3. Taenia solium
Life cycle
Cysticercosis exists world-wide but is prevalent in
Mexico, Africa, South-Est Asia and South-America.
4. 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).
6. 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.
7. 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).
10. Development of
Trichinella spiralis
in skeletal muscles
Migrated larvae
Encapsulated
larvae
Calcified larvae
11. 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).
12. 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).
13. 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).
14. Trichinella spiralis: after muscle digestion the
T.spiralis larva measures 1 mm in lenght.
(Fresh examination after muscle digestion).
17. 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.
18. 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.
19. 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).
20. 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.
21. 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.
22. 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.
23. 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.
24. 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.
25. 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).
26. 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.
27. 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.
28. 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.
29. 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)
30. 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.
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.
32. Apical aneurysm in Chagas' disease
(slide from the late Prof.Koberle, Brazil)
33. 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
36. 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)
37. 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 length and
appear with a typical C or S-shaped form.
38. 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.
39. 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.
40. 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.
41. 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.
