Unit1 Micro Flashcards
Treponema pallidum Bacteriology
syphilis
small, spirochete, don’t survive outside host, surface of spirochetes are non-immunogenic and they also are believed to down regulate the host’s TH1 response.
Treponema pallidum Pathogenesis
syphilis
Stage 1: 3 to 12 weeks,ulcer
Stage 2: 4 to 10 weeks, Macropapular rash, condylomata lata, patchy alopecia, consittutional symptoms
-High antibody titers
Latent Syphilis: either symptoms come and go pt remins infectious
Stage 3: -Granulomas (gummas) liver, brain, bones and testes
-Cardiovascular syphilis, syphilitic menegitis, meningovascular syphilis (5 to 10 yrs), parenchymal nuerosyphilis (15 to 20 yrs)
Argyll- robertson pupil
Test for nuerosyphilis:
-1 or more pupils does not constrict normally to light, but does constrict during accommodation
Treponema pallidum Lab tests
Darkfield microscopy
RPR or VDRL ( tests for Reagin through flocculation)
Reagin
Bulk nonspecific antibody population raised with a spirochete infection, detectable through RPR or VDRL
Congenital Syphilis
40-50% of babies with infected mom and spontaneously aborted
surviving babies develop sever secondary syphilis
Treponema pallidum Treatment
Single injection of benzathine penicillin G
Jarisch-Herxheimer reaction
24 flu like symptoms seen after treatment of a spirochete
Yaws (Treponema pertenue)
Ancestral form of syphilis
3 phase disease but without neuro or cardiac involvement
Gives positive RPR
Tropical disease spread by direct contact with cutaneous lesion
Pinta (Treponema carateum)
Just cutaneous involvement
Central and south america
Gives positive RPR
LOS vs LPS
LOS is a truncated form of LPS
LOS is less immunogenic than LPS
LOS causes local inflammation, LPS causes systemic
LOS in Niesseria
Differences btw N. meningitidis and N. Gonorrheae
N. gonorrhoeae is not incapsulated, even more sensitive to dehydration and cold, antibiotic resistance is more common, and there are hundreds or serotypes (no vaccine)
only N. meningococci ferment maltose
HIV introduction into humans, where,when what?
From chimpanzees
First documented case in 1902 to 1921 in Cameroon.
Three independent introduction of SIV into humans occured.
Demographics of new HIV infections in the USA
63% of new infections are in gay and bisexual men
25% other heterosexual contact
44% African American
10% of new infections are in young gay black men
Ro for HIV
Ro
Pathogenesis of initial HIV infection
1) Virus is in the mucosa
2) If there are breaks in that tissue the virus can cross into the target cells it wants to affect called the founder cells (macrophages, dendritic cells)
3) Days later there is local expansion (still susceptible to antivirals, why PEP works)
4) Drains into the lymphnodes, and propagates around the body (PEP no longer effective)
Women are more vulnerable to get HIV from Men than Men are from women
HIV microbiology
ssRNA virus, two copies of the genone in the virion (so it’s diploid and those two copies are often different from one another
Early HIV coreceptor used alongside CD4
CCR5 on marcophages
people with delta32 mutations of CCR5 can be HIV resistant
Late HIV coreceptor used alongside CD4
CXCR4 on T cells
Biggest change in antiviral therapy
when we created protease inhibitors
protease cleaves gag into its subunits MA-CA-NC
syncytium formation
Env can fuse infected T cells with uninfected T cells (lethal for T cells)
creates more virulent strains
N. gonorrhea treatment
ceftriaxone
C. trachomatis treatment
Doxycycline
If Preggers, Peds or allergic: Erythromycin
