SPIROCHETES AND SPIRILLUM TREPONEMA

1. Treponema pallidum subsp. pallidum

SPIROCHETES 2. Treponema pallidum subsp. pertenue
3. Treponema pallidum subsp. Endemicum
4. Treponema carateum

 Long, slender, helically curved, gram (-) bacilli
 Axial filaments (axial fibrils/endoflagella) facilitate
motility of the organisms (most distinctive & unusual
morphologic feature- also outer sheath)
 Composed of 2-100 axial fibrils/ endoflagella-
unusual since common bacteria have their flagella
attached outside the bacterial cell (spirochetes-
flagella is inside, responsible for motility of
organism )
 Motility is by rapid rotation around its long axis
 Infect humans and have not been cultivated for more than
one passage in vitro
 Passage- number of times a cell culture has been
subcultured
 Have to know passage number since it can make
or break an experiment of that certain organism
 In vitro- outside the body/ living organism
 Stain poorly with Gram staining or Giemsa
 Best observed with the use of dark-field or phase-contrast
microscopy
 Microaerophilic- grow in environment with 5-10% O2,
higher is detrimental

PATHOGENIC SPIROCHETES

 Genus are differentiated based on # of axial filaments/

fibrils and # of insertion disks
 Insertion disks- where the fibrils attach
 Genus:
 Treponema- tightly coiled & cork screw appearance
 Leptospira- less tightly coiled with sharp hook like  All diseases caused by these agents have relapsing clinical
bends at the end of the cells course-- the px may deteriorate since these diseases may
 Borrelia- much less tightly coiled, extremely long progress to a late stage; have prominent cutaneous
compared to other 2 genus manifestations
TREPONEMA PALLIDUM (T pallidum subsp pallidum)
 Thin, tightly coiled spirochete (corkscrew appearance)
 Difficult to stain
 Dark field microscope used instead
 Microaerophilic and cannot grow on standard culture
media (can’t grow in vitro); successfully grown in testicles
in rabbit
Clinical Infection:
Syphilis
 Acquired syphilis- organism enter the host by either
penetrating intact mucous membranes or entering through
breaks in the skin
 Transmission: sexual contact
 Incubation period: 2-6 weeks
 Invades the bloodstream and spreads to other body
sites
 Start of symptom: usually 21 days
 T pallidum- remarkable attraction to arterioles-- so
infection would lead to endarteritis (inflammation of
lining of arteries) and subsequent progressive tissue
destruction-- skin lesions
 Stages:
1. Primary syphilis
 First clinical sign of syphilis: hard chancre (a
painless ulcer)- develops at the site of
inoculation-- genitalia (penis, vagina, cervix,
anus)
 Single lesion, nontender, firm, and reddish
 Extremely infectious because the lesion contains
a large number of organisms
 Bubo formation- appears 1 week after the
appearance of hard chancre (lymph nodes
enlarge but not suppurate/ formation of pus)
 10% of px may have extragenital lesions- face,
lips, tongue, tonsils, breast, fingers
2. Secondary syphilis
 2-10 weeks after primary syphilis
 Fever, weight loss, malaise, loss of appetite, sore
throat, headache (influenza-like symptoms)
 Skin is the organ most commonly affected- rash
on the face, scalp, palms of hands, and soles of
feet (with generalized lymphadenopathy)
 Condylomata lata- white mucous patches around
moist areas like anus and vagina (mucosal
lesions)
 Highly infectious state (large numbers of
spirochetes are present)
 Px seeks medical attention at this stage
 Clinical manifestations become apparent;
systemic symptoms is evident
3. Latent stage
 Disease becomes asymptomatic (subclinical) but
not necessarily inactive
 No visible s/s of syphilis
 If you do not receive treatment, you can
continue to have syphilis in your body for years
without any signs or symptoms
4. Tertiary syphilis
 Tissue destructive phase
 Appears 3-25yrs after the initial infection in up
to 35% of untreated px
 Gumma formation- granuloma-like lesions that
are soft, painless, and non-infectious and found
on the skin or in the bones or visceral organs
 Central nervous system disease (neurosyphilis),
cardiovascular abnormalities, eye disease
>Px with neurosyphilis- are infected with tertiary syphilis or
congenital syphilis
 Congenital Syphilis
 Transmission: placental (most often associated to
mothers with early syphilis); vertically from mother
to unborn fetus
 Fetus may be aborted
 Born dead or alive with syphilis
 Born asymptomatic, show evidence of syphilis
weeks, months or years later
 Born entirely free of syphilis
 Hutchinson’s triad- deafness, blindness, notched and
peg-shaped teeth
 “saber shin” bowing of the tibia and the “bulldog”
appearance of a deformed maxilla (undersized,
resemble old man)
 Vesicular skin lesions, syphilitic rhagades (linear
scars or cracks at angle of the mouth)
 Neurosyphilis (mental deterioration, insanity,
paralysis, etc)
BORRELIA
 Causes Borreliosis (relapsing fever)
 Transmission: bite of infected body louse or ticks
 Actively motile and stain well with Giemsa’s stain (view
under bright-field mx)
 Species can grow in vitro
 Microaerophilic or anaerobic
1. Borrelia recurrentis
 Causes louse-borne or epidemic relapsing fever
 Humans are the only reservoir
 Incubation period: 2-15 days
 Fever, headache, myalgia (last 4-10 days), petechiae,
diffuse abdominal tenderness, and conjunctival effusion
 Petechiae- small red spots/rashes
2. Borrelia burgdorferi SPIRILLUM
SPIRILLUM MINUS
 Gram (-) thick, spirilla with tapering ends
 Actively motile w/ polytrichous polar flagella
 Strictly aerobic
 Normal flora of URT of rats
 Causes Rat bite fever (Sodoku)
 Causes Lyme disease- most common vector-borne disease  So- rat
in North America and Europe and is an emerging problem  Doku- poison
in northern Asia  Transmission: bites or scratches from infected rodents
 Tick-borne (through bite wound, open skin, mucous membranes in
 Not all stages occur in px (not altogether) eyes, nose, mouth), consuming food or drinks that have
 First stage= erythema migrans (EM)- red, ring-shaped skin been contaminated with droppings or urine from a rodent
lesion with a central clearing that first appears at the site of carrying the bacteria
the tick bite but may develop at distant sites as well  Clinical infection:
 Second stage= weeks to months after infection-- arthritis,  Fever, swelling or formation of an ulcer at the bite
neurologic disorders (ie meningitis, neurologic deficits) wound, swollen lymph nodes, maculopapular rash
and carditis (inflammation of the heart)  This disease is common in Asia
 Third stage= chronic arthritis or acrodermatitis chronica  Organism can be observed under the mx:
atrophicans (ACA)-a diffuse skin rash -- may continue for  Darkfield microscopy
years  Giemsa stain

LEPTOSPIRA
 Spiral-shaped, right handed helices with hooked ends
 Contain 2 axial filaments- spinning or a rapid back-and-
forth movement
1. Leptospira interrogans
 Most pathogenic Leptospira spp
 Can infect most mammals, reptiles, amphibians, fish, birds,
and invertebrates
 Cause Leptospirosis- contact with infected animals or
water contaminated with urine or blood of infected animals
 Zoonotic disease
 Most common in developing countries and warm
climates
 Incubation period: 2-20 days
 Transmission: enters the human host through breaks in the
skin, mucous membranes or conjunctivae
 Clinical infection:
 Symptoms begin abruptly from 2-20 days after
infection
 Fever, headache, myalgia, muscular pains
(gastrocnemius muscle- calves), redness of
conjunctiva, jaundice
 Anicteric leptospirosis- most common; self-limiting,
high fever and severe headache that lasts 3-7days; not
affected by jaundice; mild type
 Weil’s disease or icteric leptospirosis- most severe
illness; liver, kidney, or vascular dysfunction with
lethal pulmonary hemorrhage; death can occur in up
to 10% of cases; affects the liver=jaundice