Liver and biliary tree parasites (69)


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Liver and biliary tree parasites (69)

  2. 2. CESTOIDEAOrder: CyclophyllideaEchinococcus granulosusEchinococcus multilocularisEchinococcus vogeli
  4. 4. Echinococcus granulosus infection has a world-wide distribution with a higher prevalence inSouth-America (Argentina, Uruguay), Europe(mediterranean bassin), Northern Africa, MiddleEast, South-Central and East Asia.
  5. 5. Echinococcus granulosus: hydatidosis is caused bythe larval stage of E.granulosus.After ingestion of eggs the onchospheres penetratethe intestinal mucosa and reach host organs(mainly liver and lung) where they encyst within aweek reaching 1 cm in diameter in about 5 months.
  6. 6. Echinococcus granulosus: the cysts (2 to 30 cm)are constituted by an external acellular cuticuleand an inner cellular "germinal" layer (10-25 µ)that produces the brood capsules containing 6-12protoscolices or single protoscolices. (Germinallayer with a protoscolex).
  7. 7. Echinococcus granulosus: the larvae (scolices)develop from the germinal layer.The protoscolices are at first evaginated andmeasure 120-220 by 70-120 µ.
  8. 8. Echinococcus granulosus: the mature rotoscoliceshave 4 suckers and a rostellum with hooklets andcan be observed in the hydatid fluid.
  9. 9. Echinococcus granulosus: detail of the rostellum.
  10. 10. Echinococcus granulosus: the protoscolices thenbecome invaginated and measure 90-140 by 70-120µm.They can transform into daughter cysts.These cysts can proliferate both internally andexternally giving exogenous cysts.Spontaneous orsurgical rupture of the cyst can originate asecondary hydatidosis.
  11. 11. Echinococcus granulosus: the liver is the mostcommon site of development of cysts (50-75%).Lesions can be detected by CT scan orechography;a septate structure is a characteristicof active cysts.Treatment is based on surgical and/or medicaltherapy (albendazole)
  12. 12. Echinococcus granulosus: definitive diagnosis isobtained by means of serologic tests (EIA, IHA,CIEP/Western Blot);the last two are confirmatorytests and are useful for the follow-up of treatedpatients.-Detail of liver lesion, CT-scan with septa.-Western blot analysis: both Ag5 (55 and 65 Kd)and AgB (8, 16, 24 Kd) bands are present.
  13. 13. Echinococcus granulosus: pulmonary infection isobserved in about 20-30% of patients.Roentgenografic examination shows round masslesions and CT scan demonstrates the fluidcontent of the lesion.Serology has a lower sensitivity in extrahepatichydatidosis.
  14. 14. Echinococcus granulosus: any other organ can beaffected:nervous system, heart, bones, spleeneyes, muscles are the most common sites.Multiple involvement is frequent.Symptoms andsigns depend on the size,the site and the pressureof the cyst on host structures.-CT scan of a spleen cyst.-MRI scans of a muscular cyst.
  15. 15. Echinococcus granulosus: medullary hydatidosisis a severe form of the infection.In this case themechanical pressure of host tissues causedparaplegia.The surgical treatment allowedresolution of symptoms.The infection relapsedand responded partially to medical treatment.
  16. 16. Echinococcus granulosus: MRI imaging candemonstrate the relationship between the cystand the medulla on the longitudinal axis.The serology is often negative in infections in sitesother than liver or lung.(Medullary hydatidosis)
  17. 17. ECHINOCOCCUS MULTILOCULARIS( 1 ) E.multilocularis is a small tapeworm (1,2-4,5 mm inlenght)that parasites red and arctic foxes (dogs and cats arethe definitive hosts).Definitive hosts are always carnivores.( 2 ) In the definitive hosts the adult tapeworm, consisting of 2to 6 proglottids, lives attached to the luminal surface of thesmall intestine.The terminal proglottid contains mature eggs(ovoid, 30-40 µm in diameter).( 3 ) The embryonated eggs, the infectious stage, are long-livedand highly resistant to high and low temperature (more than50° C and down to -40° C).The mature eggs are shed with faecesand are spread in the environment.It is assumed that theintermediate host acquires the infections through the ingestionof contaminated fruits and vegetables.( 4 ) When the intermediate hosts (predominantly rodentsor other small mammals, or, accidentaly, humans) ingesteggs,the onchosphere hatches from the egg in the duodenum.( 5 ) The activated oncosphere penetrates the small intestine,enters blood vessels and reaches primarly the liver via the portalvein;In the liver the oncosphere proliferates into themetacestode surrounded by an inner germinative membrane andan outer laminated layer.( 6 ) The lifecycle is completed when an intermediate host,carrier of viable protoscolices within the cysts, is devoured by adefinite host.
  18. 18. Geographical distributionHuman AE is prevalent in North America (Alaskaand northern Canada), in Europe (France,Switzerland, Austria and Germany),in Asia (fromthe White Sea to the Behring strait in the north andfrom Turkey, through Afghanistan, Iran, India,China, Mongolia to north Japan in the south).The annual incidence of human disease varies from28 cases/100.000 inhabitants in Western Alaska(St. Lawrence Island included),to 0.18-4,4/100.000in Central Europe.
  19. 19. The diseaseThe liver is the organ primarily affected;metastasesare mainly observed in cases of advanced diseaseand may affect almost any organ.The disease either spreads via direct contact or viablood vessels.Secondary AE mostly affects the brain,the lungs, soft tissue, the spine and other bonystructures.The disease is primarily characterized byan expansive and infiltrative growth in the liver.Clinical features may be absent for many yearsand mostly become apparent in advanced disease.They may include hepatomegaly, jaundice,abdominal pain, weight loss,fever andmanifestations of secondarily affected organs.
  20. 20. DiagnosisFor diagnosing AE the clinician mainly relies onmorphological criteria together with serology andepidemiological aspects.On ultrasound a typical lesion demarcates asa heterogeneous hypoechoic lesion with irregularlyshaped margin and often contains focal areas ofcalcification ( 50% of cases). The appearance onultrasound is highly variable between cases as canbe appreciated on the images above.It is the idealmethod for screening purposes and short-termfollow-up.
  21. 21. Computedtomography (CT) andmagnetic-resonance-imaging (MRI)areused for furthercharacterization ofthe lesion.They areindispensable for theevaluation ofextrahepaticaffection in AE andthey are used for apreoperativeevaluation.CT bestdepicts the typicalcalcifications and it isused for follow-upexaminations atlonger intervalls. Forserology an ELISAwas establishedbased on the purifiedE.multiloculariscarbohydrate antigenEm2 (derived fromthe laminated layer).It is the referencetest for diagnosis andit may allowdiscrimination of AEfrom E.granulosusinfection.However, ina significantpercentage of casesthe two species cannot be differentiatedsimply by serologicalmeans.
  22. 22. TreatmentThe only curative treatment for AE to dateis total surgical resection combined withchemotherapy. Drugs used for the treatmentof AE are benzimidazoles (mebendazole50mg/KG and albendazole 10-15mg/KG).Chemotherapy is mainly parasitostatic andmay therefore not be considered curative.In inoperable or incompletely resected caseschemotherapy has to be administered forextended periods of time and often results inlife-long treatment.
  23. 23. ECHINOCOCCUS VOGELIEchinococcus vogeli: E.vogeli is the agent of thepolycystic hydatidosis.The larval stage proliferatesexternally from the germinal layer and forms septawithin the cyst generating microcysts.Endemic inCentral and South America.(Cysts, macro)
  24. 24. Echinococcus vogeli: protoscolices similar to thatof E.granulosus are present in the cysts fluid.
  25. 25. TREMATODAOrder: Strigeata-Schistosoma japonicum-Schistosoma mansoni
  27. 27. Schistosoma spp.: cercarae are the infective forms.They measure about 500 micron. After encounteringthe skin,the cercariae penetrate and lose the tailtransforming into schistosomulae.
  28. 28. S.japonicun: geographic distribution.S.japonicum occurs in Southeast Asia and westernPacific countries(including China, the Philipinesand Indonesia).S.mekongi has been reported fromCambodia and Laos.
  29. 29. S.japonicum: adult schistosomes live in pairsin the portal system and in mesenteric venules;adults of S.japonicum are bigger than adults ofS.mansoni.Males are 12-20 mm in lenght and 0,5wide,and have a ventral infolding from the ventralsucker to the posterior end forming thegynecophoric canal.Adult male with female in thecopulatory groove.Females are slender ( 0,3 mm in diameter)and longer (up to 26 mm in length),and are heldin the gynecophoric canal during copulation.Eachfemale may lay up to 2.000-3.000 eggs per day.
  30. 30. S.japonicum egg: eggs measure 70-90 my 55-60µm in diameter,are oval to round in shape withsubterminal spine.(Formol-ether concentration).
  31. 31. S.japonicum egg: eggs are usually round and havea small spine or no spine.Other small knobby-spined or not spined schistosomes that affecthumans are S.mekongi and S.malaysiensis.
  32. 32. S.japonicum: intermediate host of S.japonicum aresnails of the genus Onchomelania, hupensis spp.
  34. 34. Schistosoma spp.: cercarae are the infective forms.They measure about 500 micron. After encounteringthe skin,the cercariae penetrate and lose the tailtransforming into schistosomulae. Cercaria of Schistosoma mansoni from snail.
  35. 35. S.mansoni: intermediate host of S. mansoniare snails of the genus Biomphalaria.
  36. 36. S.mansoni: geographical distribution.S.mansoni isendemic in 43 countries in Africa and occurs inthe americas in Brazil,Suriname, Venezuela andin the Caribbean.
  37. 37. S.mansoni: adult schistosomes live in pairs in theportal system and in the mesenteric venules;malesare shorter (7-12 mm in lenght and 2 mm wide)andhave a ventral infolding from the ventral suckerto the posterior end forming the gynecophoriccanal.Adult male with female in the copulatory groove.
  38. 38. Adult male and female of S.mansoni.
  39. 39. S.mansoni : Females are slender (1 mm indiameter)and longer (9-17 mm in length),and areheld in the ginecophoric canal during copulation.Each female lays about 300 eggs per day.Adult male with female in the copulatory groove.Adult of S.mansoni in mesenteric veins of hamster.
  40. 40. S.mansoni egg: S.mansoni eggs measure 110-175by 45-70 µm;the colour is yellow, with a thintransparent shell and a strong lateral spine.Freshexamination of intestinal biopsy with one egg inthe mucosa.
  41. 41. S.mansoni egg: viable eggs contain the motilelarva, the miracidium.After breaking the shell theciliated miracidium moves in the water andreaches the mollusca.Fresh examination.
  42. 42. S.mansoni egg: egg with typical spine in stools(formol-ether concentration). Demonstration ofeggs in faeces and urine is the standard methodof diagnosis of schistosomiasis.Sensitivity of onestool examination does not exceed 60%.
  43. 43. S.mansoni egg: lateral spine at higher magnification.Other diagnostic methods include intestinal or liverbiopsy.Serology is useful in travellers from endemicareas before shedding of eggs or in extraintestinalforms (spinal) but not in natives.
  44. 44. S.mansoni: hepatosplenic schistosomiasis occursin S.mansoni and S.japonicum infections; itresults by eggs embolization in hepatic venuleswith formation of granulomas and portal fibrosis.Epatosplenomegaly, bleeding oesophageal varicesand hepatic insufficiency are the more severemanifestations. Praziquantel is the drug of choice.Liver biopsy: egg surrounded by granuloma andfibrosis of portal space.
  45. 45. Polyposis due to S.mansoni infection.Egyptian with Brazilian with portalsplenomegaly due to hypertension andinfection with ascites due toS.mansoni. S.mansoni.
  46. 46. S.mansoni: different schistosome stages are usedas antigen source(cercariae, schistosomula,adults, eggs) for standard immunodiagnostictests:enzyme linked immunosorbent assay(ELISA), indirect immunofluorescence test(IFAT), radioimmunoassay (RIA), indirecthaemoagglutination (IHA), circumovale precipitinassay.Serological tests may be useful fortravellers returning from endemic areas and inpatients with light or ectopic infection, with nodetectable eggs in the faeces,urine or intestinalbiopsies (i.e. hepatic, CNS infections).On thecontrary, in patients living in endemic areas, thepositive test may reflect previous exposure to theagent rather than an active infection;a slowdecrease in titer after effective treatment isusually observed.Recently, new tests for thedetection of schistosome antigens have beenprepared using monoclonal antibodies.The larvalstage of S.mansoni used as antigen in theindirect fluorescence test.
  47. 47. TREMATODAOrder: Echinostomata-FASCIOLA HEPATICA
  48. 48. FASCIOLA HEPATICAF.hepatica infection is found in rural areas oftemperate and tropical regions, related to cattleherding.High prevalence is described in Europeand Latin America.
  49. 49. F.hepatica, adult worm, macroscopic examination: adults measure 2-5 cm by 8-13 mm, are flat, oval in shape with a cephalic cone containing the oral sucker.The adults live in biliary ducts for up to 10 years.Fasciola hepatica, living adult in bile duct of sheep.
  50. 50. F.hepatica, adult worm, macroscopic examination:higher magnification: particular of the cephaliccone with the oral sucker.
  51. 51. F.hepatica, adult worm, liver biopsy: afterexcistation in the small intestine, metacercariaepenetrate the intestinal wall and the Glissoncapsule, cross the liver parenchima to the bileducts.Eggs can be found in faeces 3-4 monthsafter penetration.
  52. 52. F.hepatica, adult worm: the diagnosis is confirmedby the presence of eggs in faeces.Repeatedexaminations and concentration techniques arerecommended.Serology is useful when the clinicalpicture is compatible and eggs are not found.
  53. 53. F.hepatica, egg: eggs measure 140 by 80 µm andare operculated. The colour is yellow to brown.(Formol-ether concentration).
  54. 54. F.hepatica, egg: the opercular end is more visible athigher magnification;sometimes it can present ashell irregularity. F.hepatica, egg: the open operculum at higher magnification.F.hepatica, egg: the operculum can be open.Eggsare unembrionated and contain a granularmaterial.
  55. 55. Fasciola hepatica: although direct diagnosis byobservation of eggs in faecal smears it thereference method, indirect diagnostic tests such asIF may allow diagnosis when direct observation isnegative.Immunodiagnosis by indirect mmunofluorescence.Antigen: frozen sections of Fasciola hepatica.
  56. 56. TREMATODA Order:Opisthorchiata-Clonorchis sinensis / Opisthorchis viverrini-Opisthorchis felineus
  58. 58. Clonorchis sinensis/Opisthorchis viverrini:geographic distribution.
  59. 59. Clonorchis sinensis, liver biopsy:Clonorchis sinensis adults are 10-25 mm by 3-5mm,O.viverrini is 5,4-10 by 0,8-1,9 mm.The adultslive in the distal bile ducts and may survive for30-40 years, causing irritation to biliary cells andinflammation. Clonorchis sinensis adult.
  60. 60. Clonorchis sinensis, liver biopsy: most infectionsare asymptomatic.Clinical manifestations can beobserved in adults due to obstruction anddilatation of biliary ducts, cholangitis and insome cases cholangiocarcinoma.Cholangiocarcinoma caused by chronic infectionwith C.sinensis.
  61. 61. Clonorchis sinensis/ O.viverrini egg: eggs of thetwo species are similar.They measure 30-35 by12-20 µm, are operculated at one end and have asmall knob on the other end. The colour is yellow.
  62. 62. OPISTHORCHIS FELINEUSOpisthorchis felineus: an estimated 17 million ofpeople on our planet are infected with fishborneOpisthorchiidae trematode infections:Opisthorchis felineus, O.viverrini, Clonorchissinensis [1].Despite being preventable fishbornetrematode infection Opisthorchis felineus iswidespread in the Russia.Opisthorchis felineus: adult fluke
  63. 63. Opisthorchis felineus was first found in 1884in cat liver in the Northern Italy by Rivolta andin 1891 in man in Siberia by the Russianscientist K.N.Vinogradov who named it“Siberian liver fluke”Opisthorchis felineus: adult fluke, detail
  64. 64. Opisthorchis felineus (Rivolta, 1884) is the mostprevalent food-borne liver-fluke infection of manin the Russia, Ukraine and Kazahstan.Estimated number of persons infected withO.felineus in Russia is about 1,500,000 [2].Opisthorchis felineus: adult fluke, detail
  65. 65. Opisthorchis felineus: opisthorchiasis is mostprevalent in Western Siberian region in the Ob andIrtish river valleys where the prevalence amongstlocal natives (Hanti, Mansi, Nensi - Mongoloidrace)in some settlements of this region reaches100% and up to 80 amongst nonaborigeneindigenous population [3,4].In the EuropeanRussia the endemic area is located betweenVolga and Kama rivers and in some other regionswhere prevalence of this infection varies fromsporadic cases to 10% [2].Opisthorchis felineus: adult fluke, detail
  66. 66. Opisthorchis felineus: first intermediate hosts arefreshwater snails - Bithyniidae; secondintermediate hosts are freshwater fish -Cyprinidae.In Russia the most important second intermediatehosts are Leuciscus idus L., Leuciscus leuciscus L.and Rutilus rutilus L..Main second intermediatehosts from Ob and Irtish river valleys:Leuciscus idus L. (in the middle); Leuciscusleuciscus L.(at the bottom)and Rutilus rutilus L. (at the top).
  67. 67. Opisthorchis felineus: final hosts are dogs, cats andother fish-eating mammals.People in Siberia and someEuropean regions acquire infection by consumption ofraw, slightly salted and frozen fish (a locally so-called“stroganina”)because of it natural availability andbecause freezing is the most easy and cheap method ofpreserving fish in the North [3].Metacercaria in muscletissue of Leuciscus idus;compression between twoslides.(o.s.- oral suker; v.s.- ventral suker; e.v. - excretoryvisicle).
  68. 68. Opisthorchis felineus: pathological manifestationsof initial phase of O.felineus infection are multipleand vary in both quality and intensity from non-apparent form and acute cases with clinicalmanifestations.The major pathology in O.felineusinfection is chronic inflammation of the bile ducts.Opisthorchis felineus. Metacercarias in culture(artificial digestion procedure).
  69. 69. Opisthorchis felineus: opisthorchiasis varies in severity fromasymptomatic infection to severe illness with appreciablemorbidity and mortality.In heavily infected patients recurrentpyogenic cholangitis, liver abscesses,cholecystitis,pancreatitis, biliary stones may occur.The absence ofpathognomic clinical manifestations and confounding ofdiagnosis with other prevalent diseases lead to under-reporting [3,5].Opisthorchiasis is linked to holangiocarcinoma,but the pathogenesis is still unclear and liver cancer is one ofmost common malignancies that occurs in endemic areas [1].The outcome in patients with opisthorchiasis is dependent onearly treatment and hence the early detection of infection isimportant.Opisthorchiasis parasitological techniques:- stool and duodenal fluid surveys ,examination of suspected fish- artificial digestion procedure ,tissue compression betweentwo slides .Praziquantel is the drug of choice for treatment ofopisthorchiasis and clonorchiasis.Opisthorchis felineus eggs(at x 400 magnification) in duodenal fluid on the transparentpolycarbonate Nucleopore membrane (arrow indicates a filterpore (8 mm) )Duodenal fluid was obtained by duodenal aspiration.