Taenia solium L ife cycle Cysticercosis exists world-wide but is prevalent in Mexico, Africa, South-Est Asia and South-America.
Taenia solium (cysticercosis): the cysticercus appears as a white opalescent vescicle, ovoid to round, measuring 8-15 mm by 5-8 containing only one protoscolex. Many organs may be infected (subcutaneous tissue, brain, eye, muscles).
T.solium: cysticercus cellulosae with invaginated scolex T.solium: cysticercus cellulosae with evaginated scolex
Cysticercosis: nervous cysticercosis is the most severe manifestation of the disease. MRI showing an occipital lesion. Diagnosis of cysticercosis, suspected on a clinical-radiological basis, is confirmed by serology.
Cysticercosis: the onchospheres migrate to the tissues and develop to cysticerci. The cysticercus dies and becomes calcified. Calcified cysticerci in muscle. Localization in muscles depends on the geographical origin (unfrequent in american patients).
Development of Trichinella spiralis in skeletal muscles Migrated larvae Encapsulated larvae Calcified larvae
Trichinella spiralis : Trichinella spiralis larvae encysted in striated muscle. The cyst, elongated in shape, measures 0.3-0.6 by 0.2-0.3 mm. (H&E stain).
Trichinella spiralis: the cyst is formed outside by a fibrous capsule and inside by an eosinophil infiltration around the tightly coiled larvae. (H&E stain).
Trichinella spiralis: massive infection may cause acute enteritis; the migration and the later muscle encystation of larvae may be asymptomatic or cause serious generalized disease with possible miocardial and brain pathology. ( T.s. larvae).
Trichinella spiralis: after muscle digestion the T.spiralis larva measures 1 mm in lenght. (Fresh examination after muscle digestion).
TRYPANOSOMA CRUZI (Chagas' disease) T. cruzi: american trypanosomiasis was first described by Carlos Chagas in Brasil in 1909. The infection, Chagas' disease, is caused by the haemoflagellate Trypanosoma cruzi. tc1: T.cruzi in blood sample, Giemsa.
T. cruzi: the disease is a public health threat in most Latin American countries,although cases due to blood derivatives or blood transfusion has been reported in non-endemic regions. According to WHO the overall prevalence of human T.cruzi infection is estimated in 18 million cases and 100 million people are living at risk. tc2: T. cruzi: geographical distribution.
T. cruzi: the vectors are reduvidae bugs which are haematophagus and the most important are Triatoma 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).
T. cruzi: the transmission by the vector is faecal. T.cruzi infective metacyclic trypomastigotes are shed in the faeces of the bug and are inoculated into the human host by scratching infected faeces into skin abrasions usually caused by the bug in the process of feeding (blood-sucking). T.cruzi metacyclic trypomastigote: scanning electron microscopy showing T.cruzi trypomastigotes recovered from an infected Triatoma spp. in Pedro Carbo, Ecuador.
T. cruzi: infective metacyclic trypomastigotes are shed in the faeces of the bug and inoculated into the vertebrate host not only by skin lesions but also through the mucosa of the mouth and,in humans, through the conjunctiva of the eyes.
T. cruzi: trypomastigotes can infect most of the vertebrate cells,polymorphonuclear leucocytes and macrophages are probably among the first vertebrate host cells with which T.cruzi interacts in vivo. tc7a: In vitro T.cruzi infection of macrophages showing the presence of amastigotes: Wright-Giemsa stain, showing replicating T.cruzi amastigotes within host cell.
T. cruzi: this invasive step is crucial for the life cycle of the parasite since it has to become intracellular to multiply. tc7b: In vitro T.cruzi infection of macrophages showing the presence of amastigotes: immunofluorescence assay showing T.cruzi amastigotes after treatment with anti-T.cruzi polyclonal mouse sera.
T. cruzi: trypomastigotes in the host cell transform into amastigotes,which multiply intracellularly by binary division inducing inflammatory and immunological responses in vivo, and destroy cells in vitro. Amastigotes are then released into the blood stream as trypomastigotes.The latter are nondividing forms which are able to infect a wide range of new host cells but muscle and glia seem most often parasitized,or they have to be ingested by another reduviid bug in order to continue the parasite life cycle in the invertebrate host. tc8: Trypomastigotes reach the myocardial cells and after penetration they multiply as amastigotes with formation of a pseudocyst.
T. cruzi: in the Reduvidae bug the bloodstream derived trypomastigote forms pass along the digestive tract through irreversible morphological transformations in sequence;each developmental stage occurs in a specific portion of the insect's gut. Thus, in the stomach, most blood trypomastigotes change into epimastigotes and rounded forms (sphaeromastigotes). tc9: T.cruzi epimastigote. Immunofluorescence studies using antibodies to a T.cruzi protein named Tc52(immunosuppressive factor which also express a thiol-transferase activity)and confocal microscopy. An intense labeling located at the posterior end of an epimastigote indicate that Tc52 is targeted to the reservosomes(These organelles are small vesicles inside multivesicular structures being formed predominantly at the posterior end of epimastigotes).
T. cruzi: epimastigotes divide actively in the vector's intestine and reach the rectum where a final differentiation results in the infective metacyclic trypomastigotes which are eliminated in the bug's faeces. tc10: T.cruzi epimastigote. Epimastigote reacting with a monoclonal antibody against T.cruzi.
T. cruzi: some researchers have postulated that sphaeromastigotes may change either into short epimastigotes,dividing forms in the intestine, or into long epimastigotes which are nondividing forms but are able to reach the rectum where they transform into the final metacyclic trypomastigote form.In any case, this hypothesis remains controversial. tc10b: T.cruzi epimastigote. Scanning electron microscopyshowing T.cruzi epimastigote.
T. cruzi: there are three phases of the infection. The acute phase usually passes unnoticed but there may be an inflamed swelling or chagoma at the site of entry of the trypanosomes. Romanas'sign is when this swelling involves the eyelids but it occurs only in about 1-2% of the cases.In the acute phase, mortality is less than 5% and death may result from acute heart failure or meningoencephalitis in children less than two years old.Romana’s sign, clinical manifestation tipically observed in the acute phase of some Chagas’ disease patients.
T. cruzi: general symptoms in acute Chagas' disease may also include fever, hepatosplenomegaly, adenopathies and myocarditis.Electrocardiographic changes involve sinus tachycardia, prolongation of the P-R interval, primary T-wave changes and low QRS voltage.Chest X-ray can reveal cardiomegaly of different degrees. The intermediate phase is clinically asymptomatic and is detected by the presence of specific antibodies.No parasites are found in bloostream smears but xenodiagnosis could be positive in some cases. Acute Chagas myocarditis (Haematoxylin and Eosin X 160) tc12 : Posteroanterior chest radiograph showing enlarged heart due to T.cruzi infection. tc12a: Acute Chagas' disease myocarditis (Haematoxylin and Eosin X160)
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. T. cruzi: the chronic phase of Chagas'disease develops 10 - 20 years after infection and affects internal organs such as the heart,oesophagus and colon as well as the peripheral nervous system. The lesions of Chagas’ disease are incurable and in severe cases patients may die as result of heart failure.
Chagas' disease megacardia (slide from the late Prof.Koberle, Brazil)
Apical aneurysm in Chagas' disease (slide from the late Prof.Koberle, Brazil)
T. cruzi: on the other side, megacolon is associated with abnormal constipation (weeks).Faecal impaction and sigmoid volvulus are side-effects of megacolon.Neurological changes in chronic Chagas' disease include changes at the level of the central, peripheral or autonomic nervous system. Chagasic megacolon with enlargement of the sigmoid;patient from Morona Santiago province, southeastern Ecuador
X-ray showing megaoesophagus in Chagas' disease
T. cruzi: can be observed in the peripheral blood only in the acute case of the disease.Its presence is the best definition of the acute phase as all other signs are variable. - Wright-Giemsa staining of T.cruzi trypomastigote in peripheral blood smear from an acute infected patient. - T.cruzi in mouse blood (Giemsa stain)
T. cruzi: trypomastigotes have a prominent subterminal kinetoplast that often distort the membrane of the cell,an elongated nucleus and an undulating membrane. - T.cruzi trypomastigote: blood stream trypomastigotes are 15-20 µm in leng th and appear with a typical C or S-shaped form.
T. cruzi: multiplication only occurs in the amastigote phase, which grows in a variety of tissue cells especially muscle. - In vitro infected fibroblast showing a large number of intracellular amastigotes.
T. cruzi: laboratory diagnostic tests based on serology (IFA, ELISA) and Polymerase Chain Reaction (PCR) specific for T.cruzi, have been developed. - T.cruzi trypomastigotes reacting with monoclonal Ab.
T. cruzi: serological cross-reactions can occur with infections such as leprosy, leishmaniasis, treponematoses, malaria and multiple myeloma. Trypanosoma rangeli is also an important cause of false-positive testing, especially in areas where T.cruzi coexists with T.rangeli. - In vitro T.cruzi infection of macrophages showing the presence of amastigotes: confocal microscopy showing T.cruzi amastigotes after treatment with anti-Tc24 mouse sera.
T. cruzi: two drugs are in common use. Nifurtimox (Lampit, production was discontinued in 1991)and Benznidazole (Rochagan). The latter which is now the drug of choice, is given in an oral dose of 6 mg/kg body weight for 30 or 60 days.Both drugs produce anorexia, weight loss, headache and dizziness,gastric irritation, and sometimes peripheral neuritis.Experimental drugs are under evaluation.Treatment of patients in the intermediate or chronic phase is controversial. Congenital Chagas'disease and transfusion-associated acute disease require Rochagan therapy.Transfusion infection can be prevented by donor screening or,by mixing the blood with gentian violet (0,25 gr./L for 24 hours) to kill T.cruzi.Vector control programmes involving insecticide spraying with modern pyretroids and new tools for delivery in endemic areas is being carried out in some Latin American countries. tc20: TEM microphotograph of T.cruzi epimastigote.