Spirochete

1) Treponema
2) Borrelia
3) Leptospira
 Taxonomy
Order: Spirochaetales
Family: Treponemataceae
Genus: -Treponema
(Treponema pallidum)
- Borrelia
(B. recurentis, B.
burgdoferi)
-Leptospira
(L. interrogans-patogenik, L.
biflexa-nonpastogenis yang
hidup bebas)
 Gram-negative spirochetes
• Spirochete from Greek for “coiled hair”
Extremely thin and can be very long
 Motile by periplasmic flagella (axial fibrils or
endoflagella)
 Outer sheath encloses axial fibrils
• Axial fibrils originate from insertion pores at both poles of cell
Periplasmic Flagella Diagram
 Spirochaetales Associated
Human Diseases
Genus Species Disease
Treponema pallidum ssp. pallidum Syphilis
pallidum ssp. endemicum Bejel
pallidum ssp. pertenue Yaws
carateum Pinta
Borrelia burgdorferi Lyme disease (borreliosis)
recurrentis Epidemic relapsing fever
Many species Endemic relapsing fever
Leptospira interrogans Leptospirosis
(Weil’s Disease)
Treponema pallidum ssp.
pallidum
 Venereal Treponemal Disease
- T. pallidum are slender spirals with spiral coils spaced at a
distance of 1 μm from one another.
- Pathogenic T. pallidum has never been cultured on artificial
media, in fertile eggs, or in tissue culture.
- Nonpathogenic treponemes (Reiter strain) can be cultured
anaerobically in vitro.
-T. pallidum is a microaerophilic organism; it survives best in 3–
5% oxygen.
- Cause Syphilis
 Primarily sexually transmitted disease
 May be transmitted congenitally
Darkfield Microscopy of
Treponema pallidum
 General Characteristics of
Treponema pallidum
 Too thin to be seen with light microscopy in
specimens stained with Gram stain or Giemsa stain
• Motile spirochetes can be seen with darkfield
micoscopy
• Staining with anti-treponemal antibodies labeled with
fluorescent dyes
 Intracellular pathogen
 Cannot be grown in cell-free cultures in vitro
• Koch’s Postulates have not been met
 Do not survive well outside of host
 Epidemiology of T. pallidum
 Transmitted from direct sexual contact or from
mother to fetus
 Long incubation period during which time host is
non-infectious
Virulence Factors of T. pallidum
 Outer membrane proteins promote adherence
 Hyaluronidase may facilitate perivascular
infiltration
 Antiphagocytic coating of fibronectin
 Tissue destruction and lesions are primarily result
of host’s immune response (immunopathology)
 Pathogenesis of T. pallidum
Primary disease
Spirochetes multiply locally at the site of entry, and some spread to
nearby lymph nodes and then reach the bloodstream.
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, anogenital
region, axillas, and mouth. There may also be syphilitic
meningitis, chorioretinitis, hepatitis, nephritis.
 Latent Stage Syphilis &
Tertiary

 In Latent syphilis, which can last for years, there are little to no
symptoms.
•First 4 years = Early latent
•Subsequent period = Late latent

 In Tertiary syphilis there are Gummas (soft swelling,

granulomatous lesions) which occurs in the connective tissue of
the liver, brain, testes, and heart, skin, bones, and liver; degenerative
changes in the central nervous system (meningovascular syphilis); or
cardiovascular
 Congenital Syphilis

 Congenital syphilis results from transplacental

infection
 T. pallidum septicemia in the developing fetus and
widespread dissemination
Some of the infected fetuses die, miscarriages result; others are
stillborn at term.
Others are born live but develop the signs of congenital
syphiliswith variety of central nervous system anomalies.
 Diagnostic Tests for Syphilis

(Original Wasserman Test)

NOTE: Treponemal antigen tests indicate experience with a treponemal

infection, but cross-react with antigens other than T. pallidum ssp.
pallidum. Since pinta and yaws are rare in USA, positive treponemal
antigen tests are usually indicative of syphilitic infection.
Cardiolipin
is an important component of the treponemal
antigens.
the spirochetes cause the development of antibody-
like substance, reagin, which gives positive
flocculation tests
Treatment
Penicillin in concentrations of 0.003 U/mL.
Syphilis of less than 1 year’s duration is treated by a single
injection of benzathine penicillin G 2.4 million units
intramuscularly.
In neurosyphilis, the same therapy is acceptable, but larger
amounts of intravenous penicillin are sometimes
recommended.
Other antibiotics (eg, tetracyclines or erythromycin)
can occasionally be substituted. Treatment of gonorrhea
is thought to cure incubating syphilis.
Nonvenereal Treponemal
Diseases
 Bejel, Yaws & Pinta
 Primitive tropical and subtropical
regions
 Primarily in impoverished children
Treponema pallidum ssp. endemicum
Bejel (a.k.a. endemic syphilis)
• Initial lesions: nondescript oral lesions
• Secondary lesions: oral papules and mucosal patches
• Late: gummas (granulomas) of skin, bones &
nasopharynx
 Transmitted person-to-person by contaminated
eating utensils
 Primitive tropical/subtropical areas (Africa, Asia &
Australia)
Treponema pallidum ssp. pertenue
(May also see T. pertenue)
Yaws: granulomatous disease
• Early: skin lesions (see below)
• Late: destructive lesions of skin, lymph nodes & bones
 Transmitted by direct contact with lesions
containing abundant spirochetes
 Primitive tropical areas (S. America, Central Africa, SE Asia)

Papillomatous Lesions of
Yaws: painless nodules widely
distributed over body with
abundant contagious
spirochetes.
 Treponema carateum
Pinta: primarily restricted to skin
• 1-3 week incubation period
• Initial lesions: small pruritic papules
• Secondary: enlarged plaques persist for
months to years
• Late: disseminated, recurrent
hypopigmentation or depigmentation of
skin lesions; scarring & disfigurement
 Transmitted by direct contact with skin lesions
 Primitive tropical areas
(Mexico, Central & South America)

Hypopigmented Skin Lesions of

Pinta: depigmentation is commonly
seen as a late sequel with all
treponemal diseases
Borrelia spp.
Giemsa Stain of Borrelia
recurrentis in Blood

Light Microscopy Phase Contrast Microscopy

 Epidemiology of Borrelia Infections

Pediculus humanus
Borrelia
recurrentis

Ornithodoros.pps
Borrelia spp.

Ixodes spp.
Borrelia
burgdorferi
Borrelia species & relapsing fever
Relapsing fever (epidemic) is caused by Borrelia
recurrentis, transmitted by the human body louse

Antigenic structure
The antigenic structure of the organisms changes in
the course of a single infection.
Ultimate recovery (after 3 to 10 relapses) is
associated with the presence of antibodies against
several antigenic variants.
PATHOLOGY
fatal cases show spirochetes in great numbers in the spleen and
liver, necrotic and hemorrhagic lesions in the kidneys,
gastrointestinal tract, spinal fluid and brain of persons who have
had meningitis.
PATHOGENESIS & CLINICAL FINDINGS
- The incubation period is 3–10 days
- The onset is sudden, with chills and an abrupt rise of temperature.
During this time, spirochetes found in the blood. The fever persists for 3–5
days and then declines, leaving the patient weak but not ill.
- Afebrile period lasts 4–10 days and is followed by a second attack of chills,
fever, intense headache, and malaise.
- during the febrile stages, organisms are present in the blood; during the
afebrile periods, they are absent.
 Borrelia burgdorferi & Lyme Disease
Lyme disease is named after the town of Lyme, where
clusters of cases in children were identified.
Lyme disease is caused by the spirochete B. burgdorferi and
is transmitted to humans by the bite of a small ixodes tick.

The most common sign of infection is an expanding area of

redness on the skin, known as erythema migrans, that begins
at the site of a tick bite about a week after it has occurred.

In addition, flu-like symptoms, and late manifestations often

with arthralgia and arthritis.
B burgdorferi is a spiral organism, highly motile.

Transmission of B burgdorferi to humans is by injection of the

organism in tick saliva or by regurgitation of the tick's midgut
contents.

After injection by the tick, the organism migrates out from the
site, producing the characteristic skin lesion.

Dissemination occurs by lymphatics or blood to other skin and

musculoskeletal sites and to many other organs.
A unique skin lesion that begins 3 days to 4 weeks after a tick
bite often marks
Leptospirosis is an infection caused by corkscrew-
shaped bacteria called Leptospira interrogans

Signs and symptoms can range from none to mild

such as headaches, muscle pains, and fever; to
severe with bleeding from the lungs or meningitis.
Leptospira interrogans
Silver Stain of Leptospira interrogans
serotype icterohaemorrhagiae

 Obligate aerobes
 Characteristic hooked ends
(like a question mark, thus the
species epithet – interrogans)
 Leptospirosis Clinical Syndromes
 Mild virus-like syndrome
 (Anicteric leptospirosis) Systemic with aseptic
meningitis
 (Icteric leptospirosis) Overwhelming disease
(Weil’s disease)
Vascular collapse
Thrombocytopenia
Hemorrhage
Hepatic and renal dysfunction
NOTE: Icteric refers to jaundice (yellowing of skin and mucus
membranes by deposition of bile) and liver involvement
Pathogenesis of Icteric Leptospirosis
 Leptospirosis, also called Weil’s disease in humans
 Direct invasion and replication in tissues
 Characterized by an acute febrile jaundice &
immune complex glomerulonephritis
 Incubation period usually 10-12 days with flu-like
illness usually progressing through two clinical
stages:
i. Leptospiremia develops rapidly after infection (usually
lasts about 7 days) without local lesion
ii. Infects the kidneys and organisms are shed in the urine
(leptospiruria) with renal failure and death not
uncommon
 Hepatic injury & meningeal irritation is common
Clinical Progression of Icteric (Weil’s
Disease) and Anicteric Leptospirosis

(pigmented
part of eye)
 Epidemiology of Leptospirosis
 Mainly a zoonotic disease
• Transmitted to humans from a variety of wild and
domesticated animal hosts
• In USA most common reservoirs rodents (rats), dogs,
farm animals and wild animals
 Transmitted through breaks in the skin or intact
mucus membranes
 Indirect contact (soil, water, feed) with infected urine
from an animal with leptospiruria
 Occupational disease of animal handling
Comparison of Diagnostic Tests
for Leptospirosis
Rickettsia