Spirochetes-Treponemes  Flashcards

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
Q

Name the stage of Neurosyphilis:

Dementia, aphasia, muscle weakness, hallucinations

A

Late (Tertiary) - General paresis

26
Q

Name the stage of Neurosyphilis:

Chronic meningoencephalitis leading to brain atrophy

A

Late (Tertiary) - General paresis

27
Q

Name the stage of Neurosyphilis:

Infection/inflammation of the spinal cord

Demyelination of spinal cord posterior columns and dorsal roots

A

Late (Tertiary) - Tabes dorsalis

28
Q

Name the stage of Neurosyphilis:

Imbalance and Ataxia

Loss of pain and temperature sensation

A

Late (Tertiary) - Tabes dorsalis

29
Q

Symptoms of congenital syphilis:

A

Rhinitis (‘snuffles’ - heavy nasal discharge)

Widespread rash, hepatomegaly

30
Q

Long-term effects of congenital syphilis:

A

Bone and teeth malformation – frontal ‘bossing’

Facial abnormalities – ‘saddle nose’

Blindness, deafness, cardiovascular disease

31
Q

Methods of non-serological diagnosis of Treponema pallidum:

A

Darkfield microscopy
Direct fluorescent antibody
PCR

32
Q

Unique qualities of non-treponemal tests:

A

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
Q

Unique qualities of treponemal tests:

A

Tests remain positive for life, regardless of treatment

Cannot be used to monitor response to treatment

34
Q

3 types of serologic specific treponemal tests:

A

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
Q

2 types of serologic non-treponemal tests:

A

VDRL (serum & CSF) – Venereal Disease Research Laboratory

RPR (serum) – Rapid Plasma Reagin

36
Q

True or False: A positive non-treponemal test is always confirmed with a specific treponemal test

A

True

37
Q

When are non-treponemal tests likely to be negative?

A

Early primary stage, late-latent and tertiary syphilis, following treatment, or after many years

38
Q

What is unique about a reverse sequence diagnostic algorithm for syphilis?

A

Begins with a specific treponemal test (EIA or CIA)

39
Q

Best treatment of treponema pallidum? Alternatives?

A

IM injection of Benzathine penicillin G (long acting)

Doxycycline is an alternative, but is not as effective

40
Q

Treatment for neurosyphilis:

A

IV penicillin G

41
Q

What is the Jarisch-Herxheimer reaction?

A

Reaction related to the release of toxic products from dying spirochetes due to Abx.

42
Q

When are both non-treponemal and treponemal tests likely to be positive?

A

Secondary stage

43
Q

Describe transmission of Borrelia.

A

Larger spirochete that is spread from a mammalian reservoir to humans by tick or louse vectors

44
Q

Name the 2 clinical infections caused by Borrelia species.

A

Causes Relapsing fever and Lyme borreliosis (Lyme disease)

45
Q

Is Borrelia gram-positive or gram-negative?

A

Neither

46
Q

How are Borrelia species visualized?

A

Stain with Giemsa or Wright’s stain

47
Q

Why is little know about pathogenesis of diseases caused by spirochetes?

A

They are very difficult to culture due to complex nutritional needs.

48
Q

How does B. recurrentis escapes immune recognition?

A

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
Q

2 most common geographic areas for Borrelia burgdorferi cases :

A

Northeast and Mid-Atlantic states (Maine to Virginia)

Upper Midwest (Minnesota and WI)

50
Q

Primary Animal reservoirs of Borrelia burgdorferi:

A

White-tailed deer and white-footed mouse

51
Q

Name the hard tick that transmits Borrelia burgdorferi in the NE and Midwestern U.S.

A

Ixodes scapularis

52
Q

Name the hard tick that transmits Borrelia burgdorferi in the Western U.S.

A

Ixodes pacificus

53
Q

Most lyme disease is transmitted by the bite of a ________.

A

Most lyme disease is transmitted by the bite of a nymph

54
Q

Risk of human infection by Lyme disease is greatest in _________ and __________.

A

Risk of human infection is greatest in late spring and early summer

55
Q

Clinical Manifestations of Early Stage (3-30 days post bite) Lyme Disease:

A

Erythema migrans: expanding erythematous target-shaped lesion at site of tick bite

Flu-like illness: fever, chills, malaise, myalgias

56
Q

Clinical Manifestations of Early Disseminated (weeks days post bite) Lyme Disease:

A

Arthritis and arthralgia
Cardiac dysfunction (conduction block)
Facial nerve paralysis or other cranial neuropathies

57
Q

Clinical Manifestations of late-stage Lyme Disease:

A

Recurrent/relapsing arthritis in large joints

Acrodermatitis chronica atrophicans -hyperpigmented rash on the dorsal surface of the hands

58
Q

Describe the two-tiered testing system for Lyme disease:

A

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
Q

What evidence would suggest the Borrelia burgdorferi infection of the CNS?

A

Elevated lymphocytic pleocytosis and elevated protein in CSF

Specific serology testing (IgG and IgM) from CSF

PCR from CSF (reference laboratory)