Micro: the Syph

Question 1

What are the microbiological features of treponema pallidum?

Answer 1

outer and inner membranes - endoflagella between
NO gram stain - no LPS
*cannot be cultivated in vitro
syph exclusively human dz

Question 2

What is important to know about the treponema species in general?

Answer 2

cause disseminated dz - CNS
host immune response responsible for manifestations
cannot be distinguished from pallidum

Question 3

What is the relationship b/w syphilis and HIV?

Answer 3

genital ulcers increase risk of HIV transmission

Question 4

What is the basic pathogenesis of syph?

Answer 4

organisms penetrate abraded skin or intact mucus membranes and begins to replicate in dermal tissue –>primary stage chancre when immune cells come in
very invasive - small inoculum establishes dz, and disseminates soon after

Question 5

What are the clinical manifestations of the primary stage of syph?

Answer 5

3-8 wks incubation
chancre, indurated painless ulcer at site of inoculation - firm, well-demarcated
regress spontaneously but latent w Ab production

Question 6

How does syph disseminate?

Answer 6

for unknown reason, some escape during primary and home to vasculature endothelium - pass through tight jxns

Question 7

What are the features of the secondary stage of syph?

Answer 7

w/i 6 months - rash, *mimics other dzs, heaviest bacterial burden = most Abs
also regress spontaneously

Question 8

What are the outcomes of secondary syph?

Answer 8

1/3 spontaneously cure
1/3 latent for life
1/3 progress to tertiary

Question 9

What are the features of tertiary syph?

Answer 9

benign gunnas
CV (thoracic aortic aneurysm)
neurosyphilis

Question 10

Which syphilis pts are or aren’t infectious?

Answer 10

soon after inoculation through early latency are

late latent and tertiary usually not

Question 11

How does congenital syph occur?

Answer 11

transplacental transmission - after 18 wks and women inf for two years or less

Question 12

How does immunity to syph work?

Answer 12

overlapping acute and chronic inflammation account for majority of symptoms of all stages
membrane lipoproteins on organsim main proinflammatory mediators*
strong Ab response - but NO protective immunity - major immunogens not on outer surface
no vaccine

Question 13

How is diagnosis of syph done?

Answer 13

dark field microscopy - primary, secondary, some early congenital lesions/exudates
nonspecific then specific serologies - all stages
biopsies

Question 14

What are the nonspecific serologies for syph?

Answer 14

VDRL or RPR measure anti-cardiolipin Abs

good for tracking dz progression/response to therapy since specific Abs don’t fall

Question 15

What are the specific serologies for syph?

Answer 15

reactive denote present or past inf - remain + for life
if negative, VRDL was false +
+ means you must treat - can’t tell past from active

Question 16

How can spirochetes be observed on biopsy?

Answer 16

silver stain

usually lymphocytic infiltrate w plasma cells

Question 17

How can congenital syph be diagnosed?

Answer 17

routine serologies not helpful because detect moms IgG

detection of fetal IgM can help

Question 18

What is the treatment for syph?

Answer 18

IM penicillin (tetracycline is alternative)
allergic can be de-sensitized 
neurosyph gets high dose, parenteral pen

Question 19

What is an important side effect of treatment for syph?

Answer 19

Jarish-Herxheimer rxn - during therapy of primary or secondary = w/i several hours, due to release of large amounts of bacterial constituents as they die in mass and provoke cytokine cascade (give TNFalpha)
sudden fever, flushing, tachycardia, vasomotor instability