Syphillis Flashcards

1
Q

Describe the Treponema pallidum subspecies.

A

T. endemicum: Bejel – Causes mouth sores and destructive lumps in bones. Mainly occurs in hot and dry countries of the eastern Mediterranean region, southwest Asia and north Africa.
T. pertenue: Yaws – Causes skin sores and disfiguring growths on the legs and around the nose and mouth. Occurs in humid, equatorial countries in Africa, Asia and South America.
T. carateum: Pinta – Causes itchy, thickened, discoloured patches on the skin. Common among the natives of Mexico, Central America and South America.

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2
Q

Describe the total prevalence of syphilis and where is it most common?

A

The total prevalence of syphilis is 36 million and the total incidence is 11 million cases per year. Prevalence is highest in African and south-east Asian regions which prevalence is lowest in European and east Mediterranean regions.
Within Europe there are increasing numbers of reported syphilis cases in the west, mainly Spain, Norway and Sweden (MSM predominate)

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3
Q

Describe the stages of invasion of syphilis?

A

Attachment: Non-pathogenic treponemes (spiral-shaped bacteria) are non-adherent. ECM components fibronectin, laminin seem key in attachment.Gene analysis has revealed 2 potential T. pallidum fibronectin binding proteins.
Motility: Propels along by rotating along its long axis, facilitated by endoflagella (axial filaments) with typical hook, collar and basal knob structure.
Chemotaxis (Movement of an organism in response to chemical stimuli):T. pallidum has homologues of both Methyl-accepting chemotaxis and cytoplasmic chemotaxis systems common to gram –ve bacteria.Most likely move along nutrient gradients.

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4
Q

Describe the immune evasion of T. pallidum?

A

it’s able to evade the hosts immune responses due to: LIPID
Having a low rate of division-Having immune privileged sites
Being non-iron dependent-Having low immunogenicity of bacterial surface
Having no LPS, causing no septic response
Having proteins anchored to inner membrane extending into the periplasm (not the outer membrane)

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5
Q

How has the T. pallidum evolvedtogenerateclinical disease?

A

T. pallidum is able to change the TPR-K proteins by rearranging the genes from donor sites to expression sites.
This enables then to switch the protein overtime and therefore and evade the immune response due to the new chimeric sequence, which has different immunogens.

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6
Q

Describe the stages of syphilis?

A

Primary stage: Chancre formation (hard, firm, painless), LAD, and fever.
Secondary: Palladium spreads to feet and hands; Rash, LAD, fever. Formation of snail-track ulcer and fleshy region near the bottom, containing the bacteria causing lumps and hair loss, Affects the nervous system (e.g. loss the nerve controlling the eye lid)
Latent: Asymptomatic, Aneurysm formation,
Tertiary: Gomma formation, Neurosyphillis, syphilitic aortitis.
Inflammatory granulomatous destructive lesions to any organ, commonly to bone and skin, leading to destruction of the knee and the loss of feature and loss of sensation due to destruction of the neveres.

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7
Q

What are the symptoms of neurosyphilis?

A

Meningovascular: Headache, optic neuritis, tinnitus and stroke
Parenchymal: GPI (dementia paralytica) - general paralysis of the insane -general paresis, or tabes dorsals-Argyll Robertson pupils, optic neuritis

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8
Q

Name 3 specific test of diagnosis?

A

ELISA (Enzyme linked immunosorbent assay) – serologivcal test to detect antibodies (IgM and IgG) against T. pallidum. If found then there’s a positive results. -TPPA (T. pallidum particle agglutination)-Dark field microscopy.

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9
Q

Name non-2 specific test?

A
RPR  (Rapid  plasma  reagin)
VDRL  test  (Venereal  disease  research  lab  test):  uses  ox  heart.
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10
Q

Treatment

A

Benzathine penicillin, doxycycline and azithromycin.-Neurosyphilis - procaine pencillin and benzylpenicillin

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11
Q

How has resistance emerged?

A

T. pallidum can’t recombine between species as it doesn’t have transposomes e.g. plasmid. therefore resistance can only develop via mutation.
It’s thought that when a single mutant strain is introduced into a specific sexual network it can become endemic.

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12
Q

Give examples of resistance.

A

The pattern seen in Seattle may support this and the fact that there are similar types of T. pallidum in geographic regions/populations.
Few clinical failures seen wit azithromycin in African trials and no mutants in Madagascar
Increased risk of resistance with previous macrolide exposure
MSM: MAI prophylaxis in those co-effect with HIV and CT and NSU treatments therefore gaining drug resistan

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13
Q

Describe the first ever typing method (CDC)?

A

Based on 2 genes

amplify arp, tar genes with PCR

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14
Q

What trends were concluded from the CDC typing?

A

When this CDC method was used, started to see particular types are common in certain regions. For example, type 14d/14df is the most common in most areas.
They found 57 subtypes from 14 studies in 8 geographical areas and no epidemic consists of a single strain

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15
Q

Why is typing difficult?

A

T. pallidum is unable to be phenotypically typed for two reasons:-All subspecies are morphologically identical, causing inability to discriminate serologically-The bacteria cannot be sustained in artificial culture-Therefore, serotypes, biotypes, phage-typing and antibiograms all don’t work.

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