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ER Week 4 > Sexually Transmitted Diseases > Flashcards

Sexually Transmitted Diseases Flashcards

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1
Q

What are the most common presentations of an STD?

A

urethritis
cervicitis
vaginitis/vaginosis
genital ulcers

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2
Q

What are the three main causes of urethritis?

A

N. gonorrhoeae
C. trachomatis
M. hominis

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3
Q

What are the two main causes of cervicitis?

A

C. trachomatis (D-K)

M. genitalium

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4
Q

What are the two main causes of vaginitis?

A

T. vaginalis

C. albicans

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5
Q

What are the two main causes of Vaginosis?

A

Gardnerella spp.

Mobiluncus spp.

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6
Q

What bug causes syphilis?

A

Treponema pallidum

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7
Q

Which is the main HSV that causes genital infections?

A

HSV-2

but also some HSV-1

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8
Q

What bug causes chancroids/

A

H. ducreyi

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9
Q

What bug causes lymphogranuloma venerum?

A

C. trachomatis (subclass L)

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10
Q

What causes genital warts?

A

HPV

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11
Q

What are the SYSTEMIC STIs?

A

HIV-1 and HIV-2

Pelvic inflammatory disease from N. gonorrheoa, C. trachomatis or anerobes

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12
Q

What are the two STIs that lead to cancer?

A

HPV - cervical carcinoma

KSHV - Kaposi sarcoma

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13
Q

What is the main way to break down the organisms causeing genital ulcers?

A

is it painful?

painless - syphilis
painful - HSV

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14
Q

What do the cells that suggest HPV infection look like/

A

large atypical cells with lots of cytoplasm. can be binucleated - koilocytes

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15
Q

What are the two main wart diseases?

A

HPV and Molluscum contagiosum

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16
Q

How do we identify the different strains of HPV?

A

PCR

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17
Q

Describe the morphology of HPV.

A

dsDNA
circular genome
icosahedral
nonenveloped

in the papilomavirus family

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18
Q

True or false - the HPV virus goes systemic eventually.

A

false - it’s usually only local

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19
Q

In the first host cell for infection, what is necessary for the HPV to take off?

A

The host cell has to be replicating so that the virus can go along for the ride and replicate it’s genome. Then once viral replication progresses, certain strains can produce oncogenes which leads to uncontrolled growth that makes its way up to the surface

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20
Q

What urethritis bug is most likely to have purulent discharge?

A

gonorrhea

chlamydia, mycoplasma hominis and ureaplasma typically have clear discharge

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21
Q

Describe the morphology of gonorrhea

A

gram negative diplococci

they are NOT obligate intracellular, but you do typically find them in neutrophils or epithelial cells during infection

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22
Q

Is gonorrhea oxidase positive or negative?

A

positive

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23
Q

What fuel does neisseria gonorrhea use?

A

ONLY glucose

N. meningitidis does both maltose and glucose

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24
Q

What is the main virulence factor for neisseria?

A

specialized pili that allows for attachment to mucosal surface

antigenic variation of this can evade host defences and prevents killing by phagocytosis

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25
Q

What other virulence factors does neisseria have?

A

endotoxin
IgA protease

note - this neisseria gonorrhea has no capsule, but neisseria meningitidis does

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26
Q

What media do you grow Neisseria on?

A

Thayer-Martin Media

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27
Q

Why Thayer-Martin?

A

It’s’ highly specific

inhibits the growth of almost everything else wtih vancomycin, colistin, nystatin and SXT to kill most other gram + and _ along with fungi

nutrients include chocolate sheep’s blood, beef influsion, casein hydroxylase and starch

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28
Q

What is the general treatment for STD neisseria?

A

ceftriaxone

but you usually give doxycyclin too for the probably concurrent chlamydia infection

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29
Q

What do we use prophylactically in newborns?

A

erythromycin eye drops

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30
Q

Can neisseria gonorrhoae infect any other species?

A

nope - obligate human

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31
Q

What are all the clinical presentations of neisseria gonorrhoaea?

A
  1. local infection - asymptomatic, urethritis, dysuria, cervicit,s opthalmia neonatorum in infnats
  2. systemic infection with septic arthritis

c

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32
Q

What are the complications if neisseria is not treated?

A

PID with risk for ectopic pregnancy and sterility

Fitz-Hugh-Curtis - infection of the liver capsule

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33
Q

What kind of cells does neisseria killw ith its endotoxin?

A

ciliated cells

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34
Q

How does te neisseria gain access to the liver capsule for Fitx=Hugh-Curtis syndrome?

A

it can do all the way up through the fallopian tubes into the peritoneal cavity

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35
Q

There are higher incidences of neisseris infection in women who…

A

are menstruating or have an IUD

36
Q

Why don’t you get lasting immunity to neisseria?

A

antigen variation on that pili

37
Q

Painful blisters and painful lymphagenpathy….

A

HSV-2

38
Q

What is the main treatment for HSV_2

A

acyclovir

39
Q

What is the risk to a fetus with HSV-2

A

blindness

disseminated HSV

40
Q

What smear is used to diagnosed SHV-2? What would you see?

A

Multinucleated giant cell on Tzanck smear

41
Q

What kind of herpes virus is HSV-2?

A

alphaherpesviruses (which includes simplex and vavricella)

CMV is the beta
EBV is the gamma

42
Q

What type of cell does HSV-2 develop latency in?

A

neurons

43
Q

What are the ways to transmit HSV?

A

direct contact with rash

note VZV can be airborn if alveoli infected

44
Q

Describe the morphology of HSV

A

dsDNA linear genome (class 1)
icosahedral
enveloped

45
Q

What is the most important viral genes for treatment putposes?

A

thymidine kinase

and viral DNA-dependent DNA polymerase

46
Q

What type of immunity is essential for the control of HSV?

A

cell-mediated

47
Q

How does acyclovir work?

A

it’ a nuclotide analog that is only activated by viral thymidine kinase, after which it’s further activated by cellular kinases to acyclovir triphosphate which is a chain terminator

48
Q

Acyclovir is hugely selective. what’s the other reasonf or this besides needing viral thymidine kinase?

A

has a binding potential for the viral DNA 100x higher than the host cell DNA polymerase

49
Q

How does resistance to ayclovir come about?

A

mutations to the thymidine kinase and/or the viral DNA polymerase

50
Q

What are the three likely causes of vaginal discharge?

A

bacterial vaginosis - Gardnerella

candida albicans

trichomonas vaginalis

51
Q

What is the discharge like in bacterial vaginosis?

A

white to gray, moderate amount, very malodorous

52
Q

Whati s the discharge like in candida?

A

itchiness present, discharge typically white, small amount, clumped

cottage cheese

53
Q

What is the discharge like in trich?

A

discharge is yellowish - greenish in large amoutns

54
Q

WHat is included int he diagnostic workup for vaginal discharge?

A

vaginal pH and a KOH amine test

alsto wet mount and gram stain

55
Q

WHat is normal vaginal pH?

A

4.5

56
Q

If vaginal pH is elevated, what are the two likely possibilities?

A

trichomoniasies and bacterial vaginosis

57
Q

What presence of volatil aminds on the KOH amin test suggests which diagnosis?

A

bacterial vaginosis

58
Q

What would you see on gram stain in the bacterial vaginosis?

A

a clue cell - it’s a vaginal epithelial cells covered with attached microorganisms

59
Q

What would you see on wet mount in trichomonis?

A

large, pear-shaped motile flagellated protozoa

4 anterior flagella and an undulating membrane of 5 more flagella

60
Q

What proportion of tric infections are asympoatic?

A

50%

61
Q

What symtoms will show up in females?

A

vaginitis with yellowish green discharge

women who become infected during pregnancy are predisposed to premature labor and low birth weight

chronic infeciton can lead to infertility

62
Q

True or false: trichomonas is a protozoan, so it has a cyst form?

A

false - no cyst form and it does not survive long out of the host

63
Q

True or false: trichomonas, unlike candida, has no opportunistic shifts within the host

A

true

64
Q

What’s the drug of choice for trich?

A

metronidazole

damages DNA in anaerobes

65
Q

What should show up on wet prep in candida?

A

few yeast cells and pseudohyphae

66
Q

THe presence of those pseudohyphae is indicative of what?

A

that the yeast is growing rapidly and likely causing infection

67
Q

What groups of women are particularly pronte to active yeast infections?

A

diabetics
pregnancy women
some prone to this during mentrustion
HIV positive

a small percentage of women with no underlying immune disease can experience chronic or recurrent vaginal infection with candida

68
Q

What are the drugs used in yeast infections?

A

topical and oral azole drugs

69
Q

What other STD makes HIV transmission much more likely?

A

any ulcerative disease like HSV

70
Q

Painless ulcers, goes through remission, comes back as a systemic rash including on palmss…

A

syphilis

71
Q

How do we confirm syphilis infection?

A

serology

72
Q

What bacteria causes syphilis/

A

treponema pallidum

73
Q

WHat are the stages of syphilis?

A

primary secondary and tertiary separated by latent periods

74
Q

WHen is the person infectious? all the time?

A

no - only during the primary stage. not during the latent stages

75
Q

Describe presentation of primary syphilis?

A

appearancr of a hard painless chancre at the site of pathogen entry

small red, hard bump that enlarges and breaks down to elave a shallow crater with firm margins

the base of the chancre will have organisms for infecting others

76
Q

What areas are chancres usually located?

A

genitalis, lips, oral cavity, hipples, fingers or around anus

77
Q

Describe the presentation of secondary syphilis?

A

2-6 months after the chacre heals…

fever, headche, sore throat, followed by lymphadenopathy and a rash that breaks out on ALL skin surfaces, including palms and soles of the feet

person’s hair often falls out

78
Q

What’s actually causing the rash in secondary syphilis?

A

Type III HSR - immune complex

79
Q

Describe the presentation of tertiary syphilis.

A

cardiovascular syphilis - damage to small arteries in aortic wall - can distend and rupture leading to heart failure

formation of gummas - painful swollen syphilitic tumors in liver, skin, bone and cartilage

neurosyphilis - severe headaches, convulsions, atrophy of optic nerve, blindness, dementia, Argyll-Robertson pupil, and spinothalamic tract issues I think (that’s from memory, not on PP)

80
Q

Can tertiary syphilis be treated?

A

nope - fatal

fortunately we don’t see it much anymroe because of antibiotics

81
Q

Describe the presentation of congenital syphilis.

A

inhibited fetal growth
teeth notching
systemic infections with profuse nasal discharge, skin eruptions, bone deformations and nervos system abnormalities

82
Q

Describe the morphology of treponema pallidum?

A

spirochete gram negative bacteria

83
Q

How do we detect this spirochete?

A

dark-field microscopy of the suspeted lesion

also do blood tests for the antibody

84
Q

What are the antigens these antibodies are usually against?

A
  1. spirochete atngiens
  2. cardiolipin antibodies (which is a host cell constituent that the body makes ABs to in a syphilis infection)

detected with VDRL, Kolmer, and Wasserman tests

85
Q

What is the immunofluorescent method for treponema pallidum

A

FTA-ABS

fluorescent treponemal antibody absorbance test

86
Q

What is the drug of choice for syphilis/ how long?

A

penicillin G for all stages

give parenterally in large doses to maintain blood level lethal to the spirochete for at least 7 days

tetracycline and erythromycin are less effective but can be used in penicillin allergy

ER Week 4 (15 decks)

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