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DERS (reproductive) > L39- Urogenital Infections II > Flashcards

L39- Urogenital Infections II Flashcards

1
Q

UTIs are mostly caused by (exogenous/endogenous) microbes

A

endogenous- mostly from urinary tract microbiota

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2
Q

list some major concerns of STIs beyond the actual infection

A
  • some STIs like HSV2, Syphilis an inc risk of HIV acquisition
  • reproductive health consequences: i) PID –> infertility, ii) gonococcal opthalmia of fetus from mother
  • drug resistance, main gonorrhea
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3
Q

Trichomonas vaginalis microbial features

A

(sexually transmitted, fomite transmission possible)

  • protozoa (parasite) –> no cyst form
  • 4 flagella –> may lose it for ability to cross barriers
  • short undulating membrane for motility
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4
Q

Trichomonas vaginalis:

  • (1) commonly affected group
  • (2) infection site in men
  • (3) infection site in women
A

1- young, sexually active women (for asymp. and symp. disease)

2- urethra
3- vagina

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5
Q

Trichomonas vaginalis:

  • (1) clinical presentations
  • inc risk of (2)
A

1:

  • asymptomatic
  • genital inflammation = vulvovaginal trichomoniasis: fishy odor, green-white discharge, itching

2- HIV transmission

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6
Q

Trichomoniasis Dx:

  • (1) first check
  • (2) gold standard test
  • (3) non-culture tests
  • (4) other DDx
A

1- vaginal pH, >4.5 is suggestive of disease (+ BV, not candidiasis)

2- Culture: modified Modified Diamond’s Media –> add 10% NaCl (look for **motile trophozoites) + 10% KOH whiff test (fishy odor)

3- NAAT (amplified test), DNA probe (non-amplified test), gram-stain smear

4- candidiasis: yeasts and pseudohyphae

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7
Q

Urethritis, UTI male presentation

A

burning sensation, dysuria

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8
Q

Urethritis, UTI female presentation

A

frequency, urgency, dysuria

fever, chills

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9
Q

Urethritis, STI male presentation

A

hematuria. hematospermia, penile discharge
dysorgasmia, itching, tenderness, penile swelling
lymphadenopathy

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10
Q

Urethritis, STI female presentation

A

vaginal discharge, itching

pelvic / abdominal pain, dyspareunia, stomach pain

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11
Q

Neisseria gonorrhea microbial features

A
  • Gram- diplococci
  • non-motile
  • fastidious growth
  • oxidase+
  • multiple outer surface Ags
  • sexual transmission, inc risk of HIV infection

reservoirs: only humans, rare fomite transmission

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12
Q

list results of all N. gonorrhea infections

A

1a) oropharyngeal infection –> pharyngitis –> 1% systemic spread (arthritis, endocarditis, meningitis)
1b) anal / genital infection –> local irritation w/ discharge OR asymptomatic (*women) —> 1% systemic spread
2) cervical infection (+/- Sxs) –> ascending infection –> uterine cavity, fallopian tube (PID, infertility, ectopic pregancy)
3) surface colonization during birth –> eye infection –> blindness or conjunctivitis

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13
Q

Gonorrhea male and female presentation

A

Men (95% symptomatic)

  • mainly restricted to urethra
  • purulent discharge: yellowish pus
  • dysuria
Women
-cervix infection
-dysuria
-vaginal discharge
-abdominal pain
(*inc risk of dissemination b/c more asymptomatic)
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14
Q

describe the risk of gonorrhea infections in women (hint- 2)

A

-more likely asymptomatic (Sxs in 95% males) –> inc risk of dissemination
(+ inc risk HIV transmission)

-vertical transmission during birth => eye infection (blindness or conjunctivitis)

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15
Q

list the attachment factors for N. gonorrhea

A

-pili: unusual, specialized mechanism of Ag variation by DNA rearrangement

  • Opa (opacity protein)
  • por protein (creates pore for nutrient extraction)
  • Fe-binding proteins
  • lipooligosaccharide (LOS)- induces TNFα
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16
Q

N. gonorrhea:

  • attachment factors bind to (1), using (2) as the anchor
  • replication occurs in (3) manner (include main resulting Sx)
A

1- columnar epithelial cells of distal urethra (males) or cervix (females)

2- pili + outer surface proteins

3- in situ –> large numbers in virulent cells –> shed in secretions (men + women)

17
Q

N. gonorrhea:

  • spread of infection occurs as (1)
  • dissemination in to blood is common in (2) patients
  • (3) is the result of chronic infection (men and women)
A

1: (Note- nonmotile, no flagella)
- males limited to urethra
- females –> as far as fallopian tube migration via urethral/uterine contractions

2- defective complement

3- scarring and stricture of fallopian tube or urethra

18
Q

N. gonorrhea Dx:

  • (1) first properties tested for
  • (2) next non-culture lab tests
  • (3) describe culture (describe agar)
A

1- pus sample –> smear -> intracellular Gram- diplococci

2- NAATs- PCR (amplified test) or DNA probe (non-amplified test)

3- Thayer-Martin: chocolate agar w/ vancomycin, colistin, nystatin) –> oxidase+ colonies

19
Q

Chlamydia Trachomatis virulence factors

A

Atypical bacterium:

  • Gram-
  • EB infectious form, RB replicative form
  • small obligate intracellular parasites
  • entry via abrasions / lacerations
  • may increase HIV transmission
20
Q

list the clinical presentations of C. trachomatis by serotype

A

A,B,Ba,C –> trachoma

D-K –> conjunctivitis, infant pneumonia, urogenital disease

LGV-1,2,3 –> lymphogranuloma venerum

21
Q

Chlamydia trachomatis clinical presentations

A

-usually no Sxs

Sxs: vaginal discharge, dysuria (burning- direct cell destruction, host inflammatory response)

  • ~40% women –> PID = infertility, ectopic pregnancy, chronic pelvic pain
  • uncommon male complications –> epididymitis, urethritis
22
Q

Chlamydia pathogenesis mainly involves the presence of (1) on (2) cells

A

1- EB receptors (epithelial cells)

2- mucous membranes urethra, endocervix, endometrium, fallopian tubes, anorectum, respiratory tract, conjunctiva

Note- no long lasting immunity post-infection

23
Q

Chlamydia Dx

A

NAATs- most sensitive method, urine sample (some for vaginal swab)

specimens: urine/urethra males, endocervix/female females, rectum, oropharynx

24
Q

describe distribution of genital ulcers based on geographic locations

A 
USA:
i) HSV2
ii) syphilis (Treponema pallidum)
iii) chancroid (hemophilus ducreyi)
[iv) LGV / lymphogranuloma venereum- chlamydia trachomatis]

India, West Indies, Africa, S. America:
-Klebsiella granulomatis –> donovanosis / granuloma inguinale

25
Q

describe genital ulcers based on characteristics:

  • (1) number
  • (2) tenderness
A

1:
HSV- clusters
Syphilis- 1-2
others: 1

2:
Tender: HSV, chancroid, 1/3 syphilis
Painless: LGV, Donovanosis

26
Q

describe adenopathy of genital ulcers:

  • (1) HSV
  • (2) syphilis
  • (3) chancroid
  • (4) LGV
  • (5) donovanosis
A 
1- inguinal, very tender
2- rubbery, mildly tender
3- inguinal, fluctuant, very tender
4- fluctuant, 'groove sign'
5- firm, mimics LGV
27
Q

HSV1/2 viral features

A

large enveloped dsDNA icosahedral

Note- highest spread during outbreaks, but there is spread between outbreaks

28
Q 
HSV1/2- 1st episode, primary
-(1) lesions / Sxs
(at presentation)
-(+/-) HSV-1 Ab
-(+/-) HSV-2 Ab
A

1- lesions present, severe, bilateral

2- neg.
3- neg.

29
Q 
HSV2- 1st episode, non-primary
-(1) lesions / Sxs
(at presentation)
-(+/-) HSV-1 Ab
-(+/-) HSV-2 Ab
A

1- lesions present, moderate

2- pos.
3- neg.

30
Q 
HSV2- 1st episode, recurrence
-(1) lesions / Sxs
(at presentation)
-(+/-) HSV-1 Ab
-(+/-) HSV-2 Ab
A

1- lesions present, mild

2- pos. or neg.
3- pos.

31
Q 
HSV2- symptomatic, recurrence
-(1) lesions / Sxs
(at presentation)
-(+/-) HSV-1 Ab
-(+/-) HSV-2 Ab
A

1- lesions present, mild, unilateral

2- pos. or neg.
3- pos.

32
Q 
HSV2- asymptomatic infection
-(1) lesions / Sxs
(at presentation)
-(+/-) HSV-1 Ab
-(+/-) HSV-2 Ab
A

1- no lesions present, no Sxs

2- pos. or neg.
3- pos.

33
Q

describe the cells HSV invades and the types of infections

A

Lytic: most cells- Cowdry type A inclusion bodies, syncytia

Persistent: lymphocytes, macrophages

Latent: neurons

34
Q

(1) HSV mechanism to evade immune system

(2) recurrence triggers and severity

A

1- blocks IFN effects, prevents Tc/CD8+ recognition of infected cells, escapes Ig neutralization by latent (neuron) infection

2- stress usually, but triggers poorly understood –> episodes dec in severity

35
Q

HSV Dx:

  • (1) sample
  • (2) testing during outbreak
  • (3) testing between outbreaks
A

1- ulcers

2- PCR, cell culture, serology tests (glycoprotein G)

3- Ab testing

36
Q

Treponema pallidum microbial features

A
  • thin, tightly coiled
  • **spirochetes
  • motile, endoflagellum
  • slow replication
  • obligate human pathogen
  • unusual outer membrane (no LPS, no porins)
  • inc likelihood of HIV transmission
37
Q

describe presentation and time course of primary Syphilis

A

(treponema pallidum)

  • 9-90 days post-infection
  • hard, painless ulcer –> thin, greyish crust
  • disappears 1wk after proper Tx
  • disappears 4-12 wks w/o Tx
  • 75% untreated infections do not progress
38
Q

describe presentation and time course of secondary Syphilis

A

(treponema pallidum)

  • 2-8 wks after ulcer (primary)
  • flu-like syndrome
  • 80% generalized maculopapular rash (copper color) + multiple Sxs indicative of systemic infection
  • condylomata lata lesions (swarming with organism): wet mucous patches, contagious
39
Q

describe presentation and time course of tertiary Syphilis

A

(treponema pallidum)

  • 15-20 yrs post-infection
  • diffuse chronic inflammation
  • neurosyphilis => dementia, meningitis, hallucinations
  • CVS: aortic aneurysm
  • Gummatous: hypersensitive granulomatous reaction (destructive to viscera or mucocutaneous areas)

DERS (reproductive) (14 decks)

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