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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_182_библиотеки_им_акад_М_И_Перельмана.pdf
FREE-LIVING AMEBIASIS
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Gross and Microscopic Images
(Left) Lung tissue from an
autopsy of a patient who
died of Balamuthia infection
demonstrates infiltrates in
the parenchyma, which are
mostly trophozoites, necrosis,
and limited inflammation.
(Right) High magnification
of lung tissue from a
disseminated Balamuthia case
on PAS stain demonstrates
the purple rim of ruffled
membrane surrounding the
nucleus of a trophozoite.
(Left) Medium-power view
of the lungs at autopsy of a
atient with disseminated
Balamuthia shows a large
trophozoite admixed
with inflammation and
necrosis. Note the large size
of the trophozoite, which
may be much larger than
canthamoeba and Naegleria.
(Right) Low-power view of a
skin biopsy from a patient with
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
disseminated Acanthamoeba
infection shows apparent
anniculitis , cellulitis ,
hemorrhage , and necrosis
. Inflammation is limited at
high power.
(Left) High magnification
of a skin biopsy from a
atient with disseminated
canthamoeba infection
demonstrates perivascular
and periadnexal spread of
trophozoites with necrosis and
apoptotic debris. Note the
lack of inflammation. (Right)
Large vessels with diffuse
infiltration by trophozoites
of Acanthamoeba are shown
surrounded by necrosis and
apoptotic debris.
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Microscopic Features
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FREE-LIVING AMEBIASIS
(Left) High magnification of
canthamoeba trophozoites
in tissue
surrounded by mostly
apoptotic
cells. Note the lack of
inflammation, indicating
this patient is severely
immunosuppressed. (Right)
In contrast to macrophages,
amebic trophozoites
, here of Balamuthia
mandrillaris, have lower
nuclear:cytoplasmic ratios,
smaller and rounder nuclei,
and more prominent
nucleoli. (From DP: Neuro.)
is shown
and necrotic
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
(Left) PAS staining can
highlight cytoplasmic
lycogen in amebae ,
helping to differentiate
them from macrophages.
(From DP: Nonneoplastic
Pediatrics.) (Right) Shrinkage
artifact produces the
artifactual pentagonal
shape in an encysted
canthamoeba. (Courtesy A.
Yachnis, MD.)
(Left) GMS highlights cyst
walls of Acanthamoeba
species. Cysts are often
found in chronic GAE due to
canthamoeba, occasionally
in chronic examples due
to Balamuthia mandrillaris,
and not in primary amebic
meningoencephalitis due to
Naegleria fowleri. (Courtesy
. Yachnis, MD.) (Right)
Trichrome stain of tissue
infected with Balamuthia
shows the large trophozoites
admixed with necrosis
around a vessel. Note the
distinctive pink color of the
arasite nucleus.
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AMERICAN TRYPANOSOMIASIS
Amastigotes are seen in cardiac myocytes during
acute Chagas myocarditis. Note the characteristic
"dot" (nucleus ) and "dash" (kinetoplastid ),
which are diagnostic.
TERMINOLOGY
Synonyms
Chagas disease
Named after Brazilian physician Carlos Chagas (1909)
Definitions
Trypano: Greek "trypano" (borer)
Soma: Greek "soma" (body)
Named after Brazilian physician Oswaldo Cruz
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
ETIOLOGY/PATHOGENESIS
Infectious Agents
Trypanosoma cruzi, a flagellate protozoa
Member of the class Kinetoplastida
Vector-borne, zoonotic disease
Triatomine bug (reduviid bugs)
Found in southern USA, Central America, and South
America
Live in cracks and holes in cement housing, animal
kennels, chicken coops, and other areas
Cases are also reported from contaminated food and
water, blood transfusions, and organ transplants, and
vertical transmission from mother to child
Severe acute Chagas myocarditis is seen, with amastigotes
, severe inflammation, and interstitial edema .
(Courtesy Franz von Lichtenberg Collection of Infectious
Disease Pathology, BWH.)
Nonspecific symptoms such as malaise, fever;
therefore, most acute infections are not diagnosed
Chagoma, a swelling at site of inoculation
Romaa sign: Parasite enters conjunctiva, causing
periorbital swelling
Very rarely may cause acute myocarditis, pericardial
effusion, or meningoencephalitis
Chronic phase
Cardiomegaly with ventricular aneurysms,
megaesophagus, megacolon; any smooth muscle
structure may be affected
Indeterminate phase
Serologic testing is positive for T. cruzi antibodies,
but there is no apparent clinical disease
20-30% will progress to overt clinical disease over
years
Treatment
Antiprotozoal treatment is recommended for those
with acute infection (benznidazole or nifurtimox)
Treatment is recommended for those < age 18 with
indeterminate-phase infection
Prognosis
20-30% of those with chronic infection will develop
end-stage cardiac or other parasite-related disease
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CLINICAL ISSUES
Epidemiology
8 million people are infected in South America
Estimated 300,000 are infected in USA
Endemic in South America
Most common in rural areas
Presentation
Acute phase
Incubation: 1-2 weeks
Acute phase lasts 8-12 weeks
IMAGE FINDINGS
Radiographic Findings
Although not specific for Chagas disease, radiographic
findings include cardiomegaly, megaesophagus on
barium swallow, and megacolon on barium enema
AMERICAN TRYPANOSOMIASIS
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
Etiology
Trypanosoma cruzi, a protozoan parasite
Macroscopic Pathology
Dilated cardiomyopathy
Megaesophagus
Megacolon
Microscopic Pathology
Acute phase
MICROBIOLOGY
Culture
Although parasites can be cultured in artificial media,
it is not necessary for diagnosis and treatment
MACROSCOPIC FEATURES
Mega-Organ Appearance
Dilated cardiomyopathy, ventricular apical aneurysm
is the most common cardiac lesion
Megaesophagus, megacolon, megaureter
MICROSCOPIC PATHOLOGY
Histologic Features
Acute phase
Diffuse parasitemia throughout tissues and in blood
Brisk periparasitic inflammatory reaction
Myocarditis with necrosis, edema and vascular
dilation
Inflammation and parasitemia in smooth muscle
and Auerbach plexus of gastrointestinal tract
Chronic phase
Mild chronic myocarditis, necrosis, edema, fibrosis
Parasites are rarely found in chronic phase
Immunosuppression
Central nervous system chagoma (reactivation) may
occur
Key Facts
Chronic phase
ANCILLARY TESTS
Serologic Testing
Necessary for diagnosis of indeterminate-phase disease
due to lack of parasitemia
DIFFERENTIAL DIAGNOSIS
Cardiac Manifestations
Dilated cardiomyopathy, hypertrophic
cardiomyopathy, atrioventricular block
Gastrointestinal Manifestations
Achalasia, gastroesophageal reflux disease, esophageal
malignancy, chronic megacolon, Hirschsprung disease
DIAGNOSTIC CHECKLIST
Pathologic Interpretation Pearls
"Dot-dash" pattern of nucleus and kinetoplast in
clusters within cytoplasm of cardiac myocyte is
diagnostic
SELECTED REFERENCES
1. Andrade DV et al: Acute chagas disease: new global
Diffuse parasitemia in tissues and blood
Brisk periparasitic inflammatory reaction
Myocarditis with necrosis, edema, and vascular
dilation
Inflammation and parasitemia in smooth muscle of
gastrointestinal tract
Mild chronic myocarditis, necrosis, edema
Demonstrates necrosis, numerous amastigotes
challenges for an old neglected disease. PLoS Negl Trop Dis.
8(7):e3010, 2014
MICROSCOPIC FEATURES
(Left) Severe acute Chagas myocarditis demonstrates inflammation and focal myocyte necrosis . (Center) Chronic myocarditis displays
myocyte hypertrophy, interstitial inflammation, and fibrosis. (Right) Chagas megaesophagus has an inflammatory infiltrate around the myenteric
plexus and an absence of neurons . (Courtesy Franz von Lichtenberg Collection of Infectious Disease Pathology, BWH.)
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LEISHMANIASIS
H&E section of cutaneous leishmaniasis shows an
exuberant chronic inflammation in the dermis in response
to the organisms.
TERMINOLOGY
Abbreviations
Cutaneous leishmaniasis (CL)
Mucocutaneous leishmaniasis (MCL)
Visceral leishmaniasis (VL)
Synonyms
CL
Oriental sore, Uta, chiclero ulcer, tropical sore,
Bagdad boil, Baure ulcer, Aleppo button, Delhi boil
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
MCL
Forest yaws, espundia, pian bois, American
leishmaniasis
VL
Kala-azar, black fever, dumdum fever
Definitions
William Leishman (1865-1926): Leishmaniasis
Charles Donovan (1863-1951): Leishmania donovani,
Leishman-Donovan bodies (protozoa seen in tissue)
Trypanosomatids (Trypanosoma species, Leishmania
species containing kinetoplastids)
From Greek: "Trypanos" (borer) + "soma" (body)
"Kineto" (movement) + "plastid" (organelle):
Extranuclear DNA containing structure at base of
flagellum
ETIOLOGY/PATHOGENESIS
Environmental Exposure
Rural >> urban areas
Climate and other environmental changes have
potential to expand geographic range of sand fly
vectors
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Clinical photograph shows mucocutaneous
leishmaniasis. Involvement of the mucous membranes is
notorious for producing destructive lesions. (From DP:
Nonneoplastic Derm.)
Infectious Agents
Vector-borne disease (Lutzomyia and Phlebotomus:
sandflies) caused by obligate intracellular protozoa of
genus Leishmania
Infection in human is caused by ~ 21 of 30 species that
infect mammals
Life cycle: Flagellate phase (promastigote) within
vector and retracted flagellum (amastigote) in infected
human tissue
L. donovani complex
L. donovani (CL, VL)
Leishmania infantum (a.k.a. Leishmania chagasi in
New World (north of South America) (CL, VL)
Leishmania mexicana complex
L. mexicana (CL)
Leishmania amazonensis (CL, MCL)
Leishmania venezuelensis (CL)
Leishmania tropica (CL)
Leishmania major (CL)
Leishmania aethiopica (CL)
Subgenus Viannia
Leishmania (Viannia) braziliensis (CL, MCL)
Leishmania (Viannia) guyanensis (CL, MCL)
Leishmania (Viannia) panamensis (CL, MCL)
Leishmania (Viannia) peruviana (CL, MCL)
CLINICAL ISSUES
Epidemiology
Incidence
90% of VL cases occur in 6 countries: Bangladesh,
Brazil, Ethiopia, India, South Sudan, and Sudan
(WHO)
CL cases occur in Afghanistan, Algeria, Brazil,
Colombia, Islamic Republic of Iran, Pakistan, Peru,
Saudi Arabia, and Syrian Arab Republic
90% of MCL cases occur in Plurinational State of
Bolivia, Brazil, and Peru
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LEISHMANIASIS
Terminology
Leishmaniasis is a parasitic disease that is found in
parts of the tropics, subtropics, and southern Europe
Spread by bite of phlebotomine sand flies
Clinical Issues
Most common form is cutaneous leishmaniasis
Visceral leishmaniasis (VL) affects spleen, liver, and
bone marrow and can be life threatening
Mucocutaneous leishmaniasis is a less common form
(South America)
90% of VL cases occur in 6 countries
Bangladesh, Brazil, Ethiopia, India, South Sudan,
and Sudan (WHO)
Key Facts
Microscopic Pathology
Amastigote forms are 2-4 m, round to oval shaped,
and can be seen within macrophages
Marked ulceration with pseudoepitheliomatous
hyperplasia and suppurative granulomata can be seen
In VL, "post kala-azar" lesions consist of macrophages,
epithelioid cells, and lymphoplasmacytic infiltrate
Ancillary Tests
PCR is important for speciation and guiding
treatment
Top Differential Diagnoses
Histoplasmosis, rhinoscleroma, granulomatous
disease
Malakoplakia, malignant neoplasms, ulcers
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
Rare cases reported in southern Texas
Classified as a neglected tropical disease (NTD,
WHO)
Presentation
Distinct clinical forms based on location and species
causing infection
CL causes skin lesions, which may change in
shape and size, and progress up lymphatic tracts
(sporotrichoid pattern)
VL causes enlargement of spleen, liver, and bone
marrow, and is life threatening
Pentad of fever, weight loss, hepatosplenomegaly,
pancytopenia, and hypergammaglobulinemia
Onset can be insidious or sudden
MCL is less common form with manifestations in
mucosal areas (possibly due to host genetic factors)
in regions overlapping with CL
Treatment
Treatment decisions should be individualized, with
expert consultation
In March 2014, FDA approved oral agent miltefosine
for treatment of cutaneous, mucosal, and visceral
leishmaniasis caused by L. donovani in adolescents and
adults who are not pregnant or breastfeeding
Prognosis
Depends on species, host immune status, Leishmania
forms, and geographic location
Outcomes of CL & MCL >> VL (where VL is often
fatal)
MICROBIOLOGY
Culture
Required for drug screening, animal inoculation
(xenodiagnosis, rarely used)
Schneider insect, M199, or Grace medium
(monophasic)
Novy-McNeal-Nicolle or Tobie medium (diphasic)
Specialized reference labs may provide media to
patient site for direct inoculation and complete testing
in reference laboratory
MACROSCOPIC FEATURES
General Features
CL
In Old World (Asia, Africa, Middle East), disease
usually presents as papules, nodules, flat plaques,
and wart-like lesion
Unusual presentations include paronychial,
chancriform, annular, zosteriform, erysipeloid
forms, and palmoplantar form
MICROSCOPIC PATHOLOGY
Histologic Features
CL has 4 forms: Acute, chronic, recidivous, and
disseminated
Acute
Ulcerated epidermis with hyperkeratosis,
acanthosis, or atrophy
Exuberant infiltrate of lymphocytes, plasma cells,
parasitized macrophages, eosinophils
Amastigote forms are 2-4 m, round to oval
shaped
Amastigotes within macrophages, demonstrate
"dot-dash" pattern (nucleus-kinetoplast, oil
immersion)
Amastigotes located at periphery of macrophages
is referred to as "marquee" sign
Chronic
Few organisms
Tuberculoid granulomata necrosis
Recidivous
Similar to lupus vulgaris
Disseminated
Mainly in immunocompromised patients with
many parasitized cells
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LEISHMANIASIS
MCL
Marked ulceration with pseudoepitheliomatous
hyperplasia
Suppurative granulomata may be present
Amastigote forms may be present
VL
"Post kala-azar" lesions consist of macrophages,
epithelioid cells, and lymphoplasmacytic infiltrate
Spleen or liver biopsy/aspirate: Amastigote forms
may be seen
Cytologic Features
Giemsa-stained direct smear can be helpful in
identifying free amastigotes
ANCILLARY TESTS
Immunohistochemistry
G2D10 antibody is more sensitive than H&E
PCR
Important for exact speciation and guidance of
treatment
DIFFERENTIAL DIAGNOSIS
Histoplasmosis
Similar size to leishmania but stains with silver stains,
shows narrow-based budding and a periorganism halo
Rhinoscleroma
Klebsiella rhinoscleromatis, which is a rod-shaped
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
bacillus and not oval like Leishmania
"Mikulicz cells" are vacuolated macrophages often with
bacteria inside
Granulomatous Disease
TB, sporotrichosis, and sarcoidosis can be in
differential diagnosis of leishmaniasis later in
granulomatous stages
SELECTED REFERENCES
1. de Paulo LF et al: Mucocutaneous leishmaniasis: mucosal
manifestations in an endemic country. Int J Infect Dis.
17(11):e1088-9, 2013
2. Singh A et al: Histopathological features in leprosy,
post-kala-azar dermal leishmaniasis, and cutaneous
leishmaniasis. Indian J Dermatol Venereol Leprol.
79(3):360-6, 2013
3. Strazzulla A et al: Mucosal leishmaniasis: an
underestimated presentation of a neglected disease.
Biomed Res Int. 2013:805108, 2013
4. Bari AU: Clinical spectrum of cutaneous leishmaniasis: an
overview from Pakistan. Dermatol Online J. 18(2):4, 2012
5. Newlove T et al: Old World cutaneous leishmaniasis.
Dermatol Online J. 18(12):32, 2012
6. Afghan AK et al: Clinical manifestations and distribution
of cutaneous leishmaniasis in pakistan. J Trop Med.
2011:359145, 2011
7. Daneshbod Y et al: Clinical, histopathologic, and cytologic
diagnosis of mucosal leishmaniasis and literature review.
Arch Pathol Lab Med. 135(4):478-82, 2011
8. El-Khalawany M et al: Clinicopathological features and the
practice of diagnosing infectious cutaneous granulomas in
Egypt. Int J Infect Dis. 15(9):e620-6, 2011
9. Mokni M et al: [Histology of cutaneous leishmaniasis.] Ann
Dermatol Venereol. 138(4):354-6, 2011
10. Ruocco E et al: The practical use of cytology for diagnosis
in dermatology. J Eur Acad Dermatol Venereol. 25(2):125-9,
2011
11. Clem A: A current perspective on leishmaniasis. J Glob
Infect Dis. 2(2):124-6, 2010
12. Petersen CA: Leishmaniasis, an emerging disease found in
companion animals in the United States. Top Companion
Anim Med. 24(4):182-8, 2009
13. Mittal R et al: Post-kala-azar dermal leishmanasis occurring
after 10 years of treated kala azar. Int J Dermatol.
41(12):875-6, 2002
14. Landau M et al: Leishmaniasis recidivans mimicking lupus
vulgaris. Int J Dermatol. 35(8):572-3, 1996
15. Azulay RD et al: Immune-clinical-pathologic spectrum of
leishmaniasis. Int J Dermatol. 34(5):303-7, 1995
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Malakoplakia
Aggregates of histiocytes containing small, round to
oval, targetoid structures (Michaelis-Gutmann bodies)
Negative for organism
Malignant Neoplasms
Primary skin lesions or metastases
Lymphoma (e.g., angiocentric NK/T-cell lymphoma)
Lethal midline granuloma
Negative for classic histological features and organisms
Ulcers
Traumatic ulcers, stasis ulcers
Other Infectious Diseases
Fungal: Chromoblastomycosis, lobomycosis, deep
fungal infection
Bacterial: Cutaneous diphtheria, tropical pyoderma,
and other mycobacterioses
Viral: Orf
Microscopic and Gross Features
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p
A
p
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
LEISHMANIASIS
(Left) Microscopic
examination shows chronic
inflammatory and vacuolate
histocytic cellular infiltrate
throughout the dermis.
Most histocytes are filled
with amastigotes. (Right)
There are numerous
vacuolated histocytes filled
with amastigotes that are
spherical and 2-4 m in
diameter. Amastigotes
have a thin cell membrane,
cytoplasm, a delicate
spherical nucleus, and a rodshaped kinetoplast .
(Left) This slide demonstrates
eripheralization of
amastigotes within
histiocytes, or the
"marquee" sign. Note the
nucleus and opposite
small kinetoplast in
one of the amastigotes.
(From DP: Nonneoplastic
Derm.) (Right) Giemsa
stain demonstrates multiple
amastigotes within the
cytoplasm of histiocytes.
lthough hard to appreciate
here, nuclei were evident
within these organisms
when viewed through the
microscope. (From DP:
Nonneoplastic Derm.)
(Left) This lesion of
cutaneous leishmaniasis
demonstrates numerous
amastigotes within the
cytoplasm of numerous
histiocytes that filled
the dermis. (From DP:
Nonneoplastic Derm.)
(Right) Cutaneous
leishmaniasis manifests
as a typical round to oval
ainless ulcer with a welldelineated elevated border
on an exposed area of skin.
This patient spent 3 months
in Peru and did not recall a
bite. (Courtesy T. Sofarelli,
PA-C.)
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TOXOPLASMOSIS
Toxoplasma immunohistochemical stain highlights
bradyzoites of Toxoplasma gondii on a brain biopsy of an
immunocompromised patient. Inflammation can range
from frank necrosis to minimal reaction.
TERMINOLOGY
Synonyms
Piringer-Kuchinka lymphadenitis
Definitions
Greek: "Toxon" (bow shaped) + "plasma" (shape or
form)
ETIOLOGY/PATHOGENESIS
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
Infectious Agents
Disease caused by obligate intracellular parasite,
Toxoplasma gondii
Member of Apicomplexa parasites (Coccidia, Plasmodia)
containing an apicoplast used for cell penetration
CLINICAL ISSUES
Epidemiology
Toxoplasmosis is 2nd to only nontyphoidal Salmonella
as a leading cause of death attributed to food-borne
illness in United States
Humans can become infected by
Eating undercooked meat of animals harboring
tissue cysts (food borne)
Consuming food/water contaminated with cat
feces (zoonotic)
Contaminated environmental samples, blood
transfusion, or organ transplantation, or
transplacentally from mother to fetus (congenital)
1 of 5 neglected parasitic infections in USA along with
Chagas disease, neurocysticercosis, toxocariasis, and
trichomoniasis
Age-adjusted seroprevalence rate in USA is 22.5%
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Most common cause of lymphadenitis in USA and
commonly presents as cervical unilateral or bilateral
lymphadenopathy
1
Intraoperative frozen section smear from a brain biopsy
shows the slow-growing protozoan forms of Toxoplasma
bradyzoites encased in cysts with a cyst wall . Cysts
are rare in the immunocompetent.
Definitive hosts for T. gondii are members of family
Felidae (e.g., lions, cats)
Risk of congenital toxoplasmosis infection is lowest in
1st trimester of pregnancy and highest in last trimester
Congenital toxoplasmosis is more clinically severe if
infection occurs in 1st trimester
Life cycle
Sexual component that occurs only within cats
Asexual component that can occur within virtually
all warm-blooded animals, including humans, cats,
and birds
Presentation
Congenital toxoplasmosis
Characterized by ocular lesions, cerebral
calcification, and hydrocephalus
Visualization of organisms in placenta relates to fetal
outcome (more cysts and pseudocysts are present in
severe cases)
Ocular disease is the most common manifestation of
congenital toxoplasmosis
Toxoplasma lymphadenitis in immunocompetent
adults is usually self-limited
Differential diagnosis of tonsillitis, adenoid
hyperplasia, and chronic neck lymphadenopathy
should include Toxoplasma
Cerebral toxoplasmosis in immunocompromised
persons
Causes encephalitis and abscess (usually in HIVpositive patients)
Immunodeficient patients are at risk for more severe
manifestations
Multisystem disease occurs
Laboratory Tests
IgM and IgG titers against Toxoplasma are diagnostic of
acute exposure and past exposure
Important screening tool for women prior to
pregnancy/childbirth
Negative PCR does not rule out active infection
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TOXOPLASMOSIS
Etiology
Disease caused by obligate intracellular parasite,
Toxoplasma gondii
Clinical Issues
Leading cause of death attributed to food-borne
illness in United States; can be multisystem disease
Definitive hosts for T. gondii are members of family
Felidae (e.g., lions, cats)
Congenital toxoplasmosis
Toxoplasma lymphadenitis in immunocompetent
adults is usually self-limited
Cerebral toxoplasmosis in immunocompromised
persons
Multisystem disease occurs
Treatment
Usually self-limited in immunocompetent adults
Pyrimethamine and either sulfadiazine or clindamycin
are usually used in symptomatic patients
Treatment of infection in fetus and infant during 1st
year of life has been demonstrated to significantly
improve clinical outcome
Prognosis
Immunocompetent: Self-limited
Immunosuppressed: Severe manifestations can result
in prolonged neurological deficits and death
Congenital: Severe manifestations lead to neurological
deficits, visual problems, and death
Prevention
Change and dispose of cat litter daily
Avoid drinking untreated water and unpasteurized
milk
Cook food to safe temperatures
Pregnant or immunocompromised should not change
or handle cat litter boxes
MICROBIOLOGY
Culture
HeLa cells (research)
MACROSCOPIC FEATURES
Lymph Node
Lymph nodes involved by toxoplasmosis are < 3 cm in
diameter
Cut sections of biopsied lymph nodes are firm, white
MICROSCOPIC PATHOLOGY
Histologic Features
Lymph nodes
Well-preserved nodal architecture
Key Facts
Microscopic Pathology
Toxoplasma lymphadenitis shows classic triad of
florid follicular hyperplasia, monocytoid B cells, and
phagocytosing macrophages
Cerebral toxoplasmosis may show widespread
microglial nodules containing bradyzoites and
tachyzoites of T. gondii with multinucleated giant
cells and necrosis
Pap stain may demonstrate organism &/or epithelioid
microgranulomas on FNA
Top Differential Diagnoses
Lymphoma, sinus histiocytosis with massive
lymphadenopathy, cat scratch disease, and
sarcoidosis or tuberculosis
CNS
Liver
Lung
Stomach
Classic triad: Florid follicular hyperplasia, prominent
parasinusoidal and parafollicular monocytoid B
cells, clustered macrophages engulfing debris
Monocytoid B cells are CD20(+), CD5(-), CD23(-),
Bcl-2(-), Bcl-6(-), and CD10(-)
Presence of cyst is diagnostic but rarely identified in
affected lymph nodes
Organisms are rarely seen in infected lymph node
Granulomata are unusual in toxoplasmosis
lymphadenitis, and giant cells are not seen
Clusters of epithelioid histiocytes in toxoplasmosis
lymphadenitis generally contain < 25 nuclei
"Triad" histologic diagnosis has an excellent
correlation with serology
Cerebral toxoplasmosis may show widespread
microglial nodules, containing bradyzoites and
tachyzoites with multinucleated giant cells and
necrosis
Rare CNS manifestations include nonnecrotizing,
diffuse, "encephalitic" ventriculitis in HIV and
hematological malignancy
May affect vessels walls and cause thrombotic
occlusion and vasculitis
May be within pseudocysts (bradyzoites) or as free
forms (tachyzoites)
Diffuse hepatitis with infiltration of portal tracts and
sinusoids by mononuclear cells with focal abscess
Toxoplasma cysts can be seen in histocytes and
granulomata
Pulmonary involvement is indicative of
disseminated disease in immunosuppressed patients
Toxoplasma can present in histiocytes, alveolar
lining cells, endothelial cells, and pseudocysts
containing tachyzoites
True cysts containing bradyzoites can be seen
Acute and chronic inflammatory infiltrates and
trophozoites
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
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