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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_182_библиотеки_им_акад_М_И_Перельмана.pdf
CHLAMYDOPHILA AND CHLAMYDIA SPECIES INFECTIONS
Chlamydia trachomatis in tissue culture is shown with
elementary bodies . Standard microbiology culture
techniques do not detect Chlamydia. Confirmatory
diagnosis is made with PCR or serology.
TERMINOLOGY
Synonyms
Trachoma
Lymphogranuloma venereum
Psittacosis, parrot fever
Definitions
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
Greek: "Chlamys/khlamus" (cloak)
Chlamydophila: Genus that includes Chlamydophila
pneumoniae and Chlamydophila psittaci
Chlamydia: Genus that includes Chlamydia trachomatis
ETIOLOGY/PATHOGENESIS
Environmental Exposure
C. trachomatis exclusively infects humans, while C.
pneumoniae also infects horses, marsupials, and frogs
C. psittaci also infects birds and numerous mammalian
species
Infectious Agents
Chlamydiaceae (which includes Chlamydophila and
Chlamydia) is an ancient group of obligate intracellular
organisms with tiny genomes
All species share a biphasic lifestyle with 2 different
developmental forms
Elementary bodies (EB) are metabolically sloweddown, spore-like forms that are specialized for
environmental survival and host cell attachment
EBs generally attach to nonphagocytic cells via
a number of different receptors (CFTR, mannose
receptor, etc.)
Upon uptake (clathrin-mediated endocytosis) by an
epithelial cell, EBs differentiate into reticulate bodies
(RB) within host cell vacuoles
II
RBs are the germinal forms, which actively divide
8-10x before differentiating back into EBs
2
Chlamydia trachomatis in tissue culture demonstrates
reticulate bodies . Reticulate bodies indicate
replication of the bacteria, while elementary bodies are
infectious and transmit disease.
EBs can exit cell by slow extrusion or cell lysis and
reinfect new cells
Virulence determinants include numerous
mechanisms to utilize host cell nutrients and building
blocks for cellular machinery
Differences between chlamydial species are mostly
rooted in difference in "plasticity zone" of genome
Clinically relevant species of Chlamydia include C.
trachomatis, C. pneumoniae, and C. psittaci
C. trachomatis
Divided into 15 serovars (based on OmpA [MOMP]
antigenicity)
Group 1 causes trachoma, genital tract disease,
and conjunctivitis (trachoma biovar)
Group 2 causes lymphogranuloma venereum
(LGV) and proctocolitis (LGV biovar)
Plasticity zone encodes a perforin and
phospholipase D proteins
Strains of trachoma biovar bind to squamocolumnar
cells or conjunctiva, urethra, and rectum in women
and men, endocervix and upper genital tract in
women, and respiratory tract in infants
Contact with host cells induces IL-8 and a
neutrophilic response
Strains of LGV biovar are able to invade beyond
mucosal epithelium and enter lymphatics where
they multiply inside monocytes and macrophages
Spread is by sexual contact, childbirth, or hand-toeye contact (trachoma)
C. pneumoniae
Virulence factors poorly characterized
Transmission poorly described
Evidence for person-to-person spread as well as
zoonoses
C. psittaci
Pathogenesis is less well characterized, but genomic
analysis of plasticity zone indicates that a toxin gene
may be partially responsible for the more virulent
strains
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CHLAMYDOPHILA AND CHLAMYDIA SPECIES INFECTIONS
Etiology
Chlamydia are an ancient group of obligate
intracellular organisms with tiny genomes
All species share a biphasic lifestyle with 2 different
developmental forms (elementary and reticulate
bodies)
Clinically relevant species of Chlamydia include C.
trachomatis, C. pneumoniae, and C. psittaci
C. psittaci was developed as an agent of biological
warfare by both United States and former Soviet
Union in early 20th century
Clinical Issues
Clinical manifestations include trachoma, genital
infection in men and women (upper and lower),
lymphogranuloma venereum, atypical pneumonia,
and psittacosis
Developed as an agent of biological warfare by both
United States and former Soviet Union in early 20th
century
Spread is by contact with birds (even casual) or other
domestic animals
CLINICAL ISSUES
Epidemiology
Trachoma: Most common among young children in
developing countries
Genital infection: Most common in young, sexually
active men and women (most common bacterial
sexually transmitted disease)
LGV is most common in developing countries
C. pneumoniae has been demonstrated by serology to
have infected sizable percentages of adult populations
in several countries (e.g., 9% of 6 week to 19 year olds
in USA)
Presentation
C. trachomatis
Trachoma
Chronic keratoconjunctivitis
Sequelae from scarring can cause trichiasis with
ulceration, scarring, and eventual blindness
Genital infection in males
Major cause of nongonococcal urethritis: Whitish/
clear discharge, may be scant; 1% develop reactive
arthritis
Epididymitis, prostatitis, and proctitis
Genital infection in women
Often asymptomatic, sometimes mucopurulent
cervicitis/urethritis
Endometritis/salpingitis/peritonitis (pelvic
inflammatory disease [PID])
Sequelae can include infertility and ectopic
pregnancy
Lymphogranuloma venereum (3 stages)
Formation of a small genital papule
Key Facts
Nucleic acid amplification tests (NAATs) are preferred
method for detecting Chlamydia in clinical specimens
Trachoma: Most common among young children in
developing countries
Genital infection: Most common in young, sexually
active men and women (most common bacterial
sexually transmitted disease)
LGV is most common in developing countries
C. pneumoniae has been demonstrated by serology to
have infected sizable percentages of adult populations
in several countries (e.g., 9% of 6 week to 19 year olds
in USA)
C. pneumoniae
C. psittaci
Laboratory Tests
Nucleic acid amplification tests (NAATs) are preferred
method for detecting Chlamydia in clinical specimens
16S PCR may also be used
Adenitis (buboes) and development of systemic
symptoms (fever, headache, myalgia) and
lymphadenopathy (may be severe)
Chronic disease that can include fistulas, fibrosis,
scarring, and elephantiasis of genitalia due to
lymphatic obstruction
Alternatively, may present as severe proctitis,
generally in men who have sex with men
Typically mild respiratory infections
Common cause of atypical pneumonia
Several described presentations with wide range in
severity (subclinical to rapidly fatal)
Subclinical or mild nonspecific viral-like
symptoms
Fever, pharyngitis, hepatosplenomegaly,
adenopathy
Fever, bradycardia, malaise, and splenomegaly
Atypical pneumonia (more severe than that
caused by C. pneumoniae)
Common symptoms and signs are diverse and wide
ranging
Fever, headache, myalgias, reactive arthritis
Pharyngeal erythema, cough, rales
Peri-/myocarditis, endocarditis
Hepatomegaly, hepatitis, jaundice
Hemolytic anemia, DIC
Glomerulonephritis, acute tubulointerstitial
nephritis, and acute tubular necrosis
Multiple neurological and dermatological
manifestations (e.g., Horder spots)
Gestational psittacosis
Severe, progressive febrile illness
Headache, disseminated intravascular coagulation,
hepatitis, renal failure
Significant fetomaternal morbidity and mortality
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
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CHLAMYDOPHILA AND CHLAMYDIA SPECIES INFECTIONS
As an intracellular pathogen, Chlamydia has to be
cultured in cells, which is rarely done for diagnostic
purposes
Serologies may be used to diagnose some types of
chlamydial disease (e.g., C. pneumoniae)
Treatment
Drugs
Macrolides, tetracycline, and quinolones are
mainstays of treatment
Prognosis
Mortality is generally low (up to 1% with C. psittaci
infection), though several manifestations have
significant long-term morbidity
MICROBIOLOGY
Morphologic and Biochemical
Characteristics
Chlamydia are pleomorphic organisms with the basic
components of a gram-negative envelope, though they
do not express peptidoglycan
Culture
Chlamydia are obligate intracellular pathogens and
must be cultured within eukaryotic cells, which is not
routinely done in most clinical laboratories
Microbiologic Identification
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
Gold standard for identification is by NAAT
MACROSCOPIC FEATURES
Trachoma
Initial infection may present with "pink eye" or mild
irritation
Lymphoid hyperplasia may produce large white
nodules on mucosa surface of eyelid in early stages
Advanced stages (repeated infection) leads to scarring
with eyelash inversion and corneal ulceration
(blindness)
MICROSCOPIC PATHOLOGY
Histologic Features
General: Organisms may be observable in intracellular
vacuoles
Silver staining and IHC are optimal means to
visualization
Can also do 16S PCR
Trachoma
Chronic follicular conjunctivitis with papillary
hypertrophy
Giemsa-stained smear from conjunctiva should
demonstrate large intracellular (bacterial) inclusions
in cytoplasm of histiocytes
II
Genital disease
Urethritis and cervicitis specimens are rarely sent for
surgical pathology
2
IHC is more informative than morphology on
such specimens
Upper genital tract infection in women may
demonstrate endometritis, salpingitis, and tuboovarian abscess
Epididymitis in men is usually characterized by
suppurative inflammation with fibrin covering
Lymphogranuloma venereum
Cutaneous lesions and proctitis demonstrate
chronic inflammation, giant cells, plasma cells,
lymphocytes, necrosis, and granulation tissue
Granulomas with epithelioid histiocytes
Fibrosis and scarring with chronicity
Lymph nodes with suppurative inflammation and
necrosis followed by plasma cell infiltration and
lymphocytic hyperplasia
Histological hallmark is "stellate abscess"
Suppurative lesions surrounded by epithelioid and
multinucleated giant cells
Psittacosis: Histopathologic features are not well
described; may include myocarditis
Pneumonia: Standard features of atypical bacterial
pneumonia
DIFFERENTIAL DIAGNOSIS
Trachoma
Bacteria conjunctivitis (culture)
Viral conjunctivitis (negative culture, concurrent
upper respiratory infection)
Advanced stages of trachoma: Squamous cell
carcinoma of the conjunctiva
Lymphogranuloma Venereum
Differentiate from chancroid (has larger, more painful
ulcers), particularly with other laboratory evidence to
identify causative pathogen
DIAGNOSTIC CHECKLIST
Clinically Relevant Pathologic Features
Sexually transmitted organisms should have
appropriate clinical history or exposure
Pathologic Interpretation Pearls
Intracytoplasmic inclusions are helpful but PCR &/or
serology should be used to confirm diagnosis
SELECTED REFERENCES
1. Knittler MR et al: Chlamydia psittaci: New insights into
genomic diversity, clinical pathology, host-pathogen
interaction and anti-bacterial immunity. Int J Med
Microbiol. 304(7):877-93, 2014
2. Voltaggio L et al: Sex, lies, and gastrointestinal tract
biopsies: a review of selected sexually transmitted
proctocolitides. Adv Anat Pathol. 21(2):83-93, 2014
3. Darville T et al: Pathogenesis of genital tract disease due to
Chlamydia trachomatis. J Infect Dis. 201 Suppl 2:S114-25,
2010
4. Lichtenberg, F: Pathology of Infectious Diseases. New York:
Raven Press, 1991
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CHLAMYDOPHILA AND CHLAMYDIA SPECIES INFECTIONS
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g
Clinical and Microscopic Features
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
(Left) This patient has stage
I trachoma demonstrating
multiple small lymphoid
follicles . At this stage,
the eye may only appear
slightly red, swollen, and
discharge. (Courtesy
D.M. Albert.) (Right) This
atient has trachoma stage
IIa, demonstrating advanced
follicular inflammation
with a grossly swollen,
red eye. As the disease
advances, scarring and
increased inflammation lead
to corneal ulcers. (Courtesy
D.M. Albert, MD.)
(Left) Conjunctiva in a
atient with trachoma
demonstrates follicular
inflammation and
neovascularization .
(Right) In later stages
of trachoma, increased
fibrosis and scarring
is seen in the cicatricial
stages. Scarring disrupts
eye lashes with inversion,
which aggravates corneal
ulcerations. (Courtesy Franz
von Lichtenberg Infectious
Disease Collection, BWH.)
(Left) In end-stage trachoma,
there is dense fibrosis
and reduced inflammation
. (Right) The histologic
signature of early stage
lymphogranuloma venereum
is a "stellate abscess"
or granuloma . In
later stages, histological
findings are nonspecific and
ranulomas are rare.
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73
RICKETTSIA SPECIES INFECTIONS
Rickettsia are able to proliferate inside of macrophages
(Macchiavello stain, oil immersion).
TERMINOLOGY
Definitions
Rickettsia from Howard Taylor Ricketts: Studied
rickettsial disease and died from typhus
Greek: "Typhos" (smoky or hazy for mental status of
patients)
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
Manifestations
Rocky Mountain spotted fever (RMSF) (formerly
spotted fever of Idaho)
Rickettsial pox (Rickettsia akari)
ETIOLOGY/PATHOGENESIS
Environmental Exposure
Ticks are main reservoir of rickettsiae in environment
as well as the vector (adult ticks) for transmission to
humans
Dermacentor variabilis (American dog tick) in eastern,
eastern Midwest, as well as western USA
Dermacentor andersoni (Rocky Mountain wood tick)
in western USA
Mites for R. akaria
Infectious Agents
Clinically relevant species form 2 groups: Spotted fever
group and typhus group
All are considered potential agents of bioterrrorism
Spotted fever group includes > 15 species, with
Rickettsia rickettsii (causative agent of RMSF) best
characterized
Obligate intracellular pathogens that escape the
phagosome (using phospholipase D and TlcY) and
replicate in cytosol
Rely on host cell for most nutrients and building
II
blocks; genome encodes numerous transporters,
which are also virulence factors and targets of host
This child with Rocky Mountain spotted fever
demonstrates the characteristic rash involving the palms.
immune response (e.g., OmpA in spotted fever
group)
Propelled from cell-to-cell by host cell actin
filaments
Spread is by tick bite, manual removal of ticks
(particularly with crushing of tick), and laboratory
acquired
After introduction into skin, organisms spread
rapidly, targeting vascular endothelium
Endothelial cell injury results in increased
permeability, edema, hypovolemia, hypotension,
and hypoalbuminemia
Typus group includes louse-borne Rickettsia
prowazekii (agent of epidemic typhus) and flea-borne
Rickettsia typhi (agent of murine typhus)
Differs from R. rickettsii by not mobilizing
host actin for intercellular spread (replication
continues until host cell bursts from burden)
Can persist in host as a latent infection and in
environment in a dormant form
CLINICAL ISSUES
Epidemiology
RMSF is most prevalent in south central and
southeastern USA
Most infections occur in late spring and summer
in children, adults > 60, and those with increased
exposure to ticks
Follows a particularly severe course in African
American men with G6PD deficiency
Epidemic typhus is most often diagnosed in
developing countries in crowded conditions, which
favor spread of lice
Exposure to flying squirrels is an additional risk
factor, which is associated with a more benign
disease course
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RICKETTSIA SPECIES INFECTIONS
Etiology
Ticks are vector for transmission to humans
Clinically relevant species form 2 groups: Spotted
fever group and typhus group
Rickettsia rickettsii (causative agent of Rocky Mountain
spotted fever, RMSF) is best characterized of spotted
fever group
Typus group includes louse-borne Rickettsia prowazekii
(agent of typhus) and flea-borne Rickettsia typhi (agent
of murine typhus)
After introduction into skin, organisms spread
rapidly, targeting vascular endothelium
Clinical Issues
Diagnosis of RMSF and typhus is mainly clinical
Key Facts
Immunohistochemistry on cutaneous biopsy may be
useful for diagnosis (should be taken before therapy,
if possible)
PCR can be done on primary specimens (targets: 17kDa lipoprotein, OmpA, etc.)
Culture is rarely performed by clinical laboratories
Microscopic Pathology
Organisms are best visualized in tissue using
immunohistochemistry and can often be seen in
infected endothelial cells
Overall pathology is connected with endothelial
injury and subsequent increased permeability/edema,
hemorrhage, thrombi, perivascular inflammation
(usually lymphohistiocytic) and vasculitis; this
picture can present in virtually any organ system
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
Murine typhus is also found predominantly in tropical
and subtropical regions, with some cases found in
Texas and southern California
Presentation
RMSF
Average 7-day incubation followed by fever,
myalgias, gastrointestinal distress, and headache
Characteristic rash occurs in 90% of patients:
Petechial macropapular rash, often starting on wrists
and ankles
Meningeal symptoms, abnormal EEG, ocular
pathology (retinal vein engorgement, arterial
occlusion, flame hemorrhage, papilledema), renal
failure, and pulmonary compromise (alveolar
infiltrates, interstitial pneumoniae, pleural effusion)
Epidemic typhus
Average 11-day incubation followed by rigors,
malaise, mental status changes, and headache
Petechial/macropapular rash usually spares palms,
soles, and face
Can remain in a latent state that can reactivate
much later in life with a milder clinical course (BrillZinsser disease)
Murine typhus
More mild disease than epidemic typhus (can range
from subclinical to severe in ill and elderly patients)
Average 1-2 week incubation period followed
by acute onset of fever, headache, nausea and
vomiting, and less commonly, headache and rash
Rash is predominantly macropapular and usually
spares palms and soles
Progression of disease can include worsening
gastrointestinal distress, pulmonary involvement,
hepatosplenomegaly, and neurological
manifestations (confusion, stupor, seizures, ataxia)
African tick-bite fever (Rickettsia africae in SubSaharan Africa and West Indies) with fever, eschar,
maculopapular rash
Rickettsia pox (Rickettsia akari in United States, South
Africa, Korea, and Russia) with fever, chills, myalgias,
vesicular rash, diaphoresis, photophobia
Tick-borne spotted fever (Rickettsia parkeri in
southeastern USA coast) with fever, headache, eschar
(multiple) and variable rash
Laboratory Tests
Diagnosis of RMSF and typhus is mainly clinical
Serology is used for retrospective confirmation (look
for 4x rise in titer over course of disease)
Cross-reactivity across rickettsial species occurs on
serological tests
Culture is rarely performed by clinical laboratories
Treatment
Drugs
Doxycycline is mainstay of treatment for both RMSF
and typhus
Prognosis
Untreated RMSF and typhus can be rapidly fatal
With treatment, mortality is usually < 5% in healthy
individuals
MICROBIOLOGY
Morphologic and Biochemical
Characteristics
Small, gram-negative, pleomorphic, obligate
intracellular organisms
Stained by Gimenez method or acridine orange
Culture
Must be cultured in eukaryotic cell lines, guinea pigs,
or embryonated hen’s eggs
Rarely done in clinical laboratory
Microbiologic Identification
Generally not identified within microbiology
laboratory
Where it is done, culture is generally followed by
molecular methods for identification
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RICKETTSIA SPECIES INFECTIONS
MICROSCOPIC PATHOLOGY
Histologic Features
General
Organisms are best visualized in tissue using
immunohistochemistry and can often be seen in
infected endothelial cells
Overall pathology is connected with endothelial
injury and subsequent increased permeability/
edema, hemorrhage, thrombi, perivascular
inflammation (usually lymphohistiocytic) and
vasculitis (present in any organ system)
RMSF
Cutaneous
Lymphohistiocytic capillaritis and venulitis
with extravasation of erythrocytes, edema, and
perivascular and interstitial infiltrates
Leukocytoclastic vasculitis with neutrophilic
infiltrate, basal layer vacuolar degeneration and
dermoepidermal interface lymphocytic exocytosis
Pulmonary
Diffuse interstitial mononuclear inflammatory
infiltrate
Pulmonary edema and intraalveolar hemorrhage
Vasculitis of arterioles and venules
Liver
Mixed inflammatory infiltrate of the portal triad
Kidney
Mixed inflammatory infiltrate of the vessels and
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
interstitium
Acute tubular necrosis
Focal segmental tuft necrosis (less common)
Epidemic typhus and murine typhus have a similar
histopathologic presentation to RMSF
ANCILLARY TESTS
Immunohistochemistry
On cutaneous biopsy, may be useful for diagnosis
(should be taken before therapy, if possible)
Immunofluorescence
For rickettsial antigens can confirm a histological
diagnosis in most organs (especially with active
vasculitis)
PCR
Can be done on primary specimens (targets: 17-kDa
lipoprotein, OmpA, etc.)
DIFFERENTIAL DIAGNOSIS
Small Vessel Vasculitis (Skin)
Insect bite reaction, drug reaction
Leukocytoclastic Vasculitis (Skin)
Sepsis, other infections, drug exposure, physical agents
II
Collagen vascular disease, mixed cryoglobulinemia,
hyperglobulinemia
Henoch-Schnlein purpura, serum sickness, urticarial
vasculitis
Malignancies
Neutrophilic Hidradenitis (Skin)
Bacterial infection, hemodialysis treatment,
chemotherapy response
Sepsis/Severe Disseminated Disease
Neisseria meningitis has similar clinical and
histological appearance (positive cultures)
Interstitial Pneumonia With Vasculitis
Myeloperoxidase antineutrophil cytoplasmic
autoantibody (ANCA) (and other ANCA) diseases
(serology)
Hepatitis
Viral hepatitis (serology)
Renal Interstitial Nephritis
Drug-induced nephritis (history of drugs)
Bacterial infections or sepsis (post infection, cultures)
SELECTED REFERENCES
1. Walker DH et al: Rickettsia prowazekii (epidemic or louseborne typhus). In Mandell et al: Mandell, Douglas, and
Bennett’s Principles and Practice of Infectious Diseases. 8th
Edition. Philadelphia: Elsevier/Saunders. 2217-20, 2015
2. Walker DH et al: Rickettsia rickettsii and other spotted
fever group rickettsiae. In Mandell et al: Mandell, Douglas,
and Bennett’s Principles and Practice of Infectious Diseases.
8th Edition. Philadelphia: Elsevier/Saunders.2198-2205,
2015
3. Walker DH et al: Rickettsia typhi (murine typhus).
In Mandell et al: Mandell, Douglas, and Bennett’s
Principles and Practice of Infectious Diseases. 8th Edition.
Philadelphia: Elsevier/Saunders. 2221-4, 2015
4. Bechah Y et al: Epidemic typhus. Lancet Infect Dis.
8(7):417-26, 2008
5. Dantas-Torres F: Rocky Mountain spotted fever. Lancet
Infect Dis. 7(11):724-32, 2007
6. Hidalgo M et al: Rocky Mountain spotted fever, Colombia.
Emerg Infect Dis. 13(7):1058-60, 2007
7. Kao GF et al: Cutaneous histopathology of Rocky
Mountain spotted fever. J Cutan Pathol. 24(10):604-10,
1997
8. Roggli VL et al: Pulmonary pathology of Rocky Mountain
spotted fever (RMSF) in children. Pediatr Pathol.
4(1-2):47-57, 1985
9. Helmick CG et al: Rocky Mountain spotted fever: clinical,
laboratory, and epidemiological features of 262 cases. J
Infect Dis. 150(4):480-8, 1984
10. Adams JS et al: The liver in Rocky Mountain spotted fever.
Am J Clin Pathol. 75(2):156-61, 1981
11. Walker DH et al: Rickettsial infection of the pulmonary
microcirculation: the basis for interstitial pneumonitis in
Rocky Mountain spotted fever. Hum Pathol. 11(3):263-72,
1980
12. Bradford WD et al: Kidney lesions in Rocky Mountain
spotted fever: a light-, immunofluorescence-, and electronmicroscopic study. Am J Pathol. 97(2):381-92, 1979
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Microscopic Features
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p
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
RICKETTSIA SPECIES INFECTIONS
(Left) This skin biopsy
from a patient with Rocky
Mountain spotted fever
demonstrates acute vasculitis
causing endothelial damage
and focal hemorrhage .
(Right) This skin biopsy
from a patient with Rocky
Mountain spotted fever
demonstrates perivascular
lymphohistiocytic
inflammation .
(Left) In the CNS, microglial
nodules form adjacent to
vessels in RMSF. (Courtesy
Franz von Lichtenberg
Collection of Infectious
Disease Pathology, BWH.)
(Right) In Rocky Mountain
spotted fever, monocytes
form nodular aggregates
but do not form epithelioid
cell granulomas.
(Left) In this autopsy of a
atient who died of Rocky
Mountain spotted fever, a
hemorrhagic pneumonia
with a predominantly
mononuclear inflammatory
attern is demonstrated.
(Right) Spotty CNS vasculitis
in a pontine arteriole with
adjacent mononuclear
"typhus nodule" is seen
in this case of Brill-Zinsser
disease.
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SECTION 1
Morphological Diagnosis
of Fungal Infections
Aspergillosis III-1-2
Blastomycosis III-1-8
Candidiasis III-1-14
Chromoblastomycosis III-1-18
Coccidioidomycosis III-1-22
Cryptococcosis III-1-24
Histoplasmosis III-1-30
Mucormycosis III-1-36
Mycetoma III-1-42
Paracoccidioidomycosis III-1-46
Penicilliosis III-1-48
Phaeohyphomycosis III-1-50
Pneumocystosis III-1-52
Sporotrichosis III-1-56
Tineasis III-1-60