HEART & MUSCLESHEART & MUSCLESPARASITESPARASITES

CESTOIDEA CESTOIDEA Order:Order: Cyclophyllidea Cyclophyllidea

Taenia soliumTaenia soliumLLife cycleife cycle

Cysticercosis exists world-wide but is prevalent in Cysticercosis exists world-wide but is prevalent in Mexico, Africa, South-Est Asia and South-America.Mexico, Africa, South-Est Asia and South-America.

Taenia solium Taenia solium (cysticercosis): the (cysticercosis): the cysticercus appears as a white opalescent cysticercus appears as a white opalescent vescicle, vescicle, ovoid to round, measuring 8-15 mm by 5-8 ovoid to round, measuring 8-15 mm by 5-8 containing only one protoscolex. containing only one protoscolex. Many organs may be infected Many organs may be infected (subcutaneous tissue, brain, eye, (subcutaneous tissue, brain, eye, muscles). muscles). 

T.solium: cysticercus cellulosae with invaginated scolexT.solium: cysticercus cellulosae with invaginated scolex

T.solium: cysticercus cellulosae with evaginated scolexT.solium: cysticercus cellulosae with evaginated scolex

Cysticercosis: nervous cysticercosis is the most Cysticercosis: nervous cysticercosis is the most severe manifestation of the disease. severe manifestation of the disease. MRI showing an occipital lesion. Diagnosis of MRI showing an occipital lesion. Diagnosis of cysticercosis, cysticercosis, suspected on a clinical-radiological basis, is suspected on a clinical-radiological basis, is confirmed by serology.confirmed by serology.

Cysticercosis:Cysticercosis: the onchospheres migrate to the the onchospheres migrate to the tissues and develop to cysticerci. tissues and develop to cysticerci. The cysticercus dies and becomes calcified. The cysticercus dies and becomes calcified. Calcified cysticerci in muscle. Calcified cysticerci in muscle. Localization in muscles depends on the Localization in muscles depends on the geographical origin geographical origin (unfrequent in american patients).(unfrequent in american patients).      

NEMATODANEMATODA Order:Order: Trichurata Trichurata

TRICHINELLA SPIRALISTRICHINELLA SPIRALIS

Development of Development of Trichinella spiralis Trichinella spiralis in skeletal musclesin skeletal muscles

Migrated larvae Migrated larvae

Encapsulated Encapsulated larvae larvae

Calcified larvae Calcified larvae

Trichinella spiralisTrichinella spiralis: Trichinella spiralis : Trichinella spiralis larvae encysted in striated muscle. larvae encysted in striated muscle. The cyst, elongated in shape, measures 0.3-The cyst, elongated in shape, measures 0.3-0.6 by 0.2-0.3 mm. 0.6 by 0.2-0.3 mm. (H&E stain).(H&E stain).

Trichinella spiralis: the cyst is formed outside by a Trichinella spiralis: the cyst is formed outside by a fibrous capsule and inside by an eosinophil fibrous capsule and inside by an eosinophil infiltration around the tightly coiled larvae. infiltration around the tightly coiled larvae. (H&E stain).(H&E stain).

Trichinella spiralis:Trichinella spiralis: massive infection may massive infection may cause acute enteritis; the migration and the cause acute enteritis; the migration and the later muscle encystation of larvae maylater muscle encystation of larvae may be be asymptomatic or cause serious generalized asymptomatic or cause serious generalized disease withdisease with possible miocardial and brain possible miocardial and brain pathology. pathology. ((T.s.T.s. larvae). larvae).

Trichinella spiralis: after muscle digestion the Trichinella spiralis: after muscle digestion the T.spiralis larvaT.spiralis larva measures 1 mm in lenght. measures 1 mm in lenght. (Fresh examination after muscle digestion). (Fresh examination after muscle digestion).

Trichinella spiralis: Electron microscopy Trichinella spiralis: Electron microscopy

ZOOMASTIGOPHOREAZOOMASTIGOPHOREA Order:Order: Kinetoplastida Kinetoplastida

TRYPANOSOMA CRUZITRYPANOSOMA CRUZI (Chagas' disease)(Chagas' disease)

T. cruzi: american trypanosomiasis was first T. cruzi: american trypanosomiasis was first described by Carlos Chagas in Brasil in 1909. described by Carlos Chagas in Brasil in 1909. The infection, Chagas' disease, is caused The infection, Chagas' disease, is caused by the haemoflagellate Trypanosoma cruzi. by the haemoflagellate Trypanosoma cruzi. tc1: T.cruzi in blood sample, Giemsa. tc1: T.cruzi in blood sample, Giemsa.

T. cruzi: T. cruzi: the disease is a public health threat in the disease is a public health threat in most Latin American countries,although cases due most Latin American countries,although cases due to blood derivatives or blood transfusionto blood derivatives or blood transfusion has been has been reported in non-endemic regions. reported in non-endemic regions. According to WHO the overall prevalence ofAccording to WHO the overall prevalence of human T.cruzi infectionhuman T.cruzi infection is estimated in 18 million is estimated in 18 million cases and 100 million people are living at risk. cases and 100 million people are living at risk. tc2: T. cruzi:tc2: T. cruzi: geographical distribution. geographical distribution.

T. cruzi: the vectors are reduvidae bugs which are T. cruzi: the vectors are reduvidae bugs which are haematophagushaematophagus and the most important are and the most important are Triatoma infestans(Argentina, Chile, Brazil, Bolivia, Triatoma infestans(Argentina, Chile, Brazil, Bolivia, Paraguay, Uruguay, Peru),T. sordida (Argentina, Paraguay, Uruguay, Peru),T. sordida (Argentina, Bolivia, Brazil, Paraguay),Rhodnius prolixus Bolivia, Brazil, Paraguay),Rhodnius prolixus (Colombia, Venezuela, Mexico, Central America),(Colombia, Venezuela, Mexico, Central America),T. dimidiata (Ecuador, Mexico, Central America),T. dimidiata (Ecuador, Mexico, Central America),and Panstrogylus megistus (northeast Brazil).and Panstrogylus megistus (northeast Brazil).

T. cruzi: the transmission by the vector is faecal. T. cruzi: the transmission by the vector is faecal. T.cruzi infective metacyclic trypomastigotes are shedT.cruzi infective metacyclic trypomastigotes are shed in the faeces of the bug and are inoculated intoin the faeces of the bug and are inoculated into the the human host by scratching infected faeces into skin human host by scratching infected faeces into skin abrasionsabrasions usually caused by the bug in the process of usually caused by the bug in the process of feeding (blood-sucking). feeding (blood-sucking). T.cruzi metacyclic trypomastigote: scanning electron T.cruzi metacyclic trypomastigote: scanning electron microscopymicroscopy showing T.cruzishowing T.cruzi trypomastigotes trypomastigotes recovered from an infectedrecovered from an infected Triatoma spp. in Pedro Triatoma spp. in Pedro Carbo, Ecuador.Carbo, Ecuador.

T. cruzi: infective metacyclic trypomastigotes are T. cruzi: infective metacyclic trypomastigotes are shed in the faecesshed in the faeces of the bug and inoculated into of the bug and inoculated into the vertebrate host not onlythe vertebrate host not only by skin lesions but by skin lesions but also through the mucosa of the mouth and,in also through the mucosa of the mouth and,in humans, through the conjunctiva of the eyes. humans, through the conjunctiva of the eyes.

T. cruzi: trypomastigotes can infect most of the T. cruzi: trypomastigotes can infect most of the vertebrate cells,polymorphonuclear leucocytes and vertebrate cells,polymorphonuclear leucocytes and macrophages are probably amongmacrophages are probably among the first the first vertebrate host cells with which T.cruzi interacts in vertebrate host cells with which T.cruzi interacts in vivo. vivo. tc7a: In vitro T.cruzi infection of macrophages tc7a: In vitro T.cruzi infection of macrophages showing the presence of amastigotes: showing the presence of amastigotes: Wright-Giemsa stain, showing replicating T.cruzi Wright-Giemsa stain, showing replicating T.cruzi amastigotes within host cell. amastigotes within host cell.

T. cruzi: this invasive step is crucial for the life T. cruzi: this invasive step is crucial for the life cycle of the parasitecycle of the parasite since it has to become since it has to become intracellular to multiply. intracellular to multiply. tc7b: In vitro T.cruzi infection of macrophages tc7b: In vitro T.cruzi infection of macrophages showing the presence of amastigotes: showing the presence of amastigotes: immunofluorescence assay showing T.cruzi immunofluorescence assay showing T.cruzi amastigotes after treatmentamastigotes after treatment with anti-T.cruzi with anti-T.cruzi polyclonal mouse sera.polyclonal mouse sera.

T. cruzi:T. cruzi: trypomastigotes in the host cell transform trypomastigotes in the host cell transform into amastigotes,which multiply intracellularly by into amastigotes,which multiply intracellularly by binary division inducing inflammatorybinary division inducing inflammatory and and immunological responses in vivo, and destroy cells immunological responses in vivo, and destroy cells in vitro. in vitro. Amastigotes are then released into the blood Amastigotes are then released into the blood stream as trypomastigotes.The latter are stream as trypomastigotes.The latter are nondividing forms which are able to infect a wide nondividing forms which are able to infect a wide rangerange of new host cells but muscle and glia seem of new host cells but muscle and glia seem most often parasitized,or they have to be ingested most often parasitized,or they have to be ingested by another reduviid bugby another reduviid bug in order to continue the in order to continue the parasite life cycle in the invertebrate host. parasite life cycle in the invertebrate host. tc8:tc8: Trypomastigotes reach the myocardial cells Trypomastigotes reach the myocardial cells and after penetrationand after penetration they multiply as amastigotes they multiply as amastigotes with formation of a pseudocyst. with formation of a pseudocyst.

T. cruzi:T. cruzi: in the in the ReduvidaeReduvidae bug the bloodstream bug the bloodstream derived trypomastigotederived trypomastigote forms pass along the forms pass along the digestive tract through irreversibledigestive tract through irreversible morphological morphological transformations in sequence;each developmental transformations in sequence;each developmental stage occurs in a specific portion of the insect's gut. stage occurs in a specific portion of the insect's gut. Thus, in the stomach, most blood trypomastigotes Thus, in the stomach, most blood trypomastigotes change intochange into epimastigotes and rounded forms epimastigotes and rounded forms (sphaeromastigotes). (sphaeromastigotes). tc9: T.cruzitc9: T.cruzi epimastigote. Immunofluorescence epimastigote. Immunofluorescence studies usingstudies using antibodies to a antibodies to a T.cruziT.cruzi protein named protein named Tc52(immunosuppressive factor which also express a Tc52(immunosuppressive factor which also express a thiol-transferase activity)and confocal microscopy. thiol-transferase activity)and confocal microscopy. An intense labeling located at the posterior end of An intense labeling located at the posterior end of an epimastigote indicate that Tc52 is targeted to the an epimastigote indicate that Tc52 is targeted to the reservosomes(These organelles are small vesicles reservosomes(These organelles are small vesicles inside multivesicular structuresinside multivesicular structures being formed being formed predominantly at the posterior end of predominantly at the posterior end of epimastigotes). epimastigotes).

T. cruzi: epimastigotes divide actively in the T. cruzi: epimastigotes divide actively in the vector's intestine and reachvector's intestine and reach the rectum where the rectum where a final differentiation results in the infective a final differentiation results in the infective metacyclicmetacyclic trypomastigotes which are trypomastigotes which are eliminated in the bug's faeces.eliminated in the bug's faeces.tc10: T.cruzi epimastigote. Epimastigote tc10: T.cruzi epimastigote. Epimastigote reacting withreacting with a monoclonal antibody against a monoclonal antibody against T.cruzi.T.cruzi.

T. cruzi:T. cruzi: some researchers have postulated that some researchers have postulated that sphaeromastigotessphaeromastigotes may change either into short may change either into short epimastigotes,dividing forms in the intestine, or epimastigotes,dividing forms in the intestine, or into long epimastigotesinto long epimastigotes which are nondividing which are nondividing forms but are able to reach the rectumforms but are able to reach the rectum where they where they transform into the final metacyclic trypomastigote transform into the final metacyclic trypomastigote form.In any case, this hypothesis remains form.In any case, this hypothesis remains controversial.controversial.tc10b: T.cruzi tc10b: T.cruzi epimastigote. Scanning electron epimastigote. Scanning electron microscopyshowing microscopyshowing T.cruziT.cruzi epimastigote. epimastigote.

T. cruzi:T. cruzi: there are three phases of the infection. there are three phases of the infection. The acute phase usually passes unnoticed but The acute phase usually passes unnoticed but there may be an inflamed swelling or chagoma there may be an inflamed swelling or chagoma at the site of entry of the trypanosomes. at the site of entry of the trypanosomes. Romanas'sign is when this swelling involves the Romanas'sign is when this swelling involves the eyelidseyelids but it occurs only in about 1-2% of the but it occurs only in about 1-2% of the cases.In the acute phase, mortality is less than 5% cases.In the acute phase, mortality is less than 5% andand death may result from acute heart failure death may result from acute heart failure or meningoencephalitis in children less than two or meningoencephalitis in children less than two years old.Romana’s sign, clinical manifestation years old.Romana’s sign, clinical manifestation tipically observedtipically observed in the acute phase of some in the acute phase of some Chagas’ disease patients.Chagas’ disease patients.

T. cruzi:T. cruzi: general symptoms in acute Chagas' general symptoms in acute Chagas' diseasediseasemay also include fever, hepatosplenomegaly, may also include fever, hepatosplenomegaly, adenopathies and myocarditis.Electrocardiographic adenopathies and myocarditis.Electrocardiographic changes involve sinus tachycardia, prolongation changes involve sinus tachycardia, prolongation of the P-R interval, primary T-wave changes and of the P-R interval, primary T-wave changes and low QRS voltage.Chest X-ray can reveal low QRS voltage.Chest X-ray can reveal cardiomegaly of different degrees. cardiomegaly of different degrees. The intermediate phase is clinically asymptomatic The intermediate phase is clinically asymptomatic and is detected by the presence of specific and is detected by the presence of specific antibodies.No parasites are found in bloostream antibodies.No parasites are found in bloostream smears butsmears but xenodiagnosis could be positive in some xenodiagnosis could be positive in some cases. cases. Acute Chagas myocarditis (Haematoxylin and Eosin Acute Chagas myocarditis (Haematoxylin and Eosin X 160)X 160)tc12tc12: Posteroanterior chest radiograph : Posteroanterior chest radiograph showing enlargedshowing enlarged heart due to heart due to T.cruziT.cruzi infection. infection.tc12a: tc12a: Acute Chagas' disease myocarditis Acute Chagas' disease myocarditis (Haematoxylin and Eosin X160)(Haematoxylin and Eosin X160)

T.cruzi parasitize mainly the cardiac muscle but T.cruzi parasitize mainly the cardiac muscle but any cell typeany cell type may be parasitized (smooth may be parasitized (smooth muscle cells, hystiocytes): cardiac muscle with muscle cells, hystiocytes): cardiac muscle with amastigotes, H&E stain. amastigotes, H&E stain. 

T. cruzi:T. cruzi: the chronic phase of Chagas'disease the chronic phase of Chagas'disease develops 10 - 20 years after infection and affects develops 10 - 20 years after infection and affects internal organs such as the heart,oesophagus and internal organs such as the heart,oesophagus and colon as well as the peripheral nervous system. colon as well as the peripheral nervous system. The lesions of Chagas’ disease are incurable and in The lesions of Chagas’ disease are incurable and in severe casessevere cases patients may die as result of heart patients may die as result of heart failure.failure.

Chagas' disease megacardia Chagas' disease megacardia (slide from the late Prof.Koberle, Brazil) (slide from the late Prof.Koberle, Brazil) 

Apical aneurysm in Chagas' disease Apical aneurysm in Chagas' disease (slide from the late Prof.Koberle, Brazil) (slide from the late Prof.Koberle, Brazil)

T. cruzi: T. cruzi: on the other side, megacolon is on the other side, megacolon is associated associated with abnormal constipation (weeks).Faecal with abnormal constipation (weeks).Faecal impaction and sigmoid volvulus are side-effects of impaction and sigmoid volvulus are side-effects of megacolon.Neurological changes in chronic megacolon.Neurological changes in chronic Chagas' disease include changesChagas' disease include changes at the level of at the level of the central, peripheral or autonomic nervous the central, peripheral or autonomic nervous system. system.

Chagasic megacolon with enlargement of the Chagasic megacolon with enlargement of the sigmoid;patient from Morona Santiago sigmoid;patient from Morona Santiago province, southeastern Ecuador province, southeastern Ecuador

X-ray showing megaoesophagus in Chagas' disease X-ray showing megaoesophagus in Chagas' disease

X-ray showing megacolon in Chagas' disease X-ray showing megacolon in Chagas' disease

T. cruzi:T. cruzi: can be observed in the peripheral blood can be observed in the peripheral blood only in the acute case of the disease.Its presence only in the acute case of the disease.Its presence is the best definition of the acute phaseis the best definition of the acute phase as all as all other signs are variable. other signs are variable. --Wright-Giemsa staining of Wright-Giemsa staining of T.cruziT.cruzi trypomastigote trypomastigote in peripheral blood smear from an acute infected in peripheral blood smear from an acute infected patient.patient.--T.cruzi T.cruzi in mouse blood (Giemsa stain) in mouse blood (Giemsa stain)

T. cruzi: T. cruzi: trypomastigotes have a prominent trypomastigotes have a prominent subterminal kinetoplastsubterminal kinetoplast that often distort the that often distort the membrane of the cell,an elongated nucleus and membrane of the cell,an elongated nucleus and an undulating membrane. an undulating membrane. --T.cruziT.cruzi trypomastigote: blood stream trypomastigote: blood stream trypomastigotes are 15-20 µmtrypomastigotes are 15-20 µm in lengin lengthth and and appear with a typical C or S-shaped form.appear with a typical C or S-shaped form.

T. cruzi: multiplication only occurs in the T. cruzi: multiplication only occurs in the amastigote phase, amastigote phase, which grows in a variety of tissue cells especially which grows in a variety of tissue cells especially muscle. muscle. --In vitro infected fibroblast showing a large In vitro infected fibroblast showing a large number of intracellular amastigotes.number of intracellular amastigotes.

T. cruzi: laboratory diagnostic tests based on T. cruzi: laboratory diagnostic tests based on serology (IFA, ELISA) and Polymerase Chain serology (IFA, ELISA) and Polymerase Chain Reaction (PCR) specific for T.cruzi, have been Reaction (PCR) specific for T.cruzi, have been developed. developed. --T.cruzi trypomastigotes reacting with monoclonal T.cruzi trypomastigotes reacting with monoclonal Ab. Ab.

T. cruzi: serological cross-reactions can occur T. cruzi: serological cross-reactions can occur with infectionswith infections such as leprosy, leishmaniasis, such as leprosy, leishmaniasis, treponematoses, malaria and multiple myeloma.treponematoses, malaria and multiple myeloma.Trypanosoma rangeli is also an important cause Trypanosoma rangeli is also an important cause of false-positive testing, especially in areas of false-positive testing, especially in areas where T.cruzi coexists with T.rangeli. where T.cruzi coexists with T.rangeli. --In vitro T.cruzi infection of macrophages In vitro T.cruzi infection of macrophages showing the presence of amastigotes: showing the presence of amastigotes: confocal microscopy showing T.cruzi amastigotes confocal microscopy showing T.cruzi amastigotes after treatment with anti-Tc24 mouse sera. after treatment with anti-Tc24 mouse sera.

T. cruzi: two drugs are in common use. T. cruzi: two drugs are in common use. Nifurtimox (Lampit, production was discontinued Nifurtimox (Lampit, production was discontinued in 1991)and Benznidazole (Rochagan). in 1991)and Benznidazole (Rochagan). The latter which is now the drug of choice, The latter which is now the drug of choice, is given in an oral dose of 6 mg/kg body weight for is given in an oral dose of 6 mg/kg body weight for 30 or 60 days.Both drugs produce anorexia, weight 30 or 60 days.Both drugs produce anorexia, weight loss, headache and dizziness,gastric irritation, and loss, headache and dizziness,gastric irritation, and sometimes peripheral neuritis.Experimental drugs sometimes peripheral neuritis.Experimental drugs are under evaluation.Treatment of patients in the are under evaluation.Treatment of patients in the intermediate or chronic phase is controversial. intermediate or chronic phase is controversial. Congenital Chagas'disease and transfusion-Congenital Chagas'disease and transfusion-associatedassociated acute disease require Rochagan acute disease require Rochagan therapy.Transfusion infection can be prevented by therapy.Transfusion infection can be prevented by donor screening or,by mixing the blood with donor screening or,by mixing the blood with gentian violet (0,25 gr./L for 24 hours) to kill gentian violet (0,25 gr./L for 24 hours) to kill T.cruzi.Vector control programmes involving T.cruzi.Vector control programmes involving insecticide sprayinginsecticide spraying with modern pyretroids and with modern pyretroids and new tools for delivery in endemicnew tools for delivery in endemic areas is being areas is being carried out in some Latin American countries. carried out in some Latin American countries. tc20: TEM microphotograph of T.cruzi tc20: TEM microphotograph of T.cruzi epimastigote.epimastigote.