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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_182_библиотеки_им_акад_М_И_Перельмана.pdf
MALARIA
ANCILLARY TESTS
Immunohistochemistry
Antibodies to Plasmodium lactate dehydrogenase
(pLDH) will stain all parasite forms (species specific)
PCR
Tissue-based PCR to detect parasite genotypes may be
helpful in epidemic outbreaks for determining origin
in fatal cases
DIFFERENTIAL DIAGNOSIS
Severe Hypoglycemia of Newborn
Produces petechial hemorrhages in white matter of
brain but without exposure history and no parasites/
pigment in tissue sections
Fat Embolism After Traumatic Bone Fracture
Produces petechial hemorrhages in white matter of
brain associated with lipid in sections but without
exposure history and no parasites/pigment in tissue
sections
Babesiosis
On peripheral blood film, all malaria infections as well
as Babesia species infections must be distinguished by
morphology &/or PCR
Chronic intervillositis (Placental)
Idiopathic/autoimmune disease with no parasites
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
DIAGNOSTIC CHECKLIST
Clinically Relevant Pathologic Features
Patients universally present with fever and an
exposure history
Pathologic Interpretation Pearls
Presence of parasites in cerebral vessels is diagnostic
Malaria pigment polarizes and does not stain with iron
stains (unlike hemosiderin)
Depending on duration of illness, intact viable
parasites may be cleared, but parasite pigment should
still be present (in macrophages)
SELECTED REFERENCES
1. Barrera V et al: Severity of Retinopathy Parallels the
Degree of Parasite Sequestration in the Eyes and Brains of
Malawian Children With Fatal Cerebral Malaria. J Infect
Dis. Epub ahead of print, 2014
2. Joice R et al: Plasmodium falciparum transmission stages
accumulate in the human bone marrow. Sci Transl Med.
6(244):244re5, 2014
3. Milner DA Jr et al: The systemic pathology of cerebral
malaria in African children. Front Cell Infect Microbiol.
4:104, 2014
4. Tembo DL et al: Differential PfEMP1 expression is
associated with cerebral malaria pathology. PLoS Pathog.
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10(12):e1004537, 2014
5. Van Tyne D et al: Plasmodium falciparum gene expression
measured directly from tissue during human infection.
Genome Med. 6(11):110, 2014
6. Milner D Jr et al: Pulmonary pathology in pediatric
cerebral malaria. Hum Pathol. 44(12):2719-26, 2013
7. Milner DA Jr et al: A histological method for quantifying
Plasmodium falciparum in the brain in fatal paediatric
cerebral malaria. Malar J. 12:191, 2013
8. Moxon CA et al: Loss of endothelial protein C receptors
links coagulation and inflammation to parasite
sequestration in cerebral malaria in African children.
Blood. 122(5):842-51, 2013
9. Prapansilp P et al: A clinicopathological correlation of the
expression of the angiopoietin-Tie-2 receptor pathway in
the brain of adults with Plasmodium falciparum malaria.
Malar J. 12:50, 2013
10. White NJ et al: Lethal malaria: Marchiafava and Bignami
were right. J Infect Dis. 208(2):192-8, 2013
11. Craig AG et al: The role of animal models for research on
severe malaria. PLoS Pathog. 8(2):e1002401, 2012
12. Mayor A et al: Placental infection with Plasmodium vivax:
a histopathological and molecular study. J Infect Dis.
206(12):1904-10, 2012
13. Milner DA Jr et al: Human cerebral malaria and
Plasmodium falciparum genotypes in Malawi. Malar J.
11:35, 2012
14. Milner DA Jr et al: Supraorbital postmortem brain sampling
for definitive quantitative confirmation of cerebral
sequestration of Plasmodium falciparum parasites. J Infect
Dis. 205(10):1601-6, 2012
15. Ponsford MJ et al: Sequestration and microvascular
congestion are associated with coma in human cerebral
malaria. J Infect Dis. 2012 Feb 15;205(4):663-71. Epub 2011
Dec 29. Erratum in: J Infect Dis. 206(9):1483, 2012
16. Taylor WR et al: Respiratory manifestations of malaria.
Chest. 142(2):492-505, 2012
17. Dorovini-Zis K et al: The neuropathology of fatal
cerebral malaria in malawian children. Am J Pathol.
178(5):2146-58, 2011
18. Medana IM et al: Coma in fatal adult human malaria is not
caused by cerebral oedema. Malar J. 10:267, 2011
19. Umbers AJ et al: Placental malaria-associated inflammation
disturbs the insulin-like growth factor axis of fetal growth
regulation. J Infect Dis. 203(4):561-9, 2011
20. Whitten R et al: Liver pathology in Malawian children with
fatal encephalopathy. Hum Pathol. 42(9):1230-9, 2011
21. Cox-Singh J et al: Severe malaria - a case of fatal
Plasmodium knowlesi infection with post-mortem
findings: a case report. Malar J. 9:10, 2010
22. Medana IM et al: Induction of the vascular endothelial
growth factor pathway in the brain of adults with fatal
falciparum malaria is a non-specific response to severe
disease. Histopathology. 57(2):282-94, 2010
23. Sutherland CJ et al: Two nonrecombining sympatric forms
of the human malaria parasite Plasmodium ovale occur
globally. J Infect Dis. 201(10):1544-50, 2010
24. Daneshvar C et al: Clinical and laboratory features of
human Plasmodium knowlesi infection. Clin Infect Dis.
49(6):852-60, 2009
25. Lee KS et al: Morphological features and differential counts
of Plasmodium knowlesi parasites in naturally acquired
human infections. Malar J. 8:73, 2009
26. Medana IM et al: Erythropoietin and its receptors in the
brainstem of adults with fatal falciparum malaria. Malar J.
8:261, 2009
27. White VA et al: Retinal pathology of pediatric cerebral
malaria in Malawi. PLoS One. 4(1):e4317, 2009
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Gross and Microscopic
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Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
MALARIA
(Left) The brain, at autopsy,
of a child with cerebral
malaria shows severe
brain swelling, purple-gray
discoloration, and vascular
congestion. (Right) A large
vessel of the brain from a
case of cerebral malaria
demonstrates innumerable
sequestered parasites in
the lumen. Although difficult
to appreciate, all vessels in
this section are packed with
arasites, evident by their
visibility at low power.
(Left) A vessel from a
cerebral malaria patient
demonstrates sequestered
arasites adherent to the
endothelium as well as
masses of parasites, which
are clustered together within
the apparently free lumen
. Infected erythrocytes
can adhere to endothelium,
uninfected red blood cells,
latelets, and each other.
(Right) Polarized light will
highlight the hemozoin
igment within each
infected red blood cell,
which is a product of
hemoglobin digestion.
(Left) A ring hemorrhage
associated with cerebral
malaria usually demonstrates
arasites or pigment
within the central vessel of
a given lesion. Note that the
red blood cells in the tissue
are uninfected. The brain
within this region is rarified
(microinfarction). (Right)
Two ring hemorrhages
are shown in cerebral
malaria, with the larger
demonstrating a fibrin
thrombus . Coagulation
activation occurs in malaria
and local effects through
ePCR binding are implicated.
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MALARIA
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Microscopic Features
(Left) Cardiac vessels show
sequestered parasites in
a cerebral malaria patient.
lthough rare events have
been reported in experimental
malaria infections, no
tissue damage is seen in
ediatric malaria. (Right) A
section of spleen on CD8
immunohistochemistry
from a patient with malaria
demonstrates enormous
quantities of pigment
representing parasites, free
igment, and macrophages.
The spleen is the primary
arasite clearance site by
hagocytosis and digestion.
(Left) A liver section from a
child who died of cerebral
malaria demonstrates
ortal triads without
significant pigment, and
many macrophages
scattered throughout
the parenchyma, with
igment suggesting a recent
infection. (Right) A section
of liver from a patient with
multiple episodes of malaria
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
infection shows scattered
igment in macrophages
(recent infection) as well as
concentrations of pigment in
the portal triad (remote
infection).
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(Left) Small bowel with
denuded epithelium
(postmortem artifact)
demonstrates dense
sequestration in the
capillary that runs along
the base of the mucosal
surface. The GI tract
including stomach, small
bowel, and colon, is a large
site for vascular parasites
sequestration. (Right) Dense
sequestration of Plasmodium
falciparum parasites is
seen within the small vessels
of the lamina propria of
the small bowel, which
correlates strongly with dense
sequestration in the brain.
Histology and Cytology
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Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
MALARIA
(Left) Dense sequestration
of parasitized red blood
cells line the villus surface
in this active placental
malaria infection. IPT during
regnancy works at the
opulation level to prevent
lacental malaria. (Right)
fibrin clot within a
lacenta shows collections o
malaria pigment consistent
with prior infection during
regnancy. There is no active
malaria.
(Left) Placenta from an
active malaria infection
demonstrates a monocyte
with pigment and many
arasitized red blood
cells in the maternal
blood space. Parasitized
cells are not found in the
fetal circulation. (Right) A
sequestered parasite ,
bound through var2CSAtype PfEMP-1 protein to
chondroitin sulfate on the
lacental surface, is shown
in the placenta of active
malaria infection. Note the
numerous other parasitized
red cells in the maternal
vascular space.
(Left) Several segments
of brain vessels from a
ostmortem smear show
redominantly parasite
igment, free and within
macrophages , in a case
of cerebral malaria. (Right)
High magnification of a
cerebral blood vessel in
a brain smear after death
demonstrates mature
Plasmodium falciparum
arasites with characteristic
igment globule (black)
and purple-blue cytoplasm
. The presence of >
50 parasites in this vessel
segment is diagnostic of
cerebral malaria.
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MALARIA
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Peripheral Blood Films
(Left) Ring-stage parasites
are shown from a peripheral
blood of a patient infected
with malaria. With these
forms, it is not possible to
definitively speciate the
arasite or differentiate
from Babesiosis. (Right) A
monocyte, neutrophil, and red
blood cells are shown with a
banana-shaped Plasmodium
falciparum gametocyte
The ring stage and mature
ametocyte stage are the only
forms of P. falciparum typically
seen in peripheral blood due
to sequestration of the later
stages.
(Left) A ring stage and
amoeboid trophozoite stage
of Plasmodium vivax is
shown with the characteristic
Schffner dots on the red cell.
Note that the infected cells
are larger than uninfected
cells, as they are reticulocytes
(younger). A lymphoid cell is
resent. (Right) The amoeboid
forms of Plasmodium
vivax are distinct from the
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
other malaria species’ more
round trophozoite forms. In
this thicker part of the smear,
morphology is more difficult to
read.
.
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(Left) Plasmodium ovale
typically infects younger cells
(reticulocytes) so that the
cell appears larger than the
uninfected cells around it.
Note the oval shape of the
infected cell and the Schffner
dots
on the surface. A
ametocyte is also present.
(Right) Plasmodium malariae
can demonstrate a "band"
form in peripheral blood as
well as schizonts with a central
olden pigment ("daisy"
forms). An early trophozoite
stage parasite is also seen.
MR Findings and Retinal Pathology
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Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
MALARIA
(Left) A child with
retinopathy-positive CM,
imaged on a 0.35T Signa
Ovation Excite MR (GE
Health Care) is shown on
axial T2 view (TR340, TE
121) with diffuse brain
swelling with complete loss
of sulcal markings. (Courtesy
T. E. Taylor, DO.) (Right)
child with retinopathy-
ositive cerebral malaria is
shown on mid-sagittal T1
FLAIR (TR2100, TE 26) with
diffuse brain swelling with
effacement of the prepontine
cistern. (Courtesy T. E.
Taylor, DO.)
(Left) The retina of a child
who died from cerebral
malaria demonstrates
sequestration in the
retinal vessels of late-stage
arasites, which parallels
sequestration in the brain.
This sequestration produces
changes visible in the
retina during life. (Courtesy
V. White, MD.) (Right)
Retina in cerebral malaria
demonstrates innumerable
white centered hemorrhages
in the retinal vessels,
which mirror the ring
hemorrhages in the brain.
(Courtesy I. MacCormick,
MD.)
(Left) The vessels of the
retina have sequestration
of parasites as is seen
in the brain in cerebral
malaria and produce
characteristic orange
or white vessels due to
decreased hemoglobin from
arasite consumption and
red cell flow. (Courtesy I.
MacCormick, MD.) (Right)
Sequestration in the retina
in cerebral malaria causes
eripheral whitening of
the retina which, by
angiography, is consistent
with reduced blood flow/
ischemia. (Courtesy I.
MacCormick, MD.)
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FREE-LIVING AMEBIASIS
High magnification of an amebic trophozoite on a
Pap stain from a brain FNA shows the heterogeneous
cell body and distinctive nucleus . The ruffled
membrane cannot be seen.
TERMINOLOGY
Synonyms
Brain-eating ameba
Free-living ameba
Definitions
Greek: "Akantha" (thorn) + "amoibe" (change)
Balamuthia mandrillaris from Balamuth, a
parasitologist + mandrill (baboon, from which it was
isolated)
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
Naegleria from Ngler, an Austrian bacteriologist +
fowleri from Fowler, who 1st described (with Carter)
Manifestations
Naegleriasis: Primary amebic meningoencephalitis
Acanthamoebiasis or balamuthiasis: Granulomatous
amebic encephalitis
ETIOLOGY/PATHOGENESIS
Environmental Exposure
Acanthamoeba are ubiquitous organisms found in
water sources as well as soil
Primary reservoir of Legionella pneumophila bacteria
Staphylococcus (including MRSA) and Campylobacter
replicate inside parasite and may be spread this way
Often found in nasal passages of normal hosts
(colonization)
Contamination of contact lens solutions, improper
disinfection of contacts, or unclean hands can lead
to keratitis
Balamuthia is found in temperate regions of world and
enters body via scrapes or inhaled dust
Unlike Acanthamoeba and Naegleria, does not feed
on bacteria
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Naegleria are found in warm fresh water sources as well
as soil
High magnification of a tissue biopsy (skin) from a patient
with disseminated amoebiasis shows the distinctive
trophozoite cell body with the ruffled membrane
amid apoptotic debris.
Exposure via nasal passages from water allows direct
entry of ameba into cribriform plate
May be reservoir of L. pneumophila and other
bacteria
Infectious Agents
Acanthamoeba species
> 20 species of Acanthamoeba exist, with 11 causing
human disease (Acanthamoeba castellanii most
commonly studied)
Causing human disease: Acanthamoeba
astronyxis, Acanthamoeba byersi, A. castellanii,
Acanthamoeba culbertsoni, Acanthamoeba hatchetti,
Acanthamoeba keratitis, Acanthamoeba lugdunensis,
Acanthamoeba palestinensis, Acanthamoeba
polyphaga, Acanthamoeba quina, Acanthamoeba
rhysodes
Not causing human disease: Acanthamoeba
comandoni, Acanthamoeba divionensis,
Acanthamoeba healyi, Acanthamoeba jacobsi,
Acanthamoeba lenticulata, Acanthamoeba
mauritaniensis, Acanthamoebaa pearcei,
Acanthamoeba pustulosa, Acanthamoeba royreba,
A. castellanii Poussard, Acanthamoeba triangularis,
Acanthamoeba tubiashi
15-35 m in length
Cyst form in tissue is resistant to immune clearance
and may lead to recurrence of infection
Unique replicative host for several viruses including
Mimivirus, Pandoravirus, and Megavirus
Balamuthia mandrillaris
Single species isolated from a baboon in 1986, fully
described and reclassified in 1993
30-120 m in length
Naegleria species
Occurs as trophozoites, cysts, or flagellated form
Trophozoite (10-35 m) is found in human tissue
Flagellated form may be found in CSF
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FREE-LIVING AMEBIASIS
Etiology
Acanthamoeba are ubiquitous organisms found in
water sources as well as soil
Balamuthia is found in temperate regions of world
and enters body via scrapes or inhaled dust
Naegleria are found in warm fresh water sources as
well as soil
Clinical Issues
Acanthamoeba and Balamuthia
400 cases of GAE due to Acanthamoeba and 200
cases due to Balamuthia reported worldwide (> 95%
mortality)
Naegleria
150 cases reported since discovery in 1965 (> 95%
mortality)
Key Facts
Microscopic Pathology
Trophozoites (15-45 m in diameter)
Cystic forms (15-20 m in diameter)
PAM
GAE
Skin lesions
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
Clear nucleus with dense central nucleolus;
heterogeneous cytoplasm with organelles and
vacuoles
Stellate endocysts with double wall (wrinkled)
Mixture of trophozoites, mononuclear cells, and
neutrophils may be present
Encephalitis with vasculitis and thrombosed vessels
Perivascular or periadnexal distribution of necrosis
and trophozoites
CLINICAL ISSUES
Epidemiology
Acanthamoeba and Balamuthia
~ 400 cases of granulomatous amebic encephalitis
(GAE) due to Acanthamoeba and 200 cases due to
Balamuthia have been reported worldwide
Occur most commonly in immunosuppressed
patients
Both can occur in several different forms of
immunosuppression
Balamuthia has shown clusters of transplantation-
associated infections via donor-organ transmission
> 95% mortality
Naegleria
~ 150 cases have been reported since discovery in
1965
Occur in any patient exposed via nasal passages to
fresh water containing the parasite
> 95% mortality
Presentation
Primary amebic encephalitis (PAM) and GAE
Headache, fever, fatigue, nausea, and vomiting
(early)
Severe headache, neck stiffness, pain on neck
movement, photophobia (late)
Neurological symptoms (late)
Movement and speech disturbances
Unilateral paralysis
Behavioral changes, hallucinations, seizures, coma
Skin lesions occur (hematogenous spread), which
are deep and form erythematous hard nodules
(Acanthamoeba and Balamuthia)
Disseminated Acanthamoeba or Balamuthia
Skin lesions occur (hematogenous spread), which are
deep and form erythematous hard nodules without
neurologic involvement
Acanthamoeba keratitis
Redness, irritation, and cloudiness of cornea with
possible ulceration and blindness
Treatment
Early diagnosis treated with miltefosine with
hypothermia for Acanthamoeba/Balamuthia
Combinations of antibiotics and antiparasitics have
been tried but with very rare survival (2 cases prior to
2013)
No effective treatment for Naegleria
Prognosis
Very few patients survive PAM or GAE, but
combination of early diagnosis, miltefosine, and
hypothermia can lead to survival
Survivors will most likely have severe brain damage or
impairment if diagnosis is delayed
IMAGE FINDINGS
CT Findings
Brain edema with diffuse enhancement of meninges
(after contrast) with no focal lesions
MICROBIOLOGY
Culture
Acanthamoeba and Naegleria
May be inoculated onto agarose plates containing
lawn of bacterial growth to propagate parasite and
identify
Balamuthia
Will grow on a range of mammalian cell culture
lines or in mice after intranasal or intraperitoneal
inoculation
Will not grow on agarose plates with bacteria
MACROSCOPIC FEATURES
Brain in PAM
Cerebral edema
Uncal or cerebellar herniation may be present
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FREE-LIVING AMEBIASIS
Meninges may appear cloudy and purulent
Brain in GAE
Diffuse meningitis with cerebral edema
Focal softening, hemorrhage, or frank necrosis may be
present
MICROSCOPIC PATHOLOGY
Histologic Features
Parasite features in tissue
Trophozoites
Clear nucleus with dense central nucleolus
Heterogeneous cytoplasm with organelles and
vacuoles
Cystic forms
Stellate endocysts with a double wall (wrinkled)
Not seen in human tissue for Naegleria
PAM
Affected areas include olfactory bulbs (site of entry),
small to midsize artery perivascular spaces, and
frontal and temporal gray matter
Mixture of trophozoites, mononuclear cells, and
neutrophils may be present
~ 50% of cases are associated with myocarditis
GAE
Subacute to chronic meningitis
Encephalitis with vasculitis and thrombosed vessels
Giant cells may be present in immunocompetent
hosts
Skin lesions
Present in perivascular or periadnexal distribution
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
Necrosis of tissue with limited inflammation (occur
in immunosuppressed) containing replicating
trophozoites
ANCILLARY TESTS
Histochemistry
Trichome stain
Similar to other amebae, highlights nucleus in red
(vs. dark brown to black of human cells)
Silver stains
Highlights ruffled membrane of trophozoites and
internal structure of cysts
Periodic acid-Schiff
Highlights ruffled membrane deep purple
Immunofluorescence
Nasal swabs from suspected patients or material for
direct sample (e.g., brain, skin lesions) can be tested by
direct fluorescent antibody assay
DIFFERENTIAL DIAGNOSIS
Encephalitis/Meningoencephalitis
Acanthamoeba, Balamuthia, and Naegleria may appear
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very similar to each other on tissue biopsies and
require culture, immunofluorescence, or molecular
testing to distinguish
1
Entamoeba histolytica, when disseminated from bowel,
may appear very similar to the free-living ameba,
but forms large, solitary abscesses rather than diffuse
processes
Skin Lesions
Panniculitis, periadnexal inflammatory conditions
If amebae are rare, inflammation may predominate
and make diagnosis challenging
Coccidioides and Blastomycosis infections
Cross sections of yeast in disseminated or primary
skin lesions may be confused with amebae
Special stains for fungi will be positive for the yeast
DIAGNOSTIC CHECKLIST
Clinically Relevant Pathologic Features
Rapid or unexplained death after exposure to fresh
water in a normal host
Pathologic Interpretation Pearls
Amebae appear as round heterogeneous bodies with
a distinct nucleus surrounded by a ruffled membrane
with limited inflammation
Can be difficult to identify in macrophage-rich
necrotic lesions; require close scrutiny
SELECTED REFERENCES
1. Baig AM et al: Novel chemotherapeutic strategies in the
management of primary amoebic meningoencephalitis
due to Naegleria fowleri. CNS Neurosci Ther. 20(3):289-90,
2014
2. Roy SL et al: Risk for transmission of Naegleria fowleri from
solid organ transplantation. Am J Transplant. 14(1):163-71,
2014
3. Schuppler M: How the interaction of Listeria
monocytogenes and Acanthamoeba spp. affects growth
and distribution of the food borne pathogen. Appl
Microbiol Biotechnol. 98(7):2907-16, 2014
4. Sood A et al: Prompt diagnosis and extraordinary survival
from Naegleria fowleri meningitis: a rare case report.
Indian J Med Microbiol. 32(2):193-6, 2014
5. Centers for Disease Control and Prevention (CDC):
Investigational drug available directly from CDC for the
treatment of infections with free-living amebae. MMWR
Morb Mortal Wkly Rep. 62(33):666, 2013
6. Diaz JH et al: Emerging trends in free-living amebic
infections of the brain: implications for organ
transplantation. J La State Med Soc. 165(6):314-8, 2013
7. Finsterer J et al: Parasitoses of the human central nervous
system. J Helminthol. 87(3):257-70, 2013
8. Kato H et al: Successful treatment of granulomatous
amoebic encephalitis with combination antimicrobial
therapy. Intern Med. 52(17):1977-81, 2013
9. LaFleur M et al: Balamuthia mandrillaris
meningoencephalitis associated with solid organ
transplantation--review of cases. J Radiol Case Rep.
7(9):9-18, 2013
10. Lobo SA et al: Diagnostic challenges in Balamuthia
mandrillaris infections. Parasitol Res. 112(12):4015-9, 2013
11. Lorenzo-Morales J et al: Acanthamoeba keratitis: an
emerging disease gathering importance worldwide? Trends
Parasitol. 29(4):181-7, 2013
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FREE-LIVING AMEBIASIS
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Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
(Left) Cross section of a
brain from the autopsy
of a patient who died
of Balamuthia infection
demonstrates cerebral
necrosis . (Right)
Parenchymal foci of amebic
infection are hemorrhagic
and necrotic , as are
these in the temporal lobe
of a child who succumbed
to the disease caused by
Balamuthia mandrillaris.
(From DP: Neuro.)
(Left) Meningoencephalitis
due to Naegleria fowleri
typically has intense
neutrophilic inflammation
and hemorrhage .
(From DP: Neuro.) (Right)
section of cerebellar
tissue from granulomatous
amebic encephalitis fatality
demonstrates innumerable
trophozoites admixed
with normal neuronal
cells . Note the lack of
inflammation.
(Left) High magnification
of a cerebellar tissue
section from a patient with
ranulomatous amebic
encephalitis demonstrates
the perivascular
distribution of the
trophozoites . Note the
distinctive nuclei of the
organisms. (Right) A ring
of trophozoites around
a vessel is shown with a
eriphery of neutrophils
and necrosis within this brain
section.
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