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BORRELIA SPECIES INFECTIONS
Spirochetes are extracellular organisms that vary from
8-30 m in length and have 3-10 helical coils as would
be seen in Borrelia recurrentis or Borrelia hermsii. (From
DP: Blood & Bone Marrow.)
TERMINOLOGY
Definitions
Borrelia named in honor of Amde Borrel
"Lyme" from Lyme, Connecticut (1st disease
description)
Manifestations
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
Tick-borne relapsing fever (TBRF, by Borrelia hermsii,
Borrelia parkerii, Borrelia turicatae)
Louse-borne relapsing fever (LBRF, by Borrelia
recurrentis)
Lyme disease (Borrelia burgdorferi)
ETIOLOGY/PATHOGENESIS
Environmental Exposure
Several animal hosts in environment, e.g., rodents
(white-footed mice and chipmunks) are among hosts
of B. burgdorferi
Borrelia species are found associated with ticks in
environment
Ticks associated with Borrelia burgdorferi group
Ixodes scapularis (deer tick): Northeastern and
midwestern United States
Ixodes pacificus: Western United States
Ixodes ricinus (sheep tick): Europe
Ixodes persulcatus (taiga tick): Asia
Ticks associated with Borrelia hermsii
Ornithodoros hermsi
In addition, B. recurrentis is spread by human body
louse
Infectious Agents
Most clinically relevant species is B. burgdorferi
Small chromosome (950 kb), relies on host for most
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nutritional needs
This colorized scanning electron micrograph
demonstrates the helical shape of Borrelia burgdorferi.
(Courtesy C. Molins, CDC/PHIL.)
Surface-exposed proteins (e.g., OspA, OspC, CRASPs,
vls) expressed during different life cycle phases are
major virulence factors
Mediate adhesion, transmission,
immunomodulation etc.
Replication occurs locally at infection site
Induces a significant inflammatory response
and characteristic, target-shaped rash (erythema
migrans)
After days to weeks, B. burgdorferi is
widely disseminated, aided by multiple
adhesions (binding to decorin, integrins,
glycosaminoglycans, etc.)
Experimental evidence points to both extra- and
intracellular persistence
B. hermsii and B. recurrentis
Causative agents of TBRF (B. hermsii) and LBRF (B.
recurrentis)
Antigenic variation is responsible for relapsing
pattern (febrile episodes during time of high
replication)
Borrelia miyamotoi: TBRF-like illness described in Japan/
Russia/Europe transmitted by ticks
Borrelia crocidurae: TBRF-like illness in West Africa with
neurological manifestations
Similar TBRF-like illnesses are caused by Borrelia
hispanica (Spain, Morocco), Borrelia duttoni (Africa),
and Borrelia turicatae (New World)
CLINICAL ISSUES
Epidemiology
Lyme disease
Most common vector-borne infection in United
States
Highest incidence in Northeast (particularly
Connecticut)
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50
BORRELIA SPECIES INFECTIONS
Etiology
Borrelia species are found associated with ticks in
environment
Life cycle involves dormancy in nymphal tick
midgut until feeding begins during spring and
summer, then transfer to mammalian host during
tick’s blood meal
Ticks associated with B. burgdorferi group
Ixodes scapularis (deer tick): Northeastern and
midwestern United States
Ixodes pacificus: Western United States
Ticks associated with B. hermsii
Ornithodoros hermsi
Key Facts
Clinical Issues
Clinical manifestations associated with Borrelia
infection include Lyme disease and tick- and louseborne relapsing fever
Microscopic Pathology
Erythema migrans
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
Lyme disease: Most common vector-borne
infection in United States
TBRF: Most commonly associated with exposure
to a rodent-infested cabin or woodpile in Rocky
Mountain region
Classically superficial and deep perivascular
infiltrate with eosinophils centrally and plasma
cells at periphery
Also found in the Midwest (Wisconsin,
Minnesota, Michigan) and West (northern
California)
Infections associated with outdoor activities from
spring until early autumn
TBRF
USA patient exposure to a rodent-infested cabin or
woodpile in Rocky Mountain region
Globally, variable exposure to ticks and, rarely,
vertical transmission
LBRF
Associated with refugee settings in developing or
displaced nations
Presentation
Lyme disease
Initial presentation is most commonly erythema
migrans at site of tick bite
May not have classic "target" appearance with
central clearing or may be absent
Center may be indurated and even vesicular and
necrotic
Systemic symptoms may be present and
include fatigue, headache, fever and chills, and
lymphadenopathy
After days to weeks, additional cutaneous lesions
may develop (indicating cutaneous spread)
After weeks to months, additional complications
may include
Lyme arthritis: Joint swelling in 1 or more large
joints
Neuroborreliosis: Meningoradiculitis, meningitis,
peripheral facial palsy
Cardiac Lyme borreliosis: Acute onset of A-V
conduction disturbances, rhythm disturbances,
myocarditis, pericarditis, congestive heart failure
(diagnosis is usually by ECG)
Rare: Borrelia lymphocytoma, conjunctivitis (and
other ocular involvement)
Chronic manifestations may include
Acrodermatitis chronica atrophicans (red/bluish
lesions on extensor surfaces of extremities)
Chronic arthritis
Neurological: Chronic encephalomyelitis, spastic
paraparesis, ataxic gait, mental status changes
(subtle), chronic axonal polyradiculopathy
TBRF & LBRF
After an average incubation of 7 days, patient
experiences cycles consisting of 3 days of fever
followed by 7 afebrile days
Without treatment, this can repeat up to 30 times
Associated symptoms include myalgias, arthralgias,
headache, dizziness, and vomiting
Less commonly reported are lymphadenopathy,
hepatosplenomegaly, rash, and myocarditis
Laboratory Tests
Lyme disease
Serology
2-tiered approach (ELISA screen followed by
western blot confirmation)
IgM and IgG testing useful to determine acute vs.
chronic infection
May need to test convalescent serum due to lower
sensitivity in acute serum
PCR
Generally more sensitive than culture from
primary specimens (particularly joint fluid)
Lumbar puncture
In Lyme meningitis, often a lymphocytic
pleocytosis, elevated protein, normal glucose,
anti-Borrelia antibodies
Synovial fluid analysis
B. burgdorferi organisms may be detected by PCR
TBRF & LBRF
A peripheral blood smear will often demonstrate
organisms during febrile periods
Serologic testing and direct PCR can also aid
diagnosis
Treatment
Drugs
Oral doxycycline is mainstay of treatment
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BORRELIA SPECIES INFECTIONS
IV ceftriaxone is standard treatment for
neuroborreliosis
Prognosis
Mortality in Lyme disease is rare and usually due to
cardiac involvement
~ 60% of untreated patients develop persistent
infection, which generally clears after several years
Mortality in untreated TBRF is ~ 10%
Jarisch-Herxheimer reactions in 10-20% of LBRF
patients (Africa) with < 5% overall mortality with
antibiotics
MICROBIOLOGY
Morphologic and Biochemical
Characteristics
Microaerophilic, helical shape, multiple endoflagella,
motile
Culture
Difficult to culture; may take up to 12 weeks
Highest sensitivity early in infection, before antibiotics
Microbiologic Identification
Most identification is done via PCR (16s, OspA, etc.)
MICROSCOPIC PATHOLOGY
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
Histologic Features
Organisms may be visualized by
immunohistochemistry or silver stain in tissue
sections
Histologic Features: Lyme Disease
Cutaneous
Erythema migrans
Classically superficial and deep perivascular
infiltrate with eosinophils centrally and plasma
cells at periphery
Also reported: Peripheral neutrophils and
eosinophils, lack of plasma cells, spongiosis,
absence of deep vascular involvement
Lymphocytoma
Often ear lobe, nipple, or scrotum
Diffuse lymphocytic infiltrate; may have follicular
structures resembling germinal centers
Interfollicular areas demonstrate lymphocytic
infiltrate, plasma cells, eosinophils, mast cells,
macrophages
Acrodermatitis chronica atrophicans
Dermal changes in absence of epidermal changes:
Superficial and deep lymphoplasmacytic infiltrate,
fibrous bands, and pseudosclerodermatous
changes sometimes with prominent telangiectasia
of lymphatics
Synovium
In acute stage, marked edema and neutrophilic
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infiltrate
In persistent stage, nonspecific chronic mixed
inflammation and fibrin deposition with
neovascularization
Cardiac
Diffuse, focal, or perivascular infiltrates composed of
either lymphocytes or mixed inflammation (highly
variable)
Myocyte necrosis may be observed
Neurologic
Central
Mild fibrosis of meninges and lymphocytic
infiltrates, intimal hyperplasia of meningeal
arteries
Spongiform changes
Diffuse and nodular microglial activation
Diffuse demyelination of cerebral and cerebellar
white matter
Diffuse astrocytosis
Peripheral
Mixed inflammatory infiltrate of epineurial vasa
nervorum and endoneurial capillaries
Axonal degeneration
Histologic Features of Relapsing Fevers
Autopsy findings may include hepatitis, miliary
splenic abscess, central nervous system hemorrhage
with perivascular infiltrate, and gastrointestinal and
renal hemorrhagic lesions
ANCILLARY TESTS
Immunohistochemistry
Spirochete antibodies may be positive on tissue
sections from skin lesions more often than deep tissue
sites (brain, heart)
DIFFERENTIAL DIAGNOSIS
Spirochetes in Tissue
Syphilis and leptospirosis
RNA Viral Infection (Noncytopathic)
Clinical history and inflammatory pattern similar to
viral myocarditis and viral encephalitis
Serology, PCR, and IHC to distinguish from arbovirus
infections
Coinfection
Borrelia is often transmitted with Anaplasma
phagocytophilum and Babesia
SELECTED REFERENCES
1. Horton JM: Relapsing fever caused by Borrelia species.
In Mandell et al: Mandell, Douglas, and Bennett’s
Principles and Practice of Infectious Diseases. 8th Edition.
Philadelphia: Elsevier/Saunders. 2721-4, 2015
2. Steere AC: Lyme disease (Lyme Borreliosis) due to Borrelia
burgdorferi. In Mandell et al: Mandell, Douglas, and
Bennett’s Principles and Practice of Infectious Diseases. 8th
Edition. Philadelphia: Elsevier/Saunders. 2725-35, 2015
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Microscopic Features
A
A
p
p
A
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
BORRELIA SPECIES INFECTIONS
(Left) Erythema chronica
migrans shows a
lymphocytic perivascular
infiltration in the
superficial and mid dermis.
lthough the clinical
appearance of ECM is often
sufficient to suggest Lyme,
biopsies may be performed
in atypical lesions. (Right)
crodermatitis chronica
atrophicans (3rd stage
of Lyme) shows slight
acanthosis with a dense,
atchy, superficial, and deep
infiltrate with dilated and
ectatic vessels . (From
DP: Nonneoplastic Derm.)
(Left) Lymphocytoma
cutis, a nonspecific skin
inflammatory pattern than
may be seen in Lyme,
shows a much more dense
superficial and deep
inflammatory infiltrate
that can simulate
lymphoma. (From DP:
Nonneoplastic Derm.)
(Right) Lyme myocarditis,
shown here, includes a wide
range of histologic findings
including locally destructive,
redominantly lymphocytic
myocarditis. This patient
was untreated and died of
myocardial complications.
(Left) High-power view of
a case of Lyme myocarditis
shows lymphoplasmacytic
infiltrate within the
myocardium proper with
splitting of muscle cells
by tracts of inflammation.
reas of myocyte necrosis
may be inconspicuous.
(Right) When Lyme disease
is untreated and progresses,
inflammatory infiltrates
may include deposition of
collagen as a sign of
destruction and chronicity.
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LEPTOSPIRA SPECIES INFECTION
The helical structure and hooked ends of Leptospira
can be visualized with dark-field microscopy. (Courtesy
M. Gatton, CDC/PHIL.)
TERMINOLOGY
Definitions
Greek: Leptos (thin) + Latin :Spira (coiled)
ETIOLOGY/PATHOGENESIS
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
Environmental Exposure
Leptospira species have a large zoonotic reservoir as
chronic renal infections in many animals, including
rodents, livestock, and companion animals
Infectious Agents
Leptospira interrogans: Most clinically relevant species
Introduction is though contact by contaminated water
and soil with cuts and scrapes in skin and mucous
membranes
CLINICAL ISSUES
Epidemiology
Global disease, but most common in warmer climates
Presentation
After incubation period of 2-30 days, week-long febrile
illness ensues: Septicemic phase
Lasts until initiation of adaptive response clears
infection in most patients
Symptoms include high fever, headache, chills,
rigors, myalgias (particularly in calf and lumbar
region), conjunctival suffusion, abdominal pain,
nausea, vomiting, cough, and pharyngitis
In 5-15% of patients, severe, late-stage presentation
can occur: Immune phase
Additional signs and symptoms: Jaundice, renal
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failure, arrhythmias, pulmonary symptoms, aseptic
meningitis, photophobia, eye pain, adenopathy,
hepatosplenomegaly, petechial rash, and DIC
2
Silver-positive intraepithelial structures consistent with
Leptospira spirochetes are seen using Warthin-Starry or
Steiner stains. (Courtesy V. Royal, MD.)
Weil disease: Severe manifestation marked by liver
and kidney failure, hemorrhagic pneumonitis,
arrhythmias, and circulatory collapse
Laboratory Tests
Leptospira can be detected in blood, CSF, and urine
during initial septicemic phase
During immune phase, organisms can be detected in
tissue and urine, but not blood or CSF
Organisms can be detected directly via dark-field
microscopy, or PCR or culture
Serology is most common means of diagnosis
Treatment
Drugs
Oral doxycycline for most cases, with IV penicillin
or ceftriaxone reserved for more severe instances
Prognosis
Most patients experience subclinical or mild disease;
mortality with severe disease approaches 40%
MICROBIOLOGY
Morphologic and Biochemical
Characteristics
Leptospira are obligately aerobic, thin, tightly coiled
spirochetes with pointed ends that may be bent into a
hook
Culture
After several weeks will grow on media supplemented
with B vitamins, long chain fatty acids, and
ammonium salts (e.g., Ellinghausen-McCulloughJohnson-Harris media [EMJH])
Microbiologic Identification
Dark-field microscopy to identify colonies
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LEPTOSPIRA SPECIES INFECTION
Clinical Issues
Global disease but most common in warmer climates
Microscopic Pathology
Intraalveolar hemorrhage, hyaline membranes,
organizing pneumonia
Acute interstitial nephritis/acute tubular necrosis
Liver: disorganization of liver cell plates, spotty
necrosis, Kupffer cell hyperplasia, cholestasis, and
portal infiltrates
Key Facts
Silver stain or IHC: filamentous or granular aggregates
of organisms
Ancillary Tests
Spirochete antibodies: cross react (Borrelia, Syphilis);
confirmatory in suspected cases
Top Differential Diagnoses
Borreliosis and syphilis (clinically distinct)
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
MICROSCOPIC PATHOLOGY
Histologic Features
Intraalveolar hemorrhage (may be massive),
sometimes with hyaline membranes, rarely with
organizing pneumonia
Acute interstitial nephritis/acute tubular necrosis with
mixed inflammatory infiltrate of lymphocytes, plasma
cells, histiocytes, and eosinophils
Interstitial myocarditis accompanied by hemorrhage;
can involve epicardium, valves, coronary arteries, and
aorta
Liver findings range from uninvolved to
disorganization of liver cell plates, spotty necrosis,
Kupffer cell hyperplasia, cholestasis, and portal
infiltrates
Submassive centrilobular hepatocellular necrosis
associated with intense hemorrhage has been
reported in Weil disease
Diffuse hemorrhage
Silver stain or IHC may reveal filamentous or granular
aggregates of organisms
ANCILLARY TESTS
Immunohistochemistry
Spirochete antibodies may cross react (Borrelia,
Treponema) and may be confirmatory in suspected
cases
DIFFERENTIAL DIAGNOSIS
Spirochetes in Tissue
Borreliosis and syphilis (clinically distinct)
Histological Organ Involvement
Culture or visualization with special stains/
immunohistochemistry
Pulmonary
Other bacterial infections and sepsis syndromes
Cardiac
Viral myocarditis, toxoplasmosis
Hepatic
Fulminant hepatitis (HSV), CMV/EBV hepatitis,
candidiasis, Hepatitis A/E
Renal
Other causes of interstitial nephritis/acute tubular
necrosis (noninfectious vs. infectious)
SELECTED REFERENCES
1. Salkade HP et al: A study of autopsy findings in 62 cases
of leptospirosis in a metropolitan city in India. J Postgrad
Med. 51(3):169-73, 2005
IMAGE GALLERY
(Left) Interstitial edema with a mononuclear infiltrate and acute tubular injury is seen in the kidney from a leptospirosis patient. (Courtesy V.
Royal, MD.) (Center) Macrophages and lymphocytes associated with atrophic tubules and focal tubulitis with breaks in the basement
membrane are seen in leptospirosis. (Courtesy V. Royal, MD.) (Right) Mononuclear inflammation, tubulitis , casts, and focal cast extrusion
can be seen in leptospirosis. (Courtesy V. Royal, MD.)
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SYPHILIS AND OTHER TREPONEMATOSES
Microscopic examination reveals lymphocytes and
plasma cells around the blood vessels (swollen
endothelium) in the dermis.
TERMINOLOGY
Synonyms
Venereal syphilis (Treponema pallidum pallidum),
yaws (Treponema pallidum pertenue), bejel (Treponema
pallidum endemicum), pinta (Treponema pallidum
carateum)
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
Definitions
Greek: "Trepein" (to turn) + "nema" (thread)
ETIOLOGY/PATHOGENESIS
Infectious Agents
Syphilis is a sexually transmitted infection caused by
bacteria T. p. pallidum
T. p. pallidum species belongs to Spirochaetaceae
family
Risk Factors
Any sexually active person can get syphilis through
unprotected anal, vaginal, or oral sex
Estimated incidence of 12 million new cases each year
(WHO)
North America and Western Europe: Men who have
sex with men (MSM), coinfection with HIV
CLINICAL ISSUES
Presentation
Primary stage
Single small, red, painless papule with ulceration
(chancre)
Lasts 3-6 weeks and heals without treatment
Without treatment, progresses to secondary stage
II
Secondary stage
3 weeks to 3 months after primary stage
Very few diseases cause an erythematous maculopapular
eruption involving the palms and soles, and clinical
history and laboratory testing is useful for confirming
syphilis. (Courtesy G. Strauch, MD.)
Widespread skin rash mainly affect soles and palms
but can spread to whole body
Differential diagnosis includes Rocky Mountain
spotted fever, graft-vs.-host disease, erythema
migrans, and meningococcemia
Raised patches (condyloma latum)
Fever, muscle and joint pains, headache, and
swollen lymph glands
Can affect any organ (e.g., CNS, liver, kidneys,
skeletal muscles)
Latent stage
Begins when all clinical symptoms disappear
With no treatment, may remain latent for years
Most people with untreated syphilis do not develop
tertiary stage syphilis
Tertiary stage
May develop 3-10 years later
Solitary lesion (gummas)
Brain involvement (neurosyphilis), spinal cord
disease
Can affect heart, eyes, or any other organs
Symptoms of late stage can include difficulty
coordinating muscle movements, paralysis,
numbness, gradual blindness, and dementia
Congenital syphilis
One of the TORCH infections
Cause of spontaneous abortion and stillbirth
Live-born neonates may present with secondary
syphilis and progress to latent stages
Other treponematoses often affect skin and present
skin lesions through contact with infected person
Almost 75% of people affected are children < 15
years
Overcrowding, poor personal hygiene and sanitation
facilitate spread of disease in warm communities
Treatment
High-dose penicillin
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SYPHILIS AND OTHER TREPONEMATOSES
Terminology
Syphilis is a sexually transmitted infection caused by
bacteria Treponema pallidum
Pathologic treponematoses: Venereal syphilis (T.
pallidum), yaws (T. pertenue), bejel (T. endemicum),
pinta (T. carateum)
Clinical Issues
Primary: Single small, red, painless papule with
ulceration (chancre)
Secondary: Widespread skin rash; mainly affect soles
and palms but can spread to whole body
Tertiary: Solitary lesion (gummas)
Key Facts
Microscopic Pathology
Primary: Acanthotic epidermis, ulceration,
endothelial swelling, and dense lymphoplasmacytic
response
Secondary: Cellular infiltrate consists of lymphocytes,
plasma cells, macrophages, some neutrophils,
epithelioid cells, and occasional giant cells
Tertiary: Necrotizing granulomatous inflammation
Top Differential Diagnoses
Psoriasis, drug reaction, and lichenoid
hypersensitivity reaction
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
Prognosis
Syphilis is easily cured in early stages
Congenital syphilis is most serious outcome of syphilis
in women
MICROBIOLOGY
Culture
Syphilis cannot be cultured
MICROSCOPIC PATHOLOGY
Histologic Features
Primary
Acanthotic epidermis, ulceration, endothelial
swelling, and dense lymphoplasmacytic response
Secondary
Cellular infiltrate consists of lymphocytes, plasma
cells, macrophages, some neutrophils, epithelioid
cells, and occasional giant cells
Psoriasiform hyperplasia
Granulomatous inflammation is an atypical feature
of secondary stage (papular or nodular clinical
presentation)
Tertiary
Necrotizing granulomatous inflammation
Congenital
Placental histological features include the triad
of enlarged hypercellular villi, proliferative fetal
vascular changes, and acute or chronic villitis
ANCILLARY TESTS
Histochemistry
Warthin-Starry
Darkfield microscopy (mainly used in early stages)
Immunohistochemistry
Spirochete antibodies: T. p. pallidum reacts
PCR
Amplification of bacterial DNA from infected tissue
In late stages, sensitivity of PCR is lower than
immunohistochemistry techniques
Serologic Testing
Screening
Venereal disease research laboratory (VDRL) test
Rapid plasma reagin (RPR) test
Enzyme immunoassay (EIA) test
Diagnosis
Fluorescent treponemal antibody absorption (FTAABS) test
T. pallidum particle agglutination assay (TPA)
Microhemagglutination assay (MA-PT)
DIFFERENTIAL DIAGNOSIS
Primary Syphilis
Candidiasis, chancroid, granuloma inguinale, herpes
simplex, herpes zoster, lymphogranuloma venereum
Microscopic features consistent with syphilis and
lacking fungal, viral, or other bacterial morphology
Secondary Syphilis
Psoriasis
Drug reaction
Lichenoid hypersensitivity reaction
Tertiary Syphilis
Neurological degenerative diseases (clinically)
SELECTED REFERENCES
1. Rysgaard C et al: Nodular secondary syphilis with
associated granulomatous inflammation: case report and
literature review. J Cutan Pathol. Epub ahead of print, 2014
2. Carlson JA et al: The immunopathobiology of syphilis:
the manifestations and course of syphilis are determined
by the level of delayed-type hypersensitivity. Am J
Dermatopathol. 33(5):433-60, 2011
3. Barrett AW et al: The histopathology of syphilis of the oral
mucosa. J Oral Pathol Med. 33(5):286-91, 2004
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SYPHILIS AND OTHER TREPONEMATOSES
Microscopic Features
(Left) High-power view of
skin biopsy shows marked
hyperkeratosis, parakeratosis,
acanthosis, and foci of
superficial erosion in a case
of condyloma latum. (Right)
Exocytosis is prominent in the
upper layer of epidermis and
surface ulceration (condyloma
latum).
(Left) Secondary syphilis
histologically shows
interface changes
with a dense perivascular
lymphoplasmacytic
dermal infiltrate that
is greater in density in
the papillary dermis and
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
diminishes toward the base.
(From DP: Nonneoplastic
Derm.) (Right) T. pallidum
immunohistochemical stain
highlights more organisms
than a traditional silver stain in
both primary and secondary
syphilis. Red chromogen
reactions are helpful in skin
samples with melanin pigment.
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(Left) Dense
lymphoplasmacytic infiltrates
and swollen blood vessels are
highly suspicious for syphilis.
(Right) Lesions of secondary
syphilis histologically often
contain numerous plasma cells
. (From DP: Nonneoplastic
Derm.)
SYPHILIS AND OTHER TREPONEMATOSES
p
g
p
p
Microscopic and Clinical Features
Bacterial Infections: Bacterial Infections Requiring Culture/Ancillary Confirmation
(Left) Spirochetes seen
on this Warthin-Starry stain
are 5-20 m long, < 0.5
m wide spirals, typical of
Treponema pallidum. (Right)
High-power view shows
endothelial swelling and
erivascular lymphocytic
and plasmacellular infiltrate
in a case of secondary
syphilis. The prominent
endothelial swelling
may be confused with
ranulomatous appearance
from other causes.
(Left) This HIV-positive
atient shows a widespread
maculopapular eruption
indicative of secondary
syphilis. (Courtesy G.
Strauch, MD.) (Right)
Primary chancre of syphilis
affects the scrotum of a male
atient . The chancre is
less depressed and softer
due to underlying anatomy.
(Courtesy D. Johnson, MD.)
(Left) Microscopic
examination of colon
biopsy reveals severe colitis
with dense plasma cell
infiltrates and varying
numbers of neutrophils
and lymphocytes. (Right)
Numerous spirochetes
are identified in this
colon biopsy using an
immunohistochemical stain
with a polyclonal antibody
against Treponema pallidum.
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