2 STIs Flashcards

1
Q

Causative agent of syphilis

A

Treponema pallidum

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2
Q

Causative agent of gonorrhea

A

Neisseria gonorrhoeae

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3
Q

Causative agent of lymphogranuloma venereum or nongonococcal urethritis

A

Chlamydia trachomatis

Ureaplasma urealyticum

Mycoplasma genitalium

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4
Q

Causative agent of chancroid

A

Haemophilus ducreyi

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5
Q

Causative agent of granuloma inguinale

A

Calymmatobacterium granulomatis

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6
Q

Which STDs are ulcerative?

A

Syphilis
Chancroid
Genital herpes

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7
Q

Which STDs are nonulcerative?

A

Gonorrhea
Trichomoniasis
Chlamydia

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8
Q

Treponema also causes non-STD diseases such as…

A

Yaws
Pinta
Bejel

Occur in developing countries and direct contact (person-to-person transmission)

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9
Q

“The great imposter”

A

Syphilis (Treponema pallidum)

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10
Q

What does the Treponema pallidum bacteria look like?

A

Gram negative spirochete w/ a slow rotational motility

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11
Q

Obligate internal parasite requiring a mammalian host

A

Treponema pallidum

No vaccine possible b/c we don’t develop good antibodies to it (since it’s intracellular)

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12
Q

Virulence factors for T. pallidum

A

Outer membrane proteins promote adherence to host cells

Hyaluronidase may facilitate perivascular infiltration

Fibronectin coat is antiphagocytic - prevents it from looking foreign to the immune system

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13
Q

Syphilitic lesions are primarily the result of …

A

The inflammatory response

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14
Q

Acquisition of syphilis is usually via …

A

Direct sexual contact w/ a person who has an active 1˚ or 2˚ lesion

Other acquisition via nongenital contact - lesion near mouth, needle sharing, transplacental transmission

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15
Q

Which stage of syphilis?

Local multiplication and dissemination to nearby lymph nodes and other sites via blood

A

Primary

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16
Q

Which stage of syphilis?

Indurated swelling develops and surface necrosis results in chancre formation (may not be visible)

A

Primary

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17
Q

Which stage of syphilis?

Untreated lesion heals in 3-8 weeks w/ fibrosis

A

Primary

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18
Q

What is the syphilis chancre?

A

Principle lesion of primary syphilis

Typically begins as a papule that passes through a series of evolutional stages

Superficial erosion —> scanty serous exudate —> thin, grayish, slightly hemorrhagic crust —> base usually smooth, and the border raised, firm, indurated

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19
Q

The period between primary and secondary stages of syphilis is usually …

A

2-10 weeks

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20
Q

Which stage of syphilis?

Development of superficial, mucocutaneous maculopapular rash

A

Secondary

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21
Q

Which stage of syphilis?

Mucosal warty lesions (condylomata lata)

A

Secondary

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22
Q

Which stage of syphilis?

Immune complexes form in arteriolar walls

A

Secondary

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23
Q

Which stage of syphilis?

Absence of clinical signs/symptoms

A

Latency

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24
Q

Early syphilis latency

A

Within 1 year of infection

Recrudescence of active secondary syphilis

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25
Late syphilis latency
>1 year after infection Immunity to relapse and reinfection
26
Spontaneous cure in _____ of syphilis cases
1/3
27
Seropositivity w/o Disease in ____ of syphilis cases
1/3
28
Tertiary syphilis develops in _____ of cases
1/3
29
Which stage of syphilis? 5-20 years after infection
Tertiary
30
Which stage of syphilis? Meningovascular changes w/ focal neurologic changes and cortical degeneration
Tertiary This specifically is neurosyphilis
31
Which stage of syphilis? Cardiovascular changes w/ aneurysm of ascending aorta
Tertiary
32
Which stage of syphilis? Granulomata (gummas) in any tissue, but especially in skin, bones, joints
Tertiary
33
When do you usually see changes in infants with congenital syphilis?
After the fourth month, but infection probably occurred earlier
34
What indicates a poor prognosis for congenital syphilis?
Earlier onset of symptoms after birth Most infants are born heathy and develop SSx at ~3 weeks of age
35
What SSx do you see in infants with congenital syphilis?
Maculopapular cutaneous lesions Nasal obstruction w/ mucous discharge (infectious) Osteitis of nasal bones Neurosyphilis
36
What is Hutchinson’s triad?
Notched incisors, interstitial keratitis, 8th nerve deafness
37
Until proven otherwise, every genital lesion should be considered ...
Syphilitic
38
What do you have to do to visualize treponema bacteria?
Darkfield microscopy or direct immunofluorescence from 1˚ or 2˚ lesions
39
Most cases of syphilis are diagnosed...
Serologically Nontreponemal tests (VDRL, RPR) are non specific screening tests but cheap first pass Treponemal tests for specific antibodies (FTA-ABS, MHA-TP) - confirmatory for positive screening tests
40
How do you treat syphilis
Penicillin
41
Gram-negative diplodocus w/ kidney bean shaped cells
Neisseria gonorrheae Has fastidious growth requirements
42
What are the virulence factors for neisseria gonorrheae?
Antigenic variation of pili (confuses immune system) Nonpiliated phase variants (no antibodies made) Porin protein and other proteins for attachment IgA protease*** Plasmid and chromosome-mediated resistance to penicillins, tetracyclines, spectinomycin, and fluoroquinolones
43
Who has the highest rate of gonorrhea infections?
Adolescents
44
What is the major reservoir for gonorrhea?
Asymptomatic patients - almost 50% of infected women are asymptomatic
45
How is gonorrhea transmitted?
Genital, oral-genital, and rectal intercourse No sexual transmission is extremely rare
46
Attachment of N. gonorrhoeae to host cell is via...
Pili and surface protein Bacteria alter their surface properties as an adaptation to the host environment
47
Nonimmunity to N. gonorrhoeae is due to ...
Antigenic variation of pili and surface proteins —> retardation of phagocytes activity
48
How do N. gonorrhoeae bacteria injury host cells?
Lipooligosaccharide and peptidoglycan It then spreads to other tissues via Pilar attachment
49
Where can you get gonorrhea?
Eyes, mouth, urethra, vagina, rectum Basically any mucosal surface
50
What is the typical present of gonorrhea in females?
Presence in endocervix (cervicitis) accompanied by urethral colonization
51
What is the typical presentation of gonorrhea in males?
Presence in anterior urethra with much purulent discharge
52
Most common complication of gonorrhea in 10-20% of acute infections
Acute salpingitis or PID Presents w/ pain, dyspareunia, abnormal menses, bleeding, etc
53
What is salpingitis?
Spread of gonorrheal infection along Fallopian tubes Can also spread into pelvic cavity —> peritonitis and abscesses
54
What are the long-term sequelae of acute salpingitis/PID?
Chronic pelvic pain, infertility, and ectopic pregnancy secondary to scarring of tubes
55
What is DGI?
Disseminated Gonococcal Infection Any of the forms of N. gonorrhoeae infection can lead to bacteremia SSx: Fever rash (arthritis-dermatitis syndrome) Metastatic infections (endocarditis, meningitis) can also occur but PURULENT ARTHRITIS is more common (30-40% of DGI)
56
Only _____ % of gonococcal infections yield gram negative results
~60% - the gram stain of the exudate varies in sensitivity
57
What is the gold standard for diagnosing Gonorrhea?
Nuclei acid amplification (PCR) Can also use agglutination, DNA probe, biochemical tests but PCR is best
58
How do you treat gonorrhea?
3rd gen cephalosporin If resistant, go with 4th gen cephalosporin or FQ Widespread resistance to penicillin and FQs so do a culture and sensitivity
59
What are the top three species that cause nongonococcal urethritis?
Chlamydia trachomatis Ureaplasma urealyticum Mycoplasma genitalium The last two are more chronic infections b/c no cell wall
60
What is Psittacosis?
Respiratory, zoonotic atypical pneumonia caused by Chlamydia psittaci
61
Which chlamydial organism can cause acute PNA?
Chlamydophila pneumoniae Hard to ID b/c very small, obligate intracellular organism No long lasting immunity or vaccine
62
Trachoma, inclusion conjunctivitis, lymphogranuloma venereum and nongonoccal urethritis are all due to...
Chlamydia trachomatis
63
Super small, gram-negative, obligate intracellular bacteria
Chlamydia trachomatis
64
This bacteria is metabolically deficient and requires host-derived ATP to survive, so you can identify it by looking for INCLUSIONS
Chlamydia trachomatis
65
What is the unique replication cycle for chlamydia trachomatis?
Infectious form = elementary body Fragile intracellular form = reticulate body
66
Highest prevalence for Chlamydia trachomatis is among...
Teenagers
67
Ascension of Chlamydia trachomatis bacteria in female patients leads to ...
Salpingitis and PID Complications of scarring in chronic/repeat infections include sterility and ectopic pregnancy
68
>50% of infants born to mothers infected with Chlamydia trachomatis show...
Evidence of infection, usually INCLUSION CONJUNCTIVITIS and 5-10% present with PNA
69
What is the clinical spectrum of chlamydia trachomatis?
Resembles that of N. gonorrhoeae Urethritis (often asymptomatic) and epididymitis in males WATERY discharge (not mucous like in gonorrhea) Cervicitis, salpingitis, and PID in women
70
Strains of Chlamydia trachomatis that become chronic may be due to...
A gene that encodes for a toxin that functions like Toxin B of C. diff Protein scaffolding of the infected cells collapse, causing mucosal cells to separate from each other
71
What is the gold standard for diagnosing Chlamydial infections?
Isolation in cell culture is technically the gold standard (but doesn’t work all the time) Have to use immortalized cell lines and detect INTRACELLULAR INCLUSIONS, then look for clearing zones Sensitivity is less than 85%
72
Nucleic acid probes are very sensitive for Chlamydial infections, but...
They are sensitive for the genes but not for the different Chlamydial species, so you need clinical SSx to diagnose this way LOTS OF FALSE POSITIVES on the antigen test so just don’t.
73
How do you treat Chlamydial infections?
Azithromycin or tetracycline (but send for MIC)
74
The main reservoir for Ureaplasma urealyticum is...
Genital tract of sexually active persons (really any mucosal surface) Colonization is present in >80% of persons who have had 3 or more sex partners Responsible for ~50% of nongonococcal, no Chlamydial urethritis in men
75
Cause of chorioamnionitis and postpartum fever in women
Ureaplasma urealyticum
76
What are the three species of trichomonas found in humans?
Trichomonas tenax - commensalism in MOUTH Trichomonas hominis - commensalism in INTESTINE Trichomonas vaginalis - STD Tenax and hominis are both part of normal flora and harmless but vaginalis is always pathogenic
77
Giant flagellated protozoan —> vaginitis
Trichomonas vaginalis It is an extracellular anaerobic trophozoite
78
What is the life cycle of Trichomonas vaginalis?
Trophozoite is acquired via sexual intercourse Parasite establishes on the mucosa and multiplies Parasite is transmitted to sexual partner Not a huge amount of tissue damage until it progresses
79
How does trichomoniasis present in males?
Usually asymptomatic Scanty, clear to mucopurulent discharge in the event they do have Sx
80
How does trichomoniasis present in females?
Profuse vaginal discharge - frothy and malodorous (smells “amine”) Creates an environment for bacterial vaginosis b/c it changes pH
81
How is trichomoniasis diagnosed?
Wet mount exam - easy to see on microscopy Culture on diamonds media is more sensitive but takes a long time Monoclonal antibody methods and DNA probe tests available as well
82
How do you treat trichomoniasis?
Metronidazole
83
Overgrowth of opportunistic pathogen in vagina due to change in pH
Bacterial Vaginosis NOT an STI but more common with Hx of previous STDs, Hx of sexual activity, and current use of intrauterine devices
84
pH in normal vagina vs vaginosis
Normal <4.5 Vaginosis 5.0-6.0
85
Presence of clue cells
Distinguishes Vaginosis from normal vaginal secretions
86
What are the criteria for diagnosing bacterial vaginosis?
(Pick any three) Homogenous quality of secretions Presence of clue cells*** Release of fishy amine odor when 10% KOH is added Vaginal pH >4.5 Presence of curved gram negative or gram variable rods
87
Color of discharge in vaginosis and trichomoniasis
``` Vaginosis = gray Trichomoniasis = yellow-gray ``` Both thin and homogenous Both respond to metronidazole
88
Most commonly encountered opportunistic mycoses worldwide
Candidiasis Normal fungal flora of the skin, mucous membranes Colonize mucosal surfaces soon after birth (~45 min)
89
Underlying causes of candidiasis
Absence of competing normal flora Introduction to abnormal site “Pathologic” change in microenvironment (ie pH change after STI) Inborn or acquired immune defect Use of broad-spectrum abx
90
80-90% of vulvovaginal candidiasis are due to...
Candida albicans Remainder are due to C. tropicalis or C. glabrata
91
Clinical presentation of candidiasis
Thick, white, frothy discharge in women with NO ODOR Can be considered an STI but usually an endogenous infection Itching, irritation, burning sensation after intercourse or urination, vaginal pain and soreness
92
What helps Candida albicans attach to host?
GERM TUBE
93
How is candida diagnosed?
Direct microscopic exam Gram stained samples —> large G(+) yeast cells
94
Culturing candida
Chromagar —> hyphae, pseudohyphae, and GERM TUBES
95
How is Candidiasis treated?
Topical cream (Miconazole) or oral fluconazole
96
What species causes chancroid?
Haemophilus ducreyi Routinely mistaken for syphilis
97
Chancroid is more common in what locations?
Tropical countries
98
Female patients with chancroid are more likely to be...
Asymptomatic or have nondescript lesion
99
What does the chancroid lesion look like?
Tender papule on the genitalia that develops into a tender ulcer with sharp margins Much angrier, painful, and more likely to spread than syphilis Ulcer is PAINFUL, bleeds readily, and LACKS INDURATION May also have regional adenoma they and bubo development
100
Chancroid development is quick or slow?
Quick - 3-5 days post infection Vesicle or papule quickly progresses to postulation and ulceration Can autoinoculate —> multiple ulcers if untreated
101
How do you diagnose chancroid?
ID of H. ducreyi from genital ulcer or swollen lymph node There’s also a PCR-based method
102
How do you treat chancroid?
Varies based on susceptibility testing 3rd gen cephalosporins are still effective
103
Syndrome unrelated to surgery or pregnancy that results when microorganisms ascend to the endometrium, Fallopian tubes, and contiguous pelvic structures
Pelvic Inflammatory Disease Produces one or more of the following - endometriosis, salpingitis, pelvic peritonitis, tuboovarian abscess Usually due to N. gonorrhoeae or C. trachomatis
104
Clinical manifestations of PID
``` Lower abdominal pain Abnormal vaginal discharge Painful intercourse Increased pain during menstruation Irregular menstruation Fever/chills Scarring ```