Spirochetes-Treponemes  Flashcards

(59 cards)

1
Q

What features do the Spirochetes share in common?

A

Flexible, spiral peptidoglycan cell well

One or more axial fibrils (“internal flagellum”) that assists in maintaining coiled shape

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2
Q

Three major genera of Spirochetes responsible for human disease:

A

Treponema, Borrelia, Leptospira

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3
Q

Structural characteristics of Treponema pallidum

A

Outer membrane does not contain lipopolysaccharide

Thin, tightly coiled

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4
Q

How is Treponema pallidum visualized?

A

Must use Darkfield microscopy or immunofluorescence for visualization

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5
Q

Describe Treponema pallidum culture and growth.

A

Can only be cultured few generations on media with rabbit epithelial cells

Very sensitive to drying and heat

Microaerophilic (only 3-5% oxygen)

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6
Q

___________________ is the 3rd most common sexually transmitted infection in U.S.

A

Treponema pallidum (syphilis) is the 3rd most common sexually transmitted infection in U.S.

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7
Q

Incidence of syphilis is particularly rising among what demographic?

A

MSM

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8
Q

Treponema pallidum is found only in ____.

A

humans

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9
Q

How is syphilis transmitted?

A

via direct sexual contact with an infective primary or secondary mucosal lesion on the genitals, anus, or lips.

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10
Q

When and how does congenital infection with syphilis occur?

A

Congenital infection occurs in utero

by transmission across the placenta

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11
Q

Clinical hallmarks of primary stage syphilis:

A

Painless ulcer (chancre) at the site of inoculation

Painless inguinal lymphadenopathy

No systemic manifestations (no fever, rash, or fatigue)

Darkfield positive - teeming with spirochetes

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12
Q

Clinical hallmarks of secondary stage syphilis:

A

Flu-like syndrome

Fever and diffuse lymphadenopathy

Generalized mucocutaneous rash (involves the palms/soles)

Condylomata lata (papules coalesce into large lesions)

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13
Q

Clinical hallmarks of latent stage syphilis:

A

Asymptomatic

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14
Q

Clinical hallmarks of tertiary stage syphilis:

A

Granulomatous lesions of skin/organs/bone (gummas)

Neurosyphilis

Cardiovascular syphilis

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15
Q

Timeframe of primary stage syphilis:

A

10-90 days after infection

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16
Q

Timeframe of secondary stage syphilis:

A

2-10 weeks after chancre

Peaks 3-4 months after infection

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17
Q

Timeframe of latent stage syphilis:

A

A few years to as many as 25 years

Progresses to tertiary syphilis if untreated

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18
Q

Timeframe of tertiary stage syphilis:

A

Generally at least 5-10 years since infection

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19
Q

Describe the syphilis chancre:

A

smooth margins and crusted base

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20
Q

Describe Cardiovascular Syphilis:

A

Cardiovascular Syphilis – chronic large vessel vasculitis that involves the wall of the aorta, causing aortic aneurysms/dissection

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21
Q

Name the stage of Neurosyphilis:

CSF inflammatory changes: pleocytosis and elevated protein

A

Early (Secondary) - Asymptomatic

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22
Q

Name the stage of Neurosyphilis:

No symptoms

A

Early (Secondary) - Asymptomatic

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23
Q

Name the stage of Neurosyphilis:

Meningitis and Vasculitis

A

Early (Secondary) - Symptomatic Meningovascular

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24
Q

Name the stage of Neurosyphilis:

Headache, neck stiffness, fever, cranial neuropathy, stroke

A

Early (Secondary) - Symptomatic Meningovascular

25
Name the stage of Neurosyphilis: | Dementia, aphasia, muscle weakness, hallucinations
Late (Tertiary) - General paresis
26
Name the stage of Neurosyphilis: | Chronic meningoencephalitis leading to brain atrophy
Late (Tertiary) - General paresis
27
Name the stage of Neurosyphilis: Infection/inflammation of the spinal cord Demyelination of spinal cord posterior columns and dorsal roots
Late (Tertiary) - Tabes dorsalis
28
Name the stage of Neurosyphilis: Imbalance and Ataxia Loss of pain and temperature sensation
Late (Tertiary) - Tabes dorsalis
29
Symptoms of congenital syphilis:
Rhinitis (‘snuffles’ - heavy nasal discharge) Widespread rash, hepatomegaly
30
Long-term effects of congenital syphilis:
Bone and teeth malformation – frontal ‘bossing’ Facial abnormalities – ‘saddle nose’ Blindness, deafness, cardiovascular disease
31
Methods of non-serological diagnosis of Treponema pallidum:
Darkfield microscopy Direct fluorescent antibody PCR
32
Unique qualities of non-treponemal tests:
Measures reaginic (lipid) antibodies - NOT directed specifically against T. pallidum Patients revert to negative results with treatment or enough time Can be used to follow treatment
33
Unique qualities of treponemal tests:
Tests remain positive for life, regardless of treatment Cannot be used to monitor response to treatment
34
3 types of serologic specific treponemal tests:
Fluorescent treponemal antibody absorption Tests (FTAAbs) T. pallidum particle agglutination (TP-PA or TP-HA) T. pallidum enzyme immunoassay (EIA) or chemiluminescence immunoassay (CIA)
35
2 types of serologic non-treponemal tests:
VDRL (serum & CSF) – Venereal Disease Research Laboratory RPR (serum) – Rapid Plasma Reagin
36
True or False: A positive non-treponemal test is always confirmed with a specific treponemal test
True
37
When are non-treponemal tests likely to be negative?
Early primary stage, late-latent and tertiary syphilis, following treatment, or after many years
38
What is unique about a reverse sequence diagnostic algorithm for syphilis?
Begins with a specific treponemal test (EIA or CIA)
39
Best treatment of treponema pallidum? Alternatives?
IM injection of Benzathine penicillin G (long acting) Doxycycline is an alternative, but is not as effective
40
Treatment for neurosyphilis:
IV penicillin G
41
What is the Jarisch-Herxheimer reaction?
Reaction related to the release of toxic products from dying spirochetes due to Abx.
42
When are both non-treponemal and treponemal tests likely to be positive?
Secondary stage
43
Describe transmission of Borrelia.
Larger spirochete that is spread from a mammalian reservoir to humans by tick or louse vectors
44
Name the 2 clinical infections caused by Borrelia species.
Causes Relapsing fever and Lyme borreliosis (Lyme disease)
45
Is Borrelia gram-positive or gram-negative?
Neither
46
How are Borrelia species visualized?
Stain with Giemsa or Wright’s stain
47
Why is little know about pathogenesis of diseases caused by spirochetes?
They are very difficult to culture due to complex nutritional needs.
48
How does B. recurrentis escapes immune recognition?
By altering antigenic structure during infection: Gene switch from silent to expression locus on plasmid Relapses are caused by emergence and multiplication of antigenic variants
49
2 most common geographic areas for Borrelia burgdorferi cases :
Northeast and Mid-Atlantic states (Maine to Virginia) Upper Midwest (Minnesota and WI)
50
Primary Animal reservoirs of Borrelia burgdorferi:
White-tailed deer and white-footed mouse
51
Name the hard tick that transmits Borrelia burgdorferi in the NE and Midwestern U.S.
Ixodes scapularis
52
Name the hard tick that transmits Borrelia burgdorferi in the Western U.S.
Ixodes pacificus
53
Most lyme disease is transmitted by the bite of a ________.
Most lyme disease is transmitted by the bite of a nymph
54
Risk of human infection by Lyme disease is greatest in _________ and __________.
Risk of human infection is greatest in late spring and early summer
55
Clinical Manifestations of Early Stage (3-30 days post bite) Lyme Disease:
Erythema migrans: expanding erythematous target-shaped lesion at site of tick bite Flu-like illness: fever, chills, malaise, myalgias
56
Clinical Manifestations of Early Disseminated (weeks days post bite) Lyme Disease:
Arthritis and arthralgia Cardiac dysfunction (conduction block) Facial nerve paralysis or other cranial neuropathies
57
Clinical Manifestations of late-stage Lyme Disease:
Recurrent/relapsing arthritis in large joints Acrodermatitis chronica atrophicans -hyperpigmented rash on the dorsal surface of the hands
58
Describe the two-tiered testing system for Lyme disease:
Initial screening immunofluorescence assay (EIA, ELISA, IFA) - must allow time for Abx to be present Confirmed with a second, more specific Western Blot test - Detects specific IgG and IgM antibodies against Borrelia burgdorferi
59
What evidence would suggest the Borrelia burgdorferi infection of the CNS?
Elevated lymphocytic pleocytosis and elevated protein in CSF Specific serology testing (IgG and IgM) from CSF PCR from CSF (reference laboratory)