Unit1 Micro Flashcards

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1
Q

Treponema pallidum Bacteriology

A

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.

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2
Q

Treponema pallidum Pathogenesis

A

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)

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3
Q

Argyll- robertson pupil

A

Test for nuerosyphilis:

-1 or more pupils does not constrict normally to light, but does constrict during accommodation

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4
Q

Treponema pallidum Lab tests

A

Darkfield microscopy

RPR or VDRL ( tests for Reagin through flocculation)

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5
Q

Reagin

A

Bulk nonspecific antibody population raised with a spirochete infection, detectable through RPR or VDRL

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6
Q

Congenital Syphilis

A

40-50% of babies with infected mom and spontaneously aborted

surviving babies develop sever secondary syphilis

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7
Q

Treponema pallidum Treatment

A

Single injection of benzathine penicillin G

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8
Q

Jarisch-Herxheimer reaction

A

24 flu like symptoms seen after treatment of a spirochete

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9
Q

Yaws (Treponema pertenue)

A

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

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10
Q

Pinta (Treponema carateum)

A

Just cutaneous involvement
Central and south america
Gives positive RPR

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11
Q

LOS vs LPS

A

LOS is a truncated form of LPS
LOS is less immunogenic than LPS
LOS causes local inflammation, LPS causes systemic
LOS in Niesseria

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12
Q

Differences btw N. meningitidis and N. Gonorrheae

A

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

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13
Q

HIV introduction into humans, where,when what?

A

From chimpanzees
First documented case in 1902 to 1921 in Cameroon.
Three independent introduction of SIV into humans occured.

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14
Q

Demographics of new HIV infections in the USA

A

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

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15
Q

Ro for HIV

A

Ro

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16
Q

Pathogenesis of initial HIV infection

A

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

17
Q

HIV microbiology

A

ssRNA virus, two copies of the genone in the virion (so it’s diploid and those two copies are often different from one another

18
Q

Early HIV coreceptor used alongside CD4

A

CCR5 on marcophages

people with delta32 mutations of CCR5 can be HIV resistant

19
Q

Late HIV coreceptor used alongside CD4

A

CXCR4 on T cells

20
Q

Biggest change in antiviral therapy

A

when we created protease inhibitors

protease cleaves gag into its subunits MA-CA-NC

21
Q

syncytium formation

A

Env can fuse infected T cells with uninfected T cells (lethal for T cells)
creates more virulent strains

22
Q

N. gonorrhea treatment

A

ceftriaxone

23
Q

C. trachomatis treatment

A

Doxycycline

If Preggers, Peds or allergic: Erythromycin