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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_182_библиотеки_им_акад_М_И_Перельмана.pdf
TOXOPLASMOSIS
T. gondii bradyzoites and tachyzoites can affect other
organs such as heart, skin, gastrointestinal tract, and
placenta
Cytologic Features
Pap stain may demonstrate organism on FNA &/or
epithelioid microgranulomas
Reactive lymphoid hyperplasia and tachyzoites within
lymphocytes
ANCILLARY TESTS
Immunohistochemistry
Toxoplasma antibody: Stains organisms in tissue
sections
Monocytoid B cells of reactive lymph node are
CD20(+), CD5(-), CD23(-), Bcl-2(-), Bcl-6(-), and
CD10(-)
DIFFERENTIAL DIAGNOSIS
Non-B-Cell Hodgkin Lymphoma, Nodular
Lymphocyte Predominant (LP)
LP cells are admixed with numerous small B
lymphocytes, epithelioid histiocytes, and CD21(+)
dendritic reticulum cells
Sinus Histiocytosis With Massive
Lymphadenopathy
Histiocytes and emperipolesis
Capsular and pericapsular inflammation and fibrosis
CNS Lymphoma in HIV
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
Nearly 100% of affected patients have evidence of
Epstein-Barr virus (EBV), usually single lesion with
solid enhancement
Toxoplasma usually presents as multiple lesions with
ring or nodular enhancement
Cat Scratch Disease
History of sustaining a scratch or bite from a cat, and
regional adenopathy proximal to site of inoculation
Stellate granulomata with central necrosis and positive
serology for Bartonella
Agents are Bartonella henselae and Afipia felis (rarely),
both gram-negative bacilli
Sarcoidosis or Tuberculosis
Larger epithelioid histiocytes clusters, presence of
multinucleated giant cells, and caseation
Clusters of epithelioid histiocytes in toxoplasmosis
lymphadenitis generally contain < 25 nuclei
Florid follicular hyperplasia is not typical of sarcoidosis
SELECTED REFERENCES
1. Butler NJ et al: Ocular toxoplasmosis II: clinical
features, pathology and management. Clin Experiment
Ophthalmol. 41(1):95-108, 2013
2. Paquet C et al: Toxoplasmosis in pregnancy: prevention,
screening, and treatment. J Obstet Gynaecol Can.
35(1):78-9, 2013
3. Fong MY et al: Unusual manifestation of cutaneous
toxoplasmosis in a HIV-positive patient. Trop Biomed.
27(3):447-50, 2010
4. Abedalthagafi M et al: Asymptomatic diffuse "encephalitic"
cerebral toxoplasmosis in a patient with chronic
lymphocytic leukemia: case report and review of the
literature. Int J Clin Exp Pathol. 3(1):106-9, 2009
5. Dubey JP et al: Toxoplasma gondii infection in humans
and animals in the United States. Int J Parasitol.
38(11):1257-78, 2008
6. Montoya JG et al: Management of Toxoplasma gondii
infection during pregnancy. Clin Infect Dis. 47(4):554-66,
2008
7. Viguer JM et al: Fine needle aspiration of toxoplasmic
(Piringer-Kuchinka) lymphadenitis: a cytohistologic
correlation study. Acta Cytol. 49(2):139-43, 2005
8.
Yarikta M et al: [Toxoplasmosis in patients with lymphoid
hyperplasia of the head and neck.] Kulak Burun Bogaz Ihtis
Derg. 13(5-6):132-4, 2004
9. Ganji M et al: Gastric toxoplasmosis in a patient with
acquired immunodeficiency syndrome. A case report
and review of the literature. Arch Pathol Lab Med.
127(6):732-4, 2003
10. Jones J et al: Congenital toxoplasmosis. Am Fam Physician.
67(10):2131-8, 2003
11. Pathan SK et al: Fine needle aspiration cytologic diagnosis
of toxoplasma lymphadenitis. A case report with detection
of a Toxoplasma bradycyst in a Papanicolaou-stained
smear. Acta Cytol. 47(2):299-303, 2003
12. Jones JL et al: Toxoplasma gondii infection in the United
States: seroprevalence and risk factors. Am J Epidemiol.
154(4):357-65, 2001
13. Hofman P et al: [Cardiac lesions in acquired
immunodeficiency syndrome (AIDS). Apropos of an
autopsy series of 25 cases.] Ann Pathol. 10(4):247-57, 1990
14. Sheibani K et al: "Monocytoid" cells in reactive follicular
hyperplasia with and without multifocal histiocytic
reactions: an immunohistochemical study of 21 cases
including suspected cases of toxoplasmic lymphadenitis.
Am J Clin Pathol. 81(4):453-8, 1984
15. Miettinen M et al: Malignant lymphoma simulating lymph
node toxoplasmosis. Histopathology. 6(2):129-40, 1982
16.
Gavrili L et al: [Value of lymph node biopsy in the
diagnosis of toxoplasmic lymphadenitis.] Rev Med Chir
Soc Med Nat Iasi. 85(1):105-8, 1981
17. Stansfeld AG: The histological diagnosis of toxoplasmic
lymphadenitis. J Clin Pathol. 14(6):565-73, 1961
IV
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Kikuchi Disease
Paracortical, well-circumscribed necrotic lesions
No follicular hyperplasia
Karyorrhexis and fibrin deposits are common
Leishmania Lymphadenitis
Leishmania have kinetoplasts in epithelioid histocytes
Microscopic Features
p
p
p
p
Protozoan Parasitic Infections: Morphologic Diagnosis of Protozoa in Anatomic Pathology
TOXOPLASMOSIS
(Left) H&E section shows
toxoplasmosis myocarditis
and lymphocytic
infiltrate. The inclusion is
typically small to just filling
the cytoplasm of the muscle
cell and is comprised of
distinctive dots without
halos. The differential for
this appearance includes
Trypanosoma cruzi (Chagas
disease), which would
have distinctive "dotdash" features of a nucleus
and kinetoplastid. (Right)
Endomyocardial biopsy from
an immunocompromised
atient shows the
intracellular organism .
(Left) H&E section of
cerebral toxoplasmosis
shows cerebritis with
lymphoplasmacytic
infiltration and gliosis. In
atients with a clinical
suspicion of toxoplasmosis,
a low threshold for
immunohistochemical
evaluation should be used
due to the rare scattered
organisms. (Right) H&E
section shows brain
with reactive gliosis and
bradyzoites in a case
of cerebral toxoplasmosis.
Necrosis should always
rompt careful evaluation.
(Left) Low-power view of
toxoplasmosis lymphadenitis
case shows a reactive follicle
with a cluster of epithelioid
histocytes within and outside
the follicle center. Scattered
throughout the lymph
node will be macrophages
with a "moth-eaten"
appearance and evident
hagocytosis of debris.
Cysts may be found with
careful sectioning; they are
not required for diagnosis.
(Right) High-power view
from a toxoplasmosis
lymphadenitis case shows
the "monocytoid" cells that
are actually B cells.
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SECTION 1
Ancylostomiasis and Necatoriasis V-1-2
Ascariasis V-1-4
V-1-6
V-1-10
Strongyloidiasis V-1-12
Trichuriasis V-1-14
Zoonotic Nematode Infections V-1-16
Helminthic Parasitic Infections: Nematodes
ANCYLOSTOMIASIS AND NECATORIASIS
V
Duodenum from a patient with hookworm demonstrates
the small 5 mm worms adherent to the mucosa with
minimal changes. These were found on resection for
other reasons. (Courtesy R. Cooke, MD.)
TERMINOLOGY
Synonyms
Hookworm disease, miner’s anemia, tunnel disease,
brickmaker’s anemia, Egyptian chlorosis
Definitions
Latin: "Necare" (to kill) + "America" (Americans)
Greek: "Angkylos" (crooked) + "stoma" (mouth)
ETIOLOGY/PATHOGENESIS
Environmental Exposure
Hookworm filariform larvae directly penetrate skin in
contact with ground or plants
Infectious Agents
Hookworms are nematodes 1 cm in length that
clamp onto mucosa of small bowel and feed on
human blood
Hookworm eggs (regardless of species) are very similar
in appearance in stool
Necator americanus: New World hookworm
Males are 7-9 mm, females are 9-11 mm in length
and produce ~ 10,000 eggs per day
Adult worms can live in human small bowel for up
to 5 years
Ancylostoma spp: Old World hookworm
Males are 8-11 mm, females are 10-13 mm in length
and produce ~ 30,000 eggs per day
Male posterior end contains a copulatory burst
Adult worms can live in human small bowel for up
to 1 year
A section from duodenum with hookworm infection
shows the worm , which was clamped to the mucosa
for feeding, and inflamed, blunted villi in the small
bowel. (Courtesy R. Cooke, MD.)
CLINICAL ISSUES
Epidemiology
Although worms have worldwide distribution,
infection is strongly associated with poor sanitation,
bare feet, and poverty
Major cause of anemia: 0.2 mL blood/worm/day are
lost with infection
Results in stunted growth, milestone loss,
comorbidities, and decreased productivity
Presentation
Mostly asymptomatic
Loeffler syndrome (larvae pass through lungs): Cough,
and eosinophils in sputum
Acute infection of mature worms: Abdominal pain,
melena, or rarely, blood per rectum
Chronic infection: Anemia, growth stunting, and
mental milestone delay
Laboratory Tests
Stool examination for hookworm eggs &/or
rhabditiform larvae is diagnostic modality of choice
Patients may show anemia on complete blood count
but eosinophilia is uncommon
Treatment
Albendazole or mebendazole
Large effort to develop a vaccine is underway due to
lack of efficacy of mass drug treatment in hookworm
disease
Prognosis
Mortality is extremely rare and most patients recover
fully with proper treatment
Reinfection will occur without exposure prevention
Chronic disease complications (such as stunted
growth) may not revert with treatment
1
2
ANCYLOSTOMIASIS AND NECATORIASIS
Etiology
Filariform larvae directly penetrate skin
Nematodes of 1 cm clamp to small bowel mucosa,
feed on human blood
Clinical Issues
Infection associated with poor sanitation, bare feet,
and poverty
Loeffler syndrome: Cough, and eosinophils in
sputum
Key Facts
Acute infection: Abdominal pain, melena, or rarely,
blood per rectum
Chronic infection: Anemia, growth stunting, and
mental milestone delay
Microscopic Pathology
Small bowel resections may incidentally demonstrate
worms on tissue section, which are attached via
cutting plates to mucosa surface
Helminthic Parasitic Infections: Nematodes
MACROSCOPIC FEATURES
Endoscopy/Small Bowel Gross Examination
Worms are large (size), easily visualized, attached to
mucosa, and do not penetrate wall of small bowel
MICROSCOPIC PATHOLOGY
Histologic Features
Small bowel resections may demonstrate worms on
tissue section, which are attached via cutting plates to
mucosa surface
Within mouth parts, damaged mucosa should be
present
May be limited mucosal inflammatory response to
diffuse small bowel inflammation
DIFFERENTIAL DIAGNOSIS
On Lung Biopsy or Sputum Sampling
Loeffler syndrome: Eosinophilic pneumonitis caused
by Ascaris lumbricoides, hookworm, or Strongyloides
stercoralis although migrating larvae may not be seen
Disseminated strongyloidiasis, caused by S. stercoralis:
Hookworm adults and rhabditiform larvae do not
leave gastrointestinal tract
On Small Bowel Biopsy/Resection
Strongyloidiasis: Small adult worms and larvae
burrowed between intestinal epithelial cells/into
lamina propria, eosinophils
On Stool Examination
Strongyloides rhabditiform larvae show a short
buccal cavity and a primordial genitalia (absent in
hookworm)
Other helminth infections: Hookworm eggs have clear
outer shell and shrunken internal structure
"Found objects": Adult hookworms have distinctive
mouth cutting plates and a copulatory burst (male) in
tail
DIAGNOSTIC CHECKLIST
Clinically Relevant Pathologic Features
Clinically history should denote clear exposure history
or signs of chronic infection
Pathologic Interpretation Pearls
Head of worm attached to damaged mucosa
SELECTED REFERENCES
1. Hotez PJ et al: Developing vaccines to combat hookworm
infection and intestinal schistosomiasis. Nat Rev Microbiol.
8(11):814-26, 2010
2. Hotez PJ et al: Hookworm infection. Sci Am. 272(6):68-74,
1995
IMAGE GALLERY
(Left) Filariform larvae of hookworm is shown with an esophagus 1/3 the body length and pointed tail . Rhabditiform larvae have a long
buccal cavity and inconspicuous genital primordium. (Courtesy M. Melvin, MD, CDC/PHIL.) (Center) The 4 sets of sharp cutting teeth
Ancylostoma duodenale are shown, distinguishing it from Necator species, which have 2 broad cutting plates. (Courtesy M. Melvin, MD, CDC/
PHIL.) (Right) Hookworm ova
from stool are shown.
of
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Helminthic Parasitic Infections: Nematodes
ASCARIASIS
V
1
A liver with a large necrotic mass demonstrates dead
adult Ascaris worms within the lesions. (Courtesy A.
Velez Hoyos, MD.)
TERMINOLOGY
Definitions
Greek: "Askaris" (intestinal worm)
Latin: "Lumbricus" (earthworm)
ETIOLOGY/PATHOGENESIS
Environmental Exposure
Ingestion of embryonated eggs originating from soil is
primary form of transmission
Worldwide distribution, and more common in areas of
poverty with increased soil exposure
Infectious Agents
Ascaris lumbricoides
Largest nematode (roundworm) infecting humans of
helminths parasites
CLINICAL ISSUES
Presentation
Vast majority of infections are asymptomatic
Chronic infection can lead to malnutrition and
stunted growth
Loeffler syndrome: Pulmonary alveolar space
eosinophilia in response to larval passage
Large burden: Abdominal pain, swollen abdomen,
intestinal obstruction, bowel infarction, and nausea/
vomiting
Adult worms pass through ampulla of Vater, become
trapped in liver, causing right upper quadrant pain,
transaminitis, cholestasis, and abscess formation
Laboratory Tests
Stool exam for ova and parasites is almost always
positive if gravid female worms are in patient due to
A section of liver from a large liver mass demonstrates a
cross section of an Ascaris worm with surrounding
dense inflammation . Eggs may be seen in the liver
parenchyma.
large burden of eggs per day produced (200,000 per
female)
Presence of only male worms will not produce
positive stool exams
Presence of only female worms will produce
unfertilized eggs at lower numbers than gravid
females
Treatment
Gastrointestinal obstruction/infarction may require
surgical decompression/resection
Liver abscess may require surgical drainage
Albendazole or mebendazole for intestinal infection
Prognosis
Most patients return to normal health after treatment
Obstruction may lead to infarction, sepsis, and death
without treatment
Liver masses may progress to frank hepatitis or lead to
scarring
MICROBIOLOGY
Parasite Characteristics
Large adult worms (15-30 cm male and 20-35 cm
female) inhabiting small bowel
Secrete molecules to protect against immune clearance
including Ascaris carboxypeptidase inhibitor (ACI)
Typically do not leave gastrointestinal tract
MACROSCOPIC FEATURES
On Colonoscopy
Ascaris worms are very large and easily identified on
visual inspection of colon
In Stool
These large worms may be passed in stool with
high burden, after treatment, or spontaneously, and
4
Etiology
Ascaris lumbricoides
Largest nematode (roundworm) infecting humans
Worldwide distribution
Ingestion of embryonated eggs
Clinical Issues
Mostly asymptomatic
Gravid female produce 200,000 eggs per day (positive
stool exam)
ASCARIASIS
Key Facts
Microscopic Pathology
Lung
Gastrointestinal tract
Liver
Helminthic Parasitic Infections: Nematodes
Eosinophils larval forms
Normal (mechanical obstruction) or ischemic with
necrosis
Adult worms and eggs, neutrophilic abscesses,
eosinophils, and giant cells
patients may attest to the presence of "common
earthworms"
In Sputum or Expectorated
Through lung passage stage, worms may mature into
adults and expire in respiratory system to be coughed
up whole or in fragments
MICROSCOPIC PATHOLOGY
Histologic Features
Lung
Eosinophils in alveolar spaces or in interstitium
larval forms
Gastrointestinal tract
Resected tissue may appear normal (mechanical
obstruction) or ischemic with necrosis
Liver
Cross sections of adult worms and eggs are admixed
with inflammation, including neutrophilic
abscesses, eosinophils, and giant cells
DIFFERENTIAL DIAGNOSIS
Trematode Infection of Liver
Clonorchis, Opisthorchis, Fasciola, and (rarely)
Fasciolopsis
Limited inflammation (natural habitat)
Echinococcosis of Liver
Entamoeba histolytica: Solitary liver abscess
Limited inflammation and extensive necrosis
Loeffler Syndrome
Strongyloides, hookworm
Other sources of pulmonary eosinophilia occur
DIAGNOSTIC CHECKLIST
Clinically Relevant Pathologic Features
Risk factors: Poverty, soil exposure, and occupational
exposure
Pathologic Interpretation Pearls
Eggs and worm identified by morphologic features
SELECTED REFERENCES
1. Tanowitz HB et al: Other helminthic infections: Ascariasis,
dracontiasis, lagochilascariasis, micronemiasis. Handb Clin
Neurol. 114:263-8, 2013
2. Hagel I et al: Ascaris lumbricoides: an overview
of therapeutic targets. Infect Disord Drug Targets.
10(5):349-67, 2010
3. Quinnell RJ: Genetics of susceptibility to human helminth
infection. Int J Parasitol. 33(11):1219-31, 2003
4. Carpenter HA: Bacterial and parasitic cholangitis. Mayo
Clin Proc. 73(5):473-8, 1998
MICROSCOPIC FEATURES
(Left) Numerous Ascaris eggs are seen in this section of liver tissue within sheets of inflammatory cells including giant cells containing
some eggs. (Center) A cross section of a gravid female Ascaris worm shows the gastrointestinal tract
longitudinal cords
eggs.
. (Right) Ascaris eggs on stool examination with iodine demonstrate the rough surface and dark center of the large
, uterus containing eggs , and lateral
V
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Helminthic Parasitic Infections: Nematodes
HUMAN FILARIASIS
V
1
Cross sections of dilated spermatic cord lymph vessels
demonstrate male W. bancrofti; note the lack of
microfilaria. (Courtesy Franz von Lichtenberg Collection
of Infectious Disease Pathology, BWH.)
TERMINOLOGY
Synonyms
Elephantiasis
Definitions
Latin: "Filum" (thread)
Wuchereria from Otto Wucherer (German physician)
Brugia from S. L. Brug (Dutch parasitologist)
Mansonella from Sir Patrick Manson (English tropical
medicine expert)
ETIOLOGY/PATHOGENESIS
Infectious Agents
Infectious disease caused by thread-like roundworms
of the Filarioidea type
Wuchereria bancrofti
Filarial nematode transmitted by bites of infected
mosquitos
Most widely distributed accounting for > 90% of
cases
Sub-Saharan Africa
Southeast Asia
India
Pacific Islands
South America
Caribbean
Brugia malayi
Filarial nematode transmitted by bites of infected
mosquitos
China
India
Southeast Asia
Brugia timori
Filarial nematode transmitted by the bite of infected
mosquitos
Timor
Cross sections of female W. bancrofti are seen in
the epididymis with inflammation. Note the abundant
microfilaria. (Courtesy Franz von Lichtenberg Collection
of Infectious Disease Pathology, BWH.)
Mansonella streptocerca
Filarial nematode transmitted by bites of infected
midge flies
Causes skin nodules in African rain forests (similar
to onchocerciasis)
Mansonella perstans and Mansonella ozzardi
Filarial nematode transmitted by bites of infected
midge flies
M. perstans is found in sub-Saharan Africa and parts
of Central and South America
M. ozzardi is found in Central and South America
Vector
Mosquito-borne disease (Wuchereria and Brugia)
Vector species vary geographically
In Africa, most common vector is Anopheles
In the Americas, most common vector is Culex
In Pacific and Asia, Aedes and Mansonia are most
common
W. bancrofti most commonly spread by Culex,
Anopheles, and Aedes species
Midge-borne disease (Mansonella species)
Culicoides species (midge flies)
M. ozzardi is also transmitted by black flies (South
America)
CLINICAL ISSUES
Epidemiology
Wucheria and Brugia species
120 million infected worldwide
Mainly in tropics and subtropics
15 million of those infected have lymphedema of
lower limbs
25 million men have genital disease
2/3 of those infected are in Asia
1st acquired in childhood, parasite burden increases
over time spent in endemic areas
6
HUMAN FILARIASIS
Etiology
Mosquito-borne disease
Brugia malayi
Brugia timori
Wuchereria bancrofti
Clinical Issues
120 million infected worldwide
1st acquired in childhood, parasite burden increases
over time spent in endemic areas
Rarely seen in travelers spending short periods of
time in endemic regions
Microscopic Pathology
Intact male and female adult filariae can be seen in
lymphatics
Key Facts
Granulomatous reaction around dead and dying
filariae
Polypoid endolymphangitis
Acute lymphangitis and chronic lymphatic dilatation
and fibrosis
Eosinophilic lymphadenitis (Meyers-Kouwenaar
syndrome)
Blood smear light microscopy can be used to
differentiate species
Diagnostic Checklist
Blood is drawn for peripheral smear at night for
maximum parasite yield
Helminthic Parasitic Infections: Nematodes
Mosquito not very effective at transmission;
therefore, rarely seen in travelers spending short
amounts of time in endemic regions
A leading cause of disfiguring morbidity worldwide
Mansonella species
> 100 million infected worldwide with gross
underestimation due to asymptomatic/mild disease
Presentation
Wuchereria and Brugia
Majority are asymptomatic but may have subclinical
lymphatic and renal disease
Acute phase
Fever
Lymphadenopathy (genital and axillary)
Orchitis/epididymitis
Lymphedema of limbs &/or genitals
Chronic phase
Irreversible lymphedema
Florid eosinophilia found in peripheral blood counts
Can present as tropical pulmonary eosinophilia
secondary to inflammatory response to infection
Mansonella species
Majority are asymptomatic
M. perstans/M. ozzardi cause body cavity filariasis
Calabar-like swellings, eosinophilia, abdominal
pain, fever, headache, pruritus
M. streptocerca causes cutaneous nodules
Laboratory Tests
Peripheral blood smear
Identified Wuchereria and Brugia species in
peripheral blood by microfilarial features
Eosinophilia may be present
Body fluid examination (pleural fluid)
Identified M. perstans or M. ozzardi species by
microfilarial features
Treatment
Diethylcarbamazine (DEC)
Contraindicated in patients with concomitant
loiasis
Albendazole
Ivermectin
Doxycycline
Surgical excision of hydroceles may be an option in
some cases
Prognosis
Chronic lymphedema is irreversible
Good prognosis if recognized and treated early
Complications
Secondary bacterial infection can be common
complication and care should be taken to hygienically
maintain affected areas
IMAGE FINDINGS
Ultrasonographic Findings
Testicular ultrasound may show movement of
echogenic particles, classically termed "filarial dance"
In patients with travel to endemic areas, may be
suggestive of filarial infection due to obstruction
In patients with no exposure, may represent
obstruction for other reasons (post vasectomy)
MICROBIOLOGY
Parasite Features
Humans are the only vertebrate host of W. bancrofti
B. malayi can infect monkeys and felines, but humans
are most common vertebrate host
M. perstans has only a human reservoir while M.
streptocerca has animal reservoirs
Life cycle has 5 larval stages in vertebrate host and
arthropod vector
3rd stage is transmitted to vertebrate host from
mosquitoes/midges
Larvae enter circulation via bite wound and
migrate to host lymphatics
Over 6-12 months, mature worms develop (females:
8-10 cm; males: 1/3 that size)
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