Diseases of GU system (sessions 19 & 20) Flashcards
1
Q
Ulcerative STDs (3)
A
- syphilis
- chancroid
- genital herpes
2
Q
Nonulcerative STDs (3)
A
- gonorrhea
- trichomoniasis
- chlamydia
3
Q
genus Treponema includes:
A
syphilis
nonpathogenic spp. that are normal flora on mucosal surgaces
spp. that cause non-STD dz (yaws, pina, bejel)
-occur in developing countries
-P-to-P transmission via direct contact
4
Q
“The Great Imposter”
A
syphilis
caused by Treponema pallidum
5
Q
Treponema pallidum: disease and morphology
A
syphilis gram NEGATIVE SPIROCHETE w/slow rotation motility OBLIGATE INTERNAL PARASITE (need mammal host) grows in primary cell culture
6
Q
What animal model is used for syphilis
A
Rabbits mimic primary and secondary syphilis (not observed in mice or monkeys)
7
Q
Treponema pallidum: virulence
A
- FIBRONECTIN COAT is antiphagocytic
hyaluronidase may facilitate perivascular infiltration (not very specific)
lesions are primarily the response on the inflammatory response-skin is being destroyed by inflammatory cells
8
Q
Syphilis Epidemiology
A
HUMAN PATHOGEN ONLY
horizontal & vertical transmission
9
Q
What are some ways is syphilis transmited?
A
(U) acquired by direct sexual contact w/person who has active primary or secondary lesion
nongenital: lesion near mouth, needle sharing, transplacental transmission
10
Q
Primary Syphilis pathogenesis (4 steps)
A
- enters subepithelial tissues through break in skin or passage btwn epithelial cells
- local multiplication & dissemination to nearby lymph nodes & other sites via blood
- PRIMARY LESION (INDURATED SWELLING) develops & surface necrosis results in CHANCRE (may be in an inapparent site)
- Untx lesion heals in 3-8 weeks w/fibrosis
11
Q
Syphilis chancre is the principle lesion of what?
A
primary syphilis
12
Q
How does a syphilitic chancre develop?
A
begins as a papule
- occurrence of superficial erosion
- scanty serious exudate may occur, w/formation of thin, grayish, slightly hemorrhagic crus
- base is (U) SMOOTH, border RAISED and INDURCATED
13
Q
What does a syphilitic chancre lool like?
A
base is (U) SMOOTH border is RAISED, FIRM & INDURATED
14
Q
Syphilis dormancy lenghth
A
short dormancy,
lasts 2-10 weeks
15
Q
Secondary syphilis a/w
A
- MACULOPAPULAR RASH (superficial lesions of high infectivity)
- CONDYLOMATA LATA (mucosal warty lesions) in ~1/3
- Immune complexes form in arteriolar walls
16
Q
Latest syphilis definitions (early and late)
A
absence of clinical symptoms Early latency (w/in 1 yr of infection)-recrudescence of active secondary syphilis Late latency (>1 yr after infection)-immunity to relapse and reinfection [spontaneous cure in ∼1/3 of cases, seropositivity w/o disease in ~1/3 of cases, tertiary syphilis in ~1/3 of cases]
17
Q
Tertiary syphilis: manifests when?
A
manifests 5-20yrs after infection
18
Q
Tertiary syphilis presentation
A
- NEUROSYPHILIS: meningovascular changes w/focal neurologic changes and cortical degeneration
- CARDIOVASCULAR SYPHILIS: cardiovascular changes w/aneurysm of ascending aorta
- GRANULOMATA (GUMMAS) in any tissue, but esp. in skin, bones and joints=late/benign syphilis
19
Q
Hutchingson’s Triad: what is it and what does it identify
A
hallmark of congenital syphilis
notched incisors, interstitial keratitis, 8th nerve deafness
20
Q
Congenital syphilis sxs
A
-maculopapular cutaneous lesions
-nasal obstruction w/infectious mucoid discharge
-osteitis of nasal bones
-neurosyphilis
Hutchingson’s triad: notched incisors, interstitial keratitis, 8th nerve deafness
21
Q
Where is the syphilis chancre found?
A
- may occur in areas other than the genitalia, anywhere on the body
- cervical chancre may be painless, and only detected with a speculum
- often more atypical than typical, plus the possibility of secondary infection and subsequent modification
22
Q
until proven otherwise, every genital lesion
A
should be considered syphilitic
23
Q
How may you detect treponemes from primary or secondary lesions
A
DARKFEILD MICROSCOPY or direct immunofluorescence
24
Q
How are most syphilitic cases diagnosed?
A
Serologically
- NONTREPONEMAL TESTS: cardiolipin flocculation tests (VDRL, RPR) are NONSEPCIFIC SCREENING TESTS
- TREPONEMAL TESTS: specific antibody tests (FTA-ABS, MHA-TP) confirm positive screening tests
25
acute syphilis tx
Penicillin
26
Neisseria gonorrhoeae causes which 9 diseases
```
Urethritis
Cervicitis
Salpingitis
Pelvic inflammatory disease
Proctitis
Bacteremia
Arthritis
Conjunctivitis
Pharyngitis
```
27
Neisseria gonorrhea morphology
gonococcus
gram-NEGATIVE DIPLOCOCCUS W/KIDNEY BEAN-SHAPED CELLS
has fastidious growth requirements
28
Neisseria gonorrhea virulence factors
-antigenic variation of pili: confuses host immune system
-nonpiliated phase variants: no antibodies made
-porin protein and other proteins aid in attachment
-IgA protease
Plasmid- & chromosome-mediated resistance to penicillins, tetracyclines, spectinomycin, and fluoroquinolones
29
Epidemiology of Gonorrhea
Adolescents have highest rate
Major reservoir is the asymptomatic patient (almost 50% of infected women are asymptomatic, untx men can become asymptomatic)
30
Transmission of gonorrhea
genital, oral-genital & rectal intercourse transmission
| -nonsexual transmission is extremely rare
31
Why the increased # of cases of gonorrhea
- Changed sexual mores and practices
- Ineffective methods for detection of asymptomatic cases
- Presence of beta-lactamase positive strains
- Lack of public appreciation of its importance
32
Neisseria gonorrhoeae pathogenesis
1. CRITICAL STEP: attachment to epithelia via pili & surface proteins
2. bacteria alter their surface props as an adaptation to host environment (causes host nonimmunity & retardation of phagocytic activity)
3. injury to cells via released lipooligosaccharide and peptidoglycan
4. spread to other tissues via pilar attachment
33
Clinical Spectrum of Gonococcal infection
wide clinical spectrum
exit & entry via mucous of eyes, mouth, urethra, vagina, rectum
Females: presence in endocervix w/urethral colonization
Males: presence in anterior urethra w/mucopurulent discharge
34
Complications of Gonorrhea (3)
1. various local effects
2. Acute salpingitis or pelvic inflammatory dz (PID) in 10-20% of acute infections)
3. Disseminated Gonococcal Infection
35
Acute salpingintis or pelvin inflammatory dz is....
most common complication in 10-20% of acute Neisseria gonorrhea infections
- presents w/pain, dyspareunia, abnormal menses, bleeding, etx
- organisms spread along fallopian tubes (salpingitis) & into pelvic cavity (peritonitis & abscesses)
- long term sequelae include chronic pelvic lain, infertility & ectopic pregnancy secondary to scarrin gof tubes
- can also be due to Chlamydis trachtomatis anaerobes
36
Disseminated Gonococcal Infection (DGI)
any forms can lead to bacteremia
ARTHRITIS-DERMATITIS SYNDROME
metastatic infections such as endocarditis & meningitis may occur but purulent arthritis is more common (30-40% of DGI)
37
Gonorrhea: diagnosis
GOLD STANDARD: Nucleic Acid amplification (PCR)-very good and sensitive
only 60% of infections yield gram negative results
Culture: agglutination, DNA probe, biochemical tests for confirmation
38
Gonorrhea tx
3rd generation cephalosporin
| widespread resistance to penicillin and FQs
39
Etiology of Nongonococcal Urethritis (3)
"wastebasket dx" includes: Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma genitalium
40
Chlamydial dzs
1. psittacosis due to Chlamydophila psittaci
2. acute pneumonia due to Chlamydophila pneumonia
3. trachoma, inclusion conjunctivitis, lymphogranuloma venereum & NGU due to Chlamydia trachomatis
41
Chlamydia trachomatis charactersitics
OBLIGATE INTRACELLULAR BACTERIA
gram-negative
metabolically deficient, require host-derived ATP
UNIQUE REPLICATIVE CYCLE consists of:
ELEMENTARY BODY (hardy infectious form)
RETICULATE BODY (fragile intracellular form)
various serotypes involved in dz
42
Chlamydia trachomatis replicative cycle
Elementary body: hardy infectious form
| Reticulate body: fragile intracellular form
43
NGU & C. trachomatis epidemiology
1. TEENAGERS-highest prevalence
2. ascension of organisms in female results in salpingitis & PID
3. complications of scarring in chronic/repeat infections include sterility & ectopic pregnancy
4. >50% of infants born to infected mothers show evidence of infection (u) inclusion conjunctivitis, 5-10% present with atyp. pneumonia
44
Chlamydia trachomatis clinical presentation
resembles gonorrhoeae
Males: urethritis (often asymptomatic) & epididymitis, watery discharge
Females: cervicitis, salpingitis & PID
(same serotypes resp for inclusion conjunctivitis in newborns)
45
Pathogenesis of Chlamydial infection
- chronic inflammation due to toxin-producing strains which have a gene that encodes for a toxin that functions like Toxin B of Clostridium difficile
- protein scaffolding of the infected cells collapses, causing mucosal cells to separate from each other
46
Chlamydial infections gold standard for dx
Gold standard: isolation in cell culture, in human immortalized cell lines, detection of intracellular inclusions, sensitivity is less than 85%
47
tests available in dx of Chlamydial infections
Gold standard: isolation in cell culture
noncultural tests:
antigen detection is less sensitive than culture
nucleic acid probes are very sensitivity (~95%)
48
Myplasma hominis a/w which dz
pyelonephritis, PID
49
Mycoplasma genitalium a/w what dz
NGU
50
Mycoplasma pneumonia a/w what dz
atypical pneumonia
51
Ureaplasm urealyticum a/w what dz
NGU
52
Ureaplasma urealyticum reservoir/epi/causes what
main reservoir: genital tract of sexually active persons
colonize >80% of ppl. who've had 3 or more sex partners
MEN: rspnsble for ~50% of NG, nonchlamydial urethritis
WOMEN: chorioamnionitis & postpartum fever
53
3 main categories of vaginitis
1. Trichomoniasis
2. Bacterial vaginosis
3. Yeast vaginitis
54
Trichomonas tenax
commensal in mouth (normal flora)
55
Trichomonas hominis
commensal in intestine (normal flora)
56
Trichomonas vaginalis causes
cause of STD
57
Trichomonas vaginalis morphology
FLAGELLATED PROTOZOAB
exists ONLY AS A TROPHOZOITE
is an EXTRACELLULAR ANAEROBE
58
Trichomoniasis Epidemiology
cosmopolitan distribution
transmitted by sexual intercourse
common STD
59
Trichomonas vaginalis lifecycle
1. trophozoite is acquired via sexual intercourse
2. parasite establishes on the mucosa & multiples
3. parasite is transmitted to sexual partner
60
Trichomoniasis clinical characterstics
MALE: (U) asymptomatic, scanty, clear to mucopurulent discharge
FEMALE: (U) symptomatic, profuse vaginal discharge, frothy & maolodorous
cresates an environment for bacterial vaginosis (changes pH in vagina)
61
Trichomoniasis dx
wet mount exam most commonly used
culture is more sensitive
monoclonal antibody methods are available
DNA probe test (Affirm VPIII) is available
62
Epidemiologic Features of Bacterial Vaginosis
NOT AN STI-caused by an overgrowth of opportunistic pathogen in vagina due to change in pH
hist of: previous STDs, sexual activity, current use of IUD, prev pregnancy or abortion, mean # of pregnancies/abortions, # of years of sexual activity
63
Vaginal secretion characteristics in vaginosis
pH 5-6 (N1
| other organisms: Mobiluncus, Gardnerella
64
Criteria for bacterial vaginosis
1. homogenous quality of secretions
2. presence of clue cells
3. release of fishy amine odor when 10%KOH is added
4. vaginal pH >4.5
5. presence of curved GRAM NEGATIVE or GRAM VARIABLE RODS
65
Similarities btwn Vaginosis & Trichomoniasis
1. THIN & HEMOGENOUS DISCHARGE: grey (vaginosis) or yellow-grey (trichomoniasis)
2. raised vaginal pH
3. increased concentrations of anaerobes plus their products
4. concomitant infections (anaerobic bacteria, STDs)
5. response to metronidazole
66
Candidiases
most common opportunistic mycoses (fugal infections) worldwide
-normal flora of skin, mucous membranes
-colonize mucosal surfaces soon after birth
Etiology: Candida spp.
67
Underlying causes of Candidiasis
- absence of competing normal flora
- introduction to abnrmal site (love sticking to plastic)
- inborn or acquired immune defect
- use of broad-spectrum antibiotics
68
Etiology of Vulvovaginal Cadidiasis
Candida albicans=80-90%
C. tropicalis or C. glabrata=remainder
non-albicans is on the ride
very common condition that can be STD
69
Cadidiases: clinical presentation
- can be considered an STI, but (U) an endogenous infection
- thick, white, frothy discharge in women (no odor)
- itching/irritation
- burning sensation during intercourse or urination
- vaginal pain and soreness
70
Varied morphology of Candida albicans
not many virulence factors
all species are capable of attachment
germ tube is more adhesive than yeast cell
71
Cadida diagnosis
```
Direct microscopic examination
gram stained samples: large GRAM POSITIVE cells
yeast cells
pseudohyphae
true hyphae
```
72
Candida dx cultures
chromagar
hyphae & pseudohyphae
germ tubes
73
Candida serology
difficult: candida is normal flora
many have had prior exposure
low titers of antibody
74
Candida tx
topical cream (Miconazole)
or
oral fluconazole
75
genus Haemophilus morphology
non-motile
GRAM NEGATIVE
COCCOBACILLUS
76
H. influenza: what may it cause?
otitis media, epiglottitis, meningitis
77
H. aegypticus: what may it cause?
conjunctivitis
78
H. ducreyi: what may it cause?
Chancroid
79
Characteristics of Chancroid
- more (C) in tropical countries
- females may be asymptomatic or have nondescript lesion
- TENDER PAPULE ON THE GENITALIA THAT DEVELOPS INTO A TENDER ULCER W/SHARP MARGINS
- SOFT CHANCRE
- regional adenopathy & bubo development
(remember: this is from H. ducreyi)
80
Chancroid development/description
- develops quickly (3-5 days post-infection)
- vesicle or papule (U) solitary->quickly progresses to postulation & ulceration
- progressive enlargement w/autoinoculation & development of multiple ulcers
- ulcer is painful & tender, bleeds readily & lacks induration
81
Chancroid: how to dx
requires identification of Haemophilus ducreyi from the genital ulcer or swollen lymph node
- direct exam can be misleading due to presence of polymicrobial flora in ulcer material, lymph material is frequently sterile
- media for primary isolation requires presence of growth supplements
- a PCR-based method is commercially available
82
Pelvic Inflammatory Disease (PID) definition
syndrome (unrelated to surgery or pregnancy) results when microorganisms ascend to the endometrium, fallopian tubes & contiguous pelvic structures producing one or more of the following conditions-endometritis, salpingitis, pelvic peritonitis or tuboovarian abscess
83
PID is usually due to which two organisms?
Neisseria gonorrhoeae
| Chlamydia trachomatis
84
PID can also be caused which other bacteria?
```
Escherichia coli
Enterobacter spp.
Enterococcus faecalis
Bacteroides spp.
Peptostreptococcus spp.
```
85
How can you increase your risk of pelvic inflammatory disease? (5)
be female (prerequisite)
1. get an STD, esp gonorrhea or chlamydial infection
2. have a prior episode of PID
3. be a sexually active adolescent
4. multiple sexual partners
5. frequent douching
86
Clinical manifestions of PID
```
lower abdominal pain
abnormal vaginal discharge
painful intercourse
increased pain during menstruation
irregular menstruation
fever & chills
scarring
```
87
PID: how is it dx?
EVIDENCE OF INFLAMMATION: fever leukocytosis or elevated ESR
| clinical criteria are commonly used, but this is often inaccurate
