Lecture 10 Flashcards
syphilis organism
Treponema Pallidum
Treponema Pallidum shape
long, very thin spirochete
Treponema Pallidum motility
endoflagella - within periplasm (3 at each end)
Treponema Pallidum covering
has glycosaminoglycan sheath surrounding whole cell
unusual envelope
-no LPS: very loosely anchored OM with cardiolipin in membrane -mostly IM lipoproteins; OM proteins very few
Treponema Pallidum culture
-cultivate in rabbit testes
Treponema Pallidum oxygen
has microaerophilic metabolism
Treponema Pallidum primary
ulcerated, defined papule at site of infection =
chancre; regional lymph nodes swell
-usually genital site, but 10-20% oral or anal or . . . -heals spontaneously, but organisms remain
Treponema Pallidum secondary
red maculopapular rash-anywhere on body, including soles and palms
condylomas-white warts in moist areas
Treponema Pallidum tertiary
lesions in tissues throughout the body (due to immune response, not bacteria)
- skin: gummas
- bones: porous, easily bent, fragile
- heart: aorta swells, ruptures
- liver
- CNS: brain = general paresis; spine = tabes dorsalis
- neurosyphilis is hard to diagnose, and may occur at 2o or 3o stage
Treponema Pallidum and infants
May also cross placenta to infect fetus in utero (few bact. do) -~20% abortion or stillbirth
-~80% congenital defects, which may not appear immediately
-Hutchinson’s triad: interstitial keratitis - blindness : VIII nerve deafness
: Hutchinson’s teeth
-also saddlenose, neural defects, bone deformation
after any stillbirth, mother should be tested for syphilis
Treponema Pallidum epidemiology
- Exclusively human, exclusively STD
- can artificially infect rabbits, but they never go beyond 1o stage
- Contagious for first 3-5 years after infection, not thereafter -Incidence in US increasing from 2005 – now (10,000 / yr)
Treponema Pallidum pathogenesis
- highly infectious (10 organisms)
- hyaluronidase facilitates spread and invasion of tissues
- rapid motility also a spread mechanism
- few surface proteins means hiding from immune system - may explain long latent period
Treponema Pallidum control
- includes finding and testing sexual contacts
- can scrape chancres to look for spirochetes, but not if latent -Serologic Tests for Syphilis (STS) (aka VDRL)
- Indirect: T. pallidum induces formation of “reagin” in host (IgM + IgA)
- add cardiolipin to patient’s serum
- if +, reagin causes cardiolipin to clump - lots of false positives (other infections)
- Direct: Fluorescent Treponema Antibody (FTA) test
- bind T. pallidum to slide and add serum from patient
- add fluorescent anti-human 2o Ab to detect 1o Ab in serum
Treponema Pallidum treatment
- treat with Penicillin G (0.003 U/ml): very sensitive -one i.m. injection for early disease (< 1 year)
- 3 injections for later disease
- in use since 1940 without resistance developing -before 1940 treatment was Salvorsan (arsenic paste)
Neisseria gonorrhea shape and stain
Gram neg, coffee-bean shaped diplococcus
Neisseria gonorrhea environment and metabolism
- fastidious (grow on MTM or Chocolate blood)
- better with selective media (vanco, colistin, etc.)
- aerobic, but prefer 5% CO2 (candle jar)
- cytochrome c oxidase positive
Neisseria gonorrhea symptoms in general
- Invades mucus membranes of UGT, rectum, eye and throat
- proctitis (fem usu from vagina, male usu from anal sex) -pharyngitis (oral sex)
- arthritis (esp of thumbs), dermatitis (rare)
Neisseria gonorrhea in males
-urethritis: painful urination, drip of pus from urethra -40% asymptomatic
Neisseria gonorrhea in females
- urethritis, vaginitis
- cervicitis, salpingitis, PID, peritonitis
- Fallopian tube scarring, sterility (15% after 1 infection, 80% after 3)
- 60% asymptomatic
Neisseria gonorrhea in infants
conjunctivitis from infected birth canal
Neisseria gonorrhea Epidemiological
-Exclusively a human STD
~75% of people who have sex with infected person get infected, ~50% after one encounter
-other co-infections contribute to symptoms (40% Chlamydia+)
-large number of asymptomatic carriers allow continued spread
-major problem in US (0.2 to 0.5% infection prevalence, 600,000 new cases / yr. reported)
Neisseria gonorrhea diagnosis
-diagnosis in males is by gram stain of urethral drip, in females by culture of cervical or vaginal swab
Neisseria gonorrhea adhesion
- initial - pili:
- pilus antigenic variation by recombinational “cassette switching” – very common, >2% of pop with variant pili
- one promoter (pilE), many genes (pilS)
- recombine new pilS gene or part of gene with pilE to make new pili (note the advantage of being diploid)
- avoid host immune response -tight - Opa (Protein II)
- named for opacity phenotype of colonies on petri dish -antigenic variation by DNA slippage of repeats
- infections in females change Opas during menstrual cycle
Neisseria gonorrhea evasion
- Por (Protein I): outer membrane porin, but also prevents phagolysosome fusion in host
- Rmp (Protein III): Host Abs bind to it, prevents Ab binding to Por and LOS in outer membrane
- IgA protease: IgA is the bactericidal, complement activating, first response Ab
