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Microbiology test 3 > Diseases of GU system (sessions 19 & 20) > Flashcards

Diseases of GU system (sessions 19 & 20) Flashcards

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Biology 101 flashcards
1
Q

Ulcerative STDs (3)

A
  1. syphilis
  2. chancroid
  3. genital herpes
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2
Q

Nonulcerative STDs (3)

A
  1. gonorrhea
  2. trichomoniasis
  3. chlamydia
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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

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4
Q

“The Great Imposter”

A

syphilis

caused by Treponema pallidum

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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
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6
Q

What animal model is used for syphilis

A

Rabbits mimic primary and secondary syphilis (not observed in mice or monkeys)

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7
Q

Treponema pallidum: virulence

A
  1. 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
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8
Q

Syphilis Epidemiology

A

HUMAN PATHOGEN ONLY

horizontal & vertical transmission

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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

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10
Q

Primary Syphilis pathogenesis (4 steps)

A
  1. enters subepithelial tissues through break in skin or passage btwn epithelial cells
  2. local multiplication & dissemination to nearby lymph nodes & other sites via blood
  3. PRIMARY LESION (INDURATED SWELLING) develops & surface necrosis results in CHANCRE (may be in an inapparent site)
  4. Untx lesion heals in 3-8 weeks w/fibrosis
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11
Q

Syphilis chancre is the principle lesion of what?

A

primary syphilis

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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
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13
Q

What does a syphilitic chancre lool like?

A 
base is (U) SMOOTH
border is RAISED, FIRM & INDURATED
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14
Q

Syphilis dormancy lenghth

A

short dormancy,

lasts 2-10 weeks

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15
Q

Secondary syphilis a/w

A
  1. MACULOPAPULAR RASH (superficial lesions of high infectivity)
  2. CONDYLOMATA LATA (mucosal warty lesions) in ~1/3
  3. Immune complexes form in arteriolar walls
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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]
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17
Q

Tertiary syphilis: manifests when?

A

manifests 5-20yrs after infection

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18
Q

Tertiary syphilis presentation

A
  1. NEUROSYPHILIS: meningovascular changes w/focal neurologic changes and cortical degeneration
  2. CARDIOVASCULAR SYPHILIS: cardiovascular changes w/aneurysm of ascending aorta
  3. GRANULOMATA (GUMMAS) in any tissue, but esp. in skin, bones and joints=late/benign syphilis
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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

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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

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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
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22
Q

until proven otherwise, every genital lesion

A

should be considered syphilitic

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23
Q

How may you detect treponemes from primary or secondary lesions

A

DARKFEILD MICROSCOPY or direct immunofluorescence

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24
Q

How are most syphilitic cases diagnosed?

A

Serologically

  1. NONTREPONEMAL TESTS: cardiolipin flocculation tests (VDRL, RPR) are NONSEPCIFIC SCREENING TESTS
  2. TREPONEMAL TESTS: specific antibody tests (FTA-ABS, MHA-TP) confirm positive screening tests
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25
Q

acute syphilis tx

A

Penicillin

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26
Q

Neisseria gonorrhoeae causes which 9 diseases

A 
Urethritis
Cervicitis 
Salpingitis 
Pelvic inflammatory disease 
Proctitis  
Bacteremia 
Arthritis 
Conjunctivitis 
Pharyngitis
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27
Q

Neisseria gonorrhea morphology

A

gonococcus
gram-NEGATIVE DIPLOCOCCUS W/KIDNEY BEAN-SHAPED CELLS
has fastidious growth requirements

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28
Q

Neisseria gonorrhea virulence factors

A

-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

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29
Q

Epidemiology of Gonorrhea

A

Adolescents have highest rate
Major reservoir is the asymptomatic patient (almost 50% of infected women are asymptomatic, untx men can become asymptomatic)

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30
Q

Transmission of gonorrhea

A

genital, oral-genital & rectal intercourse transmission

-nonsexual transmission is extremely rare

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31
Q

Why the increased # of cases of gonorrhea

A
  • 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
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32
Q

Neisseria gonorrhoeae pathogenesis

A
  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
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33
Q

Clinical Spectrum of Gonococcal infection

A

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

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34
Q

Complications of Gonorrhea (3)

A
  1. various local effects
  2. Acute salpingitis or pelvic inflammatory dz (PID) in 10-20% of acute infections)
  3. Disseminated Gonococcal Infection
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35
Q

Acute salpingintis or pelvin inflammatory dz is….

A

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
Q

Disseminated Gonococcal Infection (DGI)

A

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
Q

Gonorrhea: diagnosis

A

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
Q

Gonorrhea tx

A

3rd generation cephalosporin

widespread resistance to penicillin and FQs

39
Q

Etiology of Nongonococcal Urethritis (3)

A

“wastebasket dx” includes: Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma genitalium

40
Q

Chlamydial dzs

A
  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
Q

Chlamydia trachomatis charactersitics

A

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
Q

Chlamydia trachomatis replicative cycle

A

Elementary body: hardy infectious form

Reticulate body: fragile intracellular form

43
Q

NGU & C. trachomatis epidemiology

A
  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
Q

Chlamydia trachomatis clinical presentation

A

resembles gonorrhoeae
Males: urethritis (often asymptomatic) & epididymitis, watery discharge
Females: cervicitis, salpingitis & PID
(same serotypes resp for inclusion conjunctivitis in newborns)

45
Q

Pathogenesis of Chlamydial infection

A
  • 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
Q

Chlamydial infections gold standard for dx

A

Gold standard: isolation in cell culture, in human immortalized cell lines, detection of intracellular inclusions, sensitivity is less than 85%

47
Q

tests available in dx of Chlamydial infections

A

Gold standard: isolation in cell culture
noncultural tests:
antigen detection is less sensitive than culture
nucleic acid probes are very sensitivity (~95%)

48
Q

Myplasma hominis a/w which dz

A

pyelonephritis, PID

49
Q

Mycoplasma genitalium a/w what dz

A

NGU

50
Q

Mycoplasma pneumonia a/w what dz

A

atypical pneumonia

51
Q

Ureaplasm urealyticum a/w what dz

A

NGU

52
Q

Ureaplasma urealyticum reservoir/epi/causes what

A

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
Q

3 main categories of vaginitis

A
  1. Trichomoniasis
  2. Bacterial vaginosis
  3. Yeast vaginitis
54
Q

Trichomonas tenax

A

commensal in mouth (normal flora)

55
Q

Trichomonas hominis

A

commensal in intestine (normal flora)

56
Q

Trichomonas vaginalis causes

A

cause of STD

57
Q

Trichomonas vaginalis morphology

A

FLAGELLATED PROTOZOAB
exists ONLY AS A TROPHOZOITE
is an EXTRACELLULAR ANAEROBE

58
Q

Trichomoniasis Epidemiology

A

cosmopolitan distribution
transmitted by sexual intercourse
common STD

59
Q

Trichomonas vaginalis lifecycle

A
  1. trophozoite is acquired via sexual intercourse
  2. parasite establishes on the mucosa & multiples
  3. parasite is transmitted to sexual partner
60
Q

Trichomoniasis clinical characterstics

A

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
Q

Trichomoniasis dx

A

wet mount exam most commonly used
culture is more sensitive
monoclonal antibody methods are available
DNA probe test (Affirm VPIII) is available

62
Q

Epidemiologic Features of Bacterial Vaginosis

A

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
Q

Vaginal secretion characteristics in vaginosis

A

pH 5-6 (N1

other organisms: Mobiluncus, Gardnerella

64
Q

Criteria for bacterial vaginosis

A
  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
Q

Similarities btwn Vaginosis & Trichomoniasis

A
  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
Q

Candidiases

A

most common opportunistic mycoses (fugal infections) worldwide
-normal flora of skin, mucous membranes
-colonize mucosal surfaces soon after birth
Etiology: Candida spp.

67
Q

Underlying causes of Candidiasis

A
  • absence of competing normal flora
  • introduction to abnrmal site (love sticking to plastic)
  • inborn or acquired immune defect
  • use of broad-spectrum antibiotics
68
Q

Etiology of Vulvovaginal Cadidiasis

A

Candida albicans=80-90%
C. tropicalis or C. glabrata=remainder
non-albicans is on the ride
very common condition that can be STD

69
Q

Cadidiases: clinical presentation

A
  • 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
Q

Varied morphology of Candida albicans

A

not many virulence factors
all species are capable of attachment
germ tube is more adhesive than yeast cell

71
Q

Cadida diagnosis

A 
Direct microscopic examination
gram stained samples: large GRAM POSITIVE cells
yeast cells
pseudohyphae
true hyphae
72
Q

Candida dx cultures

A

chromagar
hyphae & pseudohyphae
germ tubes

73
Q

Candida serology

A

difficult: candida is normal flora
many have had prior exposure
low titers of antibody

74
Q

Candida tx

A

topical cream (Miconazole)
or
oral fluconazole

75
Q

genus Haemophilus morphology

A

non-motile
GRAM NEGATIVE
COCCOBACILLUS

76
Q

H. influenza: what may it cause?

A

otitis media, epiglottitis, meningitis

77
Q

H. aegypticus: what may it cause?

A

conjunctivitis

78
Q

H. ducreyi: what may it cause?

A

Chancroid

79
Q

Characteristics of Chancroid

A
  • 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
Q

Chancroid development/description

A
  • 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
Q

Chancroid: how to dx

A

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
Q

Pelvic Inflammatory Disease (PID) definition

A

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
Q

PID is usually due to which two organisms?

A

Neisseria gonorrhoeae

Chlamydia trachomatis

84
Q

PID can also be caused which other bacteria?

A 
Escherichia coli
Enterobacter spp.
Enterococcus faecalis
Bacteroides spp.
Peptostreptococcus spp.
85
Q

How can you increase your risk of pelvic inflammatory disease? (5)

A

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
Q

Clinical manifestions of PID

A 
lower abdominal pain
abnormal vaginal discharge
painful intercourse
increased pain during menstruation
irregular menstruation
fever & chills
scarring
87
Q

PID: how is it dx?

A

EVIDENCE OF INFLAMMATION: fever leukocytosis or elevated ESR

clinical criteria are commonly used, but this is often inaccurate

Microbiology test 3 (8 decks)

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