SPIRALS

Treponema spp.

Borrelia spp.

Leptospira interrogans
Leptospirosis Clinical
Syndromes
- Mild virus-like syndrome
- (Anicteric leptospirosis)
Systemic with aseptic meningitis
- (Icteric leptospirosis)
Overwhelming disease (Weils
disease)
* Vascular collapse
* Thrombocytopenia

Nonvenereal Treponemal Diseases

* Hemorrhage
* Hepatic and renal dysfunction

- Bejel, Yaws & Pinta

- Primitive tropical and subtropical

NOTE: Icteric refers to jaundice

regions

(yellowing of skin and mucus

- Primarily in impoverished children

Borrelia recurrentis

& other

- Dark Field Microscopy

Borrelia spp.
Epidemiology of Relapsing

membranes by deposition of
bile) and liver involvement

Fever
- Associated with poverty, crowding,

Pathogenesis of Icteric

and warfare

Leptospirosis

- Arthropod vectors

- Leptospirosis, also called Weils

- Louse-borne borreliosis = Epidemic

disease in humans

Relapsing Fever

- Direct invasion and replication

- Transmitted person-to-person by

in tissues

human body lice (vectors) from

- Characterized by an acute

pallidum

infected human reservoir

febrile jaundice & immune

- Too thin to be seen with light

- Infect host only when louse is

complex glomerulonephritis

microscopy in specimens stained

injured, e.g., during scratching

- Incubation period usually 10-12

with Gram stain or Giemsa stain

- Therefore, a single louse can only

days with flu-like illness usually

infect a single person

progressing through two clinical

- Lice leave host that develops a

stages:

fever and seek normal temperature

- Leptospiremia develops rapidly

antibodies labeled with fluorescent

host

after infection (usually lasts

dyes

- Tick-borne borreliosis = Endemic

about 7 days) without local

- Intracellular pathogen

Relapsing Fever

lesion

- Cannot be grown in cell-free cultures

- Sporadic cases

- Infects the kidneys and

- Transmitted by soft body ticks

organisms are shed in the urine

- Do not survive well outside of host

(vectors) from small mammal

(leptospiruria) with renal failure

- Care must be taken with clinical

reservoir

and death not uncommon

- Ticks can multiply and infect new

- Hepatic injury & meningeal

human hosts

irritation is common

General Characteristics of

Treponema

- Motile spirochetes can be seen with

darkfield micoscopy
- Staining with anti-treponemal

in vitro

specimens for laboratory culture or

testing

Epidemiology of
Leptospirosis
- Mainly a zoonotic disease
- Transmitted to humans from a
variety of wild and domesticated
Epidemiology of T. pallidum

animal hosts

- Transmitted from direct sexual contact or

- In USA most common

from mother to fetus

reservoirs rodents (rats), dogs,

- Not highly contagious (~30% chance of

farm animals and wild animals

acquiring disease after single exposure to

- Transmitted through breaks in

infected partner) but transmission rate

the skin or intact mucus

dependent upon stage of disease

membranes

- Long incubation period during which time host

- Indirect contact (soil, water,

is non-infectious

feed) with infected urine from an

- Useful epidemiologically for contact tracing

animal with leptospiruria

and administration of preventative therapy

- Occupational disease of animal

handling

Pathogenesis of Relapsing
Fever
Pathogenesis of T. pallidum

- Relapsing fever (a.k.a., tick fever,

- Tissue destruction and lesions are primarily a

borreliosis, famine fever)

consequence of patients immune response

- Acute infection with 2-14 day (~ 6

- Syphilis is a disease of blood vessels and of

day) incubation period

the perivascular areas

- Followed by recurring febrile

- In spite of a vigorous host immune response

episodes

the organisms are capable of persisting for

- Constant spirochaetemia that

decades

worsens during febrile stages

- Infection is neither fully controlled nor

- Epidemic Relapsing Fever = Louse-

eradicated

borne borreliosis

- In early stages, there is an inhibition of cell-

- Borrelia recurrentis

mediated immunity

- Endemic Relapsing Fever = Tick-

- Inhibition of CMI abates in late stages of

borne borreliosis

disease, hence late lesions tend to be localized

- Borrelia spp.

Borrelia
burgdorferi
Pathogenesis of Lyme
Borreliosis
- Lyme disease characterized by
three stages:
1. Initially a unique skin lesion
(erythema chronicum migrans
(ECM)) with general malaise
* ECM not seen in all infected hosts
* ECM often described as bullseye
rash
* Lesions periodically reoccur
2. Subsequent stage seen in 515% of patients with neurological or
Virulence Factors of T. pallidum

cardiac involvement

- Outer membrane proteins promote adherence

3. Third stage involves migrating

- Hyaluronidase may facilitate perivascular

episodes of non-destructive, but

infiltration

painful arthritis

- Antiphagocytic coating of fibronectin

- Acute illness treated with

- Tissue destruction and lesions are primarily

phenoxymethylpenicillin or

result of hosts immune response

tetracycline

(immunopathology)

- Erythema chronicum migrans of

Pathogenesis of T. pallidum (cont.)

Lyme Borreliosis: BULL'S EYE RASH

Epidemiology of Lyme

Primary Syphilis

Borreliosis

- Primary disease process involves invasion of

- Lyme disease was recognized as a

mucus membranes, rapid multiplication & wide

syndrome in 1975 with outbreak in

dissemination through perivascular lymphatics

Lyme, Connecticut

and systemic circulation

- Transmitted by hard body tick

- Occurs prior to development of the primary

(Ixodes spp.) vectors

lesion

* Nymph stage are usually more

- 10-90 days (usually 3-4 weeks) after initial

aggressive feeders

contact the host mounts an inflammatory

* Nymph stage generally too small

response at the site of inoculation resulting in

to discern with unaided eye

the hallmark syphilitic lesion, called the chancre

* For these reasons, nymph stage

(usually painless)

transmits more pathogens

> Chancre changes from hard to ulcerative with

- White-footed deer mice and other

profuse shedding of spirochetes

rodents, deer, domesticated pets

> Swelling of capillary walls & regional lymph

and hard-shelled ticks are most

nodes w/ draining

common reservoirs

> Primary lesion heals spontaneously by fibrotic

walling-off within two months, leading to false
sense of relief
Pathogenesis of T. pallidum (cont.)
Secondary Syphilis
- Secondary disease 2-10 weeks after primary
lesion
- Widely disseminated mucocutaneous rash
- Secondary lesions of the skin and mucus
membranes are highly contagious

- Generalized immunological response

- Generalized Mucocutaneous Rash of
Secondary Syphilis

Pathogenesis of T. pallidum (cont.)

Latent Stage Syphilis
- Following secondary disease, host enters
latent period
- First 4 years = early latent
- Subsequent period = late latent
- About 40% of late latent patients progress to
late tertiary syphilitic disease
Pathogenesis of T. pallidum (cont.)
Tertiary Syphilis
- Tertiary syphilis characterized by localized
granulomatous dermal lesions (gummas) in
which few organisms are present
- Granulomas reflect containment by the

immunologic reaction of the host to chronic

infection
- Late neurosyphilis develops in about 1/6
untreated cases, usually more than 5 years
after initial infection
- Central nervous system and spinal cord
involvement
- Dementia, seizures, wasting, etc.
- Cardiovascular involvement appears 10-40
years after initial infection with resulting
myocardial insufficiency and death
Pathogenesis of T. pallidum (cont.)
Congenital Syphilis
- Congenital syphilis results from transplacental
infection
- T. pallidum septicemia in the developing fetus
and widespread dissemination
- Abortion, neonatal mortality, and late mental
or physical problems resulting from scars from
the active disease and progression of the active
disease state

Prevention & Treatment of Syphilis

- Penicillin remains drug of choice
- WHO monitors treatment recommendations
- 7-10 days continuously for early stage
- At least 21 days continuously beyond the early
stage
- Prevention with barrier methods (e.g.,
condoms)
- Prophylactic treatment of contacts identified
through epidemiological tracing