be noted In Cysticercosis, cysticerci can be detected anywhere in the body – commonly in the brain, skeletal muscle, subcutaneous tissue or eyeClinical manifestations: Clinical manifestations Clinical presentation depends on the number and location of cysticerci and extent of inflammatory response or scarring Neurological manifestations are the most commonNeurological manifestations: Neurological manifestations Seizures – generalised, focal or Jacksonian Hydrocephalus by obstruction flow of CSF by cysticerci and accompanying inflammation or arachnoiditis Signs of raised ICT, headache, vomiting, changes in urine, dizziness, ataxia or confusion Papilloedema or altered mental status Chronic meningitis or arachnoiditis , communicating hydrocephalus, or strokes. Cysticerci develop at the base of brain or subarachnoid spaceDiagnosis: Diagnosis T. solium infection by detection of eggs or proglottides Cysticercosis diagnosis difficult Consensus Conference Criteria Absolute Major Minor EpidemiologicDiagnosis: Diagnosis Absolute criteria Definite demonstration of parasite By histologic observation of parasite in excised tissue Fundus examination showing parasite in eye (Anterior chamber, vitreous, or subretinal space)Diagnosis: Diagnosis Neuro Imaging Cystic lesions with scolex In most cases, a clinical diagnosis is made on the basis of clinical presentation, radiographic studies, serology and exposure historyDiagnosis: Diagnosis Major diagnostic criteria – Neuro Imaging Cystic lesions with or without enhancement (ring enhancement) One or more nodular calcification Focal enhancing lesions Cysticerci in the brain parenchyma are 5 to 20 mm and rounded Cystic lesions in the subarachnoid space or may be upto 6 cm diameter and may be lobulatedDiagnosis: Diagnosis Major diagnostic criteria – Neuro Imaging In the subarachnoid space, walls may be thin. Fluid may be isodense with CSF Enhancement of basilar meninges in CT CT more sensitive than MRI in identifying calcific lesion MRI better in identifying cystic lesions and enhancementDiagnosis: Diagnosis Major diagnostic criteria Detection of specific antibodies to cysticerci Resolution of intracranial cystic lesions spontaneously or after therapy with Albendazole or PraziquantelDiagnosis: Diagnosis Minor diagnostic criteria Lesions compatible with neurocysticercosis on imaging Clinical manifestations suggestive of Neurocysticercosis Demonstration of antibodies to cysticerci or cysticercal antigen in CSF by ELISA Evidence of cysticercosis outside CNSDiagnosis: Diagnosis Epidemiological criteria Residence in an endemic area Frequent travel to an endemic area Household contact with an individual infected with T. soliumDiagnosis: Diagnosis Confirmed by 1 absolute criteria OR 2 major criteria + 1 minor + 1 epidemiologic criteriaDiagnosis: Diagnosis Probable 1 major + 2 minor criteria 1 major + 1 minor + 1 epidemiologic criteria 3 minor + 1 epidemiological criteria CSF – Pleocytosis with predominant lymphocytes, neutrophils or eosinophils. Protein may be elevated Glucose normal or lessTreatment: Treatment Intestinal T. Solium infection is treated with a single dose of Praziquantel (10 mg / Kg) Praziquantel can evoke inflammatory response in CNS if concomitant cryptic cysticercosis is present Niclosamide (2 gm) is also effectiveTreatment - Neurocysticercosis: Treatment - Neurocysticercosis Treatment of seizures Treatment of HydrocephalusTreatment of Seizures: Treatment of Seizures Antiepileptics – If parenchymal lesions heal without calcification. If no seizure, AED may be stopped after 2 yearsAntiparasitic drugs: Antiparasitic drugs Praziquantel 50 to 60 mg/Kg daily in 3 divided doses for 15 days or 100 mg / Kg in three doses over a single day or Albendazole 15 mg / Kg / day for 8 to 28 days Inflammatory response due to dying parasite may exacerbate hydrocephalus or seizures High dose glucocorticoids can be used if symptoms worsen Glucocorticoids increase first pass metabolism of Praziquantel . It may decrease its antiparasite effect, co-administer CimetidineTreatment of Hydrocephalus: Treatment of Hydrocephalus In hydrocephalus, reduction of intracranial pressure is the mainstay of therapy In Obstructive hydrocephalus, removal of cysticercosis via endoscopic surgery Diverting procedure - ventriculoperitoneal shunting Open craniotomy for cysticerci removal rarely required Cerebral oedema and raised ICT, glucocorticoids with avoidance of antiparasite drugs Ocular and spinal medullary lesions, drug induced inflammation can cause irreversible damagePrevention: Prevention Measures to prevent intestinal Taenia Solium infection Application of precaution to pork processing Good personal hygiene Effective faecal disposal Treatment and prevention of human intestinal infectionHydatid Cyst: Hydatid CystHydatid Cyst: Hydatid Cyst Echinococcosis – Infection caused by larval stage of E. Granulosus, E. Mutulocularis, E. Vogeli E. Granulosus produces unilocular cystic lesions prevalent where livestock are raised with dogs Tapeworm species found in Australia, Argentina, Chile, africa, E. Europe, Middle East, NewZealand, mediterranean regions E. Vogeli causes polycystic hydatid disease seen in Central South America Definitive host – Dogs – eggs in faeces Intermediate Host – Cysts – Sheep, Goat, Human, Camels, HorsesEtiology: Etiology E. Granulosus worm (5 mm long) lives in jejunum of dogs has 3 proglottids – immature, mature, gravid Humans ingest the eggs, embryo escapes, penetrate the intestinal mucosa, enter portal circulation Carried to various organs, liver and lungs Larvae develop into fluid filled unilocular hydatid cyst with external membrane and an inner germinal layer Daughter cysts develop from the inner germinal layer Germinating cystic structure called brood capsules New larvae protoscolices develop in the brood cysts expand slowly over many years. E. Multilocularis – multilocular cysts with invasion of host tissueClinical Manifestation: Clinical Manifestation Asymptomatic generally Expanding size / space occupying effect in an organ elicit symptoms Liver and Lung – common organ affected Liver involved in 2/3 of E. Granulosus and all E. Multilocularis organ Cysts incidentally detected on X-Ray or UltrasoundClinical Manifestations: Clinical Manifestations Hepatic echinococcosis – abdominal pain or a palpable mass in RUQ Compression of bile duct or leakage of cyst fluid into biliary tree mimics recurrent cholelithiasis Biliary obstruction can result in jaundiceClinical Manifestations: Clinical Manifestations Rupture / leakage from cyst – fever, pruritis, urticaria, eosinophilia or anaphylaxis Pulmonary hydatid cyst rupture into bronchial tree or peritoneal cavity produce cough, chest pain or hemoptysis Rupture may lead to multifocal dissemination of protoscolices which can form additional cystsClinical Manifestations: Clinical Manifestations Rupture can occur spontaneously or at surgery Involvement of bone – Invasion of medullary cavity with slow bone erosion producing pathological fracture CNS – Space occupying lesions Heart – conduction defects, Pericarditis Pelvis – Pelvic massClinical Manifestations: Clinical Manifestations E. Multilocularis larval forms present as slow growing hepatic tumour Progressive destruction of liver Extension of vital structures Upper quadrant and Epigastric pain Obstructive jaundice Infiltration of adjoining structures, Diaphragms, Lungs, Kidney, Metastasis to spleen, lungs or brainDiagnosis: Diagnosis Plain films – Pulmonary cysts rounded mass of uniform density. Cyst wall calcification – Liver MRI, CT, USG – well defined cysts with thick / thin walls Older cysts – Hydatid sand rich in accumulated scolices Pathognomonic finding Daughter cysts within larger cyst. Egg shell / mural calcification on CT indicative of E. Granulosus infection distinguishes cyst from Carcinoma, Bacterial or Amoebic liver abscess, HemangiomaDiagnosis: Diagnosis Specific diagnosis of E. Granulosus by examiantion of aspirated fluids for protoscolices or hooklets Diagnostic aspiration not recommended as risk of dissemination Serodiagnostic assay Cysts in liver +ve in 90% Lungs – 50% are seronegative Antibodies to echinococcal antigen by immunoblotting has the highest degree of specificityTreatment: Treatment Based on Size Location Manifestations of cysts Overall health of patientTreatment: Treatment Surgery - Principal definitive method of treatment USG staging for E. granulosis For uncomplicated CE 1 lesions and for some CE2 and CE3 lesions – PAIR (Percutaneous Aspiration, Infusion of Scolicidal agents and Re-aspiration)Treatment: Treatment PAIR is contraindicated for Superficially located cysts Cysts with multiple thick internal divisions Cysts communicating with biliary treeProphylaxis: Prophylaxis Secondary Peritoneal Echinococcosis due to spillage during PAIR Albendazole 15 mg / Kg daily x 2 divided doses (4 days before till 4 weeks after procedure)Surgery: Surgery Pericystectomy – Removal of entire cyst and fibrous tissue Medical therapy Albendazole alone for 12 weeks to 6 months Cure 30% of cases Improvement in 50% Subsequently PAIR or additional courses of medical therapyTreatment: Treatment Surgical resection for Echinococcus – Multilocularis Ongoing Albendazole for 2 years after surgeryPrevention: Prevention Endemic areas Praziquantel to infected dogs Denying dogs – access to infected animals Vaccinating sheep Limiting stray dogs You do not have the permission to view this presentation. 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