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Module 2 > Syphilis and HIV > Flashcards

Syphilis and HIV Flashcards

1
Q

What family is syphilis part of?

A

spirochaetaceae

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2
Q

What are the sub species of treponema pallidum that cause disease?

A

pallidum; endemicum; pertenue ; T.carateum

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3
Q

What disease does endemicum cause?

A

Bejel

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4
Q

What disease does pertenue cause?

A

Yaws

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5
Q

What disease does T.carateum cause?

A

pinta

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6
Q

What makes diagnosis between the subspecies of treponema pallidum difficult?

A

pallidum; endemicum; pertenue are all morphologically and serologically indistinguishable

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7
Q

Where is Bejel found?

A

hot and dry climates

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8
Q

Where is Yaws foudn?

A

hot wet countries

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9
Q

Where is Pinta found?

A

Central and South America

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10
Q

What is the shape of syphilis?

A

helically-shaped

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11
Q

What is found on the outer membrane of syphilis?

A

limited OM proteins and no LPS

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12
Q

How does syphilis move?

A

spins

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13
Q

When is the infectious capacity of syphilis lost after harvesting?

A

within 2 days

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14
Q

What makes research with syphilis difficult?

A

cannot be cultivated for sustained periods on artificial media; slow doubling time (30-33hours)

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15
Q

What is the metabolic capacity of syphilis?

A

glycolysis only- no TCA or electron transport

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16
Q

What makes syphilis such a fussy organism?

A

small genome; limited metabolic capacity; no oxidase/catalase; no heat shock proteins

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17
Q

What are the oxygen/temp requirements of syphilis?

A

micro-aerophilic; doesn’t do well above 37 degress

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18
Q

What are the modes of transmission of syphilis?

A

direct contact with infectious lesions; vertical transmsiion or during pregnancy

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19
Q

What is the transmission rate of syphilis?

A

1/3rd of sexual contacts of syphilis will develop the disease

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20
Q

What is the incidence rate of syphilis in Europe in 2016?

A

6.1/100,000

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21
Q

What is the european syphilis gender ratio?

A

8:1

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22
Q

How many cases of syphilis were in HIV postiive individuals?

A

27% but HIV status unknown in 20%

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23
Q

Why are rates of syphilis increasing?

A

reduced condom use- HIV treatable; Prep; more risky sexual practicies

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24
Q

What drugs make up prep?

A

tenofovir/emtricitabine

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25
Q

What is the efficacy of prep?

A

86%

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26
Q

What is the effect of HIV on syphilis?

A

T.pallidum load is higher in patients with HIV

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27
Q

What is the ID50 for treponema pallidum?

A

57

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28
Q

What age is there a peak in MSM syphilis cases?

A

35-39 peak

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29
Q

Why is there a spike in syphilis cases in heterosexual females at 25-29?

A

first pregnancy syphilis testing

30
Q

What is the time after contact with pallidum for primary disease?

A

9-90days

31
Q

What is the time after pallidum contact for secondary disease?

A

6 weeks-6 months

32
Q

How many chancres are found in the genitals?

A

90%

33
Q

What can be a feature of secondary syphilis in the mouth?

A

snail-track ulcers

34
Q

Aside from the classical whole body rash in secondary syphilis what other skin manifestation is seen?

A

condylomata in warm moist areas

35
Q

What are the neurological complications of secondary syphilis?

A

acute meningitis and CN palsy

36
Q

What can be seen in the eyes with secondary syphilis?

A

anterior, posterior involvement; keratouveitis

37
Q

How long after initial innoculation does CVS syphilis happen?

A

15-30 years

38
Q

What is seen with CVS syphilis?

A

affects any blood vessel, usually the ascending aorta- aneurysm. get associatied aortic regurgitation

39
Q

When does gummatous syphilis occur after initial innoculation?

A

1-46years

40
Q

What organs does gummatous syphilis commonly affect?

A

skin and bone

41
Q

Waht are the 2 categories of neurosyphilis?

A

meningo-vascular and parenchymal

42
Q

What are the symptoms of meningovascular syphilis?

A

HA; optic neuritis; tinnitus- infectious arteritis may result in stroke

43
Q

What are the 2 main forms of parenchymal neurosyphilis?

A

general paresis; tabes dorsalis

44
Q

What structure is affected in general paresis?

A

cortical white matter loss

45
Q

What are the symptoms of general paresis?

A

cognitive function; personality- dementia like; hemiparesis

46
Q

What are the symtpoms of tabes dorsalis?

A

lightening pains; patchy sensory lsoss; pupil changes(Argyll-Robertson); sensory ataxia; neuropathic ulcers and joints

47
Q

What is the difference between early and late congenital syphilis?

A

early is within 2 years of life; late is presenting after 2 years

48
Q

What are the features of early CS?

A

rash; haemorrhagic rhinitis; lymphadenopathy; hepatosplenomegaly; skeletal abnormalities

49
Q

What are hte features of late CS?

A

interstitial keratitis; Clutton’s joints; hutchison’s incisors; high palatal arch; SN deafness; frontal bossing; saddlenose deformity; neuro involvement

50
Q

What is the difference in primary syphilis presentation in HIV?

A

more likely to present with >1 chancer and may have larger and deeper lesions

51
Q

How many HIV infected patients present with concomitant lesiosn of primary and secondary syphilis at diagnosis?

A

25%

52
Q

How does HIV change the incidence of neurosyphilis?

A

increases incidence generally; and neuro complications (eye and ear; and meningitis) during early syphilis

53
Q

What Cd4 and RPR titre is associated with a risk of neurosyphilis?

A

RPR >=1:32 and CD4<350

54
Q

Why are CSF results hard to diagnose in HIV patietns?

A

HIV causes a CSF pleocytosis and raised protein

55
Q

What is the effect of HIV on ocular invovlement of syphilis?

A

more severe uveitis in pateitn with HIV- panuveitis more common than isolate anterior uveitis; worse papillitis; optic neuritis and retrobulbar optic neuritis

56
Q

What are the methods of direct detection of T.pallidum?

A

dark ground microscopy and PCR

57
Q

What is the beneffit of PCR over dark ground microscopy?

A

higher sensitivty and specificity; can be used for both gential and oral lesiosn

58
Q

What are the specific trepnoemal tests

?

A

EIA (treponemal enzyme immunoassay); TPPA (T.pallidum particle agglutination assay); TPHA (T.pallidum haemoagglutination assay); FTA-abs (fluoresent treponemal antibody absorption test) ; T. pallidum immunoblot

59
Q

What are hte non-specififc serological tests for syphilis?

A

VDRL (venereal diseases research lab test) and RPR (rapid plasma reagin test)

60
Q

What is the primary screening test for syphilis?

A

EIA- if primary suspected do IgM

61
Q

What is the confirmatory test for syphilis?

A

different treponemal test; TPPA

62
Q

What test should be done if positive test isn’t confirmed by standard confirmatory test?

A

immunoblot

63
Q

What is RPR/VDRL used for?

A

to stage the infection and monitor treatment

64
Q

What are the routine screening recommendatiosn for HIV positive patients?

A

at least annually; in outbreaks 6 monthly and high risk MSM screened every 3 months for STIs

65
Q

What is the prozone phenomenon?

A

high antibody titres interferes with formation of antigen-antibody lattice network necessary to visualise a positive test

66
Q

Why is direct groun microscopy; PCR and tissue biopsy important in HIV patients?

A

increased rate of negative serological test s

67
Q

What is serofasting?

A

non treponemal antibodies persist for a long period of time rather than become completely non reactive with time

68
Q

How much should RPR drop by 3 months after treatment?

A

2-fold

69
Q

How long should patients be advised to refrain from sexual contact after syphilis treatment?

A

until lesions fully healed and 2 weeks following treatment completion

70
Q

What is the JArish-Herxheimer reaction?

A

as bacteria die they release toxin and pt gets fever and flu symtpoms

71
Q

What is the origin of macrolide resistnace in syphilis?

A

single mutant strain introduced into a specific sexual network and becomes endemic– simialr types in populations /geographical regions

Module 2 (38 decks)

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