3. Taenia solium Life cycleCysticercosis exists world-wide but is prevalent inMexico, Africa, South-Est Asia and South-America.
4. Taenia solium (cysticercosis): thecysticercus appears as a white opalescentvescicle,ovoid to round, measuring 8-15 mm by 5-8containing only one protoscolex.Many organs may be infected(subcutaneous tissue, brain, eye, muscles).
5. T.solium: cysticercus cellulosae with invaginated scolexT.solium: cysticercus cellulosae with evaginated scolex
6. Cysticercosis: nervous cysticercosis is the mostsevere manifestation of the disease.MRI showing an occipital lesion. Diagnosis ofcysticercosis,suspected on a clinical-radiological basis, isconfirmed by serology.
7. Cysticercosis: the onchospheres migrate to thetissues and develop to cysticerci.The cysticercus dies and becomes calcified. Calcifiedcysticerci in muscle.Localization in muscles depends on the geographicalorigin(unfrequent in american patients).
8. NEMATODAOrder: Trichurata
9. TRICHINELLA SPIRALIS
10. Development of Trichinella spiralis in skeletal muscles Migrated larvaeEncapsulatedlarvae Calcified larvae
11. Trichinella spiralis: Trichinella spiralislarvae encysted in striated muscle.The cyst, elongated in shape, measures 0.3-0.6by 0.2-0.3 mm.(H&E stain).
12. Trichinella spiralis: the cyst is formed outside by afibrous capsule and inside by an eosinophilinfiltration around the tightly coiled larvae.(H&E stain).
13. Trichinella spiralis: massive infection may causeacute enteritis; the migration and the latermuscle encystation of larvae may beasymptomatic or cause serious generalizeddisease with possible miocardial and brainpathology.(T.s. larvae).
14. Trichinella spiralis: after muscle digestion theT.spiralis larva measures 1 mm in lenght.(Fresh examination after muscle digestion).
15. Trichinella spiralis: Electron microscopy
16. ZOOMASTIGOPHOREA Order: Kinetoplastida
17. TRYPANOSOMA CRUZI (Chagas disease)T. cruzi: american trypanosomiasis was firstdescribed by Carlos Chagas in Brasil in 1909.The infection, Chagas disease, is causedby the haemoflagellate Trypanosoma cruzi.tc1: T.cruzi in blood sample, Giemsa.
18. T. cruzi: the disease is a public health threat inmost Latin American countries,although cases dueto blood derivatives or blood transfusion has beenreported in non-endemic regions.According to WHO the overall prevalence of humanT.cruzi infection is estimated in 18 million casesand 100 million people are living at risk.tc2: T. cruzi: geographical distribution.
19. T. cruzi: the vectors are reduvidae bugs which arehaematophagus and the most important areTriatoma infestans(Argentina, Chile, Brazil, Bolivia,Paraguay, Uruguay, Peru),T. sordida (Argentina,Bolivia, Brazil, Paraguay),Rhodnius prolixus(Colombia, Venezuela, Mexico, Central America),T. dimidiata (Ecuador, Mexico, Central America),and Panstrogylus megistus (northeast Brazil).
20. T. cruzi: the transmission by the vector is faecal.T.cruzi infective metacyclic trypomastigotes are shedin the faeces of the bug and are inoculated into thehuman host by scratching infected faeces into skinabrasions usually caused by the bug in the process offeeding (blood-sucking). T.cruzi metacyclic trypomastigote: scanning electronmicroscopy showing T.cruzi trypomastigotesrecovered from an infected Triatoma spp. in PedroCarbo, Ecuador.
21. T. cruzi: infective metacyclic trypomastigotes areshed in the faeces of the bug and inoculated intothe vertebrate host not only by skin lesions but alsothrough the mucosa of the mouth and,in humans,through the conjunctiva of the eyes.
22. T. cruzi: trypomastigotes can infect most of thevertebrate cells,polymorphonuclear leucocytes andmacrophages are probably among the firstvertebrate host cells with which T.cruzi interacts invivo.tc7a: In vitro T.cruzi infection of macrophagesshowing the presence of amastigotes:Wright-Giemsa stain, showing replicating T.cruziamastigotes within host cell.
23. T. cruzi: this invasive step is crucial for the lifecycle of the parasite since it has to becomeintracellular to multiply.tc7b: In vitro T.cruzi infection of macrophagesshowing the presence of amastigotes:immunofluorescence assay showing T.cruziamastigotes after treatment with anti-T.cruzipolyclonal mouse sera.
24. T. cruzi: trypomastigotes in the host cell transforminto amastigotes,which multiply intracellularly bybinary division inducing inflammatory andimmunological responses in vivo, and destroy cellsin vitro.Amastigotes are then released into the bloodstream as trypomastigotes.The latter arenondividing forms which are able to infect a widerange of new host cells but muscle and glia seemmost often parasitized,or they have to be ingestedby another reduviid bug in order to continue theparasite life cycle in the invertebrate host.tc8: Trypomastigotes reach the myocardial cellsand after penetration they multiply as amastigoteswith formation of a pseudocyst.
25. T. cruzi: in the Reduvidae bug the bloodstreamderived trypomastigote forms pass along thedigestive tract through irreversible morphologicaltransformations in sequence;each developmentalstage occurs in a specific portion of the insects gut.Thus, in the stomach, most blood trypomastigoteschange into epimastigotes and rounded forms(sphaeromastigotes).tc9: T.cruzi epimastigote. Immunofluorescencestudies using antibodies to a T.cruzi protein namedTc52(immunosuppressive factor which also express athiol-transferase activity)and confocal microscopy.An intense labeling located at the posterior end ofan epimastigote indicate that Tc52 is targeted to thereservosomes(These organelles are small vesiclesinside multivesicular structures being formedpredominantly at the posterior end of epimastigotes).
26. T. cruzi: epimastigotes divide actively in thevectors intestine and reach the rectum wherea final differentiation results in the infectivemetacyclic trypomastigotes which areeliminated in the bugs faeces.tc10: T.cruzi epimastigote. Epimastigotereacting with a monoclonal antibody againstT.cruzi.
27. T. cruzi: some researchers have postulated thatsphaeromastigotes may change either into shortepimastigotes,dividing forms in the intestine, orinto long epimastigotes which are nondividingforms but are able to reach the rectum where theytransform into the final metacyclic trypomastigoteform.In any case, this hypothesis remainscontroversial.tc10b: T.cruzi epimastigote. Scanning electronmicroscopyshowing T.cruzi epimastigote.
28. T. cruzi: there are three phases of the infection.The acute phase usually passes unnoticed butthere may be an inflamed swelling or chagomaat the site of entry of the trypanosomes.Romanassign is when this swelling involves theeyelids but it occurs only in about 1-2% of thecases.In the acute phase, mortality is less than 5%and death may result from acute heart failureor meningoencephalitis in children less than twoyears old.Romana’s sign, clinical manifestationtipically observed in the acute phase of someChagas’ disease patients.
29. T. cruzi: general symptoms in acute Chagas diseasemay also include fever, hepatosplenomegaly,adenopathies and myocarditis.Electrocardiographicchanges involve sinus tachycardia, prolongationof the P-R interval, primary T-wave changes andlow QRS voltage.Chest X-ray can revealcardiomegaly of different degrees.The intermediate phase is clinically asymptomaticand is detected by the presence of specificantibodies.No parasites are found in bloostreamsmears but xenodiagnosis could be positive in somecases.Acute Chagas myocarditis (Haematoxylin and EosinX 160)tc12: Posteroanterior chest radiographshowing enlarged heart due to T.cruzi infection.tc12a: Acute Chagas disease myocarditis(Haematoxylin and Eosin X160)
30. T. cruzi: the chronic phase of Chagasdiseasedevelops 10 - 20 years after infection and affectsinternal organs such as the heart,oesophagus andcolon as well as the peripheral nervous system.The lesions of Chagas’ disease are incurable and insevere cases patients may die as result of heartfailure. T.cruzi parasitize mainly the cardiac muscle but any cell type may be parasitized (smooth muscle cells, hystiocytes): cardiac muscle with amastigotes, H&E stain.
31. Chagas disease megacardia(slide from the late Prof.Koberle, Brazil)
32. Apical aneurysm in Chagas disease(slide from the late Prof.Koberle, Brazil)
33. T. cruzi: on the other side, megacolon is associatedwith abnormal constipation (weeks).Faecalimpaction and sigmoid volvulus are side-effects ofmegacolon.Neurological changes in chronicChagas disease include changes at the level of thecentral, peripheral or autonomic nervous system. Chagasic megacolon with enlargement of the sigmoid;patient from Morona Santiago province, southeastern Ecuador
34. X-ray showing megaoesophagus in Chagas disease
35. X-ray showing megacolon in Chagas disease
36. T. cruzi: can be observed in the peripheral bloodonly in the acute case of the disease.Its presence isthe best definition of the acute phase as all othersigns are variable.-Wright-Giemsa staining of T.cruzi trypomastigotein peripheral blood smear from an acute infectedpatient.-T.cruzi in mouse blood (Giemsa stain)
37. T. cruzi: trypomastigotes have a prominentsubterminal kinetoplast that often distort themembrane of the cell,an elongated nucleus andan undulating membrane.-T.cruzi trypomastigote: blood streamtrypomastigotes are 15-20 µm in length andappear with a typical C or S-shaped form.
38. T. cruzi: multiplication only occurs in theamastigote phase,which grows in a variety of tissue cells especiallymuscle.-In vitro infected fibroblast showing a largenumber of intracellular amastigotes.
39. T. cruzi: laboratory diagnostic tests based onserology (IFA, ELISA) and Polymerase ChainReaction (PCR) specific for T.cruzi, have beendeveloped.-T.cruzi trypomastigotes reacting with monoclonalAb.
40. T. cruzi: serological cross-reactions can occurwith infections such as leprosy, leishmaniasis,treponematoses, malaria and multiple myeloma.Trypanosoma rangeli is also an important causeof false-positive testing, especially in areas whereT.cruzi coexists with T.rangeli.-In vitro T.cruzi infection of macrophagesshowing the presence of amastigotes:confocal microscopy showing T.cruzi amastigotesafter treatment with anti-Tc24 mouse sera.
41. T. cruzi: two drugs are in common use.Nifurtimox (Lampit, production was discontinued in1991)and Benznidazole (Rochagan).The latter which is now the drug of choice,is given in an oral dose of 6 mg/kg body weight for30 or 60 days.Both drugs produce anorexia, weightloss, headache and dizziness,gastric irritation, andsometimes peripheral neuritis.Experimental drugsare under evaluation.Treatment of patients in theintermediate or chronic phase is controversial.Congenital Chagasdisease and transfusion-associated acute disease require Rochagantherapy.Transfusion infection can be prevented bydonor screening or,by mixing the blood withgentian violet (0,25 gr./L for 24 hours) to killT.cruzi.Vector control programmes involvinginsecticide spraying with modern pyretroids andnew tools for delivery in endemic areas is beingcarried out in some Latin American countries.tc20: TEM microphotograph of T.cruziepimastigote.