Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology Unit 3 > 2 STIs > Flashcards

2 STIs Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

Causative agent of syphilis

A

Treponema pallidum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causative agent of gonorrhea

A

Neisseria gonorrhoeae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causative agent of lymphogranuloma venereum or nongonococcal urethritis

A

Chlamydia trachomatis

Ureaplasma urealyticum

Mycoplasma genitalium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Causative agent of chancroid

A

Haemophilus ducreyi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Causative agent of granuloma inguinale

A

Calymmatobacterium granulomatis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which STDs are ulcerative?

A

Syphilis
Chancroid
Genital herpes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which STDs are nonulcerative?

A

Gonorrhea
Trichomoniasis
Chlamydia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

“The great imposter”

A

Syphilis (Treponema pallidum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does the Treponema pallidum bacteria look like?

A

Gram negative spirochete w/ a slow rotational motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Syphilitic lesions are primarily the result of …

A

The inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which stage of syphilis?

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

A

Primary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which stage of syphilis?

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

A

Primary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which stage of syphilis?

Untreated lesion heals in 3-8 weeks w/ fibrosis

A

Primary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

2-10 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which stage of syphilis?

Development of superficial, mucocutaneous maculopapular rash

A

Secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which stage of syphilis?

Mucosal warty lesions (condylomata lata)

A

Secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which stage of syphilis?

Immune complexes form in arteriolar walls

A

Secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which stage of syphilis?

Absence of clinical signs/symptoms

A

Latency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Early syphilis latency

A

Within 1 year of infection

Recrudescence of active secondary syphilis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Late syphilis latency

A

> 1 year after infection

Immunity to relapse and reinfection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Spontaneous cure in _____ of syphilis cases

A

1/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Seropositivity w/o Disease in ____ of syphilis cases

A

1/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Tertiary syphilis develops in _____ of cases

A

1/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which stage of syphilis?

5-20 years after infection

A

Tertiary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which stage of syphilis?

Meningovascular changes w/ focal neurologic changes and cortical degeneration

A

Tertiary

This specifically is neurosyphilis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which stage of syphilis?

Cardiovascular changes w/ aneurysm of ascending aorta

A

Tertiary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which stage of syphilis?

Granulomata (gummas) in any tissue, but especially in skin, bones, joints

A

Tertiary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

When do you usually see changes in infants with congenital syphilis?

A

After the fourth month, but infection probably occurred earlier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What indicates a poor prognosis for congenital syphilis?

A

Earlier onset of symptoms after birth

Most infants are born heathy and develop SSx at ~3 weeks of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What SSx do you see in infants with congenital syphilis?

A

Maculopapular cutaneous lesions

Nasal obstruction w/ mucous discharge (infectious)

Osteitis of nasal bones

Neurosyphilis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is Hutchinson’s triad?

A

Notched incisors, interstitial keratitis, 8th nerve deafness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Until proven otherwise, every genital lesion should be considered …

A

Syphilitic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What do you have to do to visualize treponema bacteria?

A

Darkfield microscopy or direct immunofluorescence from 1˚ or 2˚ lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Most cases of syphilis are diagnosed…

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How do you treat syphilis

A

Penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Gram-negative diplodocus w/ kidney bean shaped cells

A

Neisseria gonorrheae

Has fastidious growth requirements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the virulence factors for neisseria gonorrheae?

A

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
Q

Who has the highest rate of gonorrhea infections?

A

Adolescents

44
Q

What is the major reservoir for gonorrhea?

A

Asymptomatic patients - almost 50% of infected women are asymptomatic

45
Q

How is gonorrhea transmitted?

A

Genital, oral-genital, and rectal intercourse

No sexual transmission is extremely rare

46
Q

Attachment of N. gonorrhoeae to host cell is via…

A

Pili and surface protein

Bacteria alter their surface properties as an adaptation to the host environment

47
Q

Nonimmunity to N. gonorrhoeae is due to …

A

Antigenic variation of pili and surface proteins —> retardation of phagocytes activity

48
Q

How do N. gonorrhoeae bacteria injury host cells?

A

Lipooligosaccharide and peptidoglycan

It then spreads to other tissues via Pilar attachment

49
Q

Where can you get gonorrhea?

A

Eyes, mouth, urethra, vagina, rectum

Basically any mucosal surface

50
Q

What is the typical present of gonorrhea in females?

A

Presence in endocervix (cervicitis) accompanied by urethral colonization

51
Q

What is the typical presentation of gonorrhea in males?

A

Presence in anterior urethra with much purulent discharge

52
Q

Most common complication of gonorrhea in 10-20% of acute infections

A

Acute salpingitis or PID

Presents w/ pain, dyspareunia, abnormal menses, bleeding, etc

53
Q

What is salpingitis?

A

Spread of gonorrheal infection along Fallopian tubes

Can also spread into pelvic cavity —> peritonitis and abscesses

54
Q

What are the long-term sequelae of acute salpingitis/PID?

A

Chronic pelvic pain, infertility, and ectopic pregnancy secondary to scarring of tubes

55
Q

What is DGI?

A

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
Q

Only _____ % of gonococcal infections yield gram negative results

A

~60% - the gram stain of the exudate varies in sensitivity

57
Q

What is the gold standard for diagnosing Gonorrhea?

A

Nuclei acid amplification (PCR)

Can also use agglutination, DNA probe, biochemical tests but PCR is best

58
Q

How do you treat gonorrhea?

A

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
Q

What are the top three species that cause nongonococcal urethritis?

A

Chlamydia trachomatis

Ureaplasma urealyticum

Mycoplasma genitalium

The last two are more chronic infections b/c no cell wall

60
Q

What is Psittacosis?

A

Respiratory, zoonotic atypical pneumonia caused by Chlamydia psittaci

61
Q

Which chlamydial organism can cause acute PNA?

A

Chlamydophila pneumoniae

Hard to ID b/c very small, obligate intracellular organism

No long lasting immunity or vaccine

62
Q

Trachoma, inclusion conjunctivitis, lymphogranuloma venereum and nongonoccal urethritis are all due to…

A

Chlamydia trachomatis

63
Q

Super small, gram-negative, obligate intracellular bacteria

A

Chlamydia trachomatis

64
Q

This bacteria is metabolically deficient and requires host-derived ATP to survive, so you can identify it by looking for INCLUSIONS

A

Chlamydia trachomatis

65
Q

What is the unique replication cycle for chlamydia trachomatis?

A

Infectious form = elementary body

Fragile intracellular form = reticulate body

66
Q

Highest prevalence for Chlamydia trachomatis is among…

A

Teenagers

67
Q

Ascension of Chlamydia trachomatis bacteria in female patients leads to …

A

Salpingitis and PID

Complications of scarring in chronic/repeat infections include sterility and ectopic pregnancy

68
Q

> 50% of infants born to mothers infected with Chlamydia trachomatis show…

A

Evidence of infection, usually INCLUSION CONJUNCTIVITIS and 5-10% present with PNA

69
Q

What is the clinical spectrum of chlamydia trachomatis?

A

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
Q

Strains of Chlamydia trachomatis that become chronic may be due to…

A

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
Q

What is the gold standard for diagnosing Chlamydial infections?

A

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
Q

Nucleic acid probes are very sensitive for Chlamydial infections, but…

A

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
Q

How do you treat Chlamydial infections?

A

Azithromycin or tetracycline (but send for MIC)

74
Q

The main reservoir for Ureaplasma urealyticum is…

A

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
Q

Cause of chorioamnionitis and postpartum fever in women

A

Ureaplasma urealyticum

76
Q

What are the three species of trichomonas found in humans?

A

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
Q

Giant flagellated protozoan —> vaginitis

A

Trichomonas vaginalis

It is an extracellular anaerobic trophozoite

78
Q

What is the life cycle of Trichomonas vaginalis?

A

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
Q

How does trichomoniasis present in males?

A

Usually asymptomatic

Scanty, clear to mucopurulent discharge in the event they do have Sx

80
Q

How does trichomoniasis present in females?

A

Profuse vaginal discharge - frothy and malodorous (smells “amine”)

Creates an environment for bacterial vaginosis b/c it changes pH

81
Q

How is trichomoniasis diagnosed?

A

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
Q

How do you treat trichomoniasis?

A

Metronidazole

83
Q

Overgrowth of opportunistic pathogen in vagina due to change in pH

A

Bacterial Vaginosis

NOT an STI but more common with Hx of previous STDs, Hx of sexual activity, and current use of intrauterine devices

84
Q

pH in normal vagina vs vaginosis

A

Normal <4.5

Vaginosis 5.0-6.0

85
Q

Presence of clue cells

A

Distinguishes Vaginosis from normal vaginal secretions

86
Q

What are the criteria for diagnosing bacterial vaginosis?

A

(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
Q

Color of discharge in vaginosis and trichomoniasis

A 
Vaginosis = gray
Trichomoniasis = yellow-gray

Both thin and homogenous

Both respond to metronidazole

88
Q

Most commonly encountered opportunistic mycoses worldwide

A

Candidiasis

Normal fungal flora of the skin, mucous membranes

Colonize mucosal surfaces soon after birth (~45 min)

89
Q

Underlying causes of candidiasis

A

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
Q

80-90% of vulvovaginal candidiasis are due to…

A

Candida albicans

Remainder are due to C. tropicalis or C. glabrata

91
Q

Clinical presentation of candidiasis

A

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
Q

What helps Candida albicans attach to host?

A

GERM TUBE

93
Q

How is candida diagnosed?

A

Direct microscopic exam

Gram stained samples —> large G(+) yeast cells

94
Q

Culturing candida

A

Chromagar —> hyphae, pseudohyphae, and GERM TUBES

95
Q

How is Candidiasis treated?

A

Topical cream (Miconazole) or oral fluconazole

96
Q

What species causes chancroid?

A

Haemophilus ducreyi

Routinely mistaken for syphilis

97
Q

Chancroid is more common in what locations?

A

Tropical countries

98
Q

Female patients with chancroid are more likely to be…

A

Asymptomatic or have nondescript lesion

99
Q

What does the chancroid lesion look like?

A

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
Q

Chancroid development is quick or slow?

A

Quick - 3-5 days post infection

Vesicle or papule quickly progresses to postulation and ulceration

Can autoinoculate —> multiple ulcers if untreated

101
Q

How do you diagnose chancroid?

A

ID of H. ducreyi from genital ulcer or swollen lymph node

There’s also a PCR-based method

102
Q

How do you treat chancroid?

A

Varies based on susceptibility testing

3rd gen cephalosporins are still effective

103
Q

Syndrome unrelated to surgery or pregnancy that results when microorganisms ascend to the endometrium, Fallopian tubes, and contiguous pelvic structures

A

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
Q

Clinical manifestations of PID

A 
Lower abdominal pain
Abnormal vaginal discharge
Painful intercourse
Increased pain during menstruation
Irregular menstruation
Fever/chills
Scarring

Microbiology Unit 3 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions