4. Echinococcus granulosus infection has a world-
wide distribution with a higher prevalence in
South-America (Argentina, Uruguay), Europe
(mediterranean bassin), Northern Africa, Middle
East, South-Central and East Asia.
5. Echinococcus granulosus: hydatidosis is caused by
the larval stage of E.granulosus.
After ingestion of eggs the onchospheres penetrate
the intestinal mucosa and reach host organs
(mainly liver and lung) where they encyst within a
week reaching 1 cm in diameter in about 5 months.
6. Echinococcus granulosus: the cysts (2 to 30 cm)
are constituted by an external acellular cuticule
and an inner cellular "germinal" layer (10-25 µ)
that produces the brood capsules containing 6-12
protoscolices or single protoscolices. (Germinal
layer with a protoscolex).
7. Echinococcus granulosus: the larvae (scolices)
develop from the germinal layer.
The protoscolices are at first evaginated and
measure 120-220 by 70-120 µ.
8. Echinococcus granulosus: the mature rotoscolices
have 4 suckers and a rostellum with hooklets and
can be observed in the hydatid fluid.
10. Echinococcus granulosus: the protoscolices then
become invaginated and measure 90-140 by 70-120
µm.They can transform into daughter cysts.
These cysts can proliferate both internally and
externally giving exogenous cysts.Spontaneous or
surgical rupture of the cyst can originate a
secondary hydatidosis.
11. Echinococcus granulosus: the liver is the most
common site of development of cysts (50-75%).
Lesions can be detected by CT scan or
echography;a septate structure is a characteristic
of active cysts.
Treatment is based on surgical and/or medical
therapy (albendazole)
12. Echinococcus granulosus: definitive diagnosis is
obtained by means of serologic tests (EIA, IHA,
CIEP/Western Blot);the last two are confirmatory
tests and are useful for the follow-up of treated
patients.
-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. Echinococcus granulosus: pulmonary infection is
observed in about 20-30% of patients.
Roentgenografic examination shows round mass
lesions and CT scan demonstrates the fluid
content of the lesion.
Serology has a lower sensitivity in extrahepatic
hydatidosis.
14. Echinococcus granulosus: any other organ can be
affected:nervous system, heart, bones, spleen
eyes, muscles are the most common sites.
Multiple involvement is frequent.Symptoms and
signs depend on the size,the site and the pressure
of the cyst on host structures.
-CT scan of a spleen cyst.
-MRI scans of a muscular cyst.
15. Echinococcus granulosus: medullary hydatidosis
is a severe form of the infection.In this case the
mechanical pressure of host tissues caused
paraplegia.The surgical treatment allowed
resolution of symptoms.The infection relapsed
and responded partially to medical treatment.
16. Echinococcus granulosus: MRI imaging can
demonstrate the relationship between the cyst
and the medulla on the longitudinal axis.
The serology is often negative in infections in sites
other than liver or lung.(Medullary hydatidosis)
17. TAENIA SOLIUM
Taenia solium: life cycle.
Cysticercosis exists world-wide but is prevalent in
Mexico, Africa, South-Est Asia and South-America.
20. 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.
21. 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).
23. Taenia multiceps: dogs are the definitive host:
sheep, other mammals and,rarely, man are
infected by eating embryonated eggs.
World-wide distribution. The larvae penetrate via
oral route and develop to the coenurus stage in
host's tissues.(Brain lesion).
24. Taenia multiceps: the lesion can be differentiated
from the cysticercus larva for the presence in the
same cyst of hundreds of protoscolices.
Section of a protoscolex in brain cyst.
26. ANGIOSTRONGYLUS
CANTONENSIS
Angiostrongylus cantonensis: the rat lung worm is a
nematode producing human eosinophilic
meningoencephalitis.Human infections have been
described in Asia (Philippines, Indonesia, Malaisia,
Thailand, Viet-Nam, Taiwan, Hong-Kong, Japan),
Oceania [Pacific Island (Tahiti, New Caledonia),
Papua Nuova Guinea, Australia],Cuba, Puerto Rico,
Hawaii;in the USA the parasite has been found in
rats and molluscs and one human case has been
reported from New Orleans;in Africa (Madagascar)
A.cantonensis has been found in rats.
Section of A.cantonensis young adults within
pulmonary blood vessel.
The sections show the reproductive tubes (RT),
lateral chords (LR) and the intestine (I) of the
worms.(Hematoxylin and Eosin, H&E)
27. A.cantonensis: adult worms(male: 20-22 mm by
320-420 µm, female: 22-34 mm by 340-560 µm)
live in the blood vessels of the lungs of rats where
they lay eggs.Eggs lodge in the terminal branches
of the pulmonary arteries where they hatch
liberating first-stage larvae which migrate to the
intestine via the alveolar space, the trachea, the
pharynx and the esophagus; larvae are then
eliminated with faeces.
First stage larvae infect the intermediate hosts,
molluscs (snails and slugs),where they develop to
the infective third-stage larvae.Rats become
infected by eating infected snails or slugs. The
ingested larvae migrate from rat's intestine to the
CNS where they develop to adults through two
stages of development in 2-3 weeks.Adults then
migrate to the subarachnoid space, enter the
venous system and gain the pulmonary arteries
where they become mature.Larvae can be detected
in rat's faeces 40-60 days after infection.
28. A.cantonensis: several species of terrestrial
snails (Achatina fulica, the Giant African snail),
acquatic snails (Pila spp., Viviparus javanica),
or slugs (Veronicella alte and V.siamensis) may
act as intermediate hosts for the development of
the larvae to third stage.The existance of
paratenic hosts has been demonstrated:
in freshwater prawns, land crabs and frogs
which feed on snails or slugs,larvae remain
infective for a certain period of time and may
infect rats,
or humans, when eating the paratenic host.
Achatina fulica (the Giant African snail)
29. A.cantonensis: humans become infected by eating
raw or undercooked snails, slugs, contaminated
vegetables or transport hosts;in man larvae migrate
to the CNS, where the development generally stops,
and cause eosinophilic meningoencephalitis.
Section of A.cantonensis in the subarachnoid space
with inflammation and hemorrhage.
(Hematoxylin and Eosin, H&E)
30. A.cantonensis: the pathogenesis depends on
direct damage caused by the motile larvae and
young adults (7-13 mm in lenght by 100-260 µm),
and on the host's inflammatory granulomatous
reaction.
Section of A.cantonensis in the subarachnoid
space with inflammation and hemorrhage.
(Hematoxylin and Eosin, H&E)
31. A.cantonensis: histologic examination shows
sections of the worms surrounded by inflammatory
cells(histiocytes, neutrophils and eosinophils),
vascular congestion, subdural and subarachnoid
hemorrhage, focal necrosis and hemorrhage in the
brain.
Section of young adult of A.cantonensis in the
brain without any inflammatory response:
I: intestine, LC: lateral chords.
(Hematoxylin and Eosin, H&E)
32. A.cantonensis: the incubation period ranges from 1
to 5 weeks (average 2 weeks).
Symptoms consist of headache (mainly occipital and
temporal),stiff neck, nausea, vomiting, mild fever,
rash, pruritus,abdominal pain, constitutional
symptoms.
Section of young adult of A.cantonensis in the brain,
higher magnification:the intestine (I) and the lateral
chords (LC) are well identifiable.
(Hematoxylin and Eosin, H&E)
33. A.cantonensis: meningeal signs, cranial nerves
palsies (III, IV, VI, VII),paresthesias, pain and
weakness are the commonest signs.Death is
uncommon.
An ocular form with the presence of young adults of
A.cantonensis in the anterior chamber of the eye
has been described with visual loss,pain,
blepharospasm, iridocyclitis and increased ocular
tension.
Section of young adult of A.cantonensis in the
brain, higher magnification:the prominent lateral
chords (LC) and the cuticle (C) (5 µm) are well
identifiable.
(Hematoxylin and Eosin, H&E)
34. A.cantonensis: pulmonary involvement is
uncommon but rarely some worms may migrate to
the lungs causing severe pneumonia with massive
inflammation, exudation and hemorrhage.
Section of lung during pulmonary involvement by
A.cantonensis.
(Hematoxylin and Eosin, H&E)
35. A.cantonensis: several adults, male and female
may lie within the same pulmonary vessel.
Sections of adults of A.cantonensis within
pulmonary vessel:
RT: reproductive tubes; MC: muscular cells; I:
intestine.
(Hematoxylin and Eosin, H&E)
36. A.cantonensis: no treatment is recognized as
effective;moreover anthelminthics are not
recommended.
Section of adult female within pulmonary vessel:
RT: reproductive tubes; MC: muscular cells; I:
intestine; LC: lateral chord.
(Hematoxylin and Eosin, H&E)
37. A.cantonensis: laboratory diagnosis is based on
the observation of an eosinophilic CSF pleocytosis
(500-5.000 cells/mm3, with 20-90% of
eosinophils),with elevated CSF proteins and
normal or slightly decreased CSF glucose.
Section of adult female within pulmonary vessel:
RT: reproductive tubes; MC: muscular cells; I:
intestine; LC: lateral chord.
(Hematoxylin and Eosin, H&E)
38. A.cantonensis: Charcot-Leyden crystals may be
observed in the CSF. Blood leukocytosis with
eosinophilia (>10%) is common.
The diagnosis may be confirmed by serological
testing (IF or EIA).
Charcot-Leyden crystal. Bright field examination
of wet mount preparation.
41. T. gondii: T.gondii encephalitis (TE) is the most
common cerebral opportunistic infection in
patients with AIDS.
The typical lesion is an ipodense focal area with
ring contrast-enhancement and edema.
(CT scan of a toxoplasmic encephalitis).
42. T. gondii: tissue cysts, 100-300 µm, may contain
up to 3.000 bradyzoites.The wall of mature
pseudocysts is believed to represent a
combination of host and parasitic components.
43. T. gondii: diagnosis of TE is usually presumptive,
based on clinical and radiologic findings and on the
response to treatment; cerebral biopsy sometimes
allows identification of pseudocysts in tissue
sections. (H&E stain).
45. T. gondii: the pseudocysts of T.gondii can be
observed in tissue sections with monoclonal
antibodies.
46. T. gondii: direct detection of T.gondii in clinical
specimens is rare;parasites can be isolated from
blood, CSF, amniotic fluid,tissue biopsies on cell lines
(THP-1 or MRC-5).
In clinical specimens the presence of parasites can
also be demonstrated by PCR analysis.
47. T. gondii: intracellular trophozoites of T.gondii in a
cell culture.
The trophozoites proliferate within the vacuole
developing a pseudocyst.
(Trophozoites in a THP-1 cell, Giemsa stain).
48. T. gondii: in cell cultures T.gondii proliferates to
form a pseudocyst of 8-20 parasites.
(Trophozoites in a THP-1 cell, Giemsa stain).
49. T. gondii: lysis of a THP-1 cell with release of
tachizoites in culture.
(Trophozoites in a THP-1 cell, Giemsa stain).
50. T. gondii: microscopical features of tachizoites of
Toxoplasma gondii and peritoneal macrophages
of mouse in peritoneal exudate. (SEM)
51. T. gondii: microscopical features of tachizoites of
Toxoplasma gondii and peritoneal macrophages of
mouse in peritoneal exudate. (SEM)
52. T. gondii: the anterior pole of an endozoid in
tangential projection.Several subpellicular
fibrils and their insertion on the anterior polar
ring are visible.
53. T. gondii: transmision electron microscopic picture.
Longitudinal section of an endozoid.
54. T. gondii: cross-section through an endozoid
in an advanced stage of endodiogeny.
The daugther cells appear to be surrounded.
In each of these news cells there are two round
bodies that lengthen forming the first rhoptries.
57. Sleeping sickness occurs in Africa between the
15° North and the 20° South.
The T.b.rhodesiense form is found in East and
Central-East Africa whereas the T.b.gambiense
infection occurs in Central and West Africa.
59. T. b. gambiense and rhodesiense: two forms of
trypomastigote can be seen in peripheral blood:
one is long slender, 30 µm in length,and is
capable of multiplying in the host, the other is
stumpy, not dividing,18 µm in length.
60. Trypanosoma brucei gambiense and rhodesiense:
trypanosomes appear in the peripheral blood 5 to
21 days after the infecting bite.
61. Trypanosoma brucei gambiense and rhodesiense:
the terminal stage of the infection ("sleeping
sickness") is the result of a chronic
meningoencephalomyelitis. (H&E stain).
62. Trypanosoma brucei gambiense and
rhodesiense: the typical pathological lesion of
trypanosomiasis is a perivascular round-cell
infiltration (perivascular cuffing) due to glial
cells, lymphocytes and plasmocytes (Mott cells).
(H&E stain).
64. ACANTHAMOEBA SP.
Acanthamoeba spp.: free living amoebae of the
Acanthamoeba genus cause two clinical syndrome:
1) Granulomatous amoebic encephalitis (GAE)
2) Subacute and chronic amoebic keratitis
A disseminated form of GAE is described in
individuals with the Acquired Immunodeficiency
Syndrome (AIDS)
Several species of Acanthamoeba have been
identified:A.castellani, A.culberstoni, A.polyphaga,
A.zhysodes, A.hatchetti,A.astronyxis,A.palestinensis.
(Trophozoites, trichrome stain).
65. Acanthamoeba spp.: clinical manifestations include
chronic granulomatous encephalitis and keratitis
(in particular in individuals who wear contact lens);
some case of disseminated cutaneous infection
have been reported in AIDS patients.
66. Acanthamoeba spp.: the trophozoite is irregular,
15-45 µm,having micropseudopodia called
acanthopodia;in trichrome stain the cytoplasm of
trophozoites appears greenish pink,the central
located kariosome pink or red.(Trichrome stain).
67. Acanthamoeba spp.: the cysts are spherical,
15-20 µm in diameter,having a thick double
wall. The outer wall may be spherical or
wrinkled,
the inner wall appear stellate or polyhedral.
(Acanthamoeba trophozoites and a cyst,
trichrome stain).
68. Acanthamoeba spp.: both forms have a single
nucleus with a large centrally located nucleolus.
With trichrome stain, the cysts stain red.Species
identification is based on morphology of cysts
(stellate, polyhedral).
69. Acanthamoeba spp.: trophozoite as seen under
phase contrast microscope.Its big nucleolus, both
lobopodia and acanthopodia and various vacuoles
can be seen clearly.
72. NAEGLERIA FOWLERI
Naegleria fowleri is the agent of a severe purulent
meningoencephalitis: the "Primary amoebic
meningoencephalitis". N.fowleri are free living
amoebas that live in warm fresh water all over the
world.
The lyfe cycle consist of three stages: the
amoeboid growing form that lives in the mud and
at the bottom of the ponds; the rapidly motile
biflagellate trophozoite who lives in surface layers
of water (the infective form); the dormant cyst.
Primary amoebic meningoencephalitis occurs in
individuals who have been exposed to freshwater
lakes or ponds usually during swimming; the
incubation period is about 3 to 7 days (but it may
last up to 2 weeks). Invasion of the CNS occurs
after nasal inhalation of contaminated water
containig the biflagellate trophozoites;
trophozoites (in the amoeboid form once arrived in
the nasal cavity) penetrate the epithelium and
enter the CNS through the olphactory nerve
branches in the cribriform plate and cause a
purulent meningoencephalitis.
Trophozoites are 10-to 30 m m in diameter and
have a clear nucleus with a prominent dense
central nucleolus; the cytoplasm contains
mytochondria and the rough endoplasmic
reticulum; usually ingested red blood cells,
leukocytes and bacteria are visible.
Cysts are 9 m m in diameter; they are spherical
with a central nucleus.
73. N. gruberi: trophozoite as seen under phase
contrast microscope.
Its big nucleolus, four lobopod type pseudopodia
and the contractile vacuole can be clearly seen.
74. Naegleria spp.: trophozoite stained with
Greenstein’s five dye stain and observed under
dark field microscope.
