SPIROCHETES

 The spirochetes are a large, heterogeneous group of

spiral (helical), motile, and thin bacteria.
 One family (Spirochaetaceae) of the order
Spirochaetales consists of two genera whose
members are human pathogens, Borrelia and
Treponema.
 The other family (Leptospiraceae) includes one genus
of medical importance: Leptospira.
TREPONEMA
 T. pallidum subspecies pallidum is the etiologic
agent of the venereal disease syphilis; T.
pallidum subspecies endemicum causes endemic
syphilis (bejel); and T. pallidum subspecies
pertenue causes yaws.
 T. pallidum and related pathogenic treponemes are
thin, tightly coiled spirochetes with pointed, straight
ends.
 Traditional diagnostic tests such as microscopy and
culture are of little value
 these spirochetes do not grow in cell-free cultures and
limited growth (with 30 hours of doubling time) in
tissue culture.
 Microaerophilic or anaerobic and extremely sensitive
to oxygen.
 EPIDEMIOLOGY
• Worldwide  3rd most common sexually
transmitted bacterial disease in US.
• High risk : 1. Homosexual
2. Immunocompromised
• Natural syphilis is exclusive to humans and
has no other known natural hosts.
• Labile and unable to survive exposure to
drying or disinfectan.
• Transmitted by : sexual contact, congenitally,
and transfusion with contaminated blood.
PATHOGENESIS, PATHOLOGY, AND
CLINICAL
FINDINGS
 Spirochetes multiply locally at the site of entry, and
some spread to nearby lymph nodes and then reach
the bloodstream.

 Within 2–10 weeks after infection, a papule develops

at the site of infection and breaks down to form an
ulcer with a clean, hard base (“hard chancre”).
This “primary lesion” always heals spontaneously,
 but 2–10 weeks later, the “secondary” lesions appear.
These consist of a red maculopapular rash
anywhere on the body, including the hands and
feet, and moist, pale papules (condylomas) in the
anogenital region, axillae, and mouth. The patient may
also have syphilitic meningitis, chorioretinitis,
hepatitis, nephritis (immune complex type), or
periostitis.

 The secondary lesions also subside spontaneously.

Both primary and secondary lesions are rich in
spirochetes and are highly infectious. Contagious
lesions may recur within 3–5 years after infection, but
thereafter the individual is not infectious.
 In about 30% of cases, early syphilitic infection
progresses spontaneously to complete cure without
treatment. In another 30%, the untreated infection
remains latent.

 In the remainder, the disease progresses to the

“tertiary stage” characterized by the development of
gummas in the skin, bones, and liver;
degenerative changes in the central nervous
system or cardiovascular lesions

 In all tertiary lesions, treponemes are very rare,

and the exaggerated tissue response must be
attributed to hypersensitivity to the organisms.
UTERO INFECTION (CONGENITAL SYPHILIS)
 Pregnant woman can transmit T.pallidum to the
fetus through the placenta beginning in the 10th-
15th weeks of gestation.  With any stage of
syphilis
 Some of the infected fetuses die, and
miscarriages result; others are stillborn at term.
 Other born live but develop congenital defect 
interstitial keratitis, Hutchinson’s teeth,
saddlenose, periostitis, and a variety of central
nervous system anomalies.
LABORATORY DIAGNOSIS
 Darkfield microscopy or special fluorescent
stains
 PCR (rare)

 Antibody detection

“Efforts to culture T. pallidum in vitro should not be

attempted, because the organism does not grow in
artificial cultures”
TREATMENT, PREVENTION, AND CONTROL
 A single intramuscular dose of long-acting
benzathine penicillin G is used for the early
stages of syphilis, and three doses at weekly
intervals is recommended for congenital and late
syphilis.
 Doxycycline or azithromycin.

 Only penicillin can be used for the treatment of

neurosyphilis.
 Safe-sex techniques and adequate contact and
treatment of the sex partners of patients who
have been documented with infection.
BORRELIA
 Members of the genus Borrelia cause two
important human diseases: Lyme disease and
relapsing fever.
 Lyme disease  Borrelia burgdorferi , B.
garinii, and Borrelia afzelii
 Relapsing fever  Borrelia recurrentis
 considered neither gram-positive nor gram-
negative, even though they have an outer membrane
similar to gram-negative bacteria.
 stain well with aniline dyes (e.g., Giemsa or Wright
stain)
 can be easily seen by light microscopy when
present in smears of peripheral blood from patients
with relapsing fever but not those with Lyme
disease
 Microaerophilic and have complex nutritional needs.
BORRELIA SPECIES AND
RELAPSING
FEVER
 Epidemic or louse-borne relapsing fever
form caused by Borrelia recurrentis is
transmitted by the human body louse
(Pediculus humanus) ; it does not occur in the
United States.
 Endemic relapsing fever is caused by as many
as 15 species of borreliae and is spread by
infected soft ticks of the genus Ornithodoros.
 incubation period: 3-10 days.
 Sudden onset, with chills and an abrupt rise of
temperature, duration 3-5 days until declines,
leaving the patient weak but not ill. → During this
time, spirochetes abound in the blood.
 afebrile period lasts 4-10 days and is followed by a
second attack of chills, fever, intense headache,
and malaise. → episodic febrile, with diminishing
severity.
 during the afebrile periods, spirochetes are absent in
the blood.
BORRELIA BURGDORFERI
AND LYME DISEASE
 Since 1992, three species of Borrelia have been
associated with Lyme disease, Borrelia
burgdorferi , Borrelia afzelii, and Borrelia
garinii.
 The spirochete B burgdorferi is transmitted to
humans by the bite of a small Ixodes (hard tick).
 A unique skin lesion begins 3 days - 4 weeks after a
tick bite marks stage 1 → erythema migrans +
flulike symptom
 Stage 2 occurs weeks to months later and includes
arthralgia and arthritis; neurologic manifestations
with meningitis, facial nerve palsy, and painful
radiculopathy; and cardiac disease with conduction
defects and myopericarditis.
 Stage 3 begins months to years later with chronic
skin, nervous system, or joint involvement.
LABORATORY DIAGNOSIS
 Microscopy : Borreliae that cause relapsing fever
 febrile period Giemsa- or Wright-stained
preparation of blood.
 Culture (generally not performed)

 Nucleid acid-based test

 Antibody detection : serologic testing is the

diagnostic test of choice for patients with
suspected Lyme disease 
immunofluorescence assay (IFA) and EIA 
IgM antibodies appear 2 to 4 weeks after the
onset of erythema migrans in untreated patients
 igG
TREATMENT, PREVENTION, AND CONTROL
 Lyme disease  oral amoxicillin,
doxycycline, or cefuroxime.
 Lyme arthritis and acrodermatitis chronica
atrophicans  Oral cefuroxime, doxycycline, or
amoxicillin.
 Relapsing fever  tetracyclines or
penicillins.
 Prevention of tick-borne Borrelia diseases
includes avoiding ticks and their natural
habitats, wearing protective clothing, and
applying insect repellents.
LEPTOSPIRA AND LEPTOSPIROSIS
 One pathogenic species, Leptospira interrogans,
but more than 200 serovars of L interrogans.
 Leptospires are thin, coiled spirochetes with a
hook at one or both pointed ends
 Actively motile, with two periplasmic flagel

 Obligate aerobes, grow best under aerobic

conditions at 28-30°C in semisolid medium (eg,
Ellinghausen-McCullough-Johnson-Harris,
EMJH)
PATHOGENESIS AND CLINICAL FINDINGS
 the leptospires entering the body through breaks in
the skin and mucous membranes  establish in the
parenchymatous organs (particularly liver and
kidneys)  hemorrhage and necrosis of tissue 
dysfunction of those organs (jaundice, hemorrhage,
nitrogen retention A.K.A Weil disease).
 Many infection are mild or subclinical

 incubation period : 1-2 weeks

 Variable febrile onset if present in blood

 Organisms can be found in blood and CSF early in
the disease and in urine during the later stages
 aseptic meningitis
 Nephritis and hepatitis may also recur, and there may
be skin, muscle, and eye lesions.

“The degree and distribution of organ involvement vary

in the different diseases produced by different
leptospirae in various parts of the world”
LABORATORY DIAGNOSIS
 Microscopy  Gram stain nor silver stain is
reliable in the detection of leptospires.
 Culture  Leptospires can be cultured on
specially formulated media  Fletcher, EMJH
[Ellinghausen-McCullough-Johnson- Harris],
Tween 80-albumin.
 Nucleic Acid–Based Tests : PCR.

 Antibody Detection : serologic tests is the

microscopic agglutination test (MAT).
TREATMENT, PREVENTION, AND CONTROL
 usually not fatal, particularly in the absence of
icteric disease
 Intravenously administered penicillin or
doxycycline.
 Doxycycline can be used a prophylaxis

 vaccination of livestock and pets, rodent control

can help reduce the incidence