2.1 Mmi Exam3: Genital Infections Part 1

Front 1

What is the normal flora in the female genital tract responsible for creating an acidic environment?

Back 1

Lactobacillus sp.

(acidic environment helps protect against many pathogens)

Front 2

what are the five etiologic microorganisms that cause STDS?

Back 2

Neisseria Gonorrhoeae
Chlamydia trachomatis
HSV
Treponema pallidum (syphillis)
HIV

Front 3

how is Neisseria G distinguished in a culture (morphology)? What culture does it grow on?

what cells can Neisseria G be found on and w/n?

Back 3

as a gram (-) diplococcus

chocolate agar

found on and w/n leukocytes (neutrophils)

Front 4

how is Neisseria G transmitted?

how is it gaining resistance to antibiotics?

Back 4

Transmitted by direct contact (since it does not survive well outside of the host)

- resistance: increasing number of strains containing R plasmids.

Front 5

How does Neisseria G attach to host cells?

Back 5

via their pilli (fimbriae)

Front 6

what allows for N. Gonorrhoeae to attach to many different types of cells?

Back 6

antigenic variation of pilli

-different types of pilli can attach to different tissues types throughout boy

Front 7

how does N. Gonorrhoeae escape the immune system?

Back 7

antigenic variation- immune system cannot form antibodies (no future defense either)

It also produces an enzyme that breaks down IgA antibody.

Front 8

what is the main fxn of OPA proteins on the outer membrane of N. Gonorrhoea?

how do the OPA proteins prevent activation & proliferation of lymphocytes?

Back 8

fxn: increase adherence btwn gonococci & a variety of eukaryotic cells.

OPA attaches to receptors on CD4 T lymphocytes which impairs response to this infection

Front 9

what sxs are caused by gonorrhea in men?

in women?

What might be some end results for both sexes?

Back 9

men: uretheritis (pus)

end result: sterility & prostatic abscesses

women: painful urination & vaginal discharge. (Spread in the cervix and fallopian tubes)
end result: PID--> sterility or ectopic pregnancy.

Front 10

How do you tx Gonorrhea?

Back 10

Ceftriaxone

penicillins not used d/t plasmid-mediated B-lactamase production

Front 11

what other infection mimics gonorrhea (same symptoms)?

What does this organism attach to?

(gonorrhea also does this)

Back 11

Chlamydia Trachomatis

attaches to sperm

(^ this leads to PID & sterility)

Front 12

what is lymphogranuloma venerem?

Back 12

Rare STD caused by 3 types of C. Trachomatis.

Lymph nodes in the groin swell & drain pus leading to gross swelling of the genitalia.

Front 13

4 types of C. Trachomatis can cause a chronic eye disease ___________

what does this lead to?

Back 13

Trachoma

can cause blindness!

Front 14

Main differentiation of Chlamydia from Gonorhea.

Back 14

Chlamydia is a spherical obligate intracellular bacterium

(relies on host cell for ATP, etc)

Front 15

what are the different phases of C. trachomatis?

Back 15

1) elementary body-> non replicating, infectious

2) reticulate body--> non infectious, replicating

Front 16

what form attaches to the receptor cells of the epithelium, is taken in via endocytosis, & releases cytokines (causing cell-mediated immune response)?

Back 16

elementary body (dispersal form)

Once inside it germinates into a vegetative reticulate form.

Front 17

what form is contained w/i the endocytic vacole, replicates via binary fission, & expands/grows eventually leading to cell lysis (exocytosis)?

Back 17

reticulate body

Reverts back to elementary body before being released from cell via exocytosis

Front 18

how do you diagnose C. trachomatis?

how do you tx it?

Back 18

Immunofluorescence (antibody stain)

*green apple bodies w/i cell

tx: azithromycine, doxycycline

Front 19

What complication can arise if a mother w/ chlamydia has a vaginal birth?

Back 19

newborn may be infected--> conjunctivitis & pneumonia

tx: erythromycin

Front 20

what characterizes primary syphilis?

Back 20

painless, red ulcer w/ a hard rim called a hard chancre (heals after 3-6 wks).

10-90 days from exposure to appearance of 1st sxs. (usually at site of organism entry)

Front 21

Pt presents to your office with a runny nose, watery eyes, a sore throat w/ mucus patches inside mouth & a distinctive rash on palms and soles. Dx and tx

Back 21

dx: secondary syphilis (2-10 wk incubation)--> d/t immune complex formation

tx: penicillin

Front 22

pt presents to your office complaining of difficulty coordinating muscle movements, paralysis, gradual blindness and a propensity for forgetting things (mental illness, stroke likely also). Pt also presented with a gumma on the roof of their mouth. Dx and tx

Back 22

dx: tertiary syphilis

(Gumma- granulomatous necrotizing mass)
latent period btwn secondary & tertiary may last years

tx: penicillin

Front 23

Tertiary syphillis results from a hypersensitivity reaction to________________ & may result in DEATH

Back 23

Treponema pallidum

Front 24

how is syphilis transmitted?

Back 24

primary- chancre contact w partners body

secondary- rash sores (hands/feet) or mucus patches contain active bacteria

Front 25

what causes syphilis?

how do you identify this pathogen?

Back 25

Treponema pallidum- motile spirochete

id: dark field microscopy or fluorescent staining

Front 26

what are the 2 non-specific serologic tests for syphilis?

(ALWAYS do this if no chancre present)

what three conditions will give you a false positive?

(false + are common, but if - can rule out)

Back 26

RPR (rapid plasma reagin)
VDRL (Venereal disease research laboratory)
--> can detect ab to cardiolipin and other indicators of tissue damage.

FP: febrile infections, pregnancy, autoimmune disorders

Front 27

T/F

RPR & VDRL are used to identify the presence of syphillis organism in a serologic culture

Back 27

FALSE

do not detect the actual organism, only detect tissue damage

Front 28

what is the purpose of quantitative, nonspecific tests for syphilis?

Back 28

monitor efficacy of tx... ab titers decreased w/ successive txs

(check Ab levels)

Front 29

Once you have a (+) RPR of VDRL, you MUST do a confimatory test for syphillis.

What are the 2 specific treponemal antibody confirmatory tests? why can't u use these tests to follow therapy?

Back 29

FTA-ABS (fluorescent treponemal antibody absorption)
MHA-TP (microhemagglutination)

-cannot be used to follow therapy because these antibodies do not disappear, pts remain seropositive throughout their lives.

Front 30

what pathogen causes chancroid (genital ulcer disease, GUD)?

Back 30

Haemophilus ducreyi

--> gram (-) bacillus, produces cytolethal, distending toxin

Front 31

Pt presents to your office with a soft chancre that is painful, but not indurated.

Dx? what is this dx associated with?

Back 31

dx: chancroid

assoc w/ unilateral, inguinal, lymphadenitis--> untxed buboes can form), chancres rupture & form ulcer but do NOT heal

Front 32

(males/females) w/ chancroid are usually asymptomatic.

If symptomatic, how do pts present?

Back 32

females- usually asymptomatic, but can present w/ sxs such as dysuria, vaginal discharge, painful defecation, rectal bleeding.

males- symptomatic painful lesions & inguinal tenderness

Front 33

What 3 factors are used to make a probable diagnosis of Chancroid (H. ducreyi)?

Back 33

-1 or more painful, genital ulcers

- no evidence of T. pallidum (rule out syphillis chancre)

- HSV are negative (rule out herpes sores)

Front 34

T/F

Chanchroids tend to affect uncircumcised men more than circumcised men and it is closely associated w/ prostitution. It is also more common in homosexuals.

Back 34

FALSE

everything is true EXCEPT:

Chancroid is more common in HETEROSEXUALS!

Front 35

what genital ulcer disease is the major co-factor in transmission of HIV (esp in Africa)?

Back 35

Chancroid

Front 36

who common gets granuloma inguinale (Donovanosis)?

what pathogen causes it?

Back 36

commonly found in the tropics and subtropics (poor-- blacks 6x more than caucasians)

pathogen: calymmatobacterium granulomatis

Front 37

what is the morphology of calymmatobacterium granulomatis?

where is it normally found?

what happens when it comes in contact w skin (genital)?

Back 37

gram neg, non motile capsular rod

normally present in the gut flora

causes inflammatory reaction after penetrating the skin--> resides intracellularly in macrophages

Front 38

what is the key diagnostic feature of calymmatobacterium granulomatis?

Back 38

intracellular inclusions called donovan bodies

(w/i macriphageo

Front 39

What type of lesions are characteristic of calymmatobacterium granulomatis?

Back 39

lesions on the genitals & perianal regions

- start as raised nodules (look similar to chancroids) which erode into beefy-red ulcers

Front 40

what does the herpes virus encode that is an excellent target for antiviral drugs?

Back 40

DNA polymerase (promotes viral DNA replication)

(HSV is a dsDNA virus)

Front 41

what are the three immune escape proteins of the HSV genome?

What portion of the complement system and antibody are they bound to?

Back 41

gC, gE, gI

C3 is bound to gC--> inhibits complement activation

gE/gI is bound to Fc portion of the antibody--> camouflages virus & prevents immune recognition

Front 42

pt presents to your office complaining of genital itching, burning and severe pain.

On PE you notice small, red bumps on genitalia (some of which that have already turned into blisters). Dx and tx

Back 42

HSV

particularly- HSV2

Tx: acyclovir & penciclovir (resistance to these drugs results from mutations that inactivate thymidine kinase)(drugs work by acting on pseudo-building blocks during viral replication)

Front 43

T/F

Both HSV-1 and HSV-2 are capable of infecting the genitalia and mouth.

Back 43

true

Front 44

what happens when the herpes blisters/ulcers heal?

Back 44

the virus becomes latent in neurons,

may reoccur (usually same location) due to stress, etc at any time

*blisters are extremely contagious (full of virions)

Front 45

what is the most common STD in the world?

what is it responsible for?

Back 45

HPV

responsible for papillomas (warty growths on internal and external genitalia) &

non-warty lesions of mucosal surfaces (uterine & cervical cancer)

Front 46

what is the pathogenesis of papillomavirus STDS?

Back 46

believed to enter and infect the deep layers of epithelial cells through abrasions. (result--> latent infections or immune system elimination)

(different strains cause different types^, many diff strains, not all STD (30 are, 15 assoc cancer)

Front 47

what can happen to newborn infants that are infected (not common) w/ HPV at birth ?

Back 47

warts can obstruct respiratory tract

Front 48

How is papillomavirus diagnosed & treated?

Back 48

Dx: usually abnormal pap- abnormal squamous epithelial cells

Tx:

warts- removed w liquid nitrgoen

virus- imiquimod

Front 49

what virus is associated w/ cervical cancer?

Back 49

HPV

(also assoc w/ anal & penile cancer)

(vaccine is only for some of the strains*)

Front 50

Pt presents to your office complaining of an itching vulva and vagina w/ yellowish-green, frothy vaginal discharge.

dx and what else might you see on PE?

tx?

Back 50

trichomonas vaginalis- trichomaniasis

PE: strawberry cervix

tx: metronidazole

Front 51

T/F

Trichomonas vaginals remove COOH groups from pyruvate and transfer electrons to hydrogen ions forming hydrogen gas= FROTH

Back 51

true

they have no mitochondria, but they do have hydrogenosomes and this is what they do.

Front 52

What should you be concerned w/ if you find trichomonas vaginalis in a child?

Back 52

suspect for child abuse

Front 53

How can a trichomonas vaginalis be diagnostically confirmed?

Back 53

microscopically

-large protozoan w/ characteristic jerky motility

(not automatically checked for or seen in vaginal sample- only seen under microscope, ASK)

Front 54

what are the three etiologic microorganisms that cause vaginitis?

Back 54

trichomonas vaginalis
candida albicans
gardnerella vaginalis

Front 55

T/F

Bacterial vaginitis is an STD

Back 55

FALSE

* can be infected non-sexually

Front 56

how can you cause bacterial vaginosis non-sexually?

what accounts for 60% of vulvovaginal infections?

Back 56

- use of broad-spectrum antibiotics---60% (kills lactobacillus- normal flora, allows pathogens to live)
- douching
- overused, retained tampons
- Intrauterine contraceptive devices
- multiple sex partners
- hx of STDS

Front 57

what 4 signs characterize bacterial vaginosis?

Back 57

- clue cells- sloughed off epithelial cells covered w/ bacteria

- strong fishy odor

- itching, irritation
- sticky, white or gray discharge

Front 58

how do you diagnose bacterial vaginosis?

Back 58

observation and smell
-addition of 10% KOH to vaginal fluid increases intensity of the fish odor
- vaginal smear examined microscopically.

Front 59

what would you expect to see on a microscopic stain of gardnerella vaginalis?

Back 59

clue cells

Front 60

what are the complications of bacterial vaginosis?

Back 60

PID
infertility
ectopic pregnancy
premature birth
low birth weight

*recommend full STD screening if pt has this*